Tubulointerstitial Nephritis Treatment & Management

Updated: Jan 07, 2022
  • Author: A Brent Alper, Jr, MD, MPH; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Approach Considerations

Corticosteroids have been a mainstay of therapy for tubulointerstitial nephritis, but mycophenolate mofetil may also have a role. Ultimately, however, treatment depends on the underlying etiology. [2]

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.


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.

A systematic review concluded that limited evidence does not support the use of corticosteroids in the treatment of drug-induced cases. The review included eight studies with 430 patients (300 of whom received corticosteroids and 130 of whom did not): four studies showed no difference in serum creatinine levels between the corticosteroid and comparator arms, while four studies found a benefit. [28]


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. [29, 30] This was found in both diabetics and nondiabetics. [29, 30] 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 statins are expected to result in improved outcomes. There is also no effective treatment available for cholesterol microembolic disease.

Immunoglobulin G (IgG)-4–related disease

McMahon and colleagues reported a case of a 58-year-old man initially misdiagnosed with chronic interstitial nephritis secondary to renal sarcoid and treated with repeated doses of prednisone. After his third relapse, a repeat renal biopsy confirmed a diagnosis of IgG4-tubulointerstitial nephritis. The patient had become refractory to treatment with prednisone but achieved sustained improvement in renal function after receiving rituximab. At 1 year post-treatment, serum creatinine remained at baseline and a reduction in his kidney size was observed with imaging. [17]