Reversible renal-limited thrombotic microangiopathy due to gemcitabine-dexamethasone-cisplatin therapy: a case report.
Acute Kidney Injury
/ chemically induced
Antineoplastic Combined Chemotherapy Protocols
/ adverse effects
Cisplatin
/ adverse effects
Deoxycytidine
/ adverse effects
Dexamethasone
/ adverse effects
Female
Humans
Kidney
/ pathology
Lymphoma, T-Cell
/ drug therapy
Middle Aged
Thrombotic Microangiopathies
/ chemically induced
Gemcitabine
Cisplatin
Gemcitabine
Lymphoma
Proteinuria
Thrombotic microangiopathies
Urinalysis
Journal
BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793
Informations de publication
Date de publication:
12 05 2021
12 05 2021
Historique:
received:
10
03
2021
accepted:
04
05
2021
entrez:
13
5
2021
pubmed:
14
5
2021
medline:
26
2
2022
Statut:
epublish
Résumé
Gemcitabine and cisplatin are chemotherapeutic agents used for treating multiple cancers, and these agents are sometimes used in combination. Drug-induced thrombotic microangiopathy (TMA) is a rare but potentially fatal complication. It typically presents as a systemic disease with the classical triad of hemolytic anemia, thrombocytopenia, and organ damage. In contrast to systemic TMA, cases of renal-limited TMA, defined as biopsy-proven renal TMA without the classical triad, have been reported with relatively good prognosis. Most cases of renal-limited TMA are associated with calcineurin inhibitors, and cases of drug-induced renal-limited TMA due to gemcitabine-dexamethasone-cisplatin therapy have been rarely reported. A 43-year-old woman with lymphoma developed acute kidney injury with marked proteinuria, microhematuria, and abnormal urinary casts after receiving one cycle of gemcitabine-dexamethasone-cisplatin therapy. Although she did not show hemolytic anemia and thrombocytopenia, renal biopsy showed diffuse injury to the glomerular endothelial cells, supporting the diagnosis of renal-limited TMA. Her condition improved only with the cessation of gemcitabine and cisplatin treatment. She received another chemotherapy without gemcitabine and platinum agents, and no recurrence of renal-limited TMA was observed. Drug-induced TMA occurs early after gemcitabine and cisplatin use in renal-limited form and is reversible when detected and managed in a timely manner. Urinalysis, which is simple and inexpensive and can be easily performed, is a beneficial screening tool for early-onset drug-induced TMA among patients who receive gemcitabine-dexamethasone-cisplatin therapy.
Sections du résumé
BACKGROUND
Gemcitabine and cisplatin are chemotherapeutic agents used for treating multiple cancers, and these agents are sometimes used in combination. Drug-induced thrombotic microangiopathy (TMA) is a rare but potentially fatal complication. It typically presents as a systemic disease with the classical triad of hemolytic anemia, thrombocytopenia, and organ damage. In contrast to systemic TMA, cases of renal-limited TMA, defined as biopsy-proven renal TMA without the classical triad, have been reported with relatively good prognosis. Most cases of renal-limited TMA are associated with calcineurin inhibitors, and cases of drug-induced renal-limited TMA due to gemcitabine-dexamethasone-cisplatin therapy have been rarely reported.
CASE PRESENTATION
A 43-year-old woman with lymphoma developed acute kidney injury with marked proteinuria, microhematuria, and abnormal urinary casts after receiving one cycle of gemcitabine-dexamethasone-cisplatin therapy. Although she did not show hemolytic anemia and thrombocytopenia, renal biopsy showed diffuse injury to the glomerular endothelial cells, supporting the diagnosis of renal-limited TMA. Her condition improved only with the cessation of gemcitabine and cisplatin treatment. She received another chemotherapy without gemcitabine and platinum agents, and no recurrence of renal-limited TMA was observed.
CONCLUSIONS
Drug-induced TMA occurs early after gemcitabine and cisplatin use in renal-limited form and is reversible when detected and managed in a timely manner. Urinalysis, which is simple and inexpensive and can be easily performed, is a beneficial screening tool for early-onset drug-induced TMA among patients who receive gemcitabine-dexamethasone-cisplatin therapy.
Identifiants
pubmed: 33980166
doi: 10.1186/s12882-021-02386-y
pii: 10.1186/s12882-021-02386-y
pmc: PMC8114690
doi:
Substances chimiques
Deoxycytidine
0W860991D6
Dexamethasone
7S5I7G3JQL
Cisplatin
Q20Q21Q62J
Gemcitabine
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
175Références
Lancet Oncol. 2007 Jul;8(7):634-41
pubmed: 17613425
Am J Kidney Dis. 2003 Feb;41(2):471-9
pubmed: 12552512
Br J Clin Pharmacol. 2019 Feb;85(2):403-412
pubmed: 30394581
Clin J Am Soc Nephrol. 2018 Feb 7;13(2):300-317
pubmed: 29042465
J Nephrol. 2018 Feb;31(1):15-25
pubmed: 28382507
J Clin Oncol. 2014 Nov 1;32(31):3490-6
pubmed: 25267740
Expert Opin Drug Saf. 2009 May;8(3):257-60
pubmed: 19505260
Am J Kidney Dis. 1994 Mar;23(3):444-50
pubmed: 8128949
J Clin Oncol. 2006 Aug 20;24(24):3946-52
pubmed: 16921047
Clin Kidney J. 2014 Jun;7(3):311-3
pubmed: 25852897
N Engl J Med. 2010 Apr 8;362(14):1273-81
pubmed: 20375404
Am J Kidney Dis. 1996 Oct;28(4):561-71
pubmed: 8840947
Ann Oncol. 2007 Feb;18(2):370-5
pubmed: 17074972
J Clin Oncol. 2008 Jul 20;26(21):3543-51
pubmed: 18506025
Transplantation. 1999 Feb 27;67(4):539-44
pubmed: 10071024
Anticancer Drugs. 1998 Mar;9(3):191-201
pubmed: 9625429
Am J Kidney Dis. 2000 Oct;36(4):844-50
pubmed: 11007689
Kidney Int. 1999 Jun;55(6):2457-66
pubmed: 10354295
Acta Oncol. 2011 Apr;50(3):462-5
pubmed: 20799915
Cancer. 2004 Oct 15;101(8):1835-42
pubmed: 15386331
Acta Oncol. 1998;37(1):107-9
pubmed: 9572663
Anticancer Drugs. 2003 Sep;14(8):665-8
pubmed: 14501391
Clin Kidney J. 2013 Aug;6(4):421-425
pubmed: 24422172
Ann Hematol. 2008 Jun;87(6):495-6
pubmed: 18097666
J Clin Oncol. 2012 Apr 1;30(10):1107-13
pubmed: 22370319
Blood. 2015 Jan 22;125(4):616-8
pubmed: 25414441
BMC Nephrol. 2019 Jan 11;20(1):14
pubmed: 30634936