Oxidative Stress and Modification of Renal Vascular Permeability Are Associated with Acute Kidney Injury during P. berghei ANKA Infection

Author(s):Show less -

Elias, Rosa Maria ^[1] ; Correa-Costa, Matheus ^[2] ; Barreto, Claudiene Rodrigues ^[1] ; Silva, Reinaldo Correia ^[1] ; Hayashida, Caroline Y. ^[2] ; Castoldi, Angela ^[1] ; Goncalves, Giselle Martins ^[2] ; Braga, Tarcio Teodoro ^[2] ; Barboza, Renato ^[3] ; Rios, Francisco Jose ^[2] ; Keller, Alexandre Castro ^[4] ; Cenedeze, Marcos Antonio ^[1] ; Hyane, Meire Ioshie ^[2] ; D'Imperio-Lima, Maria Regina ^[2] ; Figueiredo-Neto, Antonio Martins ^[5] ; Reis, Marlene Antonia ^[6] ; Farias Marinho, Claudio Romero ^[3] ; Pacheco-Silva, Alvaro ^{[1, 7]} ; Saraiva Camara, Niels Olsen ^{[2, 1]}

Affiliation

^[1] Univ Fed Sao Paulo, Dept Med, Disciplina Nefrol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Dept Imunol, Lab Imunobiol Transplantes, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Inst Ciencias Biomed, Dept Parasitol, BR-05508 Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, Dept Imunol, Sao Paulo - Brazil

^[5] Univ Sao Paulo, Inst Fis, BR-01498 Sao Paulo - Brazil

^[6] Univ Fed Triangulo Mineiro, Div Patol, Uberaba - Brazil

^[7] Inst Israelita Ensino & Pesquisa Albert Einstein, Sao Paulo - Brazil

• Document type: Journal article
• Source: PLoS One; v. 7, n. 8 AUG 31 2012.
• Web of Science Citations: 20

Abstract

Malaria associated-acute kidney injury (AKI) is associated with 45% of mortality in adult patients hospitalized with severe form of the disease. However, the causes that lead to a framework of malaria-associated AKI are still poorly characterized. Some clinical studies speculate that oxidative stress products, a characteristic of Plasmodium infection, as well as proinflammatory response induced by the parasite are involved in its pathophysiology. Therefore, we aimed to investigate the development of malaria-associated AKI during infection by P. berghei ANKA, with special attention to the role played by the inflammatory response and the involvement of oxidative stress. For that, we took advantage of an experimental model of severe malaria that showed significant changes in the renal pathophysiology to investigate the role of malaria infection in the renal microvascular permeability and tissue injury. Therefore, BALB/c mice were infected with P. berghei ANKA. To assess renal function, creatinine, blood urea nitrogen, and ratio of proteinuria and creatininuria were evaluated. The products of oxidative stress, as well as cytokine profile were quantified in plasma and renal tissue. The change of renal microvascular permeability, tissue hypoxia and cellular apoptosis were also evaluated. Parasite infection resulted in renal dysfunction. Furthermore, we observed increased expression of adhesion molecule, proinflammatory cytokines and products of oxidative stress, associated with a decrease mRNA expression of HO-1 in kidney tissue of infected mice. The measurement of lipoprotein oxidizability also showed a significant increase in plasma of infected animals. Together, our findings support the idea that products of oxidative stress, as well as the immune response against the parasite are crucial to changes in kidney architecture and microvascular endothelial permeability of BALB/c mice infected with P. berghei ANKA. (AU)

• FAPESP's process: 07/07139-3 - The role of heme oxygenase 1 in different renal inflammatory process in experimental animal models
• Grantee: Niels Olsen Saraiva Câmara
• Support Opportunities: Research Projects - Thematic Grants
• FAPESP's process: 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches
• Grantee: Niels Olsen Saraiva Câmara
• Support Opportunities: Research Projects - Thematic Grants