Remnant nephron physiology and the progression of chronic kidney disease

H. William Schnaper*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

44 Scopus citations

Abstract

In chronic kidney disease, ongoing failure of individual nephrons leads to the progressive loss of renal function. This process results in part from a cellular and molecular response to injury that represents an attempt to maintain homeostasis but instead initiates a program that damages the nephron. As nephrons are lost, compensation by the remaining nephrons exacerbates glomerular pathophysiology. The delivery of excessive amounts of biologically active molecules to the distal nephron and tubulointerstitium generates inflammation and cellular dedifferentiation. Energy requirements of hyperfunctioning nephrons exceed the metabolic substrate available to the renal tubule, and inadequacy of the local vascular supply promotes hypoxia/ischemia and consequent acidosis and reactive oxygen species generation. In this way, mechanisms activated to maintain biological balance ultimately lead to demise of the nephron.

Original languageEnglish (US)
Pages (from-to)193-202
Number of pages10
JournalPediatric Nephrology
Volume29
Issue number2
DOIs
StatePublished - Feb 2014

Keywords

  • Chronic kidney disease
  • Fibrosis
  • Hypertrophy
  • Nephron
  • Reactive oxygen species

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology

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