A quantitative ultrastructural study of renal pathology in fatal <i>Plasmodium falciparum</i> malaria

Nguansangiam, Sudarat; Day, Nicholas P. J.; Hien, Tran Tinh; Hoang, Nguyen Thi; Chaisri, Urai; Riganti, M; Dondorp, Arjen M.; Lee, Sue J.; Phu, Nguyen Hoan; Turner, Gareth D. H.; White, Nicholas J.; Ferguson, David J. P.; Pongponratn, Emsri

doi:10.1111/j.1365-3156.2007.01881.x

Cited by 114 publications

(97 citation statements)

References 32 publications

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“…40,41 Renal pathology has been largely attributed to acute tubular necrosis secondary to sequestration of IRBC and accumulation of mononuclear cells within both glomerular and peritubular capillaries. 42 Indirect measures of parasite sequestration and monocyte activation levels have been found to correlate with renal failure requiring replacement therapy. 43 Mild to moderate glomerulonephritis has also been observed as seen by glomerular hypercellularity and collapse.…”

Section: Clinical Evidence Of Barrier Dysfunction In Severe Malariamentioning

confidence: 99%

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Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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Plasmodial species are protozoan parasites that infect erythrocytes. As such, they are in close contact with microvascular endothelium for most of the life cycle in the mammalian host. The hostparasite interactions of this stage of the infection are responsible for the clinical manifestations of the disease that range from a mild febrile illness to severe and frequently fatal syndromes such as cerebral malaria and multi-organ failure. Plasmodium falciparum, the causative agent of the most severe form of malaria, is particularly predisposed to modulating endothelial function through either direct adhesion to endothelial receptor molecules, or by releasing potent host and parasite products that can stimulate endothelial activation and/or disrupt barrier function. In this review, we provide a critical analysis of the current clinical and laboratory evidence for endothelial dysfunction during severe P. falciparum malaria. Future investigations using state-of-the-art technologies such as mass cytometry and organs-on-chips to further delineate parasite-endothelial cell interactions are also discussed.

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Section: Clinical Evidence Of Barrier Dysfunction In Severe Malariamentioning

confidence: 99%

“…Beyond the brain and lung, applying these methods to the analysis of renal tissue from patients with severe malaria could provide additional insight into acute kidney injury in both children 144 and adults 43 which is associated with renal endothelial cell hypertrophy and cytoplasmic vacuolation as well as monocyte infiltration. 42 …”

Section: Imaging Studiesmentioning

confidence: 99%

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Gillrie

2016

Tissue Barriers

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“…These findings are similar to the histopathological profile of acute renal failure caused by malaria, which manifests as acute tubular necrosis, interstitial nephritis, and glomerulonephritis 18 . Furthermore, glomerulonephritis can be characterized by glomerular cell proliferation (e.g., mesangial, podocyte, and endothelial cells) as well as changes in the basal membranes, inflammatory cell infiltration, deposition of hemozoin, presence of infected erythrocytes in the glomerulus capillaries, necrosis, and deposition of immune complexes 19 . The glomerular cell proliferation may be related to the secondary immune response to cytokines that are released by the host in response to the infection 20 .…”

Section: Discussionmentioning

confidence: 99%

Strong renal expression of heat shock protein 70, high mobility group box 1, inducible nitric oxide synthase, and nitrotyrosine in mice model of severe malaria

Fitri

Rosmarwati

Rizky

et al. 2017

Rev. Soc. Bras. Med. Trop.

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Introduction:Renal damage is a consequence of severe malaria, and is generally caused by sequestration of Plasmodium falciparum-infected erythrocytes in the renal microcirculation, which leads to obstruction, hypoxia, and ischemia. This triggers high mobility group box 1 (HMGB1) to send a danger signal through toll-like receptors 2 and 4. This signal up-regulates inducible nitric oxide (iNOS) and nitrotyrosine to re-perfuse the tissue, and also increases heat shock protein 70 (HSP70) expression. As no study has examined the involvement of intracellular secondary molecules in this setting, the present study compared the renal expressions of HSP70, HMGB1, iNOS, and nitrotyrosine between mice suffered from severe malaria and normal mice. Methods: C57BL/6 mice were divided into an infected group (intraperitoneal injection of 10 6 P. berghei ANKA) and a noninfected group. Renal damage was evaluated using hematoxylin eosin staining, and immunohistochemistry was used to evaluate the expressions of HSP70, HMGB1, iNOS, and nitrotyrosine. Results: Significant inter-group differences were observed in the renal expressions of HSP70, HMGB1, and iNOS (p=0.000, Mann-Whitney test), as well as nitrotyrosine (p=0.000, independent t test). The expressions of HSP70 and HMGB1 were strongly correlated (p=0.000, R=1.000). No correlations were observed between iNOS and HMGB, HMGB1 and nitrotyrosine, HSP70 and nitrotyrosine, or iNOS and nitrotyrosine. Conclusions: It appears that HMGB1, HSP70, iNOS, and nitrotyrosine play roles in the renal damage that is observed in mice with severe malaria. Only HSP70 expression is strongly correlated with the expression of HMGB1.

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“…Blockage of renal microcirculation due to sequestration of infected erythrocytes, immune-mediated glomerular injury and volume depletion are some of the proposed hypotheses. 9 The diagnosis of acute kidney injury has been established on the basis of clinical evidence (anuria) and biochemical characteristics (azotemia, hyponatremia, and hypokalemia). 2,7,10 The reported polyuria is a classic evolution of diuresis during treatment of acute kidney injury and is due to recovery from fluid retention, which may be likened to the removal of an obstacle.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury in a shepherd with severe malaria: a case report

Boushab¹,

Fall-Malick

Savadogo

et al. 2016

IJNRD

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Malaria is one of the main reasons for outpatient consultation and hospitalization in Mauritania. Although four Plasmodium species, ie, Plasmodium (P.) falciparum, P. vivax, P. malariae, and P. ovale, cause malaria in Mauritania, recent data on their frequency is lacking. Since infections with P. falciparum generally result in serious disease, their identification is important. We report a case of oliguric renal injury associated with malaria in a 65-year-old shepherd. Clinical manifestations included anemia, oliguria, and elevated creatinine and urea. The rapid diagnostic test for malaria and microscopic examination of blood smears were positive for P. falciparum. On the basis of this, the patient was diagnosed as having acute kidney injury as a complication of severe malaria. The patient was treated for malaria with intravenous quinine for 4 days, followed by 3 days of oral treatment. Volume expansion, antipyretic treatment, and diuretics were administered. He also had two rounds of dialysis after which he partially recovered renal function. This outcome is not always the rule. Prognosis depends much on early diagnosis and appropriate supportive treatment.

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A quantitative ultrastructural study of renal pathology in fatal Plasmodium falciparum malaria

Cited by 114 publications

References 32 publications

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Dynamic interactions ofPlasmodiumspp. with vascular endothelium

Strong renal expression of heat shock protein 70, high mobility group box 1, inducible nitric oxide synthase, and nitrotyrosine in mice model of severe malaria

Acute kidney injury in a shepherd with severe malaria: a case report

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