Interstitial nephritis medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohsen Basiri M.D.
Overview
The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agen. The majority of patients due to drug-induced interstitial nephritis, improve spontaneously, however, renal function may not return to previous condition. No additional measures is needed among patients with minimal rise in the serum creatinine or those who demonstrate betterment after discontinuation of offending agent; otherwise if renal failure persists after removing the culprit drug, obtaining a renal biopsy and attempt glucocorticoids therapy for patients with biopsy-confirmed AIN must be considered.
Medical Therapy
The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agent, as well as following measures:
- Supportive care and maintaining adequate hydration
- Symptomatic relief for fever, rash, and systemic symptoms
- Control of blood pressure
- Correct electrolyte imbalances
- Reduce exposure to other nephrotoxic agents
The majority of patients involved with drug-induced AIN, improve spontaneously, and no additional measures are needed among patients with minimal rise in the serum creatinine or those who show betterment after discontinuation of offending agent; otherwise if renal failure persists after removing the culprit drug, obtaining a renal biopsy and attempt glucocorticoids therapy for patients with biopsy-confirmed AIN must be considered.[1]
Glucocorticoid therapy
- Glucocorticoid therapy is recommended among patients with the critical rise in the serum creatinine, or those whose renal failure persists after removing the offending agents; although before the beginning of glucocorticoid therapy obtaining a kidney biopsy and confirmation the diagnosis is necessary.[2]
- Preferred regimen: Prednisone 1 mg/kg per day PO or equivalent IV dose (maximum of 40 to 60 mg) for a minimum of one to two weeks, by a gradual taper over 3-4 weeks.[3]
- Alternative regimen: In patients who do not respond to corticosteroids within 2-3 weeks, or who are glucocorticoid dependent or glucocorticoid resistant (as with NSAID-induced disease), mycophenolate mofetil may be considered.
- The manifestations and diagnosis of AIN and the approach to the management of patients diagnosed with infection-induced AIN, tubulointerstitial nephritis and uveitis, and renal sarcoidosis are presented separately.
Lead toxicity: Repeated chelation therapy may improve renal function:
Succimer 10 mg/kg PO q8h × 5 days, then q12h × 14 days, or
EDTA 2 g IV/IM; if IM, use with 2% lidocaine.
SLE nephritis: Steroids +cyclophosphamide or azathioprine
Urate nephropathy: Allopurinol to decrease urate level
Use with caution because allopurinol is nephrotoxic.
Lithium-induced nephritis: Use amiloride as the adjunct.
Cidofovir-induced nephritis: Use probenecid as the adjunct
References
- ↑ Baker, R. J.; Pusey, C. D. (2004). "The changing profile of acute tubulointerstitial nephritis". Nephrology Dialysis Transplantation. 19 (1): 8–11. doi:10.1093/ndt/gfg464. ISSN 0931-0509.
- ↑ Michael R. Clarkson, Louise Giblin, Fionnuala P. O'Connell, Patrick O'Kelly, Joseph J. Walshe, Peter Conlon, Yvonne O'Meara, Anthony Dormon, Eileen Campbell & John Donohoe (2004). "Acute interstitial nephritis: clinical features and response to corticosteroid therapy". Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 19 (11): 2778–2783. doi:10.1093/ndt/gfh485. PMID 15340098. Unknown parameter
|month=ignored (help) - ↑ J. Rossert (2001). "Drug-induced acute interstitial nephritis". Kidney international. 60 (2): 804–817. doi:10.1046/j.1523-1755.2001.060002804.x. PMID 11473672. Unknown parameter
|month=ignored (help)