Human podocyte injury in the early course of hypertensive renal injury

Abstract

BACKGROUND Hypertension is prevalent in the general population and is regarded as the second leading cause of renal damage and dysfunction, outnumbered only by diabetes. However, the mechanisms remain unclear. AIM To investigate podocyte injury induced by hypertension in the early course without massive proteinuria or renal dysfunction. METHODS The hypertension group comprised 18 patients with hypertension accompanied by microalbuminuria, diagnosed with hypertensive renal injury according to biopsy results. For a comparison of pathological changes in renal tissue, control group 1 comprised 10 healthy volunteers, and control group 2 comprised 16 patients who underwent surgery for renal trauma. RESULTS The hypertension group had significantly higher blood pressure (P = 0.000) and microalbuminuria (P = 0.000) compared with control group 1. In the hypertension group, urinary podocytes were detected following positive staining of podocytespecific nephrin and/or CD2-associated protein (CD2AP) in urine sediment. Podocyte foot process fusion and a significant decrease in nephrin and/or CD2AP expression in glomeruli were observed in the hypertension group compared with control group 2. This indicated that hypertension caused podocyte injury and detachment from the glomerular basement membrane, which was consistent with urinary detection of podocytes. CONCLUSION Our results suggest that podocyturia appears early in the course of hypertensive renal injury, and may be a sensitive marker for early prediction of hypertensive renal injury.