Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice.
BACKGROUND
Malaria is an important tropical disease and has remained a serious health problem in many countries. One of the critical complications of malarial infection is renal injury, such as acute renal failure and chronic glomerulopathy. Few animal models of nephropathy related to malarial infection have been reported. Therefore, we developed and investigated a novel malarial nephropathy model in mice infected by murine malaria parasites.


METHODS
NC mice and C57BL/6J mice were infected with Ttwo different murine malaria parasites, Plasmodium (P.) chabaudi AS and P. yoelii 17X. After the infection, renal pathology and blood and urinary biochemistry were analyzed.


RESULTS
NC mice infected by the murine malaria parasite P. chabaudi AS, but not P. yoelii 17X, developed mesangial proliferative glomerulonephritis with endothelial damage, and decreased serum albumin concentration and increased proteinuria. These pathological changes were accompanied by deposition of immunoglobulin G and complement component 3, mainly in the mesangium until day 4 and in the mesangium and glomerular capillaries from day 8. On day 21, renal pathology developed to focal segmental sclerosis according to light microscopy. In C57BL/6J mice, renal injuries were not observed from either parasite infection.


CONCLUSIONS
The clinical and pathological features of P. chabaudi AS infection in NC mice might be similar to quartan malarial nephropathy resulting from human malaria parasite P. malariae infection. The NC mouse model might therefore be useful in analyzing the underlying mechanisms and developing therapeutic approaches to malaria-related nephropathy.
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Akihito
A
Yashima
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.|Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Masashi
M
Mizuno
Department of Nephrology, School of Medicine, Fujita Health University, 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi, 470-1192, Japan. yukio-y@fujita-hu.ac.jp.
Yukio
Y
Yuzawa
Division of Experimental Animals, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Koki
K
Shimada
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Norihiko
N
Suzuki
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Hideo
H
Tawada
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Waichi
W
Sato
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Naotake
N
Tsuboi
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Shoichi
S
Maruyama
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.|Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Yasuhiko
Y
Ito
Division of Nephrology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Seiichi
S
Matsuo
Division of Experimental Animals, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Tamio
T
Ohno
D000818:Animals; D003176:Complement C3 / Q000276:immunology; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000276:immunology / Q000469:parasitology* / Q000473:pathology; D054884:Host-Pathogen Interactions; D007074:Immunoglobulin G / Q000276:immunology; D007678:Kidney Glomerulus / Q000276:immunology / Q000469:parasitology* / Q000648:ultrastructure; D008288:Malaria / Q000276:immunology / Q000469:parasitology*; D008810:Mice, Inbred C57BL; D016788:Plasmodium chabaudi / Q000276:immunology / Q000472:pathogenicity* / Q000648:ultrastructure; D013045:Species Specificity; D013997:Time Factors
C545610:C3 protein, mouse; D003176:Complement C3; D007074:Immunoglobulin G
Animal model; Glomerulonephritis; Malarial nephropathy; NC mice; Nephrotic syndrome