Nair Ranjith K, Rao Konapur Ananth, Mukherjee D, Datt Bhaskar, Sharma Sourabh, Prakash Sudeep
Department of Nephrology, Army Hospital Research and Referral, New Delhi, India.
Saudi J Kidney Dis Transpl. 2019 Jul-Aug;30(4):960-963. doi: 10.4103/1319-2442.265474.
Malaria is a parasitic infection of global importance but has a high prevalence in the developing countries. Renal failure is a common complication of severe Plasmodium falciparum malaria and has been reported in up to 40% of all cases. Acute kidney injury (AKI), however, is not commonly associated with Plasmodium vivax infection. In those patients who develop AKI following P. vivax infection, the cause is commonly attributed to mixed undiagnosed falciparum infection or coexistent sepsis, dehydration, or hypotension. Infrequently, an association of P. vivax infection with thrombotic microangiopathy (TMA) has been reported. The purpose of this report is to describe renal failure due to TMA following malaria caused by P. vivax. A 24-year-old female presented with a history of fever and jaundice of two weeks duration followed by progressive oliguria and swelling of the face and feet five days after the onset of fever. The evaluation revealed normal blood pressure, anemia, thrombocytopenia, azotemia, unconjugated hyperbilirubinemia with mildly elevated transaminases, and elevated lactate dehydrogenase. Peripheral smear was positive for P. vivax, and schistocytes were seen. She was given intravenous artesunate followed by oral primaquine for 14 days. Urine examination showed proteinuria and microscopic hematuria. She remained oliguric and dialysis dependent, and her kidney biopsy revealed patchy cortical necrosis involving 40% of sampled cortex with widespread fibrinoid necrosis of the vessel wall, red blood cell fragmentation, and luminal thrombotic occlusion. Hemodialysis was discontinued after three weeks when there was the improvement of renal function over time, and her serum creatinine decreased to 2.2 mg/dL by six weeks. Patients with P. vivax malaria developing renal failure may have TMA. Renal biopsy, if performed early in the course of the disease, may identify TMA and institution of plasma exchange in such patients could help in early recovery.
疟疾是一种具有全球重要性的寄生虫感染，但在发展中国家的患病率很高。肾衰竭是重症恶性疟原虫疟疾的常见并发症，在所有病例中报告的发生率高达40%。然而，急性肾损伤（AKI）通常与间日疟原虫感染无关。在那些间日疟原虫感染后发生AKI的患者中，病因通常归因于未诊断出的混合恶性疟原虫感染或并存的败血症、脱水或低血压。间日疟原虫感染与血栓性微血管病（TMA）的关联报道较少。本报告的目的是描述间日疟原虫引起的疟疾后因TMA导致的肾衰竭。一名24岁女性，有两周持续发热和黄疸病史，发热五天后逐渐出现少尿，面部和足部肿胀。评估显示血压正常、贫血、血小板减少、氮质血症、非结合性高胆红素血症伴转氨酶轻度升高以及乳酸脱氢酶升高。外周血涂片间日疟原虫阳性，并可见裂体细胞。给予静脉注射青蒿琥酯，随后口服伯氨喹14天。尿液检查显示蛋白尿和镜下血尿。她仍少尿且依赖透析，肾脏活检显示局灶性皮质坏死累及40%的采样皮质，血管壁广泛纤维蛋白样坏死、红细胞破碎和管腔内血栓形成阻塞。随着时间的推移肾功能有所改善，三周后停止血液透析，六周时她的血清肌酐降至2.2mg/dL。间日疟原虫疟疾患者发生肾衰竭可能患有TMA。如果在疾病早期进行肾脏活检，可能会识别出TMA，对此类患者进行血浆置换有助于早期康复。
