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Pediatric Nephritis Workup

  • Author: Sahar Fathallah-Shaykh, MD; Chief Editor: Craig B Langman, MD  more...
Updated: Oct 12, 2015

Approach Considerations

The most helpful laboratory studies include the following:

  • Electrolyte, creatinine, and blood urea nitrogen (BUN) levels
  • Complete blood count (CBC)
  • 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
  • Serum IgA measurement [1]

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.[7] 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.

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, 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.

Renal biopsy

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.


Histologic Findings

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.

Contributor Information and Disclosures

Sahar Fathallah-Shaykh, MD Associate Professor of Pediatric Nephrology, University of Alabama at Birmingham School of Medicine; Consulting Staff, Division of Pediatric Nephrology, Medical Director of Pediatric Dialysis Unit, Children's of Alabama

Sahar Fathallah-Shaykh, MD is a member of the following medical societies: American Society of Nephrology, American Society of Pediatric Nephrology

Disclosure: Nothing to disclose.


Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical and Dental Associations, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, Southwest Pediatric Nephrology Study Group

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Frederick J Kaskel, MD, PhD Director of the Division and Training Program in Pediatric Nephrology, Vice Chair, Department of Pediatrics, Montefiore Medical Center and Albert Einstein School of Medicine

Frederick J Kaskel, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, Eastern Society for Pediatric Research, Renal Physicians Association, American Academy of Pediatrics, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Federation of American Societies for Experimental Biology, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Sigma Xi, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Uri S Alon, MD Director of Bone and Mineral Disorders Clinic and Renal Research Laboratory, Children's Mercy Hospital of Kansas City; Professor, Department of Pediatrics, Division of Pediatric Nephrology, University of Missouri-Kansas City School of Medicine

Uri S Alon, MD is a member of the following medical societies: American Federation for Medical Research

Disclosure: Nothing to disclose.

  1. Wen YK, Chen ML. IgA-Dominant Postinfectious Glomerulonephritis: Not Peculiar to Staphylococcal Infection and Diabetic Patients. Ren Fail. 2011. 33(5):480-5. [Medline].

  2. Vachvanichsanong P, McNeil E. Pediatric lupus nephritis: more options, more chances?. Lupus. 2013 Apr 29. [Medline].

  3. 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].

  4. 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].

  5. 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].

  6. 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].

  7. 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].

  8. 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].

  9. 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].

  10. 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].

  11. 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].

  12. 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].

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