Thrombotic microangiopathy and acute kidney injury following vivax malaria

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• 作者：Aditi Sinha (1)
  Geetika Singh (2)
  Abdus Sami Bhat (1)
  Sarita Mohapatra (3)
  Ashima Gulati (1)
  Pankaj Hari (1)
  J. C. Samantaray (3)
  Amit Kumar Dinda (2)
  Sanjay Kumar Agarwal (4)
  Arvind Bagga (1)
  
• 关键词：Malaria ; Plasmodium ; Hemolytic uremic syndrome
• 刊名：Clinical and Experimental Nephrology
• 出版年：2013
• 出版时间：February 2013
• 年：2013
• 卷：17
• 期：1
• 页码：66-72
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• 作者单位：Aditi Sinha (1)
  Geetika Singh (2)
  Abdus Sami Bhat (1)
  Sarita Mohapatra (3)
  Ashima Gulati (1)
  Pankaj Hari (1)
  J. C. Samantaray (3)
  Amit Kumar Dinda (2)
  Sanjay Kumar Agarwal (4)
  Arvind Bagga (1)
  
  1. Division of Nephrology, Department of Pediatrics, All India Institute of Medical Sciences, 3053, Teaching Block, New Delhi, India
  2. Department of Pathology, All India Institute of Medical Sciences, New Delhi, India
  3. Department of Microbiology, All India Institute of Medical Sciences, New Delhi, India
  4. Department of Nephrology, All India Institute of Medical Sciences, New Delhi, India
  
• ISSN：1437-7799

文摘

Background Infection with Plasmodium vivax, a common human parasite, is occasionally recognized to cause severe organ dysfunction similar to P. falciparum infection. Acute kidney injury (AKI) in malaria is attributed to acute tubular necrosis; thrombotic microangiopathy is not described. Methods This observational study includes patients referred to a tertiary care center in North India during June to September 2011 with severe AKI, anemia, and thrombocytopenia following vivax malaria. Renal biopsies were processed by light, immunofluorescence, and electron microscopy. Results Nine patients (including 5 children) had persistent AKI with thrombocytopenia and variable anemia following the diagnosis of malaria. Based on peripheral smear, eight patients were diagnosed with vivax malaria and had received antimalarial therapy prior to referral; a laboratory diagnosis of P. vivax infection was made for one patient at this center. Renal histology in all cases showed features of thrombotic microangiopathy, including fibrin thrombi, subendothelial widening, and mesangiolysis, along with variable tubulointerstitial nephritis and acute tubular or cortical necrosis. Ultrastructural examination confirmed endothelial injury and subendothelial widening. All patients required hemodialysis, and six were dialysis dependent at four?weeks. Delayed presentation to the hospital (P?=?0.019), hemolysis on peripheral smear (P?=?0.083), and prolonged oligoanuria (P?=?0.036) were associated with dialysis dependence. Conclusion The association of anemia, thrombocytopenia, and renal histological evidence of thrombotic microangiopathy with vivax malaria is novel, and suggests the presence of severe endothelial injury. Further studies are necessary to confirm the association and examine the factors associated with its occurrence.