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Glomerulonephritis, Acute: Differential Diagnoses & Workup
Updated: Jul 2, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Differential Diagnoses
Other Problems to Be Considered
- Postinfectious GN must be differentiated from the following conditions:
- IgA nephritis: The latent period between infection and onset of nephritis is 1- 2 days, or it may be concomitant with upper respiratory tract infection (ie, "synpharyngitic" in contrast to 1-3 wk "postpharyngitic nephritis" in PSGN).
- MPGN (type I, type II): This is a chronic disease, but it can manifest with an acute nephritic picture with hypocomplementemia; failure of acute nephritis to resolve should prompt consideration of this possibility.
- Lupus nephritis: Gross hematuria is unusual in lupus nephritis.
- GN of chronic infection: This can manifest as acute nephritis. Unlike PSGN, in which the infection may have resolved by the time nephritis occurs, patients with nephritis of chronic infection have an active infection at the time nephritis becomes evident. Circulating immune complexes play an important role in the pathogenesis of acute GN in these diseases.
- Vasculitis: Nephritis of MRSA may have vasculitic lesions of the lower extremities.
- Predominantly nonglomerular diseases: Thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, atheroembolic renal disease, and acute hypersensitivity interstitial nephritis may present with features of acute nephritic syndrome and should be differentiated.
Workup
Laboratory Studies
- Urinalysis and sediment examination
- These tests are crucial in the evaluation of patients with acute nephritic syndrome.
- Look for protein, blood, RBCs and WBCs, dysmorphic red cells, acanthocytes, cellular (ie, RBC, WBC) casts, granular casts, and oval fat bodies. In some instances, marked sterile pyuria is present.
- Finding RBC casts is an almost pathognomonic sign of GN.
- Urine electrolytes, urine sodium, and fractional excretion of sodium (FENa) assays are needed to assess salt avidity.
- Blood, urea, and nitrogen (BUN); serum creatinine; and serum electrolytes (especially serum potassium level)
- Complete blood cell count
- Erythrocyte sedimentation rate
- Complement levels (C3, C4, CH50)
- Low C3 levels are found in almost all patients with acute poststreptococcal nephritis; C4 levels may be slightly low. Hypocomplementemia is noted in 73.9% of adult patients.
- Type III cryoglobulinemia may be present.
- Twenty-four–hour urine test for total protein and creatinine clearance: Remember that creatinine clearance is a "steady-state" measurement. The creatinine clearance may not reveal the true picture because of rapidly changing renal function; therefore, it is better to wait until renal function has stabilized before performing creatinine clearance.
- Antistreptolysin-O titer (ASOT) or streptozyme titer: Increasing titer levels confirm recent infection. In patients with skin infection, anti-DNase B titers are more sensitive than ASOT for infection with Streptococcus.
- Antibody to NAPR: Levels are elevated in streptococcal infections with GN but not in streptococcal infections without GN.
- If MRSA is the inciting agent, then hypocomplementemia is usually not present, but plasma immunoglobulins, especially IgA, are markedly elevated.
- Qualitative estimation of proteinuria: Determination of high-molecular weight (HMW) protein, like fractional excretion of IgG (FEIgG), and low-molecular weight (LMW) protein, like alpha-1-microglobulin, may help predict the clinical outcome and may help in guiding steroid and immunosuppressive therapy, especially in patients with primary glomerular diseases with nephrotic syndrome.
Imaging Studies
- Abdominal ultrasound
- Assesses renal size
- Assesses echogenicity of renal cortex
- Excludes obstruction
Procedures
- Generally, a renal biopsy is not necessary for a diagnosis of acute PSGN; however, in most cases, it is important because histology guides both prognosis and therapy.
Histologic Findings
Diffuse endocapillary proliferative changes are found (see Media files 1-2). The most common histologic patterns are diffuse (72.1%), focal (12.8%), and mesangial (8.1%) proliferative GN in adults.1 In postinfectious GN, the glomerulus is hypercellular with marked cellular infiltration (ie, polymorphonuclear neutrophils, monocytes). Immunofluorescence may show fine granular deposits of immunoglobulin G in a "starry sky" appearance (see Media file 3). Large subepithelial deposits may be observed on electron microscopy (see Media file 4). Crescents may be observed.
More on Glomerulonephritis, Acute |
| Overview: Glomerulonephritis, Acute |
 Differential Diagnoses & Workup: Glomerulonephritis, Acute |
| Treatment & Medication: Glomerulonephritis, Acute |
| Follow-up: Glomerulonephritis, Acute |
| Multimedia: Glomerulonephritis, Acute |
| References |
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References
Nasr SH, Markowitz GS, Stokes MB, et al. Acute postinfectious glomerulonephritis in the modern era: experience with 86 adults and review of the literature. Medicine (Baltimore). Jan 2008;87(1):21-32. [Medline].
Arze RS, Rashid H, Morley R, et al. Shunt nephritis: report of two cases and review of the literature. Clin Nephrol. Jan 1983;19(1):48-53. [Medline].
Baldwin DS, Gluck MC, Schacht RG, et al. The long-term course of poststreptococcal glomerulonephritis. Ann Intern Med. Mar 1974;80(3):342-58. [Medline].
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
