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Ofloxacin Induced Hemolysis in G6PD-deficient Patient: A Rare Cause of Pigment Nephropathy
Mital Parikh1, Maulin Shah1, Jekishan Hirapara2, Shailesh Soni3, Bhalendu Vaishnav4, Labani Ghosh5
1 Consultant Nephrologist, Department of Medicine, Shree Krishna Hospital, Karamsad, India
2 Resident in Medicine, Department of Medicine, Shree Krishna Hospital, Karamsad, India
3 Consultant Pathologist, Muljibhai Patel Urological Hospital, Nadiad, Gujarat, India
4 Professor and Head, Department of Medicine, Shree Krishna Hospital, Karamsad, India
5 Assistant Professor, Department of Medicine, Shree Krishna Hospital, Karamsad, India
Correspondence Address:
Mital Parikh,
A/5 Vrundavan Park Society, VIP Road, Karelibaug, Vadodara - 390018, Gujarat
India
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/ijn.IJN_138_20
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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.
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