Approach Considerations
Treatment of acute poststreptococcal glomerulonephritis (PSGN) is mainly supportive, because there is no specific therapy for renal disease. When acute glomerulonephritis (AGN) is associated with chronic infections, the underlying infections must be treated.
The expertise available in the intensive care unit may be needed for management of patients with hypertensive encephalopathy or pulmonary edema. Consultation with a nephrologist may be indicated. On an outpatient basis, kidney function, blood pressure, edema, serum albumin, and urine protein excretion rate should be monitored.
In a retrospective study from New Zealand, Wong et al examined the characteristics and treatment of acute PSGN in 27 pediatric patients and determined that the need for acute dialysis was most common among the 11 children in the study with crescentic glomerulonephritis. These authors also determined that urinary sediment abnormalities persisted in the patients with crescentic glomerulonephritis even after a mean follow-up period of 3.2 years and that the benefits of immunosuppressive therapy were unclear in these patients. [21]
Go to Emergent Management of Acute Glomerulonephritis and Acute Poststreptococcal Glomerulonephritis for complete information on these topics.
Pharmacologic Therapy
Antibiotics
Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of infection to close contacts. Antimicrobial therapy does not appear to prevent the development of glomerulonephritis, except if given within the first 36 hours. Antibiotic treatment of close contacts of the index case may help prevent development of PSGN.
Other agents
Consider the following:
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Loop diuretics may be required in patients who are edematous and hypertensive, in order to remove excess fluid and to correct hypertension.
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Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe hypertension or encephalopathy is present.
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Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN.
Diet and Activity
Sodium and fluid restriction should be advised for treatment of signs and symptoms of fluid retention (eg, edema, pulmonary edema). Protein restriction for patients with azotemia should be advised if there is no evidence of malnutrition.
Bed rest is recommended until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity is of no benefit in the patient recovery process.
Long-Term Monitoring
Long-term studies on children with PSGN have revealed few chronic sequelae. Results of such studies are controversial because homogeneous populations suitable for proper epidemiologic analysis have not been assembled.
Long-term studies show higher mortality rates in elderly patients, particularly those on dialysis. Patients may be predisposed to crescent formation.
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Light microscopy (hematoxylin and eosin stain X 25): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
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Light microscopy (periodic acid-Schiff stain X 40): Photograph showing enlargement of glomerular tuft with marked decrease of urinary space and hypercellularity. The hypercellularity is due to proliferation of endogenous cells and polymorphonuclear leukocyte infiltrate. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
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Immunofluorescence (X25): Fine granular deposits of immunoglobulin G (IgG) along the basement membrane and mesangium, with "starry sky" appearance. Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
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Ultrastructure (electron microscopy): Photograph showing proliferation of endothelial cells and mesangial cells and leukocyte infiltrate associated with presence of large, subepithelial, electron-dense deposits (ie, "hump") (see arrow). Photograph courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
