Hypertensive nephropathy. Moving from classic to emerging pathogenetic mechanisms

J Hypertens. 2017 Feb;35(2):205-212. doi: 10.1097/HJH.0000000000001170.


Hypertensive kidney disease classically entails nephroangiosclerosis and hyalinosis with glomerular damage. However, in recent years, several evidences showed that high blood pressure also injures tubular cells, inducing epithelial-to-mesenchymal transition and tubulointerstitial fibrosis. Recently investigated mechanisms are also podocyte effacement and loss, which lead to denudation of the glomerular basement membrane and focal adhesion of the tufts to the Bowman's capsule, with reduced filtration and scars. Starting from the classic concept of nephroangiosclerosis, this review examines the recently emerged knowledge of new biochemical and molecular mechanisms underlying the kidney damage in hypertension and discusses how viable podocytes or podocyte-deriving proteins are promising tools for early diagnosis of renal remodelling in hypertension.

Publication types

  • Review

MeSH terms

  • Albuminuria / urine
  • Animals
  • Arterioles / pathology
  • Biomarkers / urine
  • Epithelial-Mesenchymal Transition
  • Humans
  • Hypertension, Renal / pathology*
  • Hypertension, Renal / physiopathology
  • Kidney Glomerulus / pathology
  • Kidney Tubules / pathology*
  • Nephritis / pathology*
  • Nephritis / physiopathology
  • Podocytes*


  • Biomarkers

Supplementary concepts

  • Hypertensive Nephropathy