Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice

Akihito Yashima, Masashi Mizuno, Yukio Yuzawa, Koki Shimada, Norihiko Suzuki, Hideo Tawada, Waichi Sato, Naotake Tsuboi, Shoichi Maruyama, Yasuhiko Ito, Seiichi Matsuo, Tamio Ohno

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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. Conclusion: 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.

Original languageEnglish
Pages (from-to)589-596
Number of pages8
JournalClinical and Experimental Nephrology
Volume21
Issue number4
DOIs
Publication statusPublished - 01-08-2017

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Plasmodium chabaudi
Glomerulonephritis
Malaria
Parasites
Kidney
Infection
Inbred C57BL Mouse
Glomerular Mesangium
Pathology
Parasitic Diseases
Complement C3
Wounds and Injuries
Sclerosis
Proteinuria
Acute Kidney Injury
Serum Albumin
Biochemistry
Microscopy
Animal Models
Immunoglobulin G

All Science Journal Classification (ASJC) codes

  • Physiology
  • Nephrology
  • Physiology (medical)

Cite this

Yashima, Akihito ; Mizuno, Masashi ; Yuzawa, Yukio ; Shimada, Koki ; Suzuki, Norihiko ; Tawada, Hideo ; Sato, Waichi ; Tsuboi, Naotake ; Maruyama, Shoichi ; Ito, Yasuhiko ; Matsuo, Seiichi ; Ohno, Tamio. / Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice. In: Clinical and Experimental Nephrology. 2017 ; Vol. 21, No. 4. pp. 589-596.
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abstract = "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. Conclusion: 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.",
author = "Akihito Yashima and Masashi Mizuno and Yukio Yuzawa and Koki Shimada and Norihiko Suzuki and Hideo Tawada and Waichi Sato and Naotake Tsuboi and Shoichi Maruyama and Yasuhiko Ito and Seiichi Matsuo and Tamio Ohno",
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Yashima, A, Mizuno, M, Yuzawa, Y, Shimada, K, Suzuki, N, Tawada, H, Sato, W, Tsuboi, N, Maruyama, S, Ito, Y, Matsuo, S & Ohno, T 2017, 'Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice', Clinical and Experimental Nephrology, vol. 21, no. 4, pp. 589-596. https://doi.org/10.1007/s10157-016-1339-8

Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice. / Yashima, Akihito; Mizuno, Masashi; Yuzawa, Yukio; Shimada, Koki; Suzuki, Norihiko; Tawada, Hideo; Sato, Waichi; Tsuboi, Naotake; Maruyama, Shoichi; Ito, Yasuhiko; Matsuo, Seiichi; Ohno, Tamio.

In: Clinical and Experimental Nephrology, Vol. 21, No. 4, 01.08.2017, p. 589-596.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Mesangial proliferative glomerulonephritis in murine malaria parasite, Plasmodium chabaudi AS, infected NC mice

AU - Yashima, Akihito

AU - Mizuno, Masashi

AU - Yuzawa, Yukio

AU - Shimada, Koki

AU - Suzuki, Norihiko

AU - Tawada, Hideo

AU - Sato, Waichi

AU - Tsuboi, Naotake

AU - Maruyama, Shoichi

AU - Ito, Yasuhiko

AU - Matsuo, Seiichi

AU - Ohno, Tamio

PY - 2017/8/1

Y1 - 2017/8/1

N2 - 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. Conclusion: 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.

AB - 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. Conclusion: 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.

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