Open AccessOfloxacin Induced Hemolysis in G6PD-deficient Patient: A Rare Cause of Pigment Nephropathy
Author(s) -
Premlata Mital,
Maulin Shah,
Jekishan J. Hirapara,
Shailesh Soni,
Bhalendu Vaishnav,
Labani Ghosh
Publication year - 2021
Publication title -
indian journal of nephrology/indian journal of nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.317
H-Index - 24
eISSN - 1998-3662
pISSN - 0971-4065
DOI - 10.4103/ijn.ijn_138_20
Subject(s) - medicine , hemolysis , nephropathy , pigment , ofloxacin , endocrinology , microbiology and biotechnology , antibiotics , diabetes mellitus , chemistry , organic chemistry , ciprofloxacin , biology
Thrombotic microangiopathy (TMA) commonly presents as a triad of acute kidney injury (AKI), jaundice, and hemolysis; however, tropical infections such as malaria, dengue, leptospira, and drugs like antimalarials can also have a similar presentation. They can cause AKI for many reasons including pre-renal causes but an important yet not relatively uncommon genetic cause of hemolytic anemia, that is, glucose 6-phosphate deficiency (G6PD) manifesting as jaundice, hemolysis, and AKI secondary to pigment nephropathy after receiving offending drugs needs to be worked up while evaluating such patients. Ofloxacin is not usually included in the lists of unsafe drugs in G6PD deficiency. Herein, we report a patient developing intravascular hemolysis secondary to G6PD deficiency associated with ofloxacin administration presenting as a rare cause for pigment nephropathy.