Compensatory responses to nephron deficiency: adaptive or maladaptive?

Fong, Debra, Denton, Kate M., Moritz, Karen M., Evans, Roger and Singh, Reetu R. (2014) Compensatory responses to nephron deficiency: adaptive or maladaptive?. Nephrology, 19 3: 119-128. doi:10.1111/nep.12198


Author Fong, Debra
Denton, Kate M.
Moritz, Karen M.
Evans, Roger
Singh, Reetu R.
Title Compensatory responses to nephron deficiency: adaptive or maladaptive?
Journal name Nephrology   Check publisher's open access policy
ISSN 1320-5358
1440-1797
Publication date 2014-03-01
Year available 2014
Sub-type Article (original research)
DOI 10.1111/nep.12198
Open Access Status Not Open Access
Volume 19
Issue 3
Start page 119
End page 128
Total pages 10
Place of publication Richmond, VIC, Australia
Publisher Wiley-Blackwell Publishing Asia
Language eng
Abstract Compensatory renal growth is a characteristic adaptation to reduced renal mass that appears to recapitulate the normal pattern of maturation of the kidney during the postnatal period. Hypertrophy of tubules (predominantly the proximal tubule) and glomeruli is accompanied by increased single nephron glomerular filtration rate and tubular reabsorption of sodium. We propose that the very factors, which contribute to the increase in growth and function of the renal tubular system, are, in the long term, the precursors to the development of hypertension in those with a nephron deficit. The increase in single nephron glomerular filtration rate is dependent on multiple factors, including reduced renal vascular resistance associated with an increased influence of nitric oxide, and a rightward shift in the tubuloglomerular feedback curve, both of which contribute to the normal maturation of renal function. The increased influence of nitric oxide appears to contribute to the reduction in tubuloglomerular feedback sensitivity and facilitate the initial increase in glomerular filtration rate. The increased single-nephron filtered load associated with nephron deficiency may promote hypertrophy of the proximal tubule and so increased reabsorption of sodium, and thus a rightward shift in the pressure natriuresis relationship. Normalization of sodium balance can then only occur at the expense of chronically increased arterial pressure. Therefore, alterations/adaptations in tubules and glomeruli in response to nephron deficiency may increase the risk of hypertension and renal disease in the long-term. Summary at a Glance This is a comprehensive review on our current understanding of postnatal functional and structural maturation of a kidney. We further explore how these adaptations in the setting of abnormal kidney development or loss of a kidney which result in low nephron number can lead to maladaptive phenotypes such as renal failure and hypertension later in life.
Keyword Compensatory renal growth
Hyperfiltration
Hypertension
Nephron number
Tubular hypertrophy
Tubuloglomerular feedback
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2015 Collection
School of Biomedical Sciences Publications
 
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