Parikh Mital, Shah Maulin, Hirapara Jekishan, Soni Shailesh, Vaishnav Bhalendu, Ghosh Labani
Consultant Nephrologist, Department of Medicine, Shree Krishna Hospital, Karamsad, India.
Resident in Medicine, Department of Medicine, Shree Krishna Hospital, Karamsad, India.
Indian J Nephrol. 2021 Jul-Aug;31(4):410-413. doi: 10.4103/ijn.IJN_138_20. Epub 2021 Feb 20.
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.
血栓性微血管病（TMA）通常表现为急性肾损伤（AKI）、黄疸和溶血三联征；然而，疟疾、登革热、钩端螺旋体等热带感染以及抗疟药等药物也可能有类似表现。它们可因多种原因导致AKI，包括肾前性原因，但在评估此类患者时，需要排查一种重要且并非相对罕见的溶血性贫血的遗传原因，即葡萄糖6磷酸缺乏症（G6PD），其在服用相关药物后表现为黄疸、溶血以及继发于色素性肾病的AKI。在G6PD缺乏症患者的不安全药物清单中通常不包括氧氟沙星。在此，我们报告一例因G6PD缺乏症继发血管内溶血并与氧氟沙星给药相关的患者，其表现为色素性肾病的罕见病因。
