Published online Nov 26, 2019. doi: 10.12998/wjcc.v7.i22.3698
Peer-review started: September 8, 2019
First decision: October 24, 2019
Revised: November 3, 2019
Accepted: November 15, 2019
Article in press: November 15, 2019
Published online: November 26, 2019
Processing time: 78 Days and 18.5 Hours
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.
To investigate podocyte injury induced by hypertension in the early course without massive proteinuria or renal dysfunction.
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.
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 podocyte-specific 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.
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.
Core tip: Podocytes probably play a crucial role in the pathogenesis of hypertensive renal injury, but human data are limited. In this study, we detected podocytes from urine sediments of patients with chronic hypertension and trace proteinuria, and obtained direct evidence that podocyte loss is not only associated with severe renal damage in chronic hypertension, but also occurs in the early course of hypertensive renal injury. We found that intrarenal expression of nephrin and CD2-associated protein was downregulated and consistent with podocyte shedding.