Tubulointerstitial Nephritis Medication

  • Author: A Brent Alper Jr, MD, MPH; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jun 30, 2011
 

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.

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Glucocorticoids

Class Summary

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

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Prednisone (Sterapred)

 

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.

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Chelating agents

Class Summary

These agents promote the excretion of lead.

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Succimer (Chemet)

 

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.

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Edetate calcium disodium (Calcium Disodium Versenate)

 

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.

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Contributor Information and Disclosures
Author

A Brent Alper Jr, MD, MPH  Associate Professor of Medicine, Section of Nephrology and Hypertension, Department of Medicine, Tulane University School of Medicine

A Brent Alper Jr, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Hypertension, American Society of Nephrology, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

F John Gennari, MD  Associate Chair for Academic Affairs, Robert F and Genevieve B Patrick Professor, Department of Medicine, University of Vermont College of Medicine

F John Gennari, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ajay K Singh, MB, MRCP, MBA  Associate Professor of Medicine, Harvard Medical School; Director of Dialysis, Renal Division, Brigham and Women's Hospital; Director, Brigham/Falkner Dialysis Unit, Faulkner Hospital

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgments

We wish to thank Suzanne Meleg-Smith, MD, for her previous contributions to this article.

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Kidney biopsy. This is an example of 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).
Kidney biopsy. Shown here is an example of acute interstitial nephritis. The diagnosis 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).
Kidney biopsy. This image 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).
Kidney biopsy in interstitial nephritis. Acute crescentic glomerulonephritis. The glomerular tuft is compressed by the proliferation of epithelial cells, forming a crescent. The interstitium shows mononuclear inflammatory infiltrate and edema (periodic acid-Schiff, 40 X).
Kidney biopsy. This image 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).
Kidney biopsy. This image 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).
Kidney biopsy. This image 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).
Kidney biopsy in interstitial nephritis. This image shows a cholesterol microembolism. The 2 arterioles in the center are occluded by elongated crystals (hematoxylin and eosin, 20 X).
Kidney biopsy in interstitial nephritis. This image 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).
 
 
 
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