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 [[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.
The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agent. The majority of patients due to drug-induced interstitial nephritis, improve spontaneously with supportive care. However, [[renal function]] may not return to baseline. In conditions with persisting [[renal failure]] it is recommended to obtain a [[Biopsy|renal  biopsy]] and trial of [[glucocorticoids]] therapy for patients with AIN on biopsy.


== 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. Additional treatment measures include:
# Supportive care and maintaining adequate hydration
# Supportive care:
# Symptomatic relief for [[fever]], rash, and systemic symptoms
## Adequate hydration
# Control of blood pressure
## Symptomatic management for [[fever]], [[rash]], and systemic symptoms.
# Correct electrolyte imbalances  
# Control of blood pressure with anti-hypertensives.
# Reduce exposure to other nephrotoxic  agents
# Correction of  electrolyte imbalances  
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>
* No additional measures are recommend for patients who responded to supportive measures


 
* In conditions with persisting [[renal failure]] it is recommended to obtain a [[Biopsy|renal  biopsy]] and trial of [[glucocorticoids]] therapy for patients with AIN on biopsy..<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><ref>{{Cite journal
=== 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.<ref>{{Cite journal
  | author = [[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]]
  | author = [[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]]
  | title = Acute interstitial nephritis: clinical features and response to corticosteroid therapy
  | title = Acute interstitial nephritis: clinical features and response to corticosteroid therapy
Line 29: Line 27:
  | pmid = 15340098
  | pmid = 15340098
}}</ref>
}}</ref>
 
** '''Preferred regimen (1):''' [[Prednisone]] 1 mg/kg per day PO or equivalent IV dose (maximum of 40 to 60 mg)  
* 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.
*** Note: Recommended for 1-2 weeks, followed by gradual tappering.<ref>{{Cite journal
 
| author = [[J. Rossert]]
* 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.
| title = Drug-induced acute interstitial nephritis
* 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.
| journal = [[Kidney international]]
Lead toxicity: Repeated chelation therapy may improve renal function:
| volume = 60
 
| issue = 2
Succimer 10 mg/kg PO q8h × 5 days, then q12h × 14 days, or
| pages = 804–817
 
| year = 2001
EDTA 2 g IV/IM; if IM, use with 2% lidocaine.
| month = August
 
| doi = 10.1046/j.1523-1755.2001.060002804.x
SLE nephritis: Steroids +cyclophosphamide or azathioprine
| pmid = 11473672
 
}}</ref>
Urate nephropathy: Allopurinol to decrease urate level
** '''Alternative regimen (1)''': [[Mycophenolate sodium|Mycophenolate mofetil]]<ref>{{Cite journal
 
| author = [[Dean C. Preddie]], [[Glen S. Markowitz]], [[Jai Radhakrishnan]], [[Thomas L. Nickolas]], [[Vivette D. D'Agati]], [[Joshua A. Schwimmer]], [[Mark Gardenswartz]], [[Raquel Rosen]] & [[Gerald B. Appel]]
Use with caution because allopurinol is nephrotoxic.
| title = Mycophenolate mofetil for the treatment of interstitial nephritis
 
| journal = [[Clinical journal of the American Society of Nephrology : CJASN]]
Lithium-induced nephritis: Use amiloride as the adjunct.
| volume = 1
 
| issue = 4
Cidofovir-induced nephritis: Use probenecid as the adjunct
| pages = 718–722
| year = 2006
| month = July
| doi = 10.2215/CJN.01711105
| pmid = 17699278
}}</ref>
*** Note: Indicated in glucocorticoid resistant or contraindicated cases.


==References==
==References==

Latest revision as of 20:23, 1 August 2018

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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 agent. The majority of patients due to drug-induced interstitial nephritis, improve spontaneously with supportive care. However, renal function may not return to baseline. In conditions with persisting renal failure it is recommended to obtain a renal biopsy and trial of glucocorticoids therapy for patients with AIN on biopsy.

Medical Therapy

The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agent. Additional treatment measures include:

  1. Supportive care:
    1. Adequate hydration
    2. Symptomatic management for fever, rash, and systemic symptoms.
  2. Control of blood pressure with anti-hypertensives.
  3. Correction of electrolyte imbalances
  • No additional measures are recommend for patients who responded to supportive measures
  • In conditions with persisting renal failure it is recommended to obtain a renal biopsy and trial of glucocorticoids therapy for patients with AIN on biopsy..[1][2]
    • Preferred regimen (1): Prednisone 1 mg/kg per day PO or equivalent IV dose (maximum of 40 to 60 mg)
      • Note: Recommended for 1-2 weeks, followed by gradual tappering.[3]
    • Alternative regimen (1): Mycophenolate mofetil[4]
      • Note: Indicated in glucocorticoid resistant or contraindicated cases.

References

  1. ↑ 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.
  2. ↑ 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)
  3. ↑ 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)
  4. ↑ Dean C. Preddie, Glen S. Markowitz, Jai Radhakrishnan, Thomas L. Nickolas, Vivette D. D'Agati, Joshua A. Schwimmer, Mark Gardenswartz, Raquel Rosen & Gerald B. Appel (2006). "Mycophenolate mofetil for the treatment of interstitial nephritis". Clinical journal of the American Society of Nephrology : CJASN. 1 (4): 718–722. doi:10.2215/CJN.01711105. PMID 17699278. Unknown parameter |month= ignored (help)

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