Pathophysiology and mechanism of macrohematuria-related acute kidney injury in IgA nephropathy

2014 Fiscal Year Final Research Report

• Project/Area Number: 24791061
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pediatrics
• Research Institution: Kobe University
• Principal Investigator: KAITO Hiroshi 神戸大学, 医学(系)研究科(研究院), 助教 (60457067)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 急性腎不全 / IgA腎症 / 鉄 / アポトーシス

Outline of Final Research Achievements

My purpose of this project was to clarify the pathophysiology and mechanism of macrohematuria-related acute kidney injury. I first hypothesized that it would be the iron, which was the main source of red blood cells and hematuria, that directly resulted in acute kidney injury. Kidney biopsy samples from patients with hematuria-related acute kidney injury showed that the main site of involvement was the renal tubular epithelial cells, which was consistent with the previous reports. In iron staining, kidney tissues with acute kidney injury had significantly more positive cells than that before kidney injury. I could confirm with the human renal tubular epithelial cell line that hemin, the chief component of hemoglobin, could induce apoptosis of renal epithelial cells.

Free Research Field

小児腎臓病学