eMedicine Specialties > Pediatrics: General Medicine > Nephrology
Nephritis: Differential Diagnoses & Workup
Updated: Jul 18, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Differential Diagnoses
Other Problems to Be Considered
Glomerulonephritis (GN)
Takayasu disease
Membranoproliferative GN
Other: Conditions that produce hematuria, decreased clearance, and, sometimes, hypertension include all specific types of GN, anatomic abnormalities of the kidneys, renal stones, tumors, drugs, and infection.
Workup
Laboratory Studies
- The most helpful laboratory studies include assessment of electrolyte, creatinine, and BUN levels; CBC count; urinalysis; urine culture; lupus serologies; measurement of complement components (ie, C3, C4); antistreptolysin-O (ASO) titer; anti-DNAase B, perinuclear antineutrophil cytoplasmic antibody (P-ANCA) measurement; cellular antineutrophil cytoplasmic antibody (C-ANCA) assessment; and serum IgA measurement.
- If the child has a history consistent with acute poststreptococcal glomerulonephritis (GN), such as low C3, positive ASO, and anti-DNAase B, a provisional diagnosis of acute poststreptococcal GN can be made. Supportive care and observation for improvement within 10-14 days is reasonable.
- If a diagnosis of acute poststreptococcal GN seems unlikely, a percutaneous renal biopsy is the single most effective mechanism to arrive at a pathologic diagnosis.
- Laboratory findings with tubulointerstitial nephritis (TIN) include hematuria, eosinophilia, sterile pyuria, low-grade proteinuria, eosinophiluria, and urinary white blood cell casts.
- A percutaneous renal biopsy is the criterion standard for diagnosing TIN.
- With TIN, the hallmarks of GN (ie, edema, hypertension, sodium chloride retention) are not present. Tubular dysfunction is the predominant feature.
- The pattern of tubular dysfunction that develops depends on the tubular segment(s) involved. Proximal tubular lesions result in aminoaciduria, glucosuria, phosphaturia, uricosuria, beta2 microglobinuria, and bicarbonaturia, often producing proximal renal tubular acidosis. Lesions involving the distal tubule result in inability to acidify the urine (distal renal tubular acidosis), to regulate sodium balance, and to secrete potassium. Lesions affecting the medulla and papilla result in inability to concentrate the urine.
- These tubular functions may be tested by calculating the fractional excretion of phosphate or bicarbonate, measuring the urinary glucose excretion, and measuring the urine pH and osmolality with fasting.
Imaging Studies
- Renal ultrasonography is usually performed to exclude other causes of hypertension and hematuria, such as renal artery stenosis (ie, small abnormal kidney on one side), anatomic abnormalities, tumor, and stones. The kidneys are frequently echodense when GN is present. The kidneys may be abnormally large or small.
- No imaging tests are sensitive or specific for TIN. Renal ultrasonography may show large kidneys with normal echogenicity. Gallium scanning may reveal increased uptake.
Procedures
- If a specific diagnosis is needed for a child with hematuria, proteinuria, edema, and hypertension (ie, nephritis), a percutaneous renal biopsy usually is the criterion standard for identifying a specific pathology.
- The kidney biopsy findings are diagnostic for TIN.
Histologic Findings
- In GN, light microscopy usually reveals infiltration of the kidney by lymphocytes, polymorphonuclear leukocytes, or both. Immunofluorescence microscopy may reveal immunoglobulin G (IgG), IgA, immunoglobulin M (IgM), or complement in mesangial or vascular distribution, depending on the type of nephritis. Electron microscopy may reveal deposits in mesangial, subendothelial, subepithelial, or a combination of tissues, depending on the type of nephritis present. Replacement of renal tissue by scar tissue (tubular atrophy and interstitial fibrosis) is the final common pathway for several types of GN.
- For TIN, light microscopy reveals focal interstitial infiltrates of edema that contains lymphocytes and eosinophils. Tubular injury is usually greater than glomerular or vascular injury.
More on Nephritis |
| Overview: Nephritis |
 Differential Diagnoses & Workup: Nephritis |
| Treatment & Medication: Nephritis |
| Follow-up: Nephritis |
| References |
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References
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Eknoyan G. Tubulointerstial nephritis. In: Massry SG, Glassock RJ, eds. Massry and Glassock's Textbook of Nephrology. Philadelphia, PA: Lippincott Williams & Wilkins; 2001:746-58.
Flanc RS, Roberts MA, Strippoli GF, et al. Treatment of diffuse proliferative lupus nephritis: a meta-analysis of randomized controlled trials. Am J Kidney Dis. Feb 2004;43(2):197-208. [Medline].
Glassock RJ, Cohen AH, Adler SG. Primary glomerular diseases. In: Brenner BM, ed. The Kidney. 5th ed. Philadelphia, PA: WB Saunders Co; 1996:1392-1497.
Goda C, Kotake S, Ichiishi A, et al. Clinical features in tubulointerstitial nephritis and uveitis (TINU) syndrome. Am J Ophthalmol. 2005;140(4):637-41. [Medline].
Gonzalez B, Hernandez P, Olguin H, et al. Changes in the survival of patients with systemic lupus erythematosus in childhood: 30 years experience in Chile. Lupus. 2005;14(11):918-23. [Medline].
Lee JW, Kim HJ, Sung SH, Lee SJ. A case of tubulointerstitial nephritis and uveitis syndrome with severe immunologic dysregulation. Pediatr Nephrol. 2005;20(12):1805-8. [Medline].
Further Reading
Keywords
nephritis, glomerulonephritis, GN, Bright disease, interstitial nephritis, tubulointerstitial disease, tubulointerstitial nephritis, TIN, hypertension, hematuria, edema, systemic lupus erythematosus, SLE, membranoproliferative glomerulonephritis, membranoproliferative GN, mesangial proliferative GN, Henoch-Schönlein purpura, immunoglobulin A nephropathy, Alport syndrome, vesicoureteral reflux, oxalosis, Crohn disease, cerebral hemorrhage, hyperkalemia, pulmonary edema, heart failure, ascites, encephalopathy, polyuria
