Pediatric Nephritis Workup
- Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD more...
The most helpful laboratory studies include the following:
Electrolyte, creatinine, and blood urea nitrogen (BUN) levels
Complete blood count (CBC)
Measurement of complement components (ie, C3, C4)
Antistreptolysin-O (ASO) titer
Perinuclear antineutrophil cytoplasmic antibody (P-ANCA) measurement
Cellular antineutrophil cytoplasmic antibody (C-ANCA) assessment
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 this disorder 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 in 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 in TIN 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 an inability to acidify urine (distal renal tubular acidosis), to regulate sodium balance, and to secrete potassium. Lesions affecting the medulla and papilla result in an inability to concentrate 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.
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, a 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.
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. Kidney biopsy findings are diagnostic for TIN.
In glomerulonephritis (GN), light microscopy usually reveals infiltration of the kidney by lymphocytes, polymorphonuclear leukocytes, or both. Immunofluorescence microscopy may reveal IgG, IgA, IgM, or complement in mesangial or vascular distribution, depending on the type of GN. Electron microscopy may reveal deposits in mesangial, subendothelial, or subepithelial tissue or in a combination of tissues, depending on the type of GN present. Replacement of renal tissue by scar tissue (tubular atrophy and interstitial fibrosis) is the final common pathway for several types of GN.
For tubulointerstitial nephritis (TIN), light microscopy reveals focal interstitial infiltrates of edema that contain lymphocytes and eosinophils. Tubular injury is usually greater than glomerular or vascular injury.
Wen YK, Chen ML. IgA-Dominant Postinfectious Glomerulonephritis: Not Peculiar to Staphylococcal Infection and Diabetic Patients. Ren Fail. 2011. 33(5):480-5. [Medline].
Vachvanichsanong P, McNeil E. Pediatric lupus nephritis: more options, more chances?. Lupus. 2013 Apr 29. [Medline].
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. 2004 Feb. 43(2):197-208. [Medline].
Endo A, Fuchigami T, Hasegawa M, Hashimoto K, Fujita Y, Inamo Y, et al. Posterior reversible encephalopathy syndrome in childhood: report of four cases and review of the literature. Pediatr Emerg Care. 2012 Feb. 28(2):153-7. [Medline].
Sfaihi L, Kamoun F, Hentati Y, Tiss O, Maaloul I, Kamoun T, et al. [Posterior reversible encephalopathy syndrome induced by acute postinfectious glomerulonephritis.]. Arch Pediatr. 2013 Apr 22. [Medline].
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].
Hettinga YM, Scheerlinck LM, Lilien MR, Rothova A, de Boer JH. The value of measuring urinary β2-microglobulin and serum creatinine for detecting tubulointerstitial nephritis and uveitis syndrome in young patients with uveitis. JAMA Ophthalmol. 2015 Feb. 133 (2):140-5. [Medline].
Jahnukainen T, Saarela V, Arikoski P, Ylinen E, Rönnholm K, Ala-Houhala M, et al. Prednisone in the treatment of tubulointerstitial nephritis in children. Pediatr Nephrol. 2013 Apr 19. [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].
Medjeral-Thomas NR, O'Shaughnessy MM, O'Regan JA, Traynor C, Flanagan M, Wong L, et al. C3 glomerulopathy: clinicopathologic features and predictors of outcome. Clin J Am Soc Nephrol. 2014 Jan. 9 (1):46-53. [Medline]. [Full Text].
Zhang Y, Nester CM, Martin B, Skjoedt MO, Meyer NC, Shao D, et al. Defining the complement biomarker profile of C3 glomerulopathy. Clin J Am Soc Nephrol. 2014 Nov 7. 9 (11):1876-82. [Medline].
Nicolas C, Vuiblet V, Baudouin V, Macher MA, Vrillon I, Biebuyck-Gouge N, et al. C3 nephritic factor associated with C3 glomerulopathy in children. Pediatr Nephrol. 2014 Jan. 29 (1):85-94. [Medline].