Trimethoprim-sulfamethoxazole induced acute interstitial nephritis in renal allografts; clinical course and outcome.

Hdl Handle:
http://hdl.handle.net/10147/127236
Title:
Trimethoprim-sulfamethoxazole induced acute interstitial nephritis in renal allografts; clinical course and outcome.
Authors:
Garvey, J P; Brown, C M; Chotirmall, S H; Dorman, A M; Conlon, P J; Walshe, J J
Affiliation:
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Citation:
Trimethoprim-sulfamethoxazole induced acute interstitial nephritis in renal allografts; clinical course and outcome. 2009, 72 (5):331-6 Clin. Nephrol.
Journal:
Clinical nephrology
Issue Date:
Nov-2009
URI:
http://hdl.handle.net/10147/127236
PubMed ID:
19863874
Abstract:
Acute interstitial nephritis (AIN) secondary to trimethoprim-sulfamethoxazole (TMP-SMX) is well documented as a cause of acute renal failure in native kidneys. TMP-SMX is the standard prophylactic agent against pneumocystis carinii (PCP) used in the early post-transplant period, however, it has to date only been indirectly associated with AIN in renal allografts. DESIGN, SETTING, PARTICIPANTS AND MEASUREMENTS: We describe eleven renal transplant patients with acute allograft dysfunction in whom a transplant biopsy demonstrated primary histopathologic features of allergic AIN, all of whom were receiving TMP-SMX in addition to other medications known to cause AIN.; All cases occurred within 1 month of transplantation and accounted for 2.12% (11/518) of the total number of transplant biopsies performed during the study period. However, this figure increased to 10.1% (11/109) when those biopsies performed for early allograft dysfunction (< 1 month) were taken into account. After discontinuation of TMP- SMX alone, all patients had an immediate improvement in serum creatinine with excellent long term allograft function - mean improvement of serum creatinine from 465 micromol/l to 136 micromol/l at last follow-up (range 15 - 55 months).; AIN secondary to TMP-SMX, although an uncommon cause of allograft dysfunction over the study period, accounted for over 10% of cases of allograft dysfunction within the first month of transplantation. Therefore, a high degree of clinical suspicion for TMP-SMX-induced AIN is warranted when confronted with early acute allograft dysfunction.
Item Type:
Article
Language:
en
MeSH:
Acute Disease; Adult; Aged; Anti-Infective Agents; Creatinine; Female; Humans; Immunosuppressive Agents; Kidney; Kidney Transplantation; Male; Middle Aged; Nephritis, Interstitial; Trimethoprim-Sulfamethoxazole Combination
ISSN:
0301-0430

Full metadata record

DC FieldValue Language
dc.contributor.authorGarvey, J Pen
dc.contributor.authorBrown, C Men
dc.contributor.authorChotirmall, S Hen
dc.contributor.authorDorman, A Men
dc.contributor.authorConlon, P Jen
dc.contributor.authorWalshe, J Jen
dc.date.accessioned2011-04-05T14:44:59Z-
dc.date.available2011-04-05T14:44:59Z-
dc.date.issued2009-11-
dc.identifier.citationTrimethoprim-sulfamethoxazole induced acute interstitial nephritis in renal allografts; clinical course and outcome. 2009, 72 (5):331-6 Clin. Nephrol.en
dc.identifier.issn0301-0430-
dc.identifier.pmid19863874-
dc.identifier.urihttp://hdl.handle.net/10147/127236-
dc.description.abstractAcute interstitial nephritis (AIN) secondary to trimethoprim-sulfamethoxazole (TMP-SMX) is well documented as a cause of acute renal failure in native kidneys. TMP-SMX is the standard prophylactic agent against pneumocystis carinii (PCP) used in the early post-transplant period, however, it has to date only been indirectly associated with AIN in renal allografts. DESIGN, SETTING, PARTICIPANTS AND MEASUREMENTS: We describe eleven renal transplant patients with acute allograft dysfunction in whom a transplant biopsy demonstrated primary histopathologic features of allergic AIN, all of whom were receiving TMP-SMX in addition to other medications known to cause AIN.-
dc.description.abstractAll cases occurred within 1 month of transplantation and accounted for 2.12% (11/518) of the total number of transplant biopsies performed during the study period. However, this figure increased to 10.1% (11/109) when those biopsies performed for early allograft dysfunction (< 1 month) were taken into account. After discontinuation of TMP- SMX alone, all patients had an immediate improvement in serum creatinine with excellent long term allograft function - mean improvement of serum creatinine from 465 micromol/l to 136 micromol/l at last follow-up (range 15 - 55 months).-
dc.description.abstractAIN secondary to TMP-SMX, although an uncommon cause of allograft dysfunction over the study period, accounted for over 10% of cases of allograft dysfunction within the first month of transplantation. Therefore, a high degree of clinical suspicion for TMP-SMX-induced AIN is warranted when confronted with early acute allograft dysfunction.-
dc.language.isoenen
dc.subject.meshAcute Disease-
dc.subject.meshAdult-
dc.subject.meshAged-
dc.subject.meshAnti-Infective Agents-
dc.subject.meshCreatinine-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshImmunosuppressive Agents-
dc.subject.meshKidney-
dc.subject.meshKidney Transplantation-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshNephritis, Interstitial-
dc.subject.meshTrimethoprim-Sulfamethoxazole Combination-
dc.titleTrimethoprim-sulfamethoxazole induced acute interstitial nephritis in renal allografts; clinical course and outcome.en
dc.typeArticleen
dc.contributor.departmentDepartment of Nephrology, Beaumont Hospital, Dublin, Ireland.en
dc.identifier.journalClinical nephrologyen
dc.description.provinceLeinster-

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