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Increased expression of renin in chronic allograft nephropathy

K Oka1, T Moriyama, S Takahara

  • 1Department of Pathology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.

Transplantation Proceedings
|June 21, 2005
PubMed
Abstract

Insights

Chronic allograft nephropathy (CAN), a major cause of kidney transplant failure, is linked to increased renin in the juxtaglomerular apparatus. This suggests the intrarenal renin-angiotensin system plays a key role in CAN development.

Area of Science:

  • Nephrology
  • Transplantation Immunology
  • Renal Pathology

Background:

  • Chronic allograft nephropathy (CAN) is the primary cause of kidney transplant failure within the first decade.
  • The exact mechanisms driving CAN remain unclear.
  • Clinical evidence suggests the renin-angiotensin system (RAS) may contribute to CAN.

Purpose of the Study:

  • To investigate the role of the intrarenal RAS in the pathogenesis of CAN.
  • To quantify renin-positive cells in renal allograft biopsies from patients with CAN.

Main Methods:

  • Immunohistochemistry was used to examine renin-positive cell distribution in 23 CAN allograft biopsies.
  • Seven stable renal transplant recipients served as controls.
  • Histological evaluation followed the Banff 97 classification.

Main Results:

  • Renin-positive cells were identified in the juxtaglomerular apparatus (JGA) of both groups.
  • The renin index (number of renin-positive cells in JGA) was significantly higher in the CAN group (P = .007).
  • The CAN group showed significantly higher serum creatinine levels.

Conclusions:

  • Elevated renin-positive cells in the JGA indicate significant intrarenal RAS activation in CAN.
  • This finding supports a crucial role for the intrarenal RAS in the development of chronic allograft nephropathy.

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