Kidney involvement in malaria: an update

Abstract

Malaria is an infectious disease of great importance for Public Health, as it is the most prevalent endemic disease in the world, affecting millions of people living in tropical areas of the globe. Kidney involvement is relatively frequent in infections by P. falciparum and P. malariae, but has also been described in the infection by P. vivax. Kidney complications in malaria mainly occur due to hemodynamic dysfunction and immune response. Liver complications leading to hepatomegaly, jaundice and hepatic dysfunction can also contribute to the occurrence of acute kidney injury. Histologic studies in malaria also evidence glomerulonephritis, acute tubular necrosis and acute interstitial nephritis. It is also possible to find chronic kidney disease associated with malaria, mainly in those patients suffering from repeated episodes of infection. Plasmodium antigens have already been detected in the glomeruli, suggesting a direct effect of the parasite in the kidney, which can trigger an inflammatory process leading to different types of glomerulonephritis. Clinical manifestations of kidney involvement in malaria include proteinuria, microalbuminuria and urinary casts, reported in 20 to 50% of cases. Nephrotic syndrome has also been described in the infection by P. falciparum, but it is rare. This paper highlights the main aspects of kidney involvement in malaria and important findings of the most recent research addressing this issue.

Figure 1. Global distribution of malaria transmission, according to the Centers for Disease Control and Prevention - CDC. Available at: http://www.cdc.gov/malaria/about/distribution.html

Figure 2. Kidney biopsy from a patient with P. falcifarum-associated immunoglobulin A (IgA) nephropathy: A) The renal biopsy specimen showed mild mesangial proliferation and expansion (original magnification × 400); B) Acute and chronic inflammatory cell infiltration in the tubulointerstitium with multifocal hemosiderin casts (original magnification × 200); C) Direct immunofluorescence showed mesangial staining for IgA (2+); D) Electron microscopy showed multifocal electron-dense deposits within the mesangium and irregularly thickened glomerular basement membrane ranging from 800 nm to 1,200 nm in thickness. Diffusely effaced foot processes were also observed. Reproduced by Yoo et al., with permission. © 2012 The Korean Academy of Medical Sciences

Figure 3. Kidney biopsy from a patient with P. falcifarum-associated glomerulonephritis: A) Eosinophilic diffuse proliferative glomerulonephritis (hematoxylin and eosin staining); B) One glomerulus showing some eosinophils (arrows). Reproduced by Walker et al., with permission. ©2007 Elsevier – The International Society of Nephrology

Figure 4. Pathophysiology of kidney involvement in Malaria