Interstitial nephritis medical therapy: Difference between revisions
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==Overview== | ==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 | 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 [[Creatinine|serum creatinine]] or those who demonstrate betterment after discontinuation of offending agent; otherwise if [[renal failure]] persists after removing the culprit drug, obtaining a [[Biopsy|renal biopsy]] and attempt [[glucocorticoids]] therapy for patients with biopsy-confirmed AIN must be considered. | ||
== Medical Therapy == | == Medical Therapy == | ||
The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agent, as well as following measures: | The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agent, as well as following measures: | ||
# Supportive care and maintaining adequate hydration | # Supportive care and maintaining adequate hydration | ||
# Symptomatic relief for fever, rash, and systemic symptoms | # Symptomatic relief for [[fever]], rash, and systemic symptoms | ||
# Control of blood pressure | # Control of blood pressure | ||
# Correct electrolyte imbalances | # Correct electrolyte imbalances | ||
# Reduce exposure to other nephrotoxic agents | # 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 | 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 [[Biopsy|renal biopsy]] and attempt [[glucocorticoids]] therapy for patients with biopsy-confirmed AIN must be considered.<ref name="BakerPusey2004">{{cite journal|last1=Baker|first1=R. J.|last2=Pusey|first2=C. D.|title=The changing profile of acute tubulointerstitial nephritis|journal=Nephrology Dialysis Transplantation|volume=19|issue=1|year=2004|pages=8–11|issn=0931-0509|doi=10.1093/ndt/gfg464}}</ref> | ||
=== Glucocorticoid therapy === | === Glucocorticoid therapy === | ||
* Glucocorticoid therapy is recommended among patients with critical rise in the | * Glucocorticoid therapy is recommended among patients with critical rise in the serum creatinine, or those whose renal failure persists after removing the offending agents; although before beginning of glucocorticoid therapy obtaining a kidney biopsy and confirmation the diagnosis is necessary. | ||
* 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. | * 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. | ||
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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 critical rise in the serum creatinine, or those whose renal failure persists after removing the offending agents; although before beginning of glucocorticoid therapy obtaining a kidney biopsy and confirmation the diagnosis is necessary.
- 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.
- 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 adjunct.
Cidofovir-induced nephritis: Use probenecid as 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.