eMedicine Specialties > Nephrology > Glomerular Diseases
Glomerulonephritis, Acute: Follow-up
Updated: Jul 2, 2008
Follow-up
Further Inpatient Care
- Patients may require hospitalization for control of edema and hypertension.
Further Outpatient Care
- Monitor renal function, BP, edema, serum albumin, and urine protein excretion rate.
Inpatient & Outpatient Medications
- Patient may require medication to control BP.
Transfer
- The expertise available in the ICU may be needed for management of patients with hypertensive encephalopathy or pulmonary edema.
Deterrence/Prevention
- Early antibiotic therapy of streptococcal infection (ie, within 36 h of onset) may prevent development of PSGN.
- Antibiotic treatment of close contacts of the index case may help prevent development of PSGN.
Complications
- Renal failure (rare)
- Pulmonary edema
- Generalized anasarca and hypoalbuminemia (secondary to severe proteinuria)
- Hypertension
- Hypertensive encephalopathy
Prognosis
- Prognosis of acute PSGN is generally excellent in children.
- Within a week or so of onset, most patients with PSGN begin to experience spontaneous resolution of fluid retention and hypertension.
- C3 levels may normalize within 8 weeks after the first sign of PSGN.
- Proteinuria may persist for 6 months and microscopic hematuria for up to 1 year after onset of nephritis.
- Eventually, all urinary abnormalities should disappear, hypertension should subside, and renal function should return to normal.
- In adults with PSGN, full recovery of renal function can be expected in just over half of patients, and prognosis is dismal in patients with underlying diabetic glomerulosclerosis.
- Few patients with acute nephritis develop rapidly progressive renal failure.
- Nephritis associated with MRSA and chronic infections usually resolves after treatment of the infection.
- Immunity to type M protein is type-specific, long-lasting, and protective. Repeated episodes of PSGN are therefore unusual.
- Approximately 15% of patients at 3 years and 2% of patients at 7-10 years may have persistent mild proteinuria. Long-term prognosis is not necessarily benign. Some patients may develop hypertension, proteinuria, and renal insufficiency as long as 10-40 years after the initial illness.
Patient Education
- Counsel patients about the need for the following measures:
- Salt restriction during the acute phase to control edema and volume-related hypertension
- BP monitoring at periodic intervals
- Ongoing long-term monitoring of patients with persistent urinary abnormalities and elevated BP
- Consideration of protein restriction and angiotensin converting enzyme inhibitors (in patients who show evidence of persistent abnormalities or in those who develop late evidence of progressive disease)
- Early antibiotic treatment of close contacts
- For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Blood in the Urine.
Miscellaneous
Medicolegal Pitfalls
- Failure to consider acute GN in the differential of patients presenting with hematuria, proteinuria, hypertension, facial or leg swelling, and renal insufficiency
- Failure to perform urinalysis, especially urine microscopy examination in patients presenting with passage of discolored urine or symptoms and signs suggestive of acute GN
- Failure to monitor renal function, electrolytes, and BP in patients with acute GN
- Failure to monitor and control BP effectively in patients with volume overload
- Failure to treat close contacts of patients with acute PSGN
- Failure to recommend long-term monitoring of patients with persistent urinary abnormalities and elevated BP
More on Glomerulonephritis, Acute |
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| Treatment & Medication: Glomerulonephritis, Acute |
 Follow-up: Glomerulonephritis, Acute |
| Multimedia: Glomerulonephritis, Acute |
| References |
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References
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Bazzi C, Petrini C, Rizza V, et al. A modern approach to selectivity of proteinuria and tubulointerstitial damage in nephrotic syndrome. Kidney Int. Oct 2000;58(4):1732-41. [Medline].
Dodge WF, Spargo BH, Travis LB, et al. Poststreptococcal glomerulonephritis. A prospective study in children. N Engl J Med. Feb 10 1972;286(6):273-8. [Medline].
Neugarten J, Gallo GR, Baldwin DS. Glomerulonephritis in bacterial endocarditis. Am J Kidney Dis. Mar 1984;3(5):371-9. [Medline].
Oda T, Yamakami K, Omasu F, et al. Glomerular plasmin-like activity in relation to nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. J Am Soc Nephrol. Jan 2005;16(1):247-54. [Medline].
Rodriguez-Iturbe B. Nephritis-associated streptococcal antigens: where are we now?. J Am Soc Nephrol. Jul 2004;15(7):1961-2. [Medline].
Rodríguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int. Jan 1984;25(1):129-36. [Medline].
Ronco P, Verroust P, Morel-Maroger L. Viruses and Glomerulonephritis. Nephron. 1982;31(2):97-102. [Medline].
Yoshizawa N, Yamakami K, Fujino M, et al. Nephritis-associated plasmin receptor and acute poststreptococcal glomerulonephritis: characterization of the antigen and associated immune response. J Am Soc Nephrol. Jul 2004;15(7):1785-93. [Medline].
Further Reading
Keywords
acute glomerulonephritis, acute nephritis, Bright disease, acute poststreptococcal glomerulonephritis, PSGN, acute postinfectious glomerulonephritis
