Medication Summary

For acute allergic interstitial nephritis, if no spontaneous recovery in renal function is observed after cessation of the offending agent, implementing a short course of steroid therapy is generally recommended. No controlled studies exist on the effect of corticosteroids; therefore, no well-defined dosage and duration exist. Most practitioners recommend a relatively high dose (eg, 1 mg/kg prednisone) with a rapidly tapering regimen within several weeks.

Class Summary

Glucocorticoid agents have immunosuppressant effects and are used for treatment of autoimmune disorders.

Prednisone (Sterapred)

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Prednisone has anti-inflammatory properties and causes profound and varied metabolic effects by modifying the body's immune response to diverse stimuli. This agent may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear lymphocyte (PMN) activity. Prednisone also stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Class Summary

These agents promote the excretion of lead.

Succimer (Chemet)

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Succimer is a metal chelator, an analogue of dimercaprol that is used in lead poisoning. This agent is particularly useful in children with lead blood levels > 45 mcg/dL. Succimer is approved for chelation therapy in children for lead poisoning. However, its value in chronic lead nephropathy is not established.

Edetate calcium disodium (Calcium Disodium Versenate)

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Edetate is used for lead chelation; only the calcium disodium preparation should be used. In the context of this article, use of this medication is confined to testing (ie, to perform the ethylenediaminetetraacetic acid [EDTA] lead mobilization test for diagnosing lead as the etiology of chronic tubulointerstitial nephritis). Extended therapy with this agent to reduce body lead stores may be of possible benefit.

Questions

Bhandari J, Thada PK, Arif H. Tubulointerstitial Nephritis. 2021 Jan. [QxMD MEDLINE Link]. [Full Text].
Joyce E, Glasner P, Ranganathan S, Swiatecka-Urban A. Tubulointerstitial nephritis: diagnosis, treatment, and monitoring. Pediatr Nephrol. 2017 Apr. 32 (4):577-587. [QxMD MEDLINE Link]. [Full Text].
Harris RC, Neilson EG. Toward a unified theory of renal progression. Annu Rev Med. 2006. 57:365-80. [QxMD MEDLINE Link].
Liu Y. Renal fibrosis: new insights into the pathogenesis and therapeutics. Kidney Int. 2006 Jan. 69(2):213-7. [QxMD MEDLINE Link]. [Full Text].
Rangan GK, Wang Y, Tay YC, Harris DC. Inhibition of nuclear factor-kappaB activation reduces cortical tubulointerstitial injury in proteinuric rats. Kidney Int. 1999 Jul. 56(1):118-34. [QxMD MEDLINE Link].
Hadded S, Harzallah A, Chargui S, Hajji M, Kaaroud H, Goucha R, et al. [Etiologies and prognostic factors of acute interstitial nephritis]. Nephrol Ther. 2021 Apr. 17 (2):114-119. [QxMD MEDLINE Link].
Martínez-Valenzuela L, Draibe J, Fulladosa X, Gomà M, Gómez F, Antón P, et al. Acute Tubulointerstitial Nephritis in Clinical Oncology: A Comprehensive Review. Int J Mol Sci. 2021 Feb 26. 22 (5):[QxMD MEDLINE Link]. [Full Text].
De Broe ME, Elseviers MM. Over-the-counter analgesic use. J Am Soc Nephrol. 2009 May 7. [QxMD MEDLINE Link].
De Broe ME. Chinese herbs nephropathy and Balkan endemic nephropathy: toward a single entity, aristolochic acid nephropathy. Kidney Int. 2012 Mar. 81(6):513-5. [QxMD MEDLINE Link].
Jelaković B, Dika Ž, Arlt VM, Stiborova M, Pavlović NM, Nikolić J, et al. Balkan Endemic Nephropathy and the Causative Role of Aristolochic Acid. Semin Nephrol. 2019 May. 39 (3):284-296. [QxMD MEDLINE Link]. [Full Text].
Maripuri S, Grande JP, Osborn TG, et al. Renal involvement in primary Sjögren''s syndrome: a clinicopathologic study. Clin J Am Soc Nephrol. 2009 Sep. 4(9):1423-31. [QxMD MEDLINE Link]. [Full Text].
Jain A, Srinivas BH, Emmanuel D, Jain VK, Parameshwaran S, Negi VS. Renal involvement in primary Sjogren's syndrome: a prospective cohort study. Rheumatol Int. 2018 Aug 23. [QxMD MEDLINE Link].
Slade N, Moll UM, Brdar B, et al. p53 mutations as fingerprints for aristolochic acid: an environmental carcinogen in endemic (Balkan) nephropathy. Mutat Res. 2009 Apr 26. 663(1-2):1-6. [QxMD MEDLINE Link]. [Full Text].
Salvadori M, Tsalouchos A. Immunoglobulin G4-related kidney diseases: An updated review. World J Nephrol. 2018 Jan 6. 7 (1):29-40. [QxMD MEDLINE Link]. [Full Text].
Mbengue M, Goumri N, Niang A. IgG4-related kidney disease: Pathogenesis, diagnosis, and treatment. Clin Nephrol. 2021 Jun. 95 (6):292-302. [QxMD MEDLINE Link].
Saeki T, Nishi S, Imai N, Ito T, Yamazaki H, Kawano M, et al. Clinicopathological characteristics of patients with IgG4-related tubulointerstitial nephritis. Kidney Int. 2010 Nov. 78(10):1016-23. [QxMD MEDLINE Link].
McMahon BA, Novick T, Scheel PJ, Bagnasco S, Atta MG. Rituximab for the Treatment of IgG4-Related Tubulointerstitial Nephritis: Case Report and Review of the Literature. Medicine (Baltimore). 2015 Aug. 94 (32):e1366. [QxMD MEDLINE Link]. [Full Text].
Inoue D, Yoshida K, Yoneda N, Ozaki K, Matsubara T, Nagai K, et al. IgG4-related disease: dataset of 235 consecutive patients. Medicine (Baltimore). 2015 Apr. 94 (15):e680. [QxMD MEDLINE Link]. [Full Text].
Mackensen F, Billing H. Tubulointerstitial nephritis and uveitis syndrome. Curr Opin Ophthalmol. 2009 Sep 11. [QxMD MEDLINE Link].
Patel S, Hossain MA, Ajam F, Patel M, Nakrani M, Patel J, et al. Dabigatran-Induced Acute Interstitial Nephritis: An Important Complication of Newer Oral Anticoagulation Agents. J Clin Med Res. 2018 Oct. 10 (10):791-794. [QxMD MEDLINE Link]. [Full Text].
Roy S, Awogbemi T, Holt RCL. Acute tubulointerstitial nephritis in children- a retrospective case series in a UK tertiary paediatric centre. BMC Nephrol. 2020 Jan 14. 21 (1):17. [QxMD MEDLINE Link]. [Full Text].
Clive DM, Vanguri VK. The Syndrome of Tubulointerstitial Nephritis With Uveitis (TINU). Am J Kidney Dis. 2018 Jul. 72 (1):118-128. [QxMD MEDLINE Link].
Kanno H, Ishida K, Yamada W, Shiraki I, Murase H, Yamagishi Y, et al. Clinical and Genetic Features of Tubulointerstitial Nephritis and Uveitis Syndrome with Long-Term Follow-Up. J Ophthalmol. 2018. 2018:4586532. [QxMD MEDLINE Link]. [Full Text].
Border WA, Holbrook JH, Peterson MC. Gallium citrate Ga 67 scanning in acute renal failure. West J Med. 1995 May. 162(5):477-8. [QxMD MEDLINE Link].
Linton AL, Richmond JM, Clark WF, Lindsay RM, Driedger AA, Lamki LM. Gallium67 scintigraphy in the diagnosis of acute renal disease. Clin Nephrol. 1985 Aug. 24(2):84-7. [QxMD MEDLINE Link].
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. [QxMD MEDLINE Link].
Shi Y, Su T, Qu L, Wang C, Li X, Yang L. Evaluation of urinary biomarkers for the prognosis of drug-associated chronic tubulointerstitial nephritis. Am J Med Sci. 2013 Oct. 346(4):283-8. [QxMD MEDLINE Link].
Quinto LR, Sukkar L, Gallagher M. The effectiveness of corticosteroid compared to non-corticosteroid therapy for the treatment of drug-induced acute interstitial nephritis: A systematic review. Intern Med J. 2018 Aug 21. [QxMD MEDLINE Link].
Lin JL, Lin-Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes. N Engl J Med. 2003 Jan 23. 348(4):277-86. [QxMD MEDLINE Link].
Lin JL, Lin-Tan DT, Yu CC, Li YJ, Huang YY, Li KL. Environmental exposure to lead and progressive diabetic nephropathy in patients with type II diabetes. Kidney Int. 2006 Jun. 69(11):2049-56. [QxMD MEDLINE Link].

Media Gallery

Tubulointerstitial nephritis: Kidney biopsy reveals acute interstitial nephritis. The renal cortex shows a diffuse interstitial, predominantly mononuclear, inflammatory infiltrate with no changes to the glomerulus. Tubules in the center of the field are separated by inflammation and edema, as compared with the more normal architecture in the right lower area (periodic acid–Schiff, 40 X).
Tubulointerstitial nephritis. On a kidney biopsy, the diagnosis of acute interstitial nephritis is based on the active inflammatory infiltrate on the right with unaffected glomeruli. Interstitial edema and fibrosis are present on the left side of the field, where some tubules show thickened basement membrane (hematoxylin and eosin, 20 X).
Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The interstitium is expanded by mononuclear inflammatory infiltrate and edema. Acute tubular damage is present; some tubules are distended and contain granular casts (hematoxylin and eosin, 40 X).
Tubulointerstitial nephritis. Kidney biopsy shows acute crescentic glomerulonephritis. The glomerular tuft is compressed by the proliferation of epithelial cells, forming a crescent. In addition, the interstitium shows mononuclear inflammatory infiltrate and edema (periodic acid–Schiff, 40 X).
Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The mononuclear inflammatory infiltrate contains abundant eosinophils, suggesting an allergic etiology. Severe tubular damage is observed (hematoxylin and eosin, 40 X).
Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The inflammatory infiltrate forms an ill-defined granuloma, suggesting allergic or infectious etiologies. A partially destroyed tubule is present (periodic acid–Schiff, 40 X).
Tubulointerstitial nephritis. Kidney biopsy shows chronic tubulointerstitial nephritis. The interstitium is expanded by fibrosis, with distortion of tubules and periglomerular fibrosis. Glomeruli do not show pathologic changes (hematoxylin and eosin, 20 X).
Tubulointerstitial nephritis. Kidney biopsy in interstitial nephritis shows a cholesterol microembolism. The 2 arterioles in the center are occluded by elongated crystals (hematoxylin and eosin, 20 X).
Tubulointerstitial nephritis. Kidney biopsy in interstitial nephritis shows a cholesterol microembolism. The arteriole in the center of the field has a thickened wall. The lumen is occluded by elongated spaces, corresponding to dissolved crystals surrounded by cellular reaction. The 2 glomeruli flanking the arteriole are sclerotic and hardly recognizable (hematoxylin and eosin, 40 X).