Nguansangiam Sudarat, Day Nicholas P J, Hien Tran Tinh, Mai Nguyen Thi Hoang, Chaisri Urai, Riganti Mario, Dondorp Arjen M, Lee Sue J, Phu Nguyen Hoan, Turner Gareth D H, White Nicholas J, Ferguson David J P, Pongponratn Emsri
Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
Trop Med Int Health. 2007 Sep;12(9):1037-50. doi: 10.1111/j.1365-3156.2007.01881.x.
To use electron microscopy to examine the role of parasitized red blood cell (PRBC) sequestration in the pathogenesis of acute renal failure in severe falciparum malaria.
Ultrastructural pathological examination of renal tissues from Southeast Asian adults (n = 63) who died from severe falciparum malaria. Qualitative and quantitative determination of the major pathological features of disease, including PRBC and leukocyte sequestration. Clinico-pathological correlation with the pre-mortem clinical picture and peripheral parasite count.
There was a high incidence of malaria-associated renal failure in this population (> 40%) and a correlation between this incidence, severe malarial anaemia and shock. Pathological features included PRBC sequestration in glomerular and tubulo-interstitial vessels, acute tubular damage and mild glomerular hypercellularity resulting from the accumulation of host monocytes within glomerular capillaries. No evidence for an immune complex mediated glomerulonephritis was found. There was a correlation between parasite sequestration in the kidney and pre-mortem renal failure, although overall levels of sequestration were relatively low. Levels of sequestration (Knob+ PRBC) were significantly higher in malaria-associated renal failure than in fatal cases without renal failure (P = 0.005).
Malaria-associated renal failure is a common and serious complication of severe Plasmodium falciparum malaria in this population, associated with acute tubular injury rather than glomerulonephritis, and linked to localization of host monocytes in the kidney as well as sequestration of PRBCs.
运用电子显微镜检查寄生红细胞（PRBC）隔离在严重恶性疟原虫疟疾所致急性肾衰竭发病机制中的作用。
对死于严重恶性疟原虫疟疾的东南亚成年人（n = 63）的肾组织进行超微结构病理检查。对疾病的主要病理特征进行定性和定量测定，包括PRBC和白细胞隔离。将临床病理与死前临床表现及外周血寄生虫计数进行相关性分析。
该人群中疟疾相关性肾衰竭的发生率很高（> 40%），且该发生率与严重疟疾贫血和休克之间存在相关性。病理特征包括PRBC在肾小球和肾小管间质血管中的隔离、急性肾小管损伤以及由于肾小球毛细血管内宿主单核细胞积聚导致的轻度肾小球细胞增多。未发现免疫复合物介导的肾小球肾炎的证据。尽管总体隔离水平相对较低，但肾脏中的寄生虫隔离与死前肾衰竭之间存在相关性。疟疾相关性肾衰竭患者的隔离水平（带棘突PRBC）显著高于无肾衰竭的致命病例（P = 0.005）。
疟疾相关性肾衰竭是该人群中严重恶性疟原虫疟疾常见且严重的并发症，与急性肾小管损伤而非肾小球肾炎相关，并且与宿主单核细胞在肾脏中的定位以及PRBC的隔离有关。
