Tubulointerstitial Nephritis Treatment & Management

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

Approach Considerations

Most patients presenting with renal insufficiency, proteinuria, and/or acid-base electrolyte disorders require consultation with a nephrologist. These patients may require inpatient care until stabilization or resolution.

Hypertensive patients should be on a low-sodium diet. For all patients with early renal disease, recommend general guidelines for a healthy diet (ie, low-fat [low-cholesterol] diet rich in fresh fruits and vegetables such as the Dietary Approaches to Stop Hypertension [DASH] diet).

Provide patients with acute interstitial nephritis with follow-up care until resolution. Patients who do not recover renal function and those with chronic tubulointerstitial nephritis should receive long-term follow-up care to ensure that optimal control of blood pressure is achieved and to protect kidneys from further potentially nephrotoxic therapies and/or interventions.

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Management of Acute Tubulointerstitial Nephritis

In cases of acute tubulointerstitial nephritis due to hypersensitivity reactions (allergic interstitial nephritis), early recognition and prompt discontinuation of the offending drug are helpful; cessation of the offending agent usually, but not always, results in complete recovery in patients. However, the rate of recovery is variable, and, in some patients, renal failure persists for many weeks before renal function improves. Some patients may progress to chronic renal insufficiency.

Obtain a thorough history of previously documented drug allergies before prescribing a new drug.

If no sign of improvement is observed within a few days of discontinuation of the offending agent, consider therapy with steroids. Although controlled trials are lacking, many authors suggest using prednisone at relatively high doses (eg, 1 mg/kg for 4-6 wks with rapid tapering of the dose). This intervention may improve the outcome, speeding renal recovery and reducing the requirement for dialysis.

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Management of Chronic Tubulointerstitial Disease

Treatment of chronic tubulointerstitial nephritis depends on the etiology and generally consists of supportive measures, such as adequate blood pressure control and management of anemia.

Analgesic nephropathy

Treatment of analgesic nephropathy is supportive and also includes discontinuation of analgesic use. Long-term follow-up studies have shown progression to end-stage renal disease (ESRD) requiring dialysis, and increased incidence of uroepithelial cancers is also observed in patients with analgesic nephropathy.

Cyclosporine/tacrolimus–induced renal failure

Reduce the cyclosporine/tacrolimus doses and target trough levels. Discontinuing these medications and/or switching to other immunosuppressives (eg, rapamycin), especially in those with more advanced renal failure, should also be considered.

Lead nephropathy

Body burden of lead and bone lead concentration can be reduced by extended chelation treatment using ethylenediaminetetraacetic acid (EDTA) (versenate). Chelation therapy is of proven value and must be implemented in acute lead poisoning. Although the oral chelating agent succimer (Chemet) has proved highly successful in treating children, it has not been widely used in adults. Nevertheless, it appears effective in reducing body lead stores.

Chelation therapy with EDTA may slow progressive renal insufficiency in patients with mild lead intoxication. Several studies from Taiwan have shown that chelation therapy in patients with modest increases in body lead burden (ie, 80-600 µg of lead) significantly slowed and/or reversed the rate of decline in the glomerular filtration rate (GFR) compared with placebo.[12, 13] This was found in both diabetics and nondiabetics.[12, 13] However, given that these studies took place in Taiwan, it is difficult to generalize these results. Further study is needed before this treatment can be recommended.

Because no effective therapy reverses the long-term consequences of lead poisoning, the best therapy is prevention and awareness of potential environmental and occupational sources for lead exposure. Therefore, implement environmental measures, such as removal of lead from indoor paint and gasoline, and eliminate other sources of exposure. Use caution with imported ceramics, particularly if glazed.

In patients with established lead nephropathy, treatment consists of management of hypertension, gout, and chronic renal insufficiency. Many patients with lead nephropathy progress to end-stage kidney failure and require dialysis.

Atherosclerotic kidney disease and cholesterol microembolic disease

No specific therapy is available for atherosclerotic kidney disease, but good control of hypertension, cessation of smoking, and vigorous control of dyslipidemia with diet and with hepatic 3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are expected to result in improved outcomes. There is also no effective treatment available for cholesterol microembolic disease.

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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.

References
  1. Harris RC, Neilson EG. Toward a unified theory of renal progression. Annu Rev Med. 2006;57:365-80. [Medline].

  2. Liu Y. Renal fibrosis: new insights into the pathogenesis and therapeutics. Kidney Int. Jan 2006;69(2):213-7. [Medline]. [Full Text].

  3. Rangan GK, Wang Y, Tay YC, Harris DC. Inhibition of nuclear factor-kappaB activation reduces cortical tubulointerstitial injury in proteinuric rats. Kidney Int. Jul 1999;56(1):118-34. [Medline].

  4. De Broe ME, Elseviers MM. Over-the-counter analgesic use. J Am Soc Nephrol. May 7 2009;[Medline].

  5. Slade N, Moll UM, Brdar B, et al. p53 mutations as fingerprints for aristolochic acid: an environmental carcinogen in endemic (Balkan) nephropathy. Mutat Res. Apr 26 2009;663(1-2):1-6. [Medline].

  6. Karmaus W, Dimitrov P, Simeonov V, et al. Offspring of parents with Balkan Endemic Nephropathy have higher C-reactive protein levels suggestive of inflammatory processes: a longitudinal study. BMC Nephrol. Apr 28 2009;10:10. [Medline]. [Full Text].

  7. Maripuri S, Grande JP, Osborn TG, et al. Renal involvement in primary Sjögren's syndrome: a clinicopathologic study. Clin J Am Soc Nephrol. Sep 2009;4(9):1423-31. [Medline].

  8. 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. Nov 2010;78(10):1016-23. [Medline].

  9. Mackensen F, Billing H. Tubulointerstitial nephritis and uveitis syndrome. Curr Opin Ophthalmol. Sep 11 2009;[Medline].

  10. Border WA, Holbrook JH, Peterson MC. Gallium citrate Ga 67 scanning in acute renal failure. West J Med. May 1995;162(5):477-8. [Medline].

  11. Linton AL, Richmond JM, Clark WF, Lindsay RM, Driedger AA, Lamki LM. Gallium67 scintigraphy in the diagnosis of acute renal disease. Clin Nephrol. Aug 1985;24(2):84-7. [Medline].

  12. 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. Jan 23 2003;348(4):277-86. [Medline].

  13. 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. Jun 2006;69(11):2049-56. [Medline].

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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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