Glomerulonephritis

Glomerulonephritis is the bilateral inflammation of the glomeruli, typically following a

streptococcal infection.
Actue glomerulonephritis is also called acute post streptococcal glomerulonephritis.
It is defined as inflammation and proliferative changes in glomerular structures.

Etiology (acute)
Beta hemolytic streptococcous infection
Berger’s disease
Upper respiratory tract infection
Skin infection (Impetigo)
HIV infection
Chronic
Membranoproliferative glomerulonephritis
Nephritic syndrome
Membraneous glomerulopathy

Pathophysiology
Due to Beta hemolytic streptococcous infection or any other causes there is formation of
antibodies
Circulating antigen antibody complex becomes lodged in glomerular capillaries
Complex initiates compliment activation, release of immunologic substances that lyses
cells
Membrane damage leads to platelet aggregation, and platelet degranulation releases
substances that increase glomerular permiabilty.
Proteinuria and hematuria results.
Activation of coagulation system leads to fibrin deposits in Bowman’s space.
The result is crescent formation and diminished renal blood flow and GFR.
Glomerular bleeding causes acidic urine which transforms Hb to methemoglobin and
results in brown urine without clots.
The inflammatory response decreases GFR, which causes fluid retention and decreased
urine output, extracellularfluid volume expansion and hypertension.
After 10 to 20 years renal insufficiency develops followed by nephritic syndrome and end
stage renal failure.
(Good’s pasture’s syndrome is a rapidly progressive glomerulonephritis in which
antibodies are produced against the pulmonary capillaries and glomerular basement
membrane. Diffuse intracellular antibody proliferation in Bowman’s space leads to a
crescent shaped structure that obliterates the space. The crescent is composed of fibrin
and endothelial, mesengial, and phagocytic cells , which compress the glomerular
capillaries, diminishing blood flow, and cause extensive scarring of the glomeruli. GFR is
reduced and renal failure occurs within weeks or months.
Systemic diseases such as hepatitis B virus, systemic lupus erythematosus, or
solid malignant tumors, cause a membraneous nephropathy. An inflammatory process
causes thickening of the glomerular capillary wall. Increased permeability and proteinuria
leads to nephritic syndrome.

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 Clinical manifestations
Early clinical manifestation
a. Hematuria
b. Proteinuria
c. Azotemia
d. Oliguria
e. Increased urine specific gravity
f. Mild headache
g. Anorexia
h. Flank pain
i. Anaemia
j. Urine retention
k. Diuresis
l. malaise
Latent clinical manifestation
a. Hypertension
b. Oliguria
c. Generalized edema
d. Poteinuria
e. Nocturia
f. Circulatory congestion

Diagnostic evaluation
1. Urinalysis
 Decreased urine output
 Moderately elevated urine specific gravity
 RBC’s , leukocytes and epithelial cells in urine
 Proteinuria mild to severe
 Gross hematuria
2. Blood studies
 BUN: elevated
 Lipid: high
 Createnine: elevated
 Albumin: low
 ESR: high
 Anti streptolysin -0 titer: elevated
3. Chest x-ray: may show pulmonary congestion, cardiac enlargement during the edematous
phase.
4. Needle biopsy of kidney: proliferation of endothelial cells

Medical management
1. Antibiotics: to treat streptococci infection (penicillin)
2. Antihypertensive: to treat hypertension
3. Diuretics: to prevent edema and renal insufficiency
4. H2 receptor antagonists: to prevent stress ulcer

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 5. Corticosteroids: to decrease antibodies synthesis and suppress inflammatory
response
6. Plasmapheresis: to suppress rebound antibody production in RPGN (rapid
progressive glomerulonephritis).

Dietary management
1. Restrict fluid intake
2. Restrict dietary protein moderately.
3. Carbohydrates are increased liberally to provide energy and reduce catabolism of
protein.
4. Potassium and sodium intake is restricted in the presence of hypercalemia, edema,
CCF.

Nursing management
1. Check vital signs and electrolyte values. Monitor intake and oputput and daily
weigh the patient.
2. Assess renal function daily through serum creatinine, BUN, and urine creatinine
clearance levels.
3. Watch for and immediately report signs of acute renal failure (oliguria, azotemia,
and acidosis).
4. Monitor for ascites and edema and take abdominal girth daily to assess
progression of ascites.
5. Consult dietician to provide a diet high in calories and low in proteins, sodium,
potassium and fluids.
6. Administer medications as ordered and provide good skin care and oral hygiene.
7. Protect the debilitated patient against secondary infection by providing good
nutrition, using good hygienic technique, and preventing contact with infected
people.
8. Provide bedrest during acute phase. Allow the patient to gradually normal
activities as symptoms subsides.
9. Tell the patient that follow up examination are necessary to detect chronic renal
failure.
10. Stress the need for regular blood pressure, urinary protein and renal function
assessment during the convalescent months to detect reoccurance.
11. Instruct the patient that abnormal urinary findings may persist for years.
12. Encourage pregnant women with history of glomerulonephritis to have frequent
medical evaluations because pregnancy further stresses the kidneys and increase
the risks of chronic renal failure.

Complications
1. CCF
2. End stage renal failure