CKDfinal Part1

1 I. PERSONAL DATA Name: Mr. Bean Address: Brgy.
Bingao, San Nicolas, Ilocos Norte Birth Date: April 27, 1996 Age: 15 years old Sex: Male Place of Birth: Sinait, Ilocos Sur Nationality: Filipino Religion: Roman Catholic Date of Admission: 04 December 2011 Time of Admission: 12:30 PM Ward: Pediatrics/ Medical Hospital Number: 622557 Chief Complaint: body malaise, flank pain Admitting Diagnosis: Chronic renal failure secondary to chronic glomerulonephritis; to consider secondary to rapidly progressive glomerolunephritis (RPGN) Final Diagnosis: Chronic Renal Failure Secondary to Chronic Kidney Disease Date of Discharge: 19 December 2011 Time of Discharge: 4:15 pm
Clinical Case Study: Chronic Kidney Disease BSN III-A Group 3 SY 2011-2012
2 II. FAMILY BACKGROUND
Members of the Family Member of the Family Age Se x Religion Place of Residence Civil Status Educational Attainment Occupation Relation to the Patient Mrs.Turnip 51 F Roman Catholic Brgy. 18, San Nicolas I.N Pea 14 M Roman Catholic Brgy. 18, San Nicolas I.N Sesame 12 F Roman Catholic Brgy. 18, San Nicolas I.N Mr. Raddish 34 M Roman Catholic Brgy. 18, San Nicolas I.N Married High School Graduate Farmer Paternal Uncle Single Grade Six Pupil Sister Single Second Year High School Student Brother Married High School Graduate Farmer Mother
The family of our patient is composed of eighth members including him. He belongs to an extended type of family wherein, he lives with his mother, his paternal uncle and two siblings. He is 15 years old and currently studying as a 4th year high school student at San Nicolas National High School. He is the son of Mr.Carrot and Mrs. Turnip. He is the oldest among the 3 children in the family. They are living in Brgy. 18, Bingao, San Nicolas, Ilocos Norte. His grandmother and grandfather are working abroad as overseas Filipino workers (OFW) respectively for almost 20 years. His father is also working as a domestic helper for 8 years now.
3 His mother and his uncle are both farmers. His uncle is married but is separated with his family. The mother of the patient is the one who decides for the needs of their family. They are living in a concrete bungalow house which they claim to be their own property. They are religiously affiliated to Roman Catholic.
Sources of Income The actual earnings of the family come from the monthly estimated income of his mother and uncle. According to his mother, income ranges from Php2,000-2,750 per month only in which it is not enough for their basic needs. However, she also added that they are receiving remittances from her husband with the amount of Php 8,000 per month while her parents-in-law gives allowances for the children in the amount of Php6,000. The financial needs of the family are being supplied adequately and the money is properly utilized on their monthly estimated food expenses for about Php 2,500; electric bills for Php2,500; allowance of children for Php,6000; transportation for Php 1,000; communication for Php250; LPG Php250 (will be utilized for three months); clothings at least Php500 (set aside to be used after 3 months); agricultural expenses for an estimate of Php2,000; miscellaneous expenses for Php 750; and, with savings of about Php500.
Monthly Sources of Income Source Salary of his mother and uncle of patient Remittance of his father Remittance of his grandmother Monthly Income Php 2,750 / month Php 8,000/ month Php 6,000/ month TOTAL Php 16,750/month
BUDGETARY ALLOCATIONS OF THE FAMILY
4 When it comes in allocating of their financial resources, they claimed that their major expenses are the allowance of their 3 children in studying. The remaining income will serve as their savings for emergency purposes like hospitalization. Monthly Expenses Education Food Transportation Communication LPG Electricity Others: Agricultural Clothing Miscellaneous Savings Php 2,000.00 Php 500.00 (set aside for 3 months) Php 750.00 Php 1,333.00 Php 6,000.00 Php 2,500.00 Php 1,000.00 Php 250.00 Php 250.00 Php 2,500.00
5 III. HEALTH HISTORY A. Family Health History Our patients family peacefully lives at Brgy.18, San Nicolas, Ilocos Norte. They are eight in the family. His maternal grandfather died at the age of 86, believed to be due to natural death. On the other hand, his paternal grandfather was diagnosed of hypertension at their RHU by Dr. X and was advised to take Losartan to manage it. The cause of this hypertension was unknown but it is believes, as Mrs. Turnip relates, to be due to his fondness to eating fatty foods. The grandfathers take alcohol occasionally especially on occasions. But his uncle is a drunkard who may consume a bottle of Ginebra San Miguel (round post) a session together with his friends. His uncle is only the one who smokes, consuming about three to four sticks a day. There are no other vices in the family aside from these. According to his mother, whenever a family member gets ill, they immediately consult to their municipal rural health unit (RHU) but if they can no longer deal with the pain, they would go to the nearest hospital which is in the Mariano Marcos Memorial Hospital and Medical Center (MMMH&MC) at Batac City. If any of the family members gets unwell due to fever, they manage it by taking Paracetamol three times a day, doing tepid sponge bath and complete bed rest. If cough and colds persist, drinking plenty amount of water and taking Neozep is their management. For stomachache they prefer to take loperamide while in head ache they manage it by just having a bed rest to relieve the pain. All drugs taken when they experience minor ailments are not prescribed (or over the counter). They all have experienced childhood illnesses such as mumps and chicken pox. In treating mumps, they rely on traditional way of healing it by way of akot-akot mixed with vinegar because they believe that it will heal the disease by its cold effect and place it on the affected area. In the presence of chicken pox, they believe that it is normal that these conditions appear during childhood days and they managed it by not eating eggs, wearing black shirts and staying at home because they believe that it would speed up the healing process. Her mother claimed that all her children were able to receive their complete vaccination (expanded program for immunization) such as BCG, DPT, Hepa B, OPV, and anti-measles. But
6 on the other hand, she and her husband, together with her parents-in-law were not able to complete their vaccination. They dont have any allergy to food and medications nor have any other familial diseases other than hypertension as experienced by his paternal grandfather. Genogram
Mr. Cabbage (*)
Mrs. Cauliflower
Mr. Brocolli(^)
Mrs. Lettuce
Legend: male
Mr. Carrot
Mrs. Turnip
female (*) dead (^) HPN
Mr. Bean
Pea
Sesame
B. Past Health History Our client experienced childhood diseases such as mumps. As management of mumps, they prefer to use akot-akot and mixed it with vinegar and place it on the affected area. Likewise, his mother claimed that Mr. Bean also experienced common illnesses such as cough, colds, fever and stomach ache. She told that drinking plenty amount of water is their management for cough and colds, boiled guava leaves for stomach ache, taking paracetamol and applying a face towel
7 with warm water in the body for fever. They prefer on increased fluid intake accompanied by complete bed rest and when it worsens, they usually seek consultation in their Health Center. His mother claimed that he was able to obtain immunizations such as 1 dose BCG, 3 doses of DPT, 3 doses of OPV, 3 doses of Hepa B and 1 dose of anti-measles. He has no allergy with foods and medication. He claimed that his son was already circumcised and had no vices at all, other than his fondness of drinking soda and eating street and junk foods. His present illness caused his first hospitalization.
C. Pediatric History Mr. Bean was delivered through normal spontaneous delivery at home with a birth weight of 2.75 kilograms. He had no congenital anomalies and Mrs. Turnip did not experience to breastfeed him and Mr. Bean was bottlefed instead. His vitamin supplements then was tiki-tiki and some problems that were encountered during his feedings were vomiting, diarrhea and constipation. According to his mother, Mr. Bean started to smile when he was 5 months old, held his head up when prone at 3 months, turned self from prone to supine at 3 months, cut tooth at 5 months, sat with support at 6 months, started to crawl at 7 months, began to walk alone when he was 1 year 4 months old, and fed himself with spoon at 1 year 1 month old. He said his first word at 10 months, spoke sentences when she was 1 year old, and had undergone bowel/bladder training at 1 year 8 months old. He used to play in a clean and safe area in their maternal family house and love to swim in the beach. His parents are the one responsible to discipline the child in a nice way and he will just listen on it. He started schooling at the age of 5 in nursery, kindergarten at 6 years and first grade at the age of 7. He loves to eat pinakbet and malunggay. He has no allergies to food and medicines but he is fond of drinking softdrinks and eating junk foods and street foods. He doesnt have difficulties in defecating and usually had his bowel movement once a day. On his sleeping pattern, he doesnt any rituals and problems before and during sleeping.
8 Mr. Bean was taught to socialize well as a kid because his parents had a good child tending habits. They were taught the use of po and opo and the usual vernacular courtesy. He was a very compliant and obedient child. He was well taught in helping in household chores at an early age. He does not like to engage in quarrels or fights. He also is not a sensitive child. He loved to engage himself in games with his child playmates. There were no problems encountered with his nutrition when he was young so far.
D. Present Health History Condition started one month prior to admission as body malaise with no associated fever or weight loss. Cough, colds, edema, and presence of tea-colored urine were not appreciated. The patient would feel tired easily when going to the farm on weekends, as well as when he arrives home after school. Complaints of weakness persisted but did not prompt them for consultation. The patient also experienced on and off progressing flank pain especially when the area was touched. Two weeks prior to admission, condition persisted hence prompting the consultation to Dr. Bravo and was given Vitamin B complex which afforded no relief. One week prior to admission, the patient experienced vomiting of previously ingested food accompanied by epigastric pain. He also experienced loose watery stools and there was a marked decrease in appetite. He also experienced dizziness. Since the patient did not have fever, no consultation was done. Four days prior to admission, an edema of the lower extremities developed. Hot compress was used to relieve it. Still, no consultation was done. Three days prior to admission, the patient experienced cough and consultation was done at The Black Nazarene Hospital and was admitted on December 2, 2011. The case was managed as a case of anemia secondary to chronic kidney disease; chronic glomerolunephritis (to consider RPGN). Medications started were the following: ampicillin, captopril, omeprazole, sangobion, and sodium bicarbonate. Complete blood count (CBC)
9 revealed the following results: RBC 6.7, WBC 11.20, Hgb 10 g/dL, Platelet 139; hence, two units of packed red blood cells (PRBC) were transfused. The following diagnostic procedures were done and revealed results: a.) urine analysis, with presence of albumin, pH 8.5, specific gravity 1.016; b.) Ultrasound revealed bilateral diffuse renal parenchymal disease with chronicity; c.) BUN of 4.0 mmol/L and creatinine of 8.6 mg/dL. The case was referred to a nephrologist with an impression of uremia secondary to CKD and was advised for hemodialysis. Another unit of PRBC was transfused. On the second day, a right internal jugular catheter was inserted for emergency hemodyalysis access and opted transfer to MMMH&MC. Upon transferring to MMMH&MC, routine laboratory tests such as CBC and urinalysis were done. Other diagnostic procedures include random blood sugar (RBS), kidney profile: bood urea nitrogen (BUN) and creatinine, ASOT, serum electrolytes, arterial blood gas (ABG) studies, and fecalysis. Intravenous fluid (IVF) was changed to D5NM, an indwelling Foley catheter (IFC) was inserted, and he then went under emergency hemodialysis. During his hospitalization at MMMH&MC, he underwent hemodialysis on the following days: Date and Time December 4, 2011 6:00 PM December 5, 2011 2:30 PM December 6, 2011 1:00 PM December 7, 2011 5:00 PM December 13, 2011 7:15 PM December 16, 2011 12:10 PM December 18, 2011 8:45 PM No. of Hours 1 2 3 4 4 4 4
10 IV. ANATOMY AND PHYSIOLOGY
THE URINARY SYSTEM The Urinary System is a group of organs in the body concerned with filtering out excess fluid and other substances from the bloodstream. The substances are filtered out from the body in the form of urine. Urine is a liquid produced by the kidneys, collected in the bladder and excreted through the urethra. Urine is used to extract excess minerals or vitamins as well as blood corpuscles from the body. The Urinary organs include the kidneys, ureters, bladder, and urethra. The Urinary system works with the other systems of the body to help maintain homeostasis. The kidneys are the main organs of homeostasis because they maintain the acid base balance and the water salt balance of the blood. PARTS OF THE URINARY SYSTEM 1. THE KIDNEY The kidney is covered by a thin connective tissue capsule and consists of an outer cortex and medullary pyramid or papillae (Kidney). Within these two regions are found the components of the structural and functional unit of the kidney, the nephron. The nephron is composed of: (1) the glomerulus, a tuft of capillaries, which produces the glomerular filtrate, housed in the renal corpuscle; followed by a series of tubules, specialized for excretion and reabsorption, including (2) the proximal convoluted tubule, (3) the descending and ascending loop of Henle, and (4) the distal convoluted tubule. Each nephron drains into a collecting tubule, which serves as a duct system to conduct the urine out of the Kidney. The glomeruli and the proximal and distal convoluted tubules are found in the cortex. The descending loop of Henle leaves the cortex and enters the medulla, returning to the cortex as the ascending loop. Therefore, the medulla consists of portions of the loops of Henle and the collecting tubules.
11 2. KIDNEY CORTEX The outer most region of the kidney, which lies just below the convex surface of the organ, is the cortex, where three components of the nephron can be found. The renal corpuscles (or Bowman's capsules) containing glomeruli are surrounded by a labyrinth of proximal and distal convoluted tubules (Cortex). The collecting tubules also penetrate the cortex, to connect with the distal convoluted tubules. These extensions are called medullary rays and represent the cores of the kidney lobules (Medullary Rays). The glomeruli consist of a tuft of capillaries housed in an epithelial lined Bowman's capsule (Renal Corpuscle). The parietal epithelium of Bowman's Capsule is a layer of simple squamous epithelium lining the outer border of the corpuscle. The visceral epithelium of Bowman's capsule (or podocytes) surrounds the capillary endothelial cells, with mesangial cells filling in the spaces between closely apposed capillaries. The afferent arteriole enters the corpuscle and the efferent arteriole leaves the corpuscle, both at a region called the vascular pole. The glomerular filtrate leaves the corpuscle via the proximal convoluted tubule. The proximal convoluted tubule travels a tortuous course, therefore will appear as tubes cut in various orientations (i.e. cross-sectional or oblique). They are the most prominent tubule seen in the cortex. The cells stain highly acidophilic and possess a brush border (Proximal Tubules). The distal convoluted tubules differ from the proximal tubules in that: (1) the total diameter of the tubule is smaller, (2) but, the cells are lower producing a larger lumen, (3) the cells are less acidophilic, and (4) the cells do not have a brush border (Distal Tubules). The distal tubules also travel a tortuous course, producing different cut orientations. Before joining the collecting tubules, the distal convoluted tubules about the renal corpuscle at the vascular pole. At this site, the distal tubule wall has an increased number of nuclei, producing a structure called the macula densa (Macula Densa). 3. KIDNEY MEDULLA The medullary portion of the kidney is organized as a single medullary pyramid (unilobar kidney) or multiple pyramids (multilobar kidney). Each pyramid of medullary tissue and its associated "cap" of cortical tissue is defined as a kidney lobe (Kidney Lobe). The pyramids
12 appear striated, due to the parallel alignment of the loops of Henle and collecting tubules (Medulla 1). Histologically, the loop of Henle appear acidophilic as the descending/ascending loop (Medulla 2) and becomes a thin squamous lined tube near the tip of the papillae (Medulla 3). Collecting tubules are not considered part of the nephron; they are the duct system of the kidney. The bulk of the medullary pyramid is composed of collecting tubules. The collecting tubules are lined with simple cuboidal epithelium. They meet at the apex or papillae of the medullary pyramid, merging together to form large ducts, the ducts of Bellini which empty into the renal pelvis (Papillae). 4. URINARY TUBULAR SYSTEM The urine in the collecting tubules is collected in the renal pelvis and exits the kidney in the ureter. The ureter travels to the bladder, where the urine can be stored. The bladder is drained by the urethra which leads to the external orifice. 5. URETER The ureter is composed of a folded mucus membrane, a muscle coat, and a fibroelastic adventitia (Ureter 1). The mucus membrane consists of two layers: (1) transitional epithelium and (2) lamina propria (Ureter 2). The muscle coat consists of two layers of smooth muscle. 6. BLADDER The urinary bladder is lined with transitional epithelium underlined by a collagenous lamina propria. A submucosa of elastic fibers and a muscular layer of three coats of smooth muscle permit expansion of the structure (Bladder). 7. URETHRA In the male, the urethra runs within the prostate gland and penis, and will be studied in the male reproductive section. In the female, it is a separate tube consisting of a mucus membrane (epithelium and lamina propria), submucosa and muscular coat of two layers of smooth muscle. The epithelium varies: transitional by the bladder, changing to stratified squamous non-keratinizing (Female Urethra), and finally stratified squamous at the opening.
13 Female urethra In the human female, the urethra is about 1-2 inches long and opens in the vulva between the clitoris and the vaginal opening. Men have a longer urethra than women. This means that women tend to be more susceptible to infections of the bladder (cystitis) and the urinary tract. Male urethra In the human male, the urethra is about 8 inches long and opens at the end of the head of the penis. The length of a male's urethra, and the fact it contains a number of bends, makes catheterisation more difficult. The urethral sphincter is a collective name for the muscles used to control the flow of urine from the urinary bladder. These muscles surround the urethra, so that when they contract, the urethra is closed.

There are two distinct areas of muscle: the internal sphincter, at the bladder neck and the external, or distal, sphincter. Human males have much stronger sphincter muscles than females, meaning that they can
retain a large amount of urine for twice as long, as much as 800mL. 8. NEPHRONS A nephron is the basic structural and functional unit of the kidney. The name nephron comes from the Greek word (nephros) meaning kidney. Its chief function is to regulate water and soluble substances by filtering the blood, reabsorbing what is needed and excreting the rest as urine. Nephrons eliminate wastes from the body, regulate blood volume and pressure, control levels of electrolytes and metabolites, and regulate blood pH. Its functions are vital to life and are
14 regulated by the endocrine system by hormones such as antidiuretic hormone, aldosterone, and parathyroid hormone. Each nephron has its own supply of blood from two capillary regions from the renal artery. Each nephron is composed of an initial filtering component (the renal corpuscle) and a tubule specialized for reabsorption and secretion (the renal tubule). The renal corpuscle filters out large solutes from the blood, delivering water and small solutes to the renal tubule for modification. THERE ARE FIVE PARTS OF THE NEPHRON: 1. The glomerulus, which is the blood kidney interface, plasma is filtered from capillaries into the Bowmans capsule. 2. The proximal convoluted tubule, which reabsorbs most of the filtered load, including nutrients and electrolytes. 3. The loop of Henle, which, depending on its length, concentrates urine by increasing the osmolality of surrounding tissue and filtrate. 4. The distal convoluted tubule, which reabsorbs water and sodium depending on needs, 5. The collecting system, which collects urine for excretion. There are two types of nephrons, those localized to the cortex, and those extending into the medulla. The latter are characterized by long loops of Henle, and are more metabolically active. GLOMERULUS The glomerulus is a capillary tuft that receives its blood supply from an afferent arteriole of the renal circulation. The glomerular blood pressure provides the driving force for fluid and solutes to be filtered out of the blood and into the space made by Bowman's capsule. The remainder of the blood not filtered into the glomerulus passes into the narrower efferent arteriole. It then moves into the vasa recta, which are collecting capillaries intertwined with the convoluted tubules through the interstitial space, where the reabsorbed substances will also enter. This then
15 combines with efferent venules from other nephrons into the renal vein, and rejoins with the main bloodstream. AFFERENT OR EFFERENT ARTERIOLES The afferent arteriole supplies blood to the glomerulus. A group of specialized cells known as juxtaglomerular cells are located around the afferent arteriole where it enters the renal corpuscle. The efferent arteriole drains the glomerulus. Between the two arterioles lies specialized cells called the macula densa. The juxtaglomerular cells and the macula densa collectively form the juxtaglomerular apparatus. It is in the juxtaglomerular apparatus cells that the enzyme renin is formed and stored. Renin is released in response to decreased blood pressure in the afferent arterioles, decreased sodium chloride in the distal convoluted tubule and sympathetic nerve stimulation of receptors (beta-adrenic) on the juxtaglomerular cells. Renin is needed to form Angiotensin I and Angiotensin II which stimulate the secretion of aldosterone by the adrenal cortex. GLOMERULAR CAPSULE OR BOWMAN'S CAPSULE Bowman's capsule (also called the glomerular capsule) surrounds the glomerulus and is composed of visceral (simple squamous epithelial cells) (inner) and parietal (simple squamous epithelial cells) (outer) layers. The visceral layer lies just beneath the thickened glomerular basement membrane and is made of podocytes which send foot processes over the length of the glomerulus. Foot processes interdigitate with one another forming filtration slits that, in contrast to those in the glomeruluar endothelium, are spanned by diaphragms. The size of the filtration slits restricts the passage of large molecules (eg, albumin) and cells (eg, red blood cells and
platelets). In addition, foot processes have a negatively-charged coat (glycocalyx) that limits the filtration of negatively-charged molecules, such as albumin. This action is called repulsion. The parietal layer of Bowman's capsule is lined by a single layer of squamous epithelium. Between the visceral and parietal layers is Bowman's space, into which the filtrate enters after passing through the podocytes' filtration slits. It is here that smooth muscle cells and macrophages lie between the capillaries and provide support for them. Unlike the visceral layer,
electrostatic
16 the parietal layer does not function in filtration. Rather, the filtration barrier is formed by three components: the diaphragms of the filtration slits, the thick glomerular basement membrane, and the glycocalyx secreted by podocytes. 99% of glomerular filtrate will ultimately be reabsorbed. The process of filtration of the blood in the Bowman's capsule is ultrafiltration (or glomerular filtration), and the normal rate of filtration is 125 ml/min, equivalent to ten times the blood volume daily. Measuring the glomerular filtration rate (GFR) is a diagnostic test of kidney function. A decreased GFR may be a sign of renal failure. Conditions that can effect GFR include: arterial pressure, afferent arteriole constriction, efferent arteriole constriction, plasma protein concentration and colloid osmotic pressure. Any proteins that are roughly 30 kilodaltons or under can pass freely through the membrane.Although, there is some extra hindrance for negatively charged molecules due to the negative charge of the basement membrane and the podocytes. Any small molecules such as
water, glucose, salt (NaCl), amino acids, and urea pass freely into Bowman's space, but cells, platelets and large proteins do not. As a result, the filtrate leaving the Bowman's capsule is very similar to blood plasma in composition as it passes into the proximal convoluted tubule. Together, the glomerulus and Bowman's capsule are called the renal corpuscle. PROXIMAL CONVOLUTED TUBULE (PCT) The proximal tubule can be anatomically divided into two segments: the proximal convoluted tubule and the proximal straight tubule. The proximal convoluted tubule can be divided further into S1 and S2 segments based on the histological appearance of its cells.
Following this naming convention, the proximal straight tubule is commonly called the S3 segment. The proximal convoluted tubule has one layer of cuboidal cells in the lumen. This is the only place in the nephron that contains cuboidal cells. These cells are covered with millions of microvilli. The microvilli serve to increase surface area for reabsorption. Fluid in the filtrate entering the proximal convoluted tubule is reabsorbed into the peritubular capillaries, including approximately two-thirds of the filtered salt and water and all filtered organic solutes (primarily glucose and amino acids). This is driven by sodium
transport from the lumen into the blood by the Na+/K+ ATPase in the basolateral membrane of
17 the epithelial cells. Much of the mass movement of water and solutes occurs in between the cells through the tight junctions, which in this case are not selective. The solutes are absorbed isotonically, in that the osmotic potential of the fluid leaving the proximal tubule is the same as that of the initial glomerular filtrate. However, glucose, amino acids, inorganic phosphate, and some other solutes are reabsorbed via secondary active transport through cotransport channels driven by the sodium gradient out of the nephron. LOOP OF THE NEPHRON OR LOOP OF HENLE The loop of Henle (sometimes known as the nephron loop) is a U-shaped tube that consists of a descending limb and ascending limb. It begins in the cortex, receiving filtrate from the proximal convoluted tubule, extends into the medulla, and then returns to the cortex to empty into the distal convoluted tubule. Its primary role is to concentrate the salt in the interstitium, the tissue surrounding the loop. DESCENDING LIMB Its descending limb is permeable to water but completely impermeable to salt, and thus only indirectly contributes to the concentration of the interstitium. As the filtrate descends deeper into the hypertonic interstitium of the renal medulla, water flows freely out of the descending limb by osmosis until the tonicity of the filtrate and interstitium equilibrate. Longer descending limbs allow more time for water to flow out of the filtrate, so longer limbs make the filtrate more hypertonic than shorter limbs. ASCENDING LIMB Unlike the descending limb, the ascending limb of Henle's loop is impermeable to water, a critical feature of the countercurrent exchange mechanism employed by the loop. The ascending limb actively pumps sodium out of the filtrate, generating the hypertonic interstitium that drives countercurrent exchange. In passing through the ascending limb, the filtrate grows hypotonic since it has lost much of its sodium content. This hypotonic filtrate is passed to the distal convoluted tubule in the renal cortex.
18 DISTAL CONVOLUTED TUBULE (DCT) The distal convoluted tubule is similar to the proximal convoluted tubule in structure and function. Cells lining the tubule have numerous mitochondria, enabling active transport to take place by the energy supplied by ATP. Much of the ion transport-taking place in the distal convoluted tubule is regulated by the endocrine system. In the presence of parathyroid hormone, the distal convoluted tubule reabsorbs more calcium and excretes more phosphate. When aldosterone is present, more sodium is reabsorbed and more potassium excreted. Atrial natriuretic peptide causes the distal convoluted tubule to excrete more sodium. In addition, the tubule also secretes hydrogen and ammonium to regulate pH. After traveling the length of the distal convoluted tubule, only 3% of water remains, and the remaining salt content is negligible. 97.9% of the water in the glomerular filtrate enters the convoluted tubules and collecting ducts by osmosis.
SIX IMPORTANT ROLES OF THE KIDNEYS 1. Regulation of plasma ionic composition. Ions such as sodium, potassium, calcium, magnesium, chloride, bicarbonate, and phosphates are regulated by the amount that the kidney excretes. 2. Regulation of plasma osmolarity. The kidneys regulate osmolarity because they have direct control over how many ions and how much water a person excretes. 3. Regulation of plasma volume. Your kidneys are so important they even have an effect
on your blood pressure. The kidneys control plasma volume by controlling how much water a person excretes. The plasma volume has a direct effect on the total blood volume, which has a direct effect on your blood pressure. Salt (NaCl) will cause osmosis to happen; the diffusion of water into the blood. 4. Regulation of plasma hydrogen ion concentration (pH). The kidneys partner up with the lungs and they together control the pH. The kidneys have a major role because they control the amount of bicarbonate excreted or held onto. The kidneys help maintain the blood Ph
mainly by excreting hydrogen ions and reabsorbing bicarbonate ions as needed.
19 5. Removal of metabolic waste products and foreign substances from the plasma. One of the most important things the kidneys excrete is nitrogenous waste. As the liver breaks down amino acids it also releases ammonia. The liver then quickly combines that ammonia with carbon dioxide, creating urea which is the primary nitrogenous end product of metabolism in humans. The liver turns the ammonia into urea because it is much less toxic. We can also excrete some ammonia, creatinine and uric acid. The creatinine comes from the metabolic breakdown of creatine phospate (a high-energy phosphate in muscles). Uric acid comes from the breakdown of nucleotides. Uric acid is insoluble and too much uric acid in the blood will build up and form crystals that can collect in the joints and cause gout. 6. Secretion of Hormones The endocrine system has assistance from the kidney's when releasing hormones. Renin is released by the kidneys. Renin leads to the secretion of aldosterone which is released from the adrenal cortex. Aldosterone promotes the kidneys to reabsorb the sodium (Na+) ions. The kidneys also secrete erythropoietin when the
blood doesn't have the capacity to carry oxygen. Erythropoietin stimulates red blood cell production. The Vitamin D from the skin is also activated with help from the kidneys. Calcium (Ca+) absorption from the digestive tract is promoted by vitamin D.
B. CHRONIC KIDNEY DISEASE
Definition. Chronic kidney disease (CKD) is the gradual loss of the kidneys' ability to filter waste from the blood. It is often a result of a kidney disease. But did you know CKD could also be a result of other diseases and illnesses? Diabetes and high blood pressure are the leading causes of CKD. Because CKD usually occurs over time, you may not have any symptoms until it's time to start dialysis.
Chronic kidney disease (CKD) is the slow break down of the kidneys' ability to filter waste and fluid from the bloodstream.
20 Kidneys are made up of nephrons, tiny structures that filter waste out of the blood. When a person is diagnosed with a kidney disease or another disease that affects the kidneys (such as diabetes or high blood pressure), the nephrons will become damaged over time and lose their filtering ability.
Because there are millions of nephrons in each kidney, a person may not notice when a few nephrons become damaged. The remaining healthy nephrons are able to take up the slack. But as more and more nephrons become damaged, the remaining healthy nephrons must work harder. Eventually, the healthy nephrons become damaged as well. Kidneys can become scarred or even shrink in size.
Chronic kidney disease is divided into five stages of increasing severity (Table 1). Stage 5 chronic kidney failure is also referred to as end-stage renal disease, wherein there is total or near-total loss of kidney function and patients need dialysis or transplantation to stay alive. The term "renal" refers to the kidney, so another name for kidney failure is "renal failure." Mild kidney disease is often called renal insufficiency. Unlike chronic kidney disease, acute kidney failure develops rapidly, over days or weeks. Table I. Stages of Chronic Kidney Disease Stage Description Slight kidney damage with normal or increased filtration Mild decrease in kidney function Moderate decrease in kidney function Severe decrease in kidney function. Preparation for renal replacement therapy Kidney failure requiring dialysis or transplantation. GFR* mL/min/1.73m2 More than 90 60-89 30-59 15-29 Less than 15
1 2 3 4 5
21 *GFR is glomerular filtration rate, a measurement of the kidney's function. STAGES OF CHRONIC KIDNEY DISEASE (CKD) STAGE 1 CKD A person with Stage 1 CKD has kidney damage with a GFR at a normal or high level greater than 90 ml/min. There are usually no symptoms to indicate the kidneys are damaged. Because kidneys do a good job even when theyre not functioning at 100%, most people will not know they have Stage 1 CKD. If they do find out theyre in Stage 1, it is usually because they were being tested for another condition such as diabetes or high blood pressure (the two leading causes of kidney disease). Other ways a person may discover they are in Stage 1 CKD:

Higher than normal levels of creatinine or urea in the blood Blood or protein in the urine Evidence of kidney damage in an MRI, CT scan, ultrasound or contrast X-ray A family history of polycystic kidney disease
STAGE 2 CKD A person with Stage 2 CKD has kidney damage with a mild decrease in their GFR of 6089 ml/min. There are usually no symptoms to indicate the kidneys are damaged. Because kidneys do a good job even when theyre not functioning at 100%, most people will not know they have Stage 2 CKD. If they do find out theyre in Stage 2, its usually because they were being tested for another condition such as diabetes or high blood pressure (the two leading causes of kidney disease). Other ways a person may discover they are in Stage 2 CKD:

Higher than normal levels of creatinine or urea in the blood Blood or protein in the urine Evidence of kidney damage in an MRI, CT scan, ultrasound or contrast X-ray
22
A family history of polycystic kidney disease
STAGE 3 CKD A person with Stage 3 CKD has kidney damage with a moderate decrease in the GFR of 30-59 ml/min. As kidney function declines waste products can build up in the blood causing a condition known as uremia. In Stage 3 a person is more likely to develop complications of kidney disease such as high blood pressure, anemia (a shortage of red blood cells) and/or early bone disease. Symptoms may start to become present in Stage 3, such as:

Fatigue: Feeling tired is common for people with CKD and is often caused by anemia. Too much fluid: The kidneys may lose their ability to control how much fluid stays in the body. A person may notice swelling (edema) in their lower legs, hands or face around the eyes. With too much fluid someone could even feel short of breath.
Urination changes: Urine may be foamy if there is protein in it, or dark orange, brown, tea colored or red if it contains blood. A person may urinate more or less, or get up at night to go to the bathroom.
Kidney pain: Most people with CKD do not have kidney pain, but with some kinds of kidney problems, such as polycystic kidney disease or infections, they may have pain in their back where the kidneys are.
Sleep problems: Some people have trouble falling asleep or staying asleep. Itching, muscle cramps or restless legs can keep them awake.
STAGE 4 CKD A person with Stage 4 CKD has advanced kidney damage with a severe decrease in the GFR to 15-30 ml/min. It is likely someone with Stage 4 CKD will need dialysis or a kidney transplant in the near future. As kidney function declines waste products build up in the blood causing a condition known as uremia. In Stage 4 a person is likely to develop complications of kidney disease such
23 as high blood pressure, anemia (a shortage of red blood cells), bone disease, heart disease and other cardiovascular diseases. Symptoms that are experienced in Stage 4 include:

Fatigue: Feeling tired is common for people with CKD and is often caused by anemia. Too much fluid: The kidneys may lose their ability to control how much fluid stays in the body. A person may notice swelling (edema) in their lower legs, hands or face around the eyes. With too much fluid someone, could even feel short of breath.
Urination changes: Urine may be foamy if there is protein in it, or dark orange, brown, tea colored or red if it contains blood. A person may urinate more or less than normal, or get up at night to go to the bathroom.
Kidney pain: Most people with CKD do not have kidney pain, but with some kinds of kidney problems, such as polycystic kidney disease or infections, they may have pain in their back where the kidneys are located.
Sleep problems: Some people have trouble falling asleep or staying asleep. Itching, muscle cramps or restless legs can keep them awake.
Nausea: Vomiting or feeling nauseated may occur with CKD. Taste changes: Food may not taste like it usually does, or may have a metallic taste. Uremic breath: As urea builds up in the blood, it may be detected in the breathing causing bad breath.
Loss of appetite: People in this stage may not feel like eating, and some people report having a metallic taste in their mouth or bad breath.
Difficulty in concentrating: Having trouble balancing a checkbook or focusing on reading the newspaper can happen with CKD.
Nerve problems: Numbness or tingling in your toes or fingers is a symptom of CKD.
24 STAGE 5 CKD A person with Stage 5 CKD has end stage renal disease (ESRD) with a GFR of 15 ml/min or less. At this advanced stage of kidney disease the kidneys have lost nearly all their ability to do their job effectively, and eventually dialysis or a kidney transplant is needed to live. Symptoms that can occur in Stage 5 CKD include:

Loss of appetite Nausea or vomiting Headaches Being tired Being unable to concentrate Itching Making little or no urine Swelling, especially around the eyes and ankles Muscle cramps Tingling in hands or feet Changes in skin color Increased skin pigmentation Because the kidneys are no longer able to remove waste and fluids from the body, toxins
build up in the blood, causing an overall ill feeling. Kidneys also have other functions they are no longer able to perform such as regulating blood pressure, producing the hormone that helps make red blood cells and activating vitamin D for healthy bones. If you are diagnosed with stage 5 CKD, you will need to see a nephrologist immediately. This is a doctor who is trained in kidney disease, kidney dialysis and transplant. The doctor will help you decide which treatment is best for you hemodialysis, peritoneal dialysis or kidney transplantand will recommend an access for dialysis. Your nephrologist will develop your overall care plan and manage your health care team.
25 THERE ARE TWO TYPES OF DIALYSIS: HEMODIALYSIS AND PERITONEAL DIALYSIS Hemodialysis requires that an access be created to get the blood from your body to the dialyzer (artificial kidney) so it can be cleaned and then go back into your body. Because in Stage 5 the kidneys are no longer working, dialysis must begin soon. A catheter will be placed into a vein in the neck, chest or groin. This is considered a temporary access. If you decide to remain on hemodialysis, your nephrologist will likely recommend you get a fistula created, which is a permanent access. To create a fistula, an artery and vein are surgically connected in the forearm. It takes a few months for the fistula to mature so that it can be used for dialysis. There is another type of access called a graft that uses artificial tubing to connect the artery and vein. It takes three to six weeks to heal so that it can be used for dialysis. For Peritoneal Dialysis (PD), a catheter access is placed in the abdomen. PD is performed by running dialysate solution through the catheter into the peritoneum and then removing the solution after a time and replacing it with new dialysate. The peritoneal membrane that lines the peritoneum is a semipermeable membrane that does the filtering for the kidney. There are different methods of performing PD. Some people manually drain and fill their abdomen every four to six hours, which is called Continuous Ambulatory Peritoneal Dialysis (CAPD). Others use an automated machine, called a cycler, which works while they sleep and then do a manual exchange in the morning. This is called Continuous Cycler Peritoneal Dialysis (CCPD). There is another choice called Nocturnal Intermittent Peritoneal Dialysis (NIPD) where PD is performed at night while sleeping. With NIPD, no exchanges are done during the day. Most people report feeling much better once they begin dialysis. As the toxins are removed from their blood and they receive medicines that replace the functions the kidneys can no longer perform, they find they can enjoy a good quality of life. Changes in the Diet Once you begin dialysis, you will need to make changes in what you eat and drink. Your diet is a big part of your treatment, so you will be working with a dietitian who will coach you on
26 how you should eat. Depending on the dialysis treatment you choose and your lab test results, your dietitian will help create a meal plan based on your individual requirements to keep you feeling your best. People on hemodialysis generally need to increase their protein, and limit fluids, sodium, potassium and phosphorus, and in some cases, calcium. Those who choose PD usually need to increase their protein and limit phosphorus, but may have fewer limits on fluid and potassium. Your dietitian will explain what foods are restricted and which ones are recommended on the renal diet. A healthy diet for stage 5 CKD may recommend:
Including grains, fruits and vegetables, but limiting or avoiding whole grains and certain fruits and vegetables that are high in phosphorus or potassium
A diet that is low in saturated fat and cholesterol and moderate in total fats, especially if cholesterol is high or if you have diabetes or heart disease
Limiting intake of refined and processed foods high in sodium and prepare foods with less salt or high sodium ingredients
Aiming for a healthy weight by consuming adequate calories and including physical activity each day within your ability Increasing protein intake to the level determined by the dietitians assessment of individual needs and to replace losses in the dialysis treatment
Taking special renal vitamins high in water soluble B vitamins and limited to 100 mg of vitamin C
Vitamin D and iron tailored to individual requirements Limiting phosphorus to1000 mg or based on individual requirements Limiting calcium to 2000 mg (no more than 1500 mg from calcium based phosphorus binders).
Limiting potassium to 2000 to 3000 mg or bases on individual requirements
27 Kidney Transplant If you wish to have a kidney transplant, tell your nephrologist. Your nephrologist will explain the process of how to get on a waiting list for a cadaverous kidney or how to find a living donor. When at Stage 5 CKD, either dialysis or a kidney transplant is necessary to continue living. If you would like to see a doctor who specializes in the care of kidneys, called a nephrologist, you can use DaVita's Find a kidney doctor tool to locate a nephrologist in your area. Risks.Some of the things that lead to chronic kidney disease are related to your age and your genetic makeup. You may be able to control other things that increase your risk, such as dietary habits and exercise. Age. The kidney begins to get smaller at about age 35. By age 80, most people have lost about 30% of their kidney mass. Being male. Men have a higher risk of developing chronic kidney disease than women. Family history. Family history is a factor in the development of both diabetes and high blood pressure, the major causes of chronic kidney disease. Polycystic kidney disease is one of several inherited diseases that cause kidney failure. High blood pressure, which gradually damages the tiny blood vessels in the kidneys. Diabetes. A persistently high blood sugar level can damage blood vessels in the kidneys. Over time, kidney damage can progress, and the kidneys may stop working altogether. Eating protein and fats. Eating a diet low in protein and fat may reduce your risk of developing kidney disease. Certain medicines. Avoid long-term use of medicines that can damage the kidneys, such as pain relievers called NSAIDs and certain antibiotics. Causes.Although chronic kidney disease sometimes results from primary diseases of the kidneys themselves, the major causes are diabetes and high blood pressure.
28
Type 1 and type 2 diabetes mellitus cause a condition called diabetic nephropathy, which is the leading cause of kidney disease in the United States.
High blood pressure (hypertension), if not controlled, can damage the kidneys over time. Glomerulonephritis is the inflammation and damage of the filtration system of the kidneys and can cause kidney failure. Postinfectious conditions and lupus are among the many causes of glomerulonephritis.
Polycystic kidney disease is an example of a hereditary cause of chronic kidney disease wherein both kidneys have multiple cysts.
Use of analgesics such as acetaminophen (Tylenol) and ibuprofen (Motrin, Advil) regularly over long durations of time can cause analgesicnephropathy, another cause of kidney disease. Certain other medications can also damage the kidneys.
Clogging and hardening of the arteries (atherosclerosis) leading to the kidneys causes a condition called ischemic nephropathy, which is another cause of progressive kidney damage.
Obstruction of the flow of urine by stones, an enlarged prostate, strictures (narrowings), or cancers may also cause kidney disease.
Other causes of chronic kidney disease include HIV infection, sickle cell disease, heroin abuse, amyloidosis, kidney stones, chronic kidney infections, and certain cancers.
If you have any of the following conditions, you are at higher-than-normal risk of developing chronic renal disease. Your kidney functions may need to be monitored regularly. Incidence
Chronic kidney disease is a growing health problem in the United States. A report by the Centers for Disease Control (CDC) determined that 16.8% of all adults above the age of 20 years have chronic kidney disease. Thus, one in six individuals has kidney disease, and over 400,000 patients are on dialysis or have received kidney transplants. About 67,000 people die each year because of kidney failure.
The prevalence of chronic kidney disease has increased by 16% from the previous decade. The increasing incidence of diabetes mellitus, hypertension (high blood pressure), obesity, and an aging population have led to this increase in kidney disease.
29
The frequency of chronic kidney disease increases with age and is much more common in adults than children. Chronic kidney disease is more prevalent among individuals above 60 years of age (39.4%).Among children, chronic kidney disease is more common in children older than 6 years than in those younger than 6 years.
Kidney disease is more common among Hispanic, African American, Asian or Pacific Islander, and Native American people. In the Philippines, the stage that has the most number of CKD cases falls on the 3rd stage followed by the 5th and only a few belongs to the 4th stage. On the other hand, the age group that is affected the most is the 70+ age bracket. Next is the 60-69 group then the ages 40-49. Fourth are the ages 50-59 and only few cases on the age brackets of 20-29 and 30-39. Manifestations.The kidneys play a critical role in keeping the body healthy by cleaning
and processing the blood. Working together, the 2 million nephrons filter and process 3-4 liters of blood approximately every 5 minutes, 24 hours a day, 7 days a week. It is important to be aware of any problems you may be having with your kidneys and get treatment quickly.CKD is initially without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As the kidneyfunction decreases: High blood pressure. Due to fluid overload and production of vasoactive hormones, increasing one's risk of developing hypertension and/or suffering from congestive heart failure Urea accumulates. Leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and crystallizes on skin ("uremic frost"). Potassium accumulates in the blood. (known as hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias) Erythropoietin synthesis is decreased. (potentially leading to anemia, which causes fatigue) Anemia. Resulting in pale gums and weakness due to a low blood count
30 Fluid volume overload. Symptoms may range from mild edema to life-threatening pulmonary edema Hyperphosphatemia. Due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency). The major sign of hypocalcemia is being tetany. Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function. Metabolic acidosis.Due to accumulation of sulfates, phosphates, uric acid etc. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia) Protein or blood in the urine. This may be discovered on a routine urinalysis that is done as part of an annual physical exam, a preoperative evaluation, or a school, employment, or insurance physical. In many (but not all) types of kidney disease, kidney damage results in leakiness of the tiny glomerular filters. These leaks allow protein and red blood cells, which are normally kept in the bloodstream, to spill into the urine. Edema or swelling. Especially of the feet, lower legs, and sometimes the face and hands. This is a sign of fluid build up that can occur in several conditions, most commonly in heart failure. However, it often is the first sign of protein leakage from the kidneys. The increased volume of urine in the bladder may lead to, or worsen incontinence (leaking urine), especially at night Symptoms of a urinary tract infection. Burning on urination, frequency (the sensation of needing to urinate very frequently), urgency (the sensation of needing to urinate urgently), bloody or cloudy urine. Although urinary tract infections do not usually cause permanent or progressive kidney damage if promptly treated, they can certainly cause a patient to seek medical attention. Weakened bones can result in bone fractures.
31 Bleeding into the stomach or gut or bruising of skin. Others.Loss of appetite, nausea vomiting, fatigue, sleepiness, itching, twitching, and a metallic taste in the mouth. These are signs of far advanced chronic kidney disease (CKD). They often indicate that the person is accumulating dangerous amounts of waste products because the kidneys are not working to excrete them. Patients with these symptoms are often in need of dialysis (artificial kidney treatments). CAUSES OF KIDNEY FAILURE
Kidneys fail when they are no longer able to clean waste from the blood and balance fluid and mineral levels. Lets take a look at some of the most common causes of kidney failure.
Diabetes Diabetes can cause damage to the kidneys, which is called diabetic nephropathy, is the most common cause of kidney disease in the United States. In diabetes the body is not able to process sugar properly. As levels of sugar build up in the body, it causes damage to blood vessels, including those in the kidney. The high levels of
sugar cause more blood to flow through the kidneys and this puts an added strain on the tiny blood vessels and raises blood pressure. Damaged kidneys are not able to remove waste products and excess fluid well, so these build up in the blood. As the waste build-up continues, the damage gets worse, and the kidneys eventually fail. Because kidney failure in diabetics occurs slowly, the patient may not notice symptoms until the kidneys actually start to fail.
High Blood Pressure High blood pressure can cause damage to the kidneys. It is interesting too that kidney damage can also cause high blood pressure. If high blood pressure damages the blood vessels in the kidneys, the kidneys will not be able to remove wastes and extra fluid. The extra fluid can cause blood pressure to rise even more.
32 If kidneys produce too much of the enzyme, renin, blood pressure will rise too high. Over time, high blood pressure can cause blood vessels in the kidneys to thicken and narrow. This can lead to reduced blood supply and reduced kidney function. As with diabetes, eventually, the damage may become so great that the kidneys fail.
High blood pressure is the second leading cause of kidney failure. Every year in the United States, there are about 15,000 new cases of kidney failure due to high blood pressure.
Glomerular Diseases The kidneys contain about a million little clusters of looping blood vessels. Each cluster is called a glomerulus. When we talk about more than one glomerulus, we call them glomeruli.
Each glomerulus is connected to a small tube called a tubule, and each glomerulus and tubule unit is known as a nephron. The body has about one million nephrons in each kidney. The glomeruli work to filter the blood, and then waste products and fluid travel through the tubule and become urine. When someone suffers from a glomerular (kidney) disease, it means that their glomeruli are no longer working the way they should. Waste products build up and cause extra fluid in the body. As a result, a persons face, hands, ankles or feet may swell.
Glomerular diseases, the third leading cause of kidney failure, come in many forms, but they fall into two major categories:

Glomerulonephritis happens when the glomeruli are inflamed (swollen). Glomerulosclerosis takes place when the glomeruli become scarred or hardened.
Glomerular disease has many causes, including other diseases such as diabetes, lupus and HIV. Toxic drugs and infection also can result in glomerular disease. In some cases, the cause is not known.
33 V. READINGS
CHRONIC GLOMERULONEPHRITIS Definition.People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter. Cause. Chronic glomerulonephritis is caused when there is slow progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. Some cases are caused by specific stimuli to the body's immune system, but the precise cause of most is unknown. An as yet undefined abnormality of the immune system is believed to be responsible for most cases. It is a cause of hypertension and chronic renal failure. Damage to the glomeruli with subsequent inefficient filtering causes blood and protein to be lost in the urine. Because symptoms develop gradually, the disorder may be discovered when there is an abnormal urinalysis during routine physical or examination for unrelated disorders. It may be discovered as a cause of hypertension that is difficult to control. Glomerulonephritis is among the leading causes of chronic renal failure and end stage renal disease. With kidney biopsy, it may be possible to reach a precise diagnosis such as membranous glomerulonephritis, IgA nephropathy (Berger's disease), focal segmental glomerulosclerosis, mesangial proliferative disorder, diabetic nephropathy/sclerosis, lupus nephritis, or nephritis associated with disorders such as amyloidosis, multiple myeloma, or immune disorders including AIDS. It may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about one-fourth of people with chronic glomerulonephritis there is no prior history of kidney disease, and the disorder first appears as chronic renal failure. Manifestations. Signs and symptoms of the said diseases may include the presence of blood in the urine and having foamy urine. Chronic renal failure symptoms that gradually develop may include, unintentional weight loss, nausea, vomiting, general ill feeling or malaise, fatigue, headache, frequent hiccups, generalized itching, decreased urine output, need to urinate
34 at night, easy bruising or bleeding, decreased alertness, drowsiness, somnolence, lethargy, confusion, delirium, muscle twitching, muscle cramps, seizures, hyperpigmentation, decreased sensation in the hands, feet, or other areas. Additional symptoms that may be associated with this disease would include excessive urination, nosebleed, high blood pressure and blood in the vomit or in stools. Prognosis. The outcome varies depending on the cause. Some types of
glomerulonephritis may have spontaneous remission. If nephrotic syndrome is present and can be controlled, other symptoms may be controlled. If nephrotic syndrome is present and cannot be controlled, end-stage renal disease is likely. The disorder generally progresses at widely variable rates. END STAGE RENAL DISEASE End stage renal disease (ESRD) is the last stage (stage five) of chronic kidney disease (CKD). This means kidneys are only functioning at 10%15% of their normal capacity. Kidneys are important organs that contribute to your overall well-being. When kidney function is this low, they cannot effectively remove waste or excess fluid from your blood. Kidneys are also responsible for other functions that support the body, such as balancing electrolytes and producing certain hormones. When chronic kidney disease develops into ESRD, dialysis or a kidney transplant is necessary to stay alive. Urine Production Fully functioning kidneys clean the blood of wastes and excess fluid. These items are eliminated through urine. Because kidneys with ESRD do a very poor job of removing these items, waste and fluid buildup in the body to unhealthy levels. Accumulated waste in the bloodstream can make you feel sick. This is a condition called uremia. When fluid is not removed from the body, tissues will swell and lead to a condition called edema. Excess fluid in the bloodstream can also increase blood pressure. Electrolytes
35 Electrolytes are minerals and salts such as magnesium, sodium and potassium. They are found in foods you eat and are essential to good health. However, too much or too little of these electrolytes can make you sick. Healthy kidneys make sure these levels are balanced. But kidneys affected with ESRD cannot regulate the levels of electrolytes. When this happens, changes in your bodys functions occur. Sodium can cause tissues to retain water. Excess potassium can cause an abnormal heart rhythm, which may lead to cardiac arrest. Too little magnesium can affect your heartbeat and cause changes in your mental state; too much can leave you feeling weak. Hormones Healthy kidneys make certain hormones. One is a parathyroid hormone that activates vitamin D into a substance called calcitriol. Calcitriol helps your body absorb calcium. If your body cannot absorb calcium, your bones become weak and may break. Another hormone your kidneys manufacture is erythropoietin. Erythropoietin tells your body to make red blood cells, which carry oxygen to the cells throughout your body. If your red blood cell count is low, you may develop anemia, which will leave you feeling weak and fatigued. Enzymes Renin is an enzyme kidneys produce. Renin helps the body regulate sodium and potassium levels in the blood, as well as help regulate blood pressure. When blood pressure drops, renin is released and starts a chemical reaction in the body that will produce a substance called angiotensin. Angiotensin causes your blood vessels to narrow, or constrict. This helps raise blood pressure. Angiotensin also signals the adrenal glands (found at the top of your kidneys) to release a hormone called aldosterone. Aldosterone tells the kidneys to retain salt (sodium) and excrete potassium. By retaining salt, the body keeps more water in the system. This water raises the blood volume and blood pressure. Kidneys affected by ESRD sometimes make too much renin, which keeps blood pressure levels high. This kind of high blood pressure can be difficult to treat.
36 Regular dialysis treatment, following your renal diet and taking prescribed medications can go a long way in managing ESRD. If you have been diagnosed with end stage renal disease, it is important to follow your health care teams advices regarding treatment. C. FLUID IMBALANCES
1. DEHYDRATION
Dehydration, usually caused by diarrhea, remains a major cause of morbidity and mortality in infants and young children worldwide. Infants are particularly susceptible to the ill effects of dehydration because of their greater baseline fluid requirements (due to a higher metabolic rate), higher evaporative losses (due to a higher ratio of surface area to volume), and inability to communicate thirst or seek fluid.
Etiology: The most common source of increased fluid loss is the GI tract from vomiting, diarrhea, or both (eg, gastroenteritis). Other sources are renal (eg, diabetic ketoacidosis), cutaneous (eg, excessive sweating, burns), and 3rd-space losses (eg, into the intestinal lumen in bowel obstruction). All types of lost fluid contain electrolytes in varying concentrations, so fluid loss is always accompanied by electrolyte loss. Decreased fluid intake is common during serious illness of any kind and is particularly problematic when the child is vomiting and during hot weather. It may also be a sign of neglect. Treatment is best approached by considering separately the fluid resuscitation requirements, current deficit, ongoing losses, and maintenance requirements. The volume (eg, amount of fluid), composition, and rate of replacement differ for each. Formulas and estimates used to determine treatment parameters provide a starting place, but treatment requires ongoing monitoring of vital signs, clinical appearance, urine output and specific gravity, weight, and sometimes serum electrolyte levels. Children with severe dehydration (eg, evidence of circulatory compromise) should receive fluids IV. Those unable or unwilling to drink or who
37 have repetitive vomiting can receive fluid replacement IV, through an NGT, or sometimes orally through frequently repeated small amounts. 2. OVERHYDRATION Overhydration, also called water excess or water intoxication, is a condition in which the body contains too much water. It occurs when the body takes in more water than it excretes, and its normal sodium level is diluted. This can result in digestive problems, behavioral changes, brain damage, seizures, or coma. The condition is most common in patients whose kidney function is impaired and may occur when health care professionals administer greater amounts of water-producing fluids and medications than the patient's body can handle. Overhydration can cause acidosis (a condition in which blood and body tissues have an abnormally high acid content), anemia, cyanosis (a condition that occurs when oxygen levels in the blood drop sharply), hemorrhage, and shock. The brain is the organ most vulnerable to the effects of overhydration. If excess fluid levels accumulate gradually, the brain may be able to adapt to the demand the patient will have only a few symptoms. If the condition develops rapidly, confusion, seizures, and coma are likely to occur. Since the brain particularly susceptible, behavior changes are usually the first symptoms of water intoxication. The patient may become confused, drowsy, or inattentive. Shouting and delirium are common. Other symptoms of overhydration may include blurred vision, muscle cramps and twitching, paralysis on one side of the body, poor coordination, nausea and vomiting, rapid breathing, sudden weight gain, and weakness. Blood pressure is sometimes, but not always higher than normal. Chronic illness, malnutrition, a tendency to retain water, and kidney diseases and disorders increase the likelihood of becoming overhydrated. Infants and the elderly are at increased risk for overhydration, as are people with certain mental disorders. Before treatment can begin, a doctor must determine whether a patient's symptoms are due to overhydration, in which excess water is found inside and outside cells, or excess blood volume, in which high sodium levels prevent the body from storing excess water inside the cells.
38 Mild overhydration can generally be corrected by following a doctor's instructions to limit fluid intake. In more serious cases, diuretics may be prescribed to increase urination, although these drugs tend to be most effective in the treatment of excess blood volume. Identifying and treating any underlying condition (such as impaired heart or kidney function) is crucial.
D. ELECTROLYTE IMBALANCES
1. HYPOKALEMIA CAUSES: Hypokalemia can result from one or more of the following medical conditions: Inadequate Potassium Intake
Perhaps the most obvious cause is insufficient consumption of potassium (that is, a lowpotassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalemia.
Gastrointestinal or Integument Loss
A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhea, excessive perspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emeticbicarbonaturia that force urinary potassium excretion.
Urinary Loss
39
Certain medications can cause excess potassium loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalemia.
A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, -hydroxybutyrate.
Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity. Second, an acute rise of plasma HCO3- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate. Metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms.
Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands. Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzymes that allows cortisols to stimulate aldosterone receptors. This deficiency -- known as apparent mineralocorticoid excess syndrome -- can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies and chewing tobacco.
Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.
40 2. HYPERKALEMIA Hyperkalemia is a condition in which you have too much potassium in your blood. Most potassium in the body (98%) is found within cells and organs. Only a small amount circulates in the bloodstream. Potassium helps nerve and muscle cells, including the heart, function properly. Your kidneys usually maintain levels of potassium in the blood, but if you have kidney disease -the most common cause of hyperkalemia -- potassium levels can build up. Medications or diet may also affect the amount of potassium in the blood. Hyperkalemia can be life threatening and must be treated promptly. SIGNS AND SYMPTOMS: Sometimes hyperkalemia has no symptoms. Other times you may experience the following:

Irregular heartbeat Fatigue Weakness Tingling, numbness, or other unusual sensations Paralysis Difficulty breathing Nausea and vomiting
CAUSES: Hyperkalemia has many causes, including the following:

Kidney disease Too much acid in the blood, as is sometimes seen in diabetes Diet high in potassium (bananas, oranges, tomatoes, high protein diets, salt substitutes, potassium supplements)
Trauma, especially crush injuries or burns Addison's disease Certain medications, including beta-blockers
41 3. HYPONATREMIA Hyponatremia refers to a lower-than-normal level of sodium in the blood. Sodium is essential for many body functions including the maintenance of fluid balance, regulation of blood pressure, and normal function of the nervous system. Hyponatremia has sometimes been referred to as "water intoxication," especially when it is due to the consumption of excess water, for example during strenuous exercise, without adequate replacement of sodium. Sodium is the major positively charged ion (cation) in the fluid outside of cells of the body. The chemical notation for sodium is Na. When combined with chloride (Cl), the resulting substance is table salt (NaCl). CAUSES: A low sodium level in the blood may result from excess water or fluid in the body, diluting the normal amount of sodium so that the concentration appears low. This type of hyponatremia can be the result of chronic conditions such as kidney failure (when excess fluid cannot be efficiently excreted) and congestive heart failure, in which excess fluid accumulates in the body. SIADH (syndrome of inappropriate anti-diuretic hormone) is a disease whereby the body produces too much anti-diuretic hormone (ADH), resulting in retention of water in the body. Consuming excess water, for example during strenuous exercise, without adequate replacement of sodium, can also result in hyponatremia. Hyponatremia can also result when sodium is lost from the body or when both sodium and fluid are lost from the body, for example, during prolonged sweating and severe vomiting or diarrhea. Medical conditions that can sometimes be associated with hyponatremia are adrenal insufficiency, hypothyroidism, and cirrhosis of the liver. Finally, a number of medications can lower blood sodium levels. Examples of these include diuretics, vasopressin, and the sulfonylurea drugs. SIGNS AND SYMPTOMS:
42 When sodium levels in the body are low, water tends to enter cells, causing them to swell. When this occurs in the brain, it is referred to as cerebral edema. Cerebral edema is particularly dangerous because the brain is confined in the skull without room for expansion, and the swelling can lead to brain damage as the pressure increases within the skull. In chronic hyponatremia, in which the blood sodium levels drop gradually over time, symptoms are typically less severe than with acute hyponatremia (a sudden drop in blood sodium level). Symptoms can be very nonspecific and can include:

headache, confusion or altered mental state, seizures, and decreased consciousness which can proceed to coma and death.
Other possible symptoms include:

restlessness, muscle spasms or cramps, weakness, and tiredness. Nausea and vomiting may accompany any of the symptoms.
4. HYPERNATREMIA Hypernatremia is serum Na concentration > 145 mEq/L. It implies a deficit of total body water relative to total body Na, caused by water intake being less than water losses. A major symptom is thirst; other clinical manifestations are primarily neurologic (due to an osmotic shift of water out of brain cells), including confusion, neuromuscular excitability, seizures, and coma. Diagnosis requires measurement of serum Na and sometimes other tests. Treatment is usually controlled water replacement. When the response is poor, testing (eg, monitored water deprivation or administration of vasopressin) is directed at detecting causes other than decreased water intake. CAUSES:
43 Hypernatremia reflects a deficit of total body water (TBW) relative to total body Na content. Because total body Na content is reflected by ECF volume status, hypernatremia must be considered along with status of the ECF volume: hypovolemia, euvolemia, and hypervolemia. Note that the ECF volume is not the same as effective plasma volume. Hypernatremia usually implies either an impaired thirst mechanism or limited access to water. The severity of the underlying disorder that results in an inability to drink in response to thirst and the effects of brain hyperosmolality are thought to be responsible for a high mortality rate in hospitalized adults with hypernatremia. There are several common causes of hypernatremia. Hypovolemic hypernatremia: Hypernatremia associated with hypovolemia occurs with Na loss accompanied by a relatively greater loss of water from the body. Common extrarenal causes include most of those that cause hyponatremia and volume depletion. Either hypernatremia or hyponatremia can occur with severe volume loss, depending on the relative amounts of Na and water lost and the amount of water ingested before presentation. Renal causes of hypernatremia and volume depletion include therapy with diuretics. Loop diuretics inhibit Na reabsorption in the concentrating portion of the nephrons and can increase water clearance. Osmotic diuresis can also impair renal concentrating capacity because of a hypertonic substance present in the tubular lumen of the distal nephron occasionally urea can cause osmotic diuresis resulting in hypernatremia. The most common cause of hypernatremia due to osmotic diuresis is hyperglycemia in patients with diabetes. Because glucose does not penetrate cells in the absence of insulin, hyperglycemia further dehydrates the ICF compartment. The degree of hyperosmolality in hyperglycemia may be obscured by the lowering of serum Na resulting from movement of water out of cells into the ECF. Patients with renal disease can also be predisposed to hypernatremia when their kidneys are unable to maximally concentrate urine. Euvolemic hypernatremia: Hypernatremia with euvolemia is a decrease in TBW with near-normal total body Na (pure water deficit). Extrarenal causes of water loss, such as excessive sweating, result in some Na loss, but because sweat is hypotonic, hypernatremia can result before
44 significant hypovolemia. A deficit of almost purely water also occurs in central and nephrogenic diabetes insipidus. Essential hypernatremia (primary hypodipsia) occasionally occurs in children with brain damage and in chronically ill elderly adults. It is characterized by an impaired thirst mechanism (eg, caused by lesions of the brain's thirst center). Altered osmotic trigger for ADH release is another possible cause of euvolemic hypernatremia; some lesions cause both an impaired thirst mechanism and an altered osmotic trigger. The nonosmotic release of ADH appears intact, and these patients are generally euvolemic. Hypervolemic hypernatremia: Hypernatremia in rare cases is associated with volume overload. In this case, hypernatremia results from a grossly elevated Na intake associated with limited access to water. One example is the excessive administration of hypertonic NaHCO 3 during treatment of lactic acidosis. Hypernatremia can also be caused by the administration of hypertonic saline or incorrectly formulated hyperalimentation. Hypernatremia in the Elderly: Hypernatremia is common in the elderly, particularly postoperative patients and those receiving tube feedings or parenteral nutrition. Other contributing factors may include the following:

Dependence on others to obtain water Impaired thirst mechanism Impaired renal concentrating capacity (due to diuretics, impaired ADH release, or nephron loss accompanying aging or other renal disease)
Impaired angiotensin II production (which may contribute directly to the impaired thirst mechanism)
SIGNS AND SYMPTOMS: The major symptom of hypernatremia is thirst. The absence of thirst in conscious patients with hypernatremia suggests an impaired thirst mechanism. Patients with difficulty communicating may be unable to express thirst or obtain access to water.
45 The major signs of hypernatremia result from CNS dysfunction due to brain cell shrinkage. Confusion, neuromuscular excitability, hyperreflexia, seizures, or coma may result; cerebrovascular damage with subcortical or subarachnoid hemorrhage and venous thromboses are common in patients who died from severe hypernatremia. In chronic hypernatremia, osmotically active substances occur in CNS cells (idiogenicosmoles) and increase intracellular osmolality. Therefore, the degree of brain cell dehydration and resultant CNS symptoms are less severe in chronic than in acute hypernatremia. When hypernatremia occurs with abnormal total body Na, the typical symptoms of volume depletion or overload are present. A large volume of hypotonic urine is characteristically excreted in patients with renal concentrating defects. When losses are extrarenal, the route of water loss is often evident (eg, vomiting, diarrhea, excessive sweating), and the urinary Na concentration is low. 5. HYPOCALCEMIA Hypocalcemia is an electrolyte imbalance and is indicated by a low level of calcium in the blood. The normal adult value for calcium is 4.5-5.5 mEq/L. Calcium is important for healthy bones and teeth, as well as for normal muscle and nerve function. Normal blood calcium levels are maintained through the actions
of parathyroid hormone (PTH), your kidneys and intestines. CAUSES: There are many causes of hypocalcemia, these include:

Vitamin D deficiency Chronic renal failure Magnesium deficiency Alcoholism Biphosphonate therapy - drugs used to treat high blood calcium levels or pills used to treat osteoporosis.
46

Certain types of leukemia or blood disorders A complication of chemotherapy, tumor lysis syndrome, occurs when your body breaks down tumor cells rapidly, after chemotherapy. This may cause hypocalcemia, high blood potassium levels, and other electrolyte abnormalities. This is very serious, and if your blood test results indicate you suffer from it, your doctor or health care provider will need to closely monitor you during this time.
Drugs such as diuretics, estrogens replacement therapy, fluorides, glucose, insulin, excessive laxative use, and magnesium may also lead to hypocalcemia.
Certain things in your diet, like caffeine, phosphates (found in soda pop), and certain antibiotics may make it difficult for you to absorb calcium.
Vitamin D, however, helps you to absorb calcium in your body.
SIGNS AND SYMPTOMS:
The most common sign of hypocalcemia is what is called "neuromuscular irritability." Your nerves and muscles, which are directly related to blood calcium levels, may spasm or twitch.
If your blood test results indicate hypocalcemia, you may notice muscle cramps in your legs or your arms.
The symptoms of hypocalcemia you experience may relate to how fast or how slowly the fall in blood calcium levels occur.
o
If you have long-standing low blood calcium levels, you may notice no symptoms of hypocalcemia.
If you have an "acute" or sudden drop in your blood calcium level, you may notice more twitching.
You may notice, with mildly lowered blood calcium levels, numbness and tingling of your fingers and toes.
You may notice that you are depressed, or more irritable if you have mildly low hypocalcemia.
With severely lowered blood calcium levels, you may become confused or disoriented. Your heart muscle may contract irregularly due to the electrolyte disturbance.
47 6. HYPERCALCEMIA CAUSES: Primary hyperparathyroidism is the most common cause of hypercalcemia. It is due to excess PTH release by the parathyroid glands. This excess occurs due to an enlargement of one or more of the parathyroid glands, or a growth (usually not cancer) on one of the glands. Other medical conditions can also cause hypercalcemia:

Adrenal gland failure Being bedbound (or not being able to move) for a long period of time Calcium excess in the diet (called milk-alkali syndrome, usually due to at least 2,000 milligrams of calcium per day)
An inherited condition that affects the body's ability to regulate calcium (familial hypocalciurichypercalcemia)
Hyperthyroidism Kidney failure Medications such as lithium and thiazide diuretics (water pills) Some cancerous tumors (for example, lung cancers, breast cancer) Vitamin D excess (hypervitaminosis D) from diet or inflammatory diseases Hypercalcemia affects less than 1 percent of the population. The widespread ability to
measure blood calcium since the 1960s has improved detection of the condition, and today most patients with hypercalcemia have no symptoms. Women over age 50 are most likely to have hypercalcemia, usually due to primary hyperparathyroidism. SIGNS AND SYMPTOMS: Abdominal:

Constipation Nausea
48

Pain Poor appetite Vomiting
Kidney:

Flank pain Frequent thirst Frequent urination
Muscular:
Muscle twitches Weakness
Psychological:

Apathy Dementia Depression Irritability Memory loss
Skeletal:

Bone pain Bowing of the shoulders Fractures due to disease (pathological fractures) Loss of height Spinal column curvature
7. HYPOMAGNESEMIA Magnesium is present in greatest concentration within the cell and is the second most abundant intracellular cation after potassium. The total body content of magnesium is 2000 mEq. The intracellular concentration of magnesium is 40 mEq/L, while the serum concentration is 1.5Clinical Case Study: Chronic Kidney Disease BSN III-A Group 3 SY 2011-2012
49 2 mEq/L. Most of the body's magnesium is found in bone. Only 1% of the total body magnesium is extracellular. Of this amount, one half is ionized, and 25-30% is protein bound. SIGNS AND SYMPTOMS: The primary clinical findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias. The severity of symptoms is not related directly to the magnesium level. The reference range for serum magnesium level is 1.8-3 mEq/L. Usually, patients become symptomatic at 1.8 mEq/L. However, the physical findings may not be present in all cases. In one study of patients who were severely depleted of magnesium, abnormal physical findings were present in only 2 of 21 patients.
Neuromuscular Irritability
o o o o o
Hyperactive deep tendon reflexes Muscle cramps Muscle fibrillation Trousseau and Chvostek signs Dysarthria and dysphagia from esophageal dysmotility
CNS Hyperexcitability
o o o o
Irritability and combativeness Disorientation Psychosis Ataxia, vertigo, nystagmus, and seizures (at levels <1 mEq/L)
Cardiac arrhythmias that may be caused by hypomagnesemia alone or concomitant hypokalemia result from decreased activity of ATPase.
o o
Paroxysmal atrial and ventricular dysrhythmias Repolarization alternans
Neonates
o o o o
Apnea Weakness Seizures Jitteriness

50 CAUSES: The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses.
GI losses
o
Malabsorption of magnesium in the ileum results in hypomagnesemia. Situations of decreased absorption include malabsorption syndromes (eg, celiac sprue), radiation injury to the bowel, bowel resection, or small bowel bypass.
GI secretions in large amounts may cause hypomagnesemia. Upper GI secretions contain 1 mEq/L of magnesium, while lower GI secretions contain 15 mEq/L of magnesium. Significant losses of magnesium that result in hypomagnesemia may result from chronic diarrhea, laxative abuse, inflammatory bowel disease, or neoplasm.
Malnutrition leads to hypomagnesemia when dietary intake of magnesium is low. Dietary sources include green vegetables, fruits, fish, fresh meat, and cereal. Alcoholics are classically hypomagnesemic in part due to poor nutrition.Diabetic patients who are not receiving magnesium supplements may have dietary deficiencies in magnesium.
Renal losses from primary renal disorders or secondary causes (eg, drugs, hormones, osmotic load) may result in magnesium wasting and subsequent hypomagnesemia.
o
Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys. This condition occurs in the diuretic phase of acute tubular necrosis, postobstructive diuresis, and renal tubular acidosis.
Drugs may cause magnesium wasting.
Diuretics (eg, thiazide, loop diuretics) decrease the renal threshold for magnesium reabsorption in addition to wasting of potassium and calcium.
Cisplatin causes dose-dependent kidney damage in 100% of patients receiving this drug.
Pentamidine and some antibiotics also cause renal magnesium wasting. Fluoride poisoning similarly causes hypomagnesemia.
Endocrine disorders may cause hypomagnesemia.
51
Primary aldosteronism decreases magnesium levels by increasing renal flow.
Hypoparathyroidism and hyperthyroidism may cause renal wasting.
Osmotic diuresis results in magnesium loss in the kidney.
Diabetic patients, especially those with poor glucose control, develop hypomagnesemia from a glucose-induced osmotic diuresis.
Alcoholics become hypomagnesemic partially by an osmotic diuresis from alcohol. Urinary losses have been reported to be 2-3 times control values.
Miscellaneous
o
Extracellular volume expansion, as in cirrhosis or intravenous (IV) fluid administration, may decrease magnesium levels.
Redistribution of magnesium into cells may cause lower magnesium levels. Insulin causes this effect.
o o o
Excessive lactation may create a significant amount of magnesium loss. Hungry bone syndrome may lead to lower serum magnesium concentrations. Pregnant women have been found to be magnesium depleted, especially those women who experience preterm labor.
8. HYPERMAGNESEMIA Magnesium is absorbed in the ileum and excreted in stool and urine. The minimum daily requirement of magnesium is 300-350 mg, or 15 mmol; this amount is easily obtainable with a normal daily intake of fruits, seeds, and vegetables because magnesium is a component of chlorophyll and is present in high concentrations in all green plants. The kidney is the main regulator of magnesium concentrations. Absorption occurs primarily in the proximal tubule and thick ascending limb of the loop of Henle. Hypermagnesemia is a rare electrolyte abnormality because the kidney is very effective in excreting excess magnesium. SIGNS AND SYMPTOMS:
52 Physical findings are related to the serum magnesium levels.
Serum magnesium levels of 3.5-5.0 mEq/L are associated with the following:
o o
Disappearance of deep tendon reflexes Muscle weakness
Serum magnesium levels of 5.0-6.0 mEq/L are related to the following:

o o
Hypotension Vasodilatation
Serum magnesium levels of 8.0-10.0 mEq/L are associated with the following:
o o o
Arrhythmia, including atrial fibrillation Intraventricular conduction delay Flaccid skeletal muscle paralysis
Levels of serum magnesium greater than 10.0 mEq/L are related to the following:
o o o o o
Asystole Heart block Ventilatory failure Stupor or coma Death
Elevated levels of magnesium also are associated with the following:

o o
Delayed thrombin formation Platelet clumping
CAUSES: Most cases of hypermagnesemia are due to iatrogenic interventions and
administration,especially errors in calculating appropriate infusions. Additional causes include the following:
Ingestion of magnesium-containing substances such as vitamins, antacids, or cathartics by patients with chronic renal failure
Acute renal failure (in the absence of dialysis)
53
Excessive intravenous infusions of magnesium in patients being treated for eclampsia, asthma, torsade de pointes, or other cardiac arrhythmias
In neonates, treatment of maternal eclampsia with magnesium, which passes through the placental circulation
Decreased GI elimination and increased GI absorption of magnesium due to intestinal hypomotility from any cause
o o
GI medications that decrease motility, including narcotics and anticholinergics Hypomotility disorders such as bowel obstruction and chronic constipation
Tumor lysis syndrome, by releasing massive amounts of intracellular magnesium Adrenal insufficiency (secondary hypermagnesemia) Rhabdomyolysis, like tumor lysis syndrome, by releasing significant amounts of intracellular magnesium
Milk-alkali syndrome Hypothyroidism Hypoparathyroidism Neoplasm with skeletal muscle involvement Lithium intoxication Extracellular volume contraction, as in diabetic ketoacidosis (DKA)
9. HYPOPHOSPHATEMIA Serum phosphate or phosphorus normally ranges from 2.5-4.5 mg/dL (0.81-1.45 mmol/L) in adults. Hypophosphatemia is defined as mild (2-2.5 mg/dL, or 0.65-0.81 mmol/L), moderate (1-2 mg/dL, or 0.32-0.65 mmol/L), or severe (<1 mg/dL, or 0.32 mmol/L). Mild to moderately severe hypophosphatemia is usually asymptomatic. Major clinical sequelae usually occur only in severe hypophosphatemia. As in the case of other intracellular ions (eg, potassium, magnesium), a decrease in the level of serum phosphate (hypophosphatemia) should be distinguished from a decrease in total body storage of phosphate (phosphate deficiency).
54 SIGNS AND SYMPTOMS:
Muscle weakness is the most common physical finding; careful assessment of motor strength on neurologic examination is critical. Weakness may be subtle or profound and may involve any muscle group.
Diminished respiratory rate and tidal volume may reflect respiratory impairment due to hypophosphatemia; however, tachypnea may be present, an important clue to one of the most common etiologies of hypophosphatemia (respiratory alkalosis).
Hypotension and cardiac compromise due to severe hypophosphatemia is rare. The skin and conjunctivae may be pale secondary to the hemolytic anemia that may complicate hypophosphatemia.
Signs of rhabdomyolysis may be present on extremities. Mental status abnormalities may occur with severe hypophosphatemia, ranging from simple irritability or confusion to florid altered mental status and coma.
CAUSES:
The ED physician is most likely to encounter hypophosphatemia in patients withdrawing from alcohol and in patients undergoing treatment for DKA.
Other risk factors

o o o
Chronic alcoholism Chronic ingestion of phosphate-binding antacids Patients on total parenteral nutrition (TPN) with inadequate phosphate supplementation
Refeeding after prolonged starvation (eg, anorexia nervosa)
Hypophosphatemia may also occur in the setting of thyrotoxic periodic paralysis (TPP). If considering this diagnosis, the presence of hypophosphatemia suggests TPP rather than spontaneous periodic paralysis, in which phosphorus levels are likely to be normal.
55 10. HYPERPHOSPHATEMIA Hyperphosphatemia occurs when the phosphorus load (from GI absorption, exogenous administration, or cellular release) exceeds renal excretion and tissue uptake. Most symptoms and sequelae are due to secondary hypocalcemia. Initial care is aimed at management and correction of the hypocalcemia and its sequelae. Endpoints of therapy include resolution of symptoms and a serum calcium level within the low reference range. Oral phosphate binders are used to decrease the highly efficient GI absorption of phosphorus. Calcium salts are widely used but may produce hypercalcemia. Aluminum salts are effective binders but may induce aluminum toxicity. Newer compounds containing iron or bile acid sequestrants are replacing calcium and aluminum binders. Proximal diuretics are phosphuretic to the same extent they are natriuretic. Acetazolamide is particularly efficient in promoting renal phosphate excretion. SIGNS AND SYMPTOMS: The nervous and cardiovascular systems are most commonly affected.
CNS
o o o o o o o o
Altered mental status Delirium Obtundation Coma Convulsions and seizures Muscle cramping or tetany Neuromuscular hyperexcitability (ie, Chvostek and Trousseau signs) Paresthesias (particularly perioral and distal extremities)
Cardiovascular system
o o
Hypotension and heart failure Prolongation of the QT interval
56
Ocular - Cataracts
CAUSES: Phosphorus balance between intracellular and extracellular compartments and between bone and other tissues may be influenced by many factors. The most common cause of hyperphosphatemia is decreased renal excretion due to renal insufficiency from any cause. All marked elevations of phosphorus involve significant addition of phosphorus to the extracellular compartment, usually with some impairment of renal function.

Renal insufficiency (acute or chronic) Medications - Liposomal amphotericin B Increased catabolism or cellular injury
o o o o o o o o o o
Rhabdomyolysis Trauma, burns, crush injuries, shock Exhaustive exercise Prolonged immobilization Heat-related illnesses Malignant hyperthermia Hypothermia Massive hemolysis Severe infections Ischemic bowel
Endocrinopathies
o o o o o o
Hypoparathyroidism Pseudohypoparathyroidism Abnormal parathyroid hormone Acromegaly and other causes of growth hormone excess Thyrotoxicosis Glucocorticoid withdrawal or deficiency
Poisoning, excessive intake or administration

o
Bisphosphonate therapy
57
o o
Vitamin D intoxication or other causes of increased vitamin D (sarcoidosis) Ingestion or administration of phosphate salts (eg, oral/rectal laxatives, enemas, intravenous phosphate)
o o o o
Hyperalimentation (including lipid administration) White phosphorous burns Milk-alkali syndrome Transfusion of outdated blood
Neoplasms
o o o o
Leukemia Lymphoma Bone tumors Tumor lysis after chemotherapy
Acidosis
o o o o
Acute respiratory acidosis Lactic acidosis Diabetic ketoacidosis Alcoholic ketoacidosis
Alkalosis Miscellaneous
o o o o
Tumoralcalcinosis Cortical hyperostosis Syndrome of familial intermittent hyperphosphatemia Hyperbilirubinemia (controversial as cause)
E. ACID-BASE IMBALANCES 1. RESPIRATORY ACIDOSIS Respiratory acidosis is a clinical disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the partial arterial pressure of carbon dioxide (PaCO2). The normal reference range for PaCO2 is 36-44 mm Hg.
58 Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3-)/PaCO2, decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the lungs is less than the production of carbon dioxide in the tissues. Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH <7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate value (ie, >30 mm Hg). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, an inability to ventilate adequately owing to a neuromuscular disease (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barr syndrome, muscular
dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD). Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragmatic function due to fatigue and hyperinflation. Chronic respiratory acidosis also may be secondary to obesity-hypoventilation syndrome (ie, pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities. Lung diseases that primarily cause abnormalities in alveolar gas exchange usually do not cause hypoventilation; however, they tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue is present.
59 2. RESPIRATORY ALKALOSIS Respiratory alkalosis is a primary decrease in Pco2 with or without compensatory decrease in HCO3; pH may be high or near normal. Cause is an increase in respiratory rate or volume (hyperventilation) or both. Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes light-headedness, confusion, paresthesias, cramps, and syncope. Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and serum electrolyte measurements. Treatment is directed at the cause. Etiology: Respiratory alkalosis is a primary decrease in Pco2 (hypocapnia) from an increase in respiratory rate or volume (hyperventilation), or both. Ventilation increase occurs most often as a physiologic response to hypoxia, metabolic acidosis, and increased metabolic demands (eg, fever), and as such is present in many serious conditions. In addition, pain and anxiety and some CNS disorders can increase respirations without a physiologic need. Respiratory alkalosis can be acute or chronic. Distinction is based on the degree of metabolic compensation; excess HCO3 is buffered by extracellular hydrogen ion (H+) within minutes, but more significant compensation occurs over 2 to 3 days as the kidneys decrease H+ excretion. 3. METABOLIC ALKALOSIS Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration. This occurs as a consequence of a loss of H+ from the body or a gain in HCO3-. In its pure form, it manifests as alkalemia (pH >7.40). As a compensatory mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur. The first clue to metabolic alkalosis is often an elevated bicarbonate concentration that is observed when serum electrolyte measurements are obtained. Remember that an elevated serum bicarbonate concentration may also be observed as a compensatory response to primary respiratory acidosis. However, a bicarbonate concentration greater than 35 mEq/L is almost always caused by metabolic alkalosis.
60 4. METABOLIC ACIDOSIS Metabolic acidosis is primary reduction in HCO3, typically with compensatory reduction in Pco2; pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3 loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV NaHCO3 may be indicated when pH is very low.Metabolic acidosis is acid accumulation from increased acid production or acid ingestion; decreased acid excretion; or GI or renal HCO3 loss. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation.

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1 I. PERSONAL DATA Name: Mr. Bean Address: Brgy.

2 II. FAMILY BACKGROUND

BUDGETARY ALLOCATIONS OF THE FAMILY

Mr. Cabbage (*)

10 IV. ANATOMY AND PHYSIOLOGY

mainly by excreting hydrogen ions and reabsorbing bicarbonate ions as needed.

B. CHRONIC KIDNEY DISEASE

A family history of polycystic kidney disease

Nerve problems: Numbness or tingling in your toes or fingers is a symptom of CKD.

Limiting potassium to 2000 to 3000 mg or bases on individual requirements

Gastrointestinal or Integument Loss

CAUSES: Hyperkalemia has many causes, including the following:

Other possible symptoms include:

Vitamin D, however, helps you to absorb calcium in your body.

SIGNS AND SYMPTOMS:

Pain Poor appetite Vomiting

Flank pain Frequent thirst Frequent urination

Muscle twitches Weakness

Apathy Dementia Depression Irritability Memory loss

Paroxysmal atrial and ventricular dysrhythmias Repolarization alternans

Apnea Weakness Seizures Jitteriness

Drugs may cause magnesium wasting.

Endocrine disorders may cause hypomagnesemia.

Primary aldosteronism decreases magnesium levels by increasing renal flow.

Hypoparathyroidism and hyperthyroidism may cause renal wasting.

Osmotic diuresis results in magnesium loss in the kidney.

52 Physical findings are related to the serum magnesium levels.

Disappearance of deep tendon reflexes Muscle weakness

Serum magnesium levels of 5.0-6.0 mEq/L are related to the following:

Asystole Heart block Ventilatory failure Stupor or coma Death

Elevated levels of magnesium also are associated with the following:

Delayed thrombin formation Platelet clumping

CAUSES: Most cases of hypermagnesemia are due to iatrogenic interventions and

Acute renal failure (in the absence of dialysis)

54 SIGNS AND SYMPTOMS:

Other risk factors

Refeeding after prolonged starvation (eg, anorexia nervosa)

Hypotension and heart failure Prolongation of the QT interval

Poisoning, excessive intake or administration

Leukemia Lymphoma Bone tumors Tumor lysis after chemotherapy

Acute respiratory acidosis Lactic acidosis Diabetic ketoacidosis Alcoholic ketoacidosis

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