Chapter 1 Renal Function

When presented with patients with differing systemic blood pressure, students will explain how the
glomerulus can maintain GFR.
The kidney protects its GFR over a wide range of renal perfusion pressures. This process is called
autoregulation. The kidney accomplishes this because the glomerular capillary is located between an afferent
and an efferent arteriole and by dilating and constricting each separately it can control the pressure for filtration in
the glomerulus.
In situations where CF !olume is abnormal, students will explain the direction of change in "C# $aCl %
&'( re)absorption.
Salt and water are freely filtered at the glomerulus. The majority of Nal is reabsorbed isotonically with water in
the !T. The percent re"absorbed is variable and controlled by starling forces in the peritubular capillary and
depends on #F volume. $hen the kidney perceives a low state of #F volume the percent re"absorbed may be
as high as %&'. $hen there is e(cess #F volume this percent falls to )*'.
Gi!en a case history of a patient with abnormal serum potassium concentration, students will list the
factors causing increased * excretion in the urine.
+ is freely filtered and ,**' re"absorbed in the !T. The amount present in the final urine is determined almost
entirely by secretion into the distal parts of the nephron. Factors that increase + secretion are aldosterone-
alkalosis- high distal sodium delivery rates- and the presence of a non"absorbable anion. .acetoacetate- penicillin/
In patients with acidosis, students will be able to describe the difference between renal bicarbonate
reclamation and bicarbonate regeneration.
0icarb reclamation occurs in the !T. 1n the !T all the filtered 234 is reclaimed. The tubule secretes and 25
which combines with the filtered Na234 resulting in Na 5 2634. The Na is re"absorbed in e(change for the
secreted 25. The 2634 dissociates into 263 5 36 because of carbonic anhydrase in brush border. 263 and
36 are then absorbed into the cell and converted back to 2634 and ultimately 25 and 234. Normally all the
filtered 234 is re"absorbed by the end of the !T.
0icarb regeneration occurs in the 7T. 1n the 7T there is no 8 in the tubular lumen- and under normal
circumstances- no Na234. 1n this area- the urine contains weak acids .Na2S39- Na2!39/ which are
converted to strong acids by joining with a secreted 25 ion. 8lso- ammonia is secreted by the tubule and used to
trap 25 ions in the urine. #ach time a 25 is secreted into the urine- a 234 is secreted into the peritubular blood
and Na is re"absorbed. Thus 7T new 234 is generated and returned to the systemic circulation.
Gi!en a case history of a patient with an abnormal serum calcium, students will be able to list the ma+or
factors controlling serum calcium homeostasis.
The bulk of filtered calcium is re"absorbed in the !T in parallel with sodium. Factors that alter Na re"absorption
also alter calcium re"absorption in the same manner. Separation of sodium and calcium re"absorption occurs in
the distal nephron where !T2 increases a re"absorption and decreases phosphate re"absorption. !T2 does not
affect sodium re"absorption.
Chapter ' ,ymptoms and ,igns and Renal Function #ests
When presented with the results of a patients urinalysis the student will be able to interpret the features
that would suggest the presence of a glomerular disease or tubulointerstitial disease and describe what
further tests would be re-uired to confirm the diagnosis.
1n glomerular disease it is almost universal that patients will have significant hypertension. 2ypertension is
primarily caused by salt and water retention as the kidneys fail. 1t may also be caused by areas of renal ischemia
leading to elaboration of renin. Those patients with tubulo"interstitial disease will have significant renal failure but
no hypertension and have salt wasting rather that retention. 3ther tests that would be useful- 0:N;reatinine-
:rine 3smolality and :rinalysis looking for protein and R0 casts.
Gi!en the results of the serum ./$ interpret the possible cause of an ele!ation of urea and explain the
underlying mechanism in!ol!ed.
:rea is the end product of protein metabolism. 7ietary or endogenous body protein is broken down by the liver to
urea which is removed from the body via glomerular filtration. The serum urea level is not merely a reflection of
the GFR but is also influenced by protein breakdown- liver metabolism- GFR- and the percent of tubular urea re"
absorption. 1ncreased 0:N can occur from decreased GFR- increased protein catabolism .0urns- G1 0leeds-
Sepsis- and
Steroid Treatment/- increased tubular re"absorption .<olume ontraction/ and increased dietary protein intake.
Gi!e the results of serum creatinine explain the relationship between GFR and serum creatinine and be
able to explain the important !ariables that effect the interpretation of the serum creatinine and creatinine
clearance as a measure of GFR.
reatinine is generated from muscle and thus its production is usually constant for any given individual muscle
mass. 1t is not metaboli=ed and is freely filtered at the glomerulus. reatinine is used as and inde( or GFR.
#ach doubling of the serum creatinine means that the GFR has decreased by &*'. >uscle mass- creatinine
production and GFR fall with age thus the serum creatinine stays the same as we age but it reflects a lower GFR.
reatinine learance is based on collecting urine over a fi(ed time period. 1t is a slight overestimation of the true
GFR because of the addition or secreted creatinine to the calculation. 1n advanced renal failure .GFR ?6*ml;min/
creatinine overestimated GFR by as much as &*' due to increased secretion. 7uring the 69 hours the creatinine
concentration must not fluctuate because this will give an inaccurate result.
Gi!en their results of the serum ./$ and creatinine the student will be able to pro!ide a differential
diagnosis of the possible causes of an ele!ated ./$0Creatinine ratio and be able to explain the
mechanism in!ol!ed in each possibility.
Normal 0:N;reatinine ratio is appro(imately ,*@,. 1n states of volume contraction- the percent of urea re"
absorbed by the kidney increases along with sodium re"absorption. This causes the serum urea to increase but
the serum creatinine remains stable since GFR is autoregulated and creatinine handling by the tubule is
unchanged. Thus- the 0:N to creatinine ratio increases A ,*@,. The recognition of this change allows one to
recogni=e patients with #F volume contraction.
In the in!estigation of Renal cyst, .ladder tumor, /reteric stone the student will be able to list the
ad!antages and ris1s of !arious renal imaging techni-ues.
Renal Ultrasound
Gives info about kidney si=e- presence of cysts or tumors- obstruction or stones. This test is an e(cellent
screening test and the one that should be used first in the investigation of most patients with kidney disease since
it gives the most info at the least risk and cost
KUB
This is a routine ("ray of the abdomen. 1t can be used to assess the kidney si=e and will show %*' of renal
stones. :ric acid stones are not radio"opaBue and therefore will not be detected.
Radionuclide Scan
:ses radioactive material linked to a carrier. 1t is a good screening test for renal blood flow.
Intravenous Pyelogram (IVP)
Some physicians feel the 1<! is best for evaluating patients with recurrent :T1Cs. ontrast agents may cause an
acute deterioration in renal function. 1t is primarily used in the urologic investigations of hematuria- renal calculi
and neoplasms.
Computerized Tomograpy (CT)
ontrast material carries same risk as 1<!. 1t is useful to separate cystic from solid lesions as well as look at
causes of ureteric obstruction by disease processes in the retroperitoneum.
!rteriograpy
:ses contrast- shows blood vessels- it is used to look for renal artery stenosis and tumor vasculature in solid
masses.
Retrograde Pyelograpy
:ses contrast but only in the collecting system. 1t reBuires cystoscopy and is used to look for tumors of stones in
the collecting system and for causes of obstruction.
In a patient re-uiring renal biopsy the student will be able to explain the indications and potential ris1s of
renal biopsy.
Renal 0( is used primarily as an investigation for patients with suspected glomerular disease. 1t is occasionally
used in investigation of patients with une(plained renal failure with normal si=ed kidneys. omplications are
primarily due to hemorrhage. ontraindicated in single kidney and coagulation disorder patients.
Chapter 2 Chronic *idney 3isease and &ypertension
When faced with a patient with ele!ated blood pressure describe the ma+or differences between the
biochemical findings of patients with classic reno!ascular hypertension !s. those with renal artery
stenosis. #he student will be able to describe the two ma+or mechanisms underlying the basic
physiology of hypertension.
0lood pressure is determined by the volume of blood in the arterial tree and the capacity of that tree to hold that
volume. .0!D3 ( T!R/ The kidney adjusts both parameters of 0!. The T!R is influenced by the renin
angiotensin pathway and 3 by the kidneys ability to concentrate and dilute the urine. %&' of cases of
hypertension are idiopathic but some investigators argue that the kidney is the underlying problem in all cases of
chronic hypertension. 1n patients with renal artery stenosis there is hypertension caused by high renins-
angiotensin and aldosterone.
Gi!en a patient with microalbuminuria the student will be able to gi!e the most common causes and list
the li1ely conse-uences.
!roteinuria is another marker of renal damage. There is a relationship between increasing levels of albuminuria
and the level of blood pressure control. <ery early stages of proteinuria can be detected by looking at albumin
e(cretion in patients at risk. .diabetics- hypertensives- and < disease/ Eow levels of albumin e(cretion are called
microalbuminuria and the finding of microalbuminuria predicts those who are at risk of developing progressive
renal failure.
>icroalbuminuria 4*"4**mg;day
!roteinuria A4**mg;day
Gi!en clinical and radiological data indicating renal in+ury the student will be able to list the stages of
Chronic *idney disease.
hronic +idney disease is defined as any kidney disease that lasts greater than 4 months and is manifest by
either abnormalities detected on urinalysis or urinary tract imaging or causing a decrease in GFR. lassified
according to stages.
Stage "
+idney 7isease .abnormal blood- urine- or anatomy/ with normal GFR
Stage #
+idney disease with mild decrease in GFR )*"F%ml;min
Stage $
+idney disease with moderate decrease in GFR 4*"&%ml;min
Stage %
+idney disease with severe decrease in GFR ,&"6%ml;min
Stage &
Renal Failure GFR ? ,& ml;min
Gi!en a patient with chronic renal disease the student will be able to list the common causes of
progressi!e renal in+ury and the ma+or strategies to pre!ent progressi!e renal in+ury and renal failure.
'lomerular (yper)iltration
8s renal function is lost- the kidney adapts by increasing the amount of filtrate processed by the remaining healthy
nephrons. This adaptation leads to endothelial injury- release of cytokines- detachment of epithelial cells causing
glomerular sclerosis and more nephron loss
Systemic (ypertension
Systemic hypertension leads to macrovascular disease and hastens the deterioration of renal function because
afferent arteriolar dilatation leads to increased glomerular pressure leading to damage and fibrosis.
(yperlipidemia
2yperlipidemia contributes to macrovascular disease and hastens renal deterioration and < complications.
(yperpospatemia
7ue to renal impairment there is an elevated phosphate which leads to calcium phosphorus product causing
calcium precipitation in blood vessels and damaged tissues. This further aggravates macrovascular disease and
progressive renal scarring.
Chapter 4 3isorders of ,alt and Water Regulation
When presented with a patients electrolytes, the student will be able to describe the most appropriate
maneu!er to assess total body sodium content, the body fluid compartments and the forces go!erning
mo!ement of fluid and solutes between each compartment.
.T0$ D ,;4 #F 5 6;4 1F/ Sodium is confined almost totally to the #F space and since water moves freely
from the 1F- whenever #F is raised it is because of the sodium content. The diagnosis of total sodium content
can be done by doing a physical e(am. Sodium content is high in patients with elevated jugular venous pressure-
edema and ascites. Sodium content is low in patients with dry mucous membranes- orthostatic hypotension- and
no increase in G<!.
Forces pushing fluid from the capillary to interstitial fluid are the capillary hydrostatic pressure and the tissue
oncotic pressure. Forces pushing fluid from the interstitial fluid to capillary are tissue hydrostatic pressure and
capillary oncotic pressure.
In a patient with generali5ed edema students will list the three ma+or causes of generali5ed edema and the
changes in starling forces leading to the edema of !arious etiologies.
>ovement of fluid from the intravascular compartment to the interstitial space may be caused by too high an
intravascular hydrostatic pressure or too low an intravascular oncotic pressure.
Cardiovascular
2F with back up of venous hydrostatic pressure leads to impaired venous return. 1t also leads to decreased 3
causing salt and water retention. 0oth these processes lead to edema formation.
*iver
2epatic Fibrosis and failure of the liver to synthesi=e plasma proteins leads to hepatic venous outflow block .portal
hypertension/ and decreased intravascular oncotic pressure. Together they lead to development of acites and
later leg edema develops
Kidney
Glomerular disease leads to albuminuria which decreases intravascular oncotic pressure leading to edema. The
edema is typically seen uniformly throughout the body.
In patient !olume contraction students will be able to choose from a list of I6 solutions, the most
appropriate one to use in different states of CF !olume contraction.
'lucose and +ater (,&+)
&' de(trose in water is isotonic to #F and is eBuivalent to giving pure water to the patient since the glucose is
metaboli=ed leaving pure water behind. 1t is distributed in T0$.
Saline
.%' Nal in water is called normal saline. 1t is isotonic with respect to #F and therefore it distributes in the #F
only
!l-umin.plasma.-lood
These protein rich fluids distribute into the plasma volume only.
Gi!en a set of serum blood !alues students will be able to calculate the serum osmolality.
3smolality D 6HSerum NaI 5 0:N;6.F 5 Glucose;,F
8lmost all the osmolality of the #F is created by the serum sodium- therefore changes in serum sodium
concentration reflect a breakdown in the bodyCs osmotic regulatory system.
In a patient with an abnormal serum osmolality students will list the three factors that control serum
osmolality and explain their role.
Tirst
8nything that increases osmolality causes increase in thirst.
!,( Secretion
8nything that increases osmolality will increase 872 secretion. 872 increases renal tubular permeability to water
causing greater water re"absorption and a more concentrated urine.
Renal Concentrating and ,iluting /ecanisms
The kidney will alter its re"absorption or e(cretion of water to ensure that the osmolality stays within normal range.
In a patient with a low serum sodium students will describe one clinical condition where hyponatriemia
with hyperosmolality is commonly seen and explain the pathophysiology.
This condition is seen in states of hyperglycemia. Since glucose is osmotically active- it draws water from the 1F
to the #F and dilutes the Na. $hen you measure osmolality- you measure the number of solutes .glucose 5 Na/
in #F water- therefore- the osmolality is high but the serum Na is low.
In a patient with low serum sodium students will be able to list at least two conditions where true
hyponatriemia is associated with increased CF !olume.
Seen in edema states- 2F- liver disease with ascites- and nephrotic syndrome. 1n these conditions- volume
receptors in the atria and the large vessels in the chest sense and low circulating volume witch causes 872
secretion and renal water retention leading to hyponatriemia.
In a patient with high serum sodium students will be able to list one condition where hypernatremia with
decreased CF !olume may be seen.
This is the most common clinical condition. These patients have lost salt and water but more water than salt.
>ost body fluids are hypotonic to #F so that patients lose more water than salt.
Chapter 7 3isorders of "otassium Concentration
When presented with a report of a patient8s electrolytes students will be able to describe the ma+or
potassium containing compartments, their relati!e si5es and list three factors that go!ern the mo!ement
of * into the cells.
>ost + is intracellular .,&* m#B;E/ and only 4.&"&.6 m#B;E in in e(tracellular fluid. The large difference in #F
and 1F + concentrations is maintained by ion pumps that pump + into cells in e(change for Na. Factors that
enhance uptake of + by cells is insulin- alkalosis- and periodic paralysis.
In a patient with a low serum * students will be able to describe two diagnoses associated with
hypo1alemia and a low urine *.
7iarrhea or significant bowel mucus loss can lead to hypokalemia and low urine +.
Gi!en a set of serum electrolytes students will be able to recogni5e one clinical situation with
hypo1alemia, high urine * and acidosis.
Renal Tubular 8cidosis .RT8/ is an inability to conserve bicarbonate or e(crete 25. This leads to acidosis and
increased use of Na"+ e(change to accomplish Na re"absorption. This leads to hypokalemia and acidosis- an
unusual clinical combination.
Gi!en a set of blood gases and electrolytes students will be able to list two diagnoses associated with
hypo1alemia, high urine * and al1alosis.
2yperaldosteronism causes an increase e(change of Na"+ and Na"2. This leads to + loss and alkalosis.
2yperaldosteronism can be primary or secondary.
In a patient with high serum * students will be able to list three mechanisms which may lead to
hyper1alemia.
Pseudo.0actitious (yper1alemia
This a test tube phenomenon. 1t is seen in patients with $0 counts over &**-*** or platelet counts greater than
J&*-***. These cells release + into the collection tube when the blood coagulates resulting in a high measured +
in the tube- but there is no hyperkalemia in the patient.
Si)ts2K moves )rom IC0 to 3C0
8cidosis- 7iabetes >ellitus- 7igitalis into(ication- and ell Necrosis.
*ac1 o) K e4cretion
Renal Failure- !otassium Sparing diuretics- and 8ddisonCs 7isease.
Chapter 9 :cid).ase 3isturbances
When presented with a patient with metabolic acidosis students will be able to calculate the anion gap
and describe its use in differential diagnosis.
>etabolic acidosis may be cause either by a gain of acid .234 consumption/ or alkali loss .234 loss/ 1n both
circumstance- the serum 234 falls. 1n situations where there is pure gain of organic acid- there is a fall in
234- and thus- the anion gap increases. 1n situation of alkali loss- l is retained as 234 is lost- and therefore-
the anion gap does not change. 1t is through the calculation that one can classify the different types of metabolic
acidosis.
The 8nion Gap@ Na " Hl " 234I
Increases in te !nion 'ap
+etoacidosis- Eactic 8cidosis- :remic 8cidosis- 1nto(ications
5o2Cange !nion 'ap
Renal Tubular 8cidosis- 7iarrhea- and 2yperailementation
When presented with a patient acid)base disturbance students will be able to recogni5e the typical blood
gases of a simple metabolic acidosis.
The lungs rapidly compensate by blowing off 36. For each ,m#B;E decrease in 234- the p36 should
decrease ,mm2g.
Serum p2 down. p36 down- and 234 down.
When presented with a patient acid)base disturbance students will be able to recogni5e the typical blood
gases of a simple metabolic al1alosis.
The e(pected respiratory response is to decrease respiration. .increased p36/ This response is variable and
usually small- rarely leading to a p36 greater than &&mm2g.
Serum p2 up- p36 up- and 234 up.
When presented with a patient !omiting students will be able to explain the type of acid)base disturbance
li1ely to occur and its pathophysiology.
:pper G1 losses contain 2E- NaE- and volume. The loss of 2l leads to metabolic alkalosis. The Nal and
volume loss leads to #F volume contraction. This volume contraction maintains the alkalosis by stimulating
renal retention of Na. 0ecause of depletion of + and l only Na " 25 e(change remains perpetuating the
alkalosis.
When presented with a patient with hypertension, hypo1alemia and al1alosis students will be able to list
the possible mechanisms.
!atients with primary and secondary hyperaldosteronism have e(cess 8ldosterone with increases Na " + and Na "
2 e(change- and the + and 2 loss leads to hypokalemia and metabolic alkalosis. The increase Na absorption will
also lead to volume e(pansion and hypertension.
When presented with a patient with respiratory acidosis students will describe the type and direction of
expected compensation.
Respiratory acidosis is due to an increase in p36 secondary to 3!7- hypoventilation- or etc. 7uring the first
69 hours of respiratory acidosis- the kidney does not have time to retain 234 to any significant degree. There is
a small increase in 234 due to buffering of some 25 by intracellular proteins. This is only about an increase of
,m#B;E for every ,*mm2g increase in 36. 8fter J6 hours- the kidney can retain more 234. The 234
increases 4"9 m#B;E for every ,*mm2g increase in p36.
When gi!en a !alue for urine chloride in a patient with metabolic al1alosis students will be able to
determine the diagnostic meaning of this !alue in the diagnosis of the problem.
1f the :rine l is low R( with Nal and +l and if urine l is high look for mineralcorticoid e(cess.
Chapter ; 3iabetic $ephropathy
(b+ecti!es<
Chapter = :cute Renal Failure
When presented with a patient history the student will be able to recogni5e three features of the illness
that would suggest a diagnosis of renal failure and explain their pathophysiology.
Pre2Renal
Situations in which there is a decrease in renal perfusion. These can range from shock- heart failure- or
dehydration to obstruction of the renal artery. Eook for low plasma volume- low .3.- low plasma albumin-
vasodilatation- and renal artery stenosis.
Post2Renal26-struction o) te ureters or -ladder outlet
Suspect these causes in all patients but especially the patient with pain- no urine- or gross hematuria. Eook for
bladder outlet obstruction or bilateral ureteric obstruction.
Renal
8ll conditions where the kidney is diseased. The causes may be pre"glomerular- glomerular- interstitial or post"
glomerular. 1n the majority of patients with acute renal failure the commonest cause is acute tubular necrosis.
Gi!en the appropriate laboratory !alues the student will be able to determine the appropriate test to
distinguish between the three ma+or types of acute renal failure and discuss the rationale of each.
BU5.Creatinine Ratio
1n pre"renal conditions leading to oliguria- the amount of urea re"absorbed is increased. This leads to increased
urea without a change in serum creatinine because GFR is maintained by autoregulation. Thus- the urea to
creatinine ratio is increased beyond ,*@, in pre"renal causes of oliguria. 1n 8TN- GFR is decreased and creatinine
increases along with 0:N keeping the ratio ,*@, or less.
Urine 3lectrolytes and 6smolality
1f oliguria is due to normal renal concentration the urine will be of high osmolality. .greater than )**/ The urine
sodium concentration will be very low since the kidney concentrates urine by removing Nal and leaving behind
only that amount of 263 necessary to e(crete waste products
Urine to Plasma Ratios
1n pre"renal oliguria the u;p cr. will be 6**@, while in renal oliguria u;p cr. will be ,*@,.
In a patient with acute renal failure the student will be able to identify and describe the management of
those elements of the patient8s disease that re-uire immediate attention and explain the rationale and
mode of action of each therapeutic maneu!er.
!ssess 3C0 Volume 7 Correct any ,e)icits
The first action is to ensure that renal perfusion is adeBuate. $hen in doubt- give e(tra Nal and measure <!
or pulmonary capillary wedge pressure.
Use o) ,iuretics
3nce you are sure #F volume is normal- a trial of diuretics is warranted. Giving >annitol or Furosemide may
flush out obstruction tubular cell debris and shifts blood flow toward the corte(.
Use o) ,opamine
1nfusions of low dose dopamine increase both blood pressure and renal blood flow and thus may protect against
8TN.
Calcium Cannel Bloc1ers
alcium influ( is associated with the cellular damage of 8TN.
5aturetic Peptides
,ialysis
1f all else fails- one usually reBuires dialysis to support the patient until renal function returns.
Gi!en a patient with a renal cause of acute renal failure the student will be able to list the possible renal
causes of acute renal failure and explain the pathophysiology of each.
8cute Tubular Necrosis- 1nterstitial Nephritis- and 8cute Glomerulonephritis.
Chapter > Chronic Renal Failure
When presented with a patient history, the student will be able to list three groups of patients who are at
ris1 for the de!elopment of chronic renal failure.
hronic renal failure refers to renal failure that progresses slowly over months to years. The symptoms of RF
are often minimal until a significant proportion of the renal function is lost. .F*'/ The diagnosis is largely based
on a good history and physical looking for diseases commonly associated with RF or drugs that impair renal
function. This should be followed by a urinalysis looking for infection- porteinuria- blood and casts. Finally-
assessment of kidney si=e by ultrasound. Three groups of patients who are at risk are diabetics- hypertensives-
and progressive organ failure patients.
Gi!en a case history the student will be able to list fi!e features for the illness that would suggest a
diagnosis of chronic renal failure and explain their pathophysiology.
The accumulation of wastes- disordered homeostasis and endocrine synthetic failure leads to a host of symptoms.
"Retention of wastes urea- creatinine- Nal- 263- +5
"<olume regulation@glomerular diseases tend to lead to salt and water retention. Some tubular and interstitial
diseases cause e(cessive salt and water loss.
"8cidosis from failure to generate bicarbonate and secrete 25 ions
"2yperkalemia
"2yperphosphatemia
In a patient with an ele!ated creatinine the student will be able to determine the appropriate test to
distinguish acute from chronic renal failure and discuss the rationale of each.
!rior known increase in serum creatinine is most reliable evidence of RF. 8lso renal sonogram showing small
kidneys has a high association with RF. Eook for chronic symptoms or signs like fatigue- nausea- pruritus-
nocturia and hypertension.
In a patient with e!idence of progressi!e renal damage the student will be able to identify and describe
the management of those elements of the patient8s disease that are most li1ely to slow the progression of
renal failure.
,ietary Protein Restriction
The majority function of the kidney is to eliminate the end products of protein metabolism. 8s nephrons are lost
the remaining nephrons increase their filtration to compensate. This leads to glomerular hyperfiltration and
hypertension both of which may lead to glomerular scarring and further loss of function. 0y limiting protein in the
diet- less waste is generated and the need for hyperfiltration is lessened.
Blood Pressure Control
The majority of patients with chronic renal failure develop hypertension. 2ypertension causes vascular damage
including nephrosclerosis in the kidney. 8# inhibitors are drugs of choice to protect renal function and alcium
channel blockers may be a good substitute.
!void ,rug To4icity
>any drugs are eliminated via the kidneys. They reBuire a change in dosage in patients with renal failure.
Pospate Control
8 fall in GFR impairs phosphate e(cretion. 2igh levels of serum phosphate combine with calcium and deposit in
tissues including blood vessels and the kidney.
Gi!en a case history and laboratory data of a patient with renal failure the student will be able to identify
those elements of the disease that re-uire immediate dialysis.
1n general- dialysis is reBuired once the GFR is less than &",*' of normal " usually a creatinine over ,*mg;dl or a
0:N A,** mg;dl. Some absolute indications for dialysis are uremic coma or sei=ures- uremic pericarditis- uremic
neuropathy- and severe acidosis- hyperkalemia- or fluid overload not manageable by conservative therapy.
Chapter 1? #ubulo)Interstitial 3isease
When presented with a patient with renal dysfunction the student will be able to describe the typical
expected findings both clinically and from the laboratory that would distinguish the patient with
glomerular disease from one who has tubulointerstitial disease.
!resentation of acute tubulointerstitial nephritis varies- but 8RF- with or without oliguria- temporally related to an
offending drug or infection is typical. Fever occurs in most cases and may be accompanied by an urticarial rash.
The urine sediment usually reveals $0Cs and R0Cs. !roteinuria is usually minimal. Renal biopsy is the only
definitive method for diagnosis. Glomerular disease may be primary or secondary to systemic disease. The
major pathogenic categories are inflammatory .nephritic syndrome/ and hemodynamic .nephrotic syndrome/.
Serological markers such as anti"G0> and 8N8 suggest a specific glomerular disease or at least help narrowing
the differential.
In a patient with cystic disease of the 1idney students will describe the genetic inheritance of adult
polycystic 1idney disease.
8utosomal dominant inheritance"cysts develop progressively- patients present with slowly progressive renal
failure in their 4*Cs to &*Cs- with large cysts throughout both kidneys often with associated hypertension.
Gi!en a case history of a patient with acute renal failure related to drug allergy students will list the
typical renal lesion li1ely to be seen on renal biopsy in a patient with a rash and acute renal failure.
!atients with acute interstitial nephritis typically suffer from acute renal failure due to an allergic reaction to drugs.
They usually have other manifestations of allergy including fever- rash- and eosinophilia. 7iagnosis depends on
finding the urine full of $0- many of which are eosinophils. Gallium scanning or the kidneyCs is often positive
due to the intense interstitial inflammatory infiltrate which is evident on renal biopsy as well. 7rugs commonly
associate with this syndrome are the penicillins- sulfonamides- and NS817s.
Gi!en the case history of a patient with chronic renal insufficiency students will be able to describe two
tubulointerstitial diseases leading to chronic renal failure.
Cystic ,iseases" 8dult polycystic- >edullary ystic- and >edullary Sponge
Cronic Interstitial 5epritis patients present with progressive renal failure due to interstitial fibrosis and renal
tubular defects. 1nterstitial fibrosis leads to renal failure often associated with renal tubular acidosis or salt
wasting." !apillary necrosis- 8nalgesic nephropathy- >yeloma kidney- :ric acid nephropathy- Eithium into(ication-
cyclosporine to(icity- and heavy metal e(posure.
In a patient with acute renal failure students will be able to list two mechanisms leading to :#$.
Severe ischemic or to(ic insults to the kidney result in tubular damage which- when sufficiently severe may result
in tubular necrosis. There is a marked decrease in cortical renal blood flow and a marked decrease in GFR. This
decrease in GFR may be maintained by intrarenal elaboration of renin. There is also evidence of leakage of
tubular fluid through the damaged tubular epithelium into the peritubular capillaries.
Gi!e the appropriate lab data students will be able to recogni5e the features suggesti!e of renal tubular
disease and list two tubular diseases causing abnormalities of regulation.
Renal Tubular 8cidosis and Nephrogenic 7iabetes 1nsipidus
Chapter 11 /rinary #ract Infection
Gi!en a patient with dysuria the student will be able to describe the features that suggest a /#I and how
to distinguish upper from lower tract infection.
The clinical presentation of :T1 is usually with complaints of burning on urination .dysuria/ and other symptoms of
bladder irritation including urinary freBuency. Symptoms of upper tract infection include flank pain- nausea-
vomiting and fever. Fever is the only reliable sign of upper tract involvement.
Gi!en a case history identify the !arious factors that might predispose to /#I.
Female- 1nfants of both se(es- and older males with prostatic hypertrophy
Gi!e the case history and urine culture and sensiti!ity results students will be able to distinguish the
pattern of relapse from re)infection in a patient with recurrent /#I8s.
Re2In)ection pattern
Recurrent :T1 with different organisms with different antibiotic sensitivities occurring at intervals more that )
weeks apart. These represent new- repeated- lower- urinary tract infections. They are an inconvenience and
uncomfortable but do not lead to renal damage.
Relapse pattern
Recurrent :T1Cs with the same organism with the same antibiotic sensitivity occurring less than si( weeks apart.
They represent inadeBuately treated urinary tract infections- and if left untreated can lead to permanent renal
damage in children. This pattern often indicates the presence of abnormalities of the urinary tract anatomy of
function.
Gi!en the details of !arious patients with /#Is the student will be able to describe the appropriate
approach to diagnosis and management for patients of differing sex and age.
1n children a urinalysis should be done. 1f pyruia is found then a midsteam urine culture for sensitivity should be
done. 8ll young boys and girls under three years of age- reBuire and 1<! and voiding cystoureterogram .<:/ to
evaluate for upper tract disease and reflu(.
1n all girls over three who have pyelonephritis or women with two or more episodes of cystitis should be screened
with an ultrasound after their second episode and followed up with a 1<! and <: in those where ultrasound is
abnormal. !g. ,*& in notes for management.
Chapter 1' Calcium @etabolism and Renal Calculi
When presented with a patient with renal colic the student will be able to list three common causes of
renal calculi.
Numerous factors contribute to stone formation. >ost interest has centered around crystalloid concentration of
the urine. Factors which promote crystalli=ation are reduced urine volume- e(cess urine acidity .uric acid/ or
alkalinity .struvite/- deficiency or inhibitors of calcification- and infection or stasis. Recent evidence suggests that
dietary factors as an e(cess intake of salt- protein- and o(alate have an improtant role in causing renal calculi in
susceptible individuals.
Gi!en a patient with an abnormal serum calcium concentration the student will be able to list two ma+or
mechanisms that control serum calcium concentration.
alcium enters the body via the intestine. 1t circulates in the blood in both and ioni=ed and protein bound form. 1t
is stored in bone and is e(creted by the kidney. The control of this system is maintained through variations in
!T2 and <it 7. 8 fall in serum ioni=ed calcium will cause an increase in !T2. !T2 causes removal of calcium
from the bone and increased re"absorption from the kidney. <it 7 is ingested or made in the skin through the
action of :< light. <it 7 causes increased absorption via the gut and facilitates the action of !T2 on bone.
In a patient with renal calculi the student will be able to list two possible pathogenetic mechanisms of
1idney stones.
1diopathic hypercalciuria is defined as an increase in e(cretion of calcium greater than 9** mg;day in men and
4&*mg;day in women. 2yperuricuria is the e(cretion of greater than F**",***mg;day of uric acid. 2ypercalcemia
which results in hypercalciuria and predisposes to the formation of calcium stones. :ric acid stones.
When faced with a patient with high or low calcium the student will be able to de!elop a differential
diagnosis and recogni5e the different pathophysiologic possibilities.
Chapter 12 @agnesium and "hosphorus
(b+ecti!es <