ACUTE GLOMERULONEPHRITIS
Acute Glomerulonephritis refers to a group of kidney diseases in which there is an inflammatory reaction in the glomeruli.
Causes
A common cause if B- haemolytic strepto coccus. In most cases, the stimulus of the reaction is group A streptococcal infection of the throat, throat, [ordinarily] precedes the onset of glomerulonephritis by an interval of 2-3 weeks.
Glomerulonephritis may also be associated with other, disease Such as systemic lupus erythematosus, polyarteritis nodosa, scleroderma, DM, amyloidosis and bacterial endocarditis.
Pathophysiology
Infection elsewhere in the body or it may develop secondary to systemic disorders
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Antigen - Antibody reaction
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Production of immune complexes that lodge in the glomeruli
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Thickening of glomerular basement membrane
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Scarring and loss of filtering surface.
Clinical Manifestation
The disease may be so mild that it is discovered accidentally through a routine urinalysis or history may reveal a preceding episode of pharyngitis or tonsillitis with fever. In more severe form of the disease - headache, malaise, facial edema, flank pain,
mild to severe hypertension, tenderness over the costovertebral angle. [The angles formed on each side of the body by the bottom rib of cage and vertebral column) Proteinuria, haematuria, oliguria, edema of extremities, fatigue and anorexia; anaemia from loss of RBCs into the urine.
[The clinical course of Acute Glomerulonephritis proceeds as follows from onset of symptoms to recovery over 90% of Patients regain normal renal function within 60 days:
a Diuresis usually starts 1-2 weeks after onset of symptoms.
b. Renal clearances and blood urea concentration return to normal.
C. Edema es and hypertension lessens.
d. Microscopic proteinuria or haematuria may persist many months).
Diagnostic Evaluation
1. Urinalysis - haematuria (microscopic or gross), proteinuria, red cell casts, white blood cells, renal epithelial cells and various casts in the sediment. [early in the disease, Pt voids 50-200ml daily of a cola coloured urine with a sp. Gravity between 1.020 and 1.025 and a thick sediment of RBCs, WBCs and all kinds of casts].
2. Blood-elevated BUN and creatinine levels low albumin in level, high lipid level, absorbed antistreptolysin, (from reaction to streptococcal organism).
3. Needle biopsy of the kidney reveals obstruction of glomerular capillaries from proliferation of endothelial cells.
Management
1. Management is symptomatic and includes antihypertensives, diuretics, drugs for management of hyperkalaemia (due to renal insufficiency), H₂ blocker (to prevent stress ulcers), and phosphate binding agents (to reduce phosphate and elevate calcium).
2. Antibiotic therapy is initiated to eliminate infection (if still present) i.e. If residual streptococcal infection is suspected, penicillin is given.
3. Third intake is restricted [fluids are given according to the Patients fluid losses and daily body weight. ie 400-500ml + previous 24 hrs urine output].
4. Dietary protein is restricted moderately if there is oliguria and the BUN is elevated. [due to renal insufficiency]
5. Carbohydrates are observed [liberally] to provide energy and reduce catabolism of protein.
6. K and Na intake is restricted in presence of hyperkalaemia, edema or signs of CHE
7. Therapy for rapidly progressive glomerulonephritis may included.
a. Plasma exchange
b. Immunosuppressants (corticosteroids, cyclophosphamide)
c. Dialysis may be considered if fluid retention uraemia cannot be controlled.
Complications
1. Hypertension, Congestive Cardiac Failure, endocarditis
2. Fluid and electrolyte imbalances in the acute phase, hyperkalaemia hyperphosphatemia, hypervolemia.
3. Malnutrition
4. Hypertensive encephalopathy, seizures
5. ESRD-end stage renal disease
Nursing Management
1. Monitor vital signs, i/o and maintain dietary restriction during acute phase
2. Ensure Bed rest until urine clears and BUN, creatinine and BP normalizes (Rest also facilitates diuresis).
3. Administration Medication as ordered.
4. Monitor fluid balance; replace fluids according to the Patients fluid losses (urine, respiration, faeces) and daily body weight as prescribed.
5. Monitor CVP and pulmonary, artery Pressure. If indicated.
6. Monitor for signs and symptoms of CHF distended neck veins, tachycardia, gallop rhythm, enlarged and tender liver crackles at bases of lungs.
7. Observe for hypertensive encephalopathy and seizures.
8. Explain importance of follow up evaluation of BP, urinary protein and BUN concentration [to determine of there is exacerbation of disease activity)
9. Encourage Patient to treat any infection promptly.
10. Tell Patient to report any signs of deciding renal function and to obtain treatment immediately.
