Pathophysiology of Acute Glomerulonephritis

With the infections, an antigen-antibody complex forms that causes renal damage especially the nephrons. The damage to the nephrons allowthe passage of large molecules like the Red blood cell that causes hematuria and is the primary sign of Acute Glomerulonephritis. Another large molecule are the Proteins, that causes proteinuria. When proteinuria occurs, there is a decrese in the osmotic pressure that leads to generalized edema or anasarca. This decreases the circulating blood volume, which decreases the blood flow and affects the Renin-Angiotensin-Aldosterone-System, where the Renin promotes vasoconstriction that leads to hypertension.

Signs of Acute Glomerulonephritis

1. 2. 3. 4. 5. 6. 7. Hematuria Hypertension Generalized edema Proteinuria Oliguria Anorexia Nausea and vomiting

Diagnostic Test for Acute Glomerulo nephritis

1. 2. 3. 4. Anti streptolysin - O (ASO) Titer. Urinalysis. Renal Biopsy. Is the most confirmatory diagnostic procedure. Increased BUN and Creatinine.

Management for Acute Glomerulo nephritis

1. 2. 3. 4. Antibiotics. Anti hypertensive Bed rest. Increase oral fluid intake.

Causes of Acute Glomerulonephritis Acute nephritic syndrome is often caused by an immune response triggered by an infection or other disease. Inflammation disrupts the functioning of the glomerulus, which is the part of the kidney that controls filtering and excretion. This inefficient functioning results in blood and protein appearing in the urine, and the accumulation of excess fluid in the body. Swelling results when protein is lost from the blood stream. (Protein maintains fluid within the blood vessels, and when it is lost the fluid collects in the tissues of the body). Acute nephritic syndrome may be associated with the development of high blood pressure, interstitial inflammation (inflammation of the spaces between the cells of the kidney tissue), and acute kidney failure.

Symptoms of Acute Glomerulonephritis Many people with glomerulonephritis have no symptoms. When symptoms occur, they are often flulike, such as general fatigue, nausea, vomiting, loss of appetite, fever, and abdominal and joint pain. These types of general symptoms can continue for up to one month before symptoms of kidney failure appear. Patients whose kidneys are failing will produce only small amounts of urine and have swelling (edema) from fluid build-up. Symptoms of acute glomerulonephritis usually occur around two to three weeks after a streptococcal infection and begin with swelling. They can progress to high blood pressure, visual disturbances, shortness of breath, blood in the urine, and a reduction in urine production. Chronic glomerulonephritis develops so gradually that it is often not discovered until a routine physical exam. As this condition progresses, it causes high blood pressure, swelling, and other symptoms of kidney failure. Treatment of Acute Glomerulonephritis The goal of treatment is to reduce glomerular inflammation. Hospitalization is required for diagnosis and treatment of many forms of acute nephritic syndrome. The cause must be identified and treated. This may include antibiotics or other medications or treatment. Bedrest may be recommended. The diet may include restriction of salt, fluids, and potassium. Medications may include anti-hypertensive medications to control high blood pressure. Corticosteroids or other anti-inflammatory medications may be used to reduce inflammation.

Acute glomerulonephritis refers to a specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.[1, 2] The condition is defined as the sudden onset of hematuria, proteinuria, and red blood cell casts. This clinical picture is often accompanied by hypertension, edema, and impaired renal function. The most common causes of acute glomerulonephritis are postinfectiousStreptococcus species, but other bacteria, as well as viruses, fungi, and parasites, can be the cause. The disease can also result from systemic and renal disorders.[3]

Acute glomerulonephritis results when the capillaries in the kidney (glomeruli) that control filtering and excretion become inflamed and unable to function properly. With the selective filtering mechanism damaged, blood and protein are lost in the urine, and excess body fluids accumulate (it is the protein in the bloodstream that maintains our fluid balance). Most often, the inflammation that triggers the disease stems from an immune response to a specific bacterium called Streptococcus. Typically, the body launches this immune response when the bacteria attacks the lungs or, less commonly, the skin. Other bacteria, viruses, fungi, and parasites may also trigger such a response, but it is less usual. Acute glomerulonephritis may also stem from systemic causes that affect the body as a whole and for a variety of reasons also result in compromised glomerular function. Some of these conditions are hypersensitivity vasculitis, Wegener granulomatosis, systemic lupus erythematosus, polyarteritis nodosa, cryoglobinemia, and Goodpasture syndrome. Because it is the dominant, specific cause of acute glomerulonephritis, this topic will focus on the streptococcal origins of glomerulonephritis. There are two forms of acute glomerulonephritis: postinfectious glomerulonephritis and infectious glomerulonephritis. Postinfectious glomerulonephritis typically occurs about 21 days after a respiratory or skininfection with Streptococcus. Infectious glomerulonephritis occurs during or within a few days of streptococcal infection. The disease may result in high blood pressure (hypertension), fluid accumulation

(edema), and kidney failure. Of the two types, postinfectious glomerulonephritis (also called acute poststreptococcal glomerulonephritis) is the most common. The most common risk factor for development of postinfectious glomerulonephritis is an untreated streptococcal infection of the respiratory tract and, less commonly, of the skin (impetigo). Risk: Males are twice as likely to have the condition as females, and although glomerulonephritis can appear at any
age, 90% of cases occur in those under 40 years. The disease most often develops in boys between 2 and 14 years (Kazzi).

Incidence and Prevalence: There has been a significant decline in the incidence of acute glomerulonephritis in
developed countries such as the US, and cases are reported only sporadically. The declining incidence rates are probably related to improved nutritional status in these countries and more liberal use of antibiotics. Developing countries, such as those in Africa and the Caribbean, appear to have a higher potential for development of streptococcal infections, and the incidence of acute glomerulonephritis is proportionally higher in these areas.

Diagnosis
History: Individuals may report a recent bacterial (streptococcal) or viral illness. In some cases, symptoms are mild,
and individuals may report only vague weakness, loss of appetite (anorexia), and lethargy. In more severe cases, they may complain of cola- or tea-colored urine, fever, chills, weakness, headache, blurred vision (reduced visual acuity), abdominal or flank pain, reduced or no urine output (oliguria or anuria, respectively) for several days, nausea, and vomiting.

Physical exam: Examination usually reveals generalized swelling (edema) particularly around the face and eyes
(periorbital), fluid in the abdomen (ascites), fluid in the lungs (pulmonary edema) and chest cavity (pleural effusion), elevated blood pressure (hypertension), bloody urine, and skin rashes.

Tests: Visual examination of the urine usually provides enough information necessary for a definitive diagnosis of
acute glomerulonephritis. The urine, which may be scanty in amount, will typically be dark, smoky, or cola-colored or red or brown in hue. There is usually persistent and excessive foam in the specimen, indicating a high level of protein in the urine. A laboratory test of the urine (urinalysis) may show protein and blood, high acid levels (low pH), and midto high-normal range values for specific gravity. Other laboratory tests may include an analysis of how well the kidneys are working (renal function test) and specific blood tests for serum urea nitrogen, creatinine, hyaluronidase, deoxyribonuclease B, and serum complement. The percentage of red blood cells (hematocrit) and the amount of hemoglobin in the blood can be measured using a complete blood count (CBC). A streptozyme test and cultures of the throat and skin may show evidence of the streptococcus bacterium.

Source: Medical Disability Advisor

Treatment
Treatment for acute glomerulonephritis depends on the underlying cause of the disease. In most cases, it is designed to relieve symptoms and reduce the potential for complications. Antibiotic therapy is used to treat the infection that resulted in acute glomerulonephritis (e.g., a penicillin derivative is given for

streptococcal bacteria). Fluid retention (edema) and high blood pressure (hypertension) are treated with drugs that promote fluid loss (diuretics) and lower blood pressure (angiotensin converting enzyme [ACE] inhibitors). Other drug treatments may include anti-inflammatory drugs (corticosteroids), drugs that decrease the response of the immune system (immunosuppressive), and drugs that prevent clotting (anticoagulants or antiplatelet agents). Usually, dietary salt (sodium) and water will be restricted.
Source: Medical Disability Advisor

ACOEM

ACOEM's Practice Guidelines, the gold standard in effective medical treatment of occupational injuries and illnesses, are provided in this section to complement the disability duration guidelines.*

* The relationship between the MDGuidelines (MDA) content and ACOEM's guidelines is approximate and does not always link identical diagnoses. The user should consult the diagnostic codes in both guidelines, as well as the clinical descriptions, before assuming an equivalence.

Source: ACOEM Practice Guidelines

Prognosis
The predicted outcome is extremely variable, and the results of clinical studies regarding treatment effects are contradictory. Heart, lung, or neurological complications will worsen the outcome. Individuals who lose kidney function will have to be treated on an ongoing basis with dialysis, and if there is no meaningful recovery of kidney function, they may be a candidate for a kidney transplant. Generally, adults have a poorer prognosis for acute glomerulonephritis than do young individuals. Drug treatments are usually effective, and very few individuals die as a result of fluid in the lungs (pulmonary edema), brain inflammation (hypertensive encephalopathy), or uncontrolled infection.
Source: Medical Disability Advisor

Complications
Complications of acute glomerulonephritis include elevated blood pressure (hypertension), urinary tract or kidney infection (pyelonephritis), inflammation of the brain tissue (hypertensive encephalopathy), and decreased pumping ability of the heart (congestive heart failure). In rare cases (0.5% to 2%), the disease may progress to chronic renal failure (Kazzi).
Source: Medical Disability Advisor

Return to Work (Restrictions / Accommodations)

Rest is an important part of recovery from acute glomerulonephritis. Bed rest followed by a period of very limited activity may continue for several weeks to months. Individuals who are able to return to work will be very limited in their capacity to perform physical labor and may have to be reassigned to a desk job for a period of time. If kidney dialysis is required, the individual may require an extended leave of absence or a switch to a part-time or flex-time schedule to accommodate treatment. Individuals who are receiving dialysis treatments should be assigned more sedentary duties.
Source: Medical Disability Advisor

Failure to Recover
If an individual fails to recover within the expected maximum duration period, the reader may wish to consider the following questions to better understand the specifics of an individual's medical case.

Regarding diagnosis:

Has diagnosis of acute glomerulonephritis been confirmed? Has individual experienced any complications related to glomerulonephritis? Does individual have an underlying condition that may affect recovery? Is this condition receiving appropriate treatment?

Regarding treatment:

Is individual taking medication as prescribed? Is individual compliant with dietary modifications? Is individual receiving adequate rest for optimal recovery?

Regarding prognosis:

Do symptoms persist despite treatment? Did individual experience residual kidney impairment? Was hypertension effectively resolved? Is additional drug therapy warranted? Did individual experience permanent kidney damage? Is dialysis required? Is individual a candidate for a kidney transplant? Is individual on local/national transplant lists?

What is acute glomerulonephritis? A person with acute glomerulonephritis has inflammation of the blood vessels in the kidney, which causes the kidneys to malfunction. The most common cause of acute glomerulonephritis is a throat infection with the bacteria, Streptococcus. What are the symptoms of acute glomerulonephritis? Common symptoms of acute glomerulonephritis include blood in the urine, fever,nausea, rash, leg swelling, and high blood pressure.

Acute Glomerulonephritis Symptoms

Symptoms of acute glomerulonephritis include: o o Abnormal appearing urine: Urine may be foamy due to high protein concentration Blood in the urine: Cola colored urine

 o o o

Decreased urine production Fever Chills Nausea Rash Swelling: Leg swelling Foot swelling (bilateral) Face swelling Hand swelling (bilateral) Vomiting Hiccups Weight gain

Worsening symptoms of acute glomerulonephritis include:

o o o

Repeated vomiting Excessive fatigue High blood pressure Back pain: Low back pain Flank pain Shortness of breath: Worsens with exertion Worsens when lying flat Confusion

Acute Glomerulonephritis Evaluation

The evaluation of acute glomerulonephritis begins with a medical history and physical examination. Physical findings in those with acute glomerulonephritis may include: o Confusion Lethargy Excessive sleepiness Dry skin Pale skin

o o o o

Caused by anemia Loss of muscle tissue Muscles become smaller Leg swelling Foot swelling (bilateral) Facial swelling Worse around the eyes Enlargement of the liver High blood pressure

Blood and urine tests are required to make the diagnosis of acute glomerulonephritis. Tests that may be used to evaluate acute glomerulonephritis include:

Serum calcium level Serum phosphate level Complete blood count Erythropoietin blood levels Kidney profile: includes sodium and potassium levels Urinalysis 24 hour urine for creatinine clearance

Additional tests that may be used to evaluate the kidneys include:

Abdominal ultrasound Abdominal CT scan Intravenous pyelogram Kidney biopsy MRI scan of the abdomen Renal arteriogram Kidney biopsy

Acute Glomerulonephritis Anatomy

To better understand acute glomerulonephritis, it helps to understand the anatomy of the kidneys. The kidneys are located in the back of the abdomen, below the ribcage and on either side of the spine.

Each kidney weighs about 1/4 pound (0.6 kg) and is about the size of a fist. The kidneys filter waste from the bloodstream and produce urine. The kidneys also regulate the salt and water balance for the body. Examples: Kidney Kidney cross section Kidney cross section close-up Kidney collecting system Genitourinary system

Acute Glomerulonephritis Physiology

To better understand acute glomerulonephritis, it helps to understand what the kidneys do. Kidney Physiology The kidneys perform vital functions for the body. Functions include: Filter waste from the bloodstream and make urine Regulate blood pressure Regulate fluid balance Regulate red blood cell production Regulate salts, such as potassium and sodium, in the bloodstream

The kidneys remove waste from the bloodstream and pass it into the urine. If the waste products are allowed to accumulate, they become toxic

RHD