Glomerulonephritis PDF

Glomerulonephritis
Glomerulonephritis (GN) presents with hematuria with RBC casts, proteinuria, oliguria, hypertension, azotemia
and edema.
Acute glomerulonephritis is associated with inflammation and proliferation of the glomerular tuft. It may be rapidly
progressive.
Chronic glomerulonephritis carries the indication that permanent damage has occurred.
EPIDEMIOLOGY
Acute poststreptococcal glomerulonephritis can occur in anyone >2 years, but is most frequently found in boys between 5
15 years old.
Incidence
Incidence of acute poststreptococcal glomerulonephritis in the US has declined over the last 2 decades.
Chronic glomerulonephritis occurs more often at the end of the 1st decade of life and in adults.
RISK FACTORS
Genetics
Genetic predisposition:
Familial glomerulonephritis (e.g., Alport syndrome, X linked)

ETIOLOGY
Low serum complement level: Systemic diseases:

1. Vasculitis and autoimmune disease (e.g., systemic lupus erythematosus [SLE])
2. Subacute bacterial endocarditis (SBE)
3. Shunt nephritis
4. Cryoglobulinemia
Low serum complement level: Renal diseases:

1. Acute poststreptococcal glomerulonephritis
2. Membranoproliferative glomerulonephritis (types 1, 2, and 3)
Normal serum complement level: Systemic diseases:

1. Polyarteritis nodosa group
2. Wegener vasculitis
3. Henoch-Schnlein purpura
4. Hypersensitivity vasculitis
5. Visceral abscess
Normal serum complement level: Renal diseases:

1. IgA nephropathy
2. Idiopathic rapidly progressive glomerulonephritis

3. Immune-complex disease
4. Pauci-immune glomerulonephritis
Diagnosis
SIGNS AND SYMPTOMS
Macroscopic hematuria (dark brown urine)
Sore throat
Impetigo
A prior upper respiratory infection that persists at least 1 week or skin lesions in the proceeding 34 weeks suggests
acute poststreptococcal glomerulonephritis.
An upper respiratory infection in the previous few days suggests IgA nephropathy.
Reduced output of urine
Dyspnea, fatigue, lethargy
Headache
Seizures (hypertensive encephalopathy)
Symptoms of a systemic disease such as fever, rash (especially on the buttocks and legs, posteriorly), arthralgia,
and weight loss
History
Special questions:
Establish the time relationship between a sore throat and the acute glomerulonephritis. The onset of acute
poststreptococcal glomerulonephritis is usually associated with a time delay of >1 week.
Physical Exam
Look for:
Hypertension
Pallor
Signs of volume overload (e.g., edema, jugular venous distention, hepatomegaly, basal pulmonary crepitation, and
a triple cardiac rhythm)
Impetigo or ecthyma (pyoderma)
Signs of vasculitis such as rash, loss of fingertip pulp space tissue, Raynaud phenomenon, and vascular thrombosis
Signs of a systemic disorder (see comment on vasculitis)
Signs of chronic renal insufficiency such as short stature, pallor, sallow skin, edema, excoriations, pericardial
friction rub, pulmonary rales and effusion, breath that smells of urine, asterixis, myoclonus, and neuropathy
TESTS
LABORATORY
Urine:
1. Microscopy of the urine for crenated erythrocytes and erythrocyte castshallmark of nephritis
2. Proteinuria
Evidence of previous strep infection:

1. Throat culture for -hemolytic streptococcus (result is positive in 1520% with acute poststreptococcal
glomerulonephritis)
2. Antistreptolysin O titer: Positive result in 60% of patients with acute poststreptococcal glomerulonephritis.
3. Streptozyme test: A mixed antigen test for -hemolytic streptococcus. Together, the antistreptolysin O
titerplus streptozyme tests have a >85% sensitivity.
4. Complement C3 serum level will be low in acute poststreptococcal glomerulonephritis and in other causes
of acute glomerulonephritis as detailed herein.
Blood chemistry:
1. Can be normal in acute glomerulonephritis
2. In chronic glomerulonephritis, serum chemistries will reflect the degree of renal failure (i.e., raised
serum ureaand creatinine). The serum potassiumand phosphate levels will be elevated and the calcium
level decreased.
3. With chronic renal insufficiency: Normocytic, normochromic, or hypochromic microcytic anemia
IMAGING
Chest radiograph to look for pulmonary edema and determine cardiac size
Renal ultrasound if presentation or course not typical of acute poststreptococcal glomerulonephritis. The ultrasound
is to assess the size and parenchymal texture.
DIAGNOSTIC PROCEDURES
Electrocardiogram:
Electrocardiogram to assess ventricular size and for hyperkalemia

PATHOLOGICAL FINDINGS
In acute poststreptococcal glomerulonephritis, light microscopy reveals enlarged swollen glomerular tufts, mesangial and
epithelial cell proliferation, with polymorphonuclear cell infiltration. There is granular deposition of C3 and IgG on
immunofluorescence, and electron-dense subepithelial deposits or humps are seen on electron microscopy.
The histology varies in chronic glomerulonephritis and depends on the cause. Rapidly progressive glomerulonephritis is
associated with crescent formation.
DIFFERENTIAL DIAGNOSIS
Acute postinfectious glomerulonephritis (Lancefield group A -hemolytic streptococci Pneumococcus,

Mycoplasma, mumps, Epstein-Barr virus)
Infection related (hepatitis B and C, syphilis)
IgA nephropathy
Membranoproliferative glomerulonephritis
Autoimmune glomerulonephritis (e.g., SLE)
Familial glomerulonephritis
Acute interstitial nephritis
Hemolytic uremic syndrome
Pyelonephritis
Treatment
INITIAL STABILIZATION
Treat hypertensive encephalopathy and life-threatening electrolyte disturbances immediately.
GENERAL MEASURES
Acute poststreptococcal glomerulonephritis is a self-limiting disease. Acute therapy is usually sufficient.
The therapy of chronic glomerulonephritis depends on the underlying disease process; it may include
immunosuppressives and, ultimately, the management of chronic renal failure.
DIET
Restrictions of intake of fluid, sodium, potassium, and phosphate are initially required.
MEDICATIONS
The following may be required:
Loop diuretics (furosemide) for volume, BP, and potassium control
Antihypertensive agents; vasodilators such as calcium channel blockers (e.g., nifedipine, isradipine, amlodipine)
and loop diuretics are useful as first-line agents; IV hydralazine, labetalol, nicardipine, or nitroprusside may be
required to treat severe refractory hypertension.
Serum potassium-lowering agents (sodium polystyrene sulfonate [Kayexalate], furosemide, bicarbonate,

insulin/glucose, salbutamol). Intravenous calcium is used to stabilize the myocardium in severe hyperkalemia.
Phosphate binders
Immunosuppressive agents such as prednisone, cyclophosphamide, and sometimes azathioprine are used in the
treatment of vasculitis-associated glomerulonephritis, membranoproliferative glomerulonephritis, and rapidly
progressing glomerulone-phritis. Plasmapheresis may be used to treat rapidly progressing glomerulonephritis.
Penicillin is used in acute poststreptococcal glomerulonephritis, but does not affect the course of the disease.
Follow-up Recommendations
In acute poststreptococcal glomerulonephritis, improvement usually occurs within 37 days, hypertension is not sustained,
and macroscopic hematuria is transient. Watch for ongoing oliguria, unresolved hypertension, increasing proteinuria, or
progressive azotemia. Complement levelsreturn to normal within 68 weeks of the initial presentation.
CLINICAL:
Microscopic hematuria may be present up to two years after an episode of poststreptococcal glomerulonephritis
If complement levels do not return to normal after presumed poststreptococcal glomerulonephritis, one needs to
consider SLE and MPGN.
PATIENT MONITORING
Look for and treat hyperkalemia.
To control seizures, treat the hypertension; anticonvulsants play a secondary role.
Monitor the degree of renal failure.
Home testing: BP monitoring may be required.
Do not fail to check serum potassium levels.
Be certain to recognize fluid overload.
Be certain to recognize the severity and type of renal failure.

DISPOSITION
Admission Criteria
Hypertension , Edema, Renal failure

EXPECTED COURSE/PROGNOSIS
Prognosis is excellent in acute poststreptococcal glomerulonephritis and variable for other causes of
glomerulonephritis in childhood.
Acute poststreptococcal glomerulonephritis rarely recurs.

POSSIBLE COMPLICATIONS
Acute renal failure
Hyperkalemia
Hypertension
Volume overload (e.g., congestive cardiac failure, pulmonary edema, hypertension)
Chronic renal failure
Frequently Asked Questions
Q: When does the complement return to normal?
A: Hemolytic complement levels (C3) return to normal within a 68-week period in acute poststreptococcal
glomerulonephritis. Persistently low C3 levels suggest a cause other than acute poststreptococcal
glomerulonephritis.
Q: What are the indications for renal biopsyin acute glomerulonephritis?
A: Patients in whom there is sustained hypertension, ongoing or progressive azotemia, or persistent proteinuria of
>1.5 g/d should be biopsied.

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Glomerulonephritis

Familial glomerulonephritis (e.g., Alport syndrome, X linked)

Low serum complement level: Systemic diseases:

Low serum complement level: Renal diseases:

Normal serum complement level: Systemic diseases:

Normal serum complement level: Renal diseases:

2. Idiopathic rapidly progressive glomerulonephritis

Macroscopic hematuria (dark brown urine)

Reduced output of urine

Dyspnea, fatigue, lethargy

Seizures (hypertensive encephalopathy)

Impetigo or ecthyma (pyoderma)

Signs of a systemic disorder (see comment on vasculitis)

Evidence of previous strep infection:

Electrocardiogram to assess ventricular size and for hyperkalemia

Acute postinfectious glomerulonephritis (Lancefield group A -hemolytic streptococci Pneumococcus,

Infection related (hepatitis B and C, syphilis)

Autoimmune glomerulonephritis (e.g., SLE)

Acute interstitial nephritis

Hemolytic uremic syndrome

Acute poststreptococcal glomerulonephritis is a self-limiting disease. Acute therapy is usually sufficient.

Loop diuretics (furosemide) for volume, BP, and potassium control

Serum potassium-lowering agents (sodium polystyrene sulfonate [Kayexalate], furosemide, bicarbonate,

Look for and treat hyperkalemia.

To control seizures, treat the hypertension; anticonvulsants play a secondary role.

Monitor the degree of renal failure.

Home testing: BP monitoring may be required.

Do not fail to check serum potassium levels.

Be certain to recognize fluid overload.

Be certain to recognize the severity and type of renal failure.

Hypertension , Edema, Renal failure

Acute poststreptococcal glomerulonephritis rarely recurs.

Acute renal failure

Volume overload (e.g., congestive cardiac failure, pulmonary edema, hypertension)

Chronic renal failure

Frequently Asked Questions

Q: When does the complement return to normal?

Q: What are the indications for renal biopsyin acute glomerulonephritis?

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