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Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney
Zoe McArdle1, Michiel F Schreuder2, Karen M Moritz3
1Cardiovascular Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, VIC, Australia.
Insights
Children with a solitary functioning kidney (SFK) face higher risks of hypertension and kidney disease. Compensatory growth mechanisms, while initially protective, may lead to long-term kidney injury and elevated blood pressure.
Area of Science:
- Pediatric Nephrology
- Renal Physiology
- Hypertension Research
Background:
- Children born with a solitary functioning kidney (SFK) are at increased risk for adult-onset hypertension and kidney disease.
- Compensatory kidney growth, including tubule and glomeruli enlargement and increased single nephron glomerular filtration rate (SNGFR), normalizes total glomerular filtration rate (GFR) but may paradoxically lead to kidney injury over time.
- Early identification of biomarkers for kidney injury risk in SFK patients is crucial.
Purpose of the Study:
- To review the compensatory adaptations in SFK.
- To elucidate how these adaptations contribute to kidney injury and hypertension.
- To evaluate current and future prognostic factors for predicting adverse outcomes in SFK.
Main Methods:
- Review of compensatory mechanisms in SFK.
- Analysis of studies in an ovine model of SFK.
- Investigation of the roles of the renal nitric oxide system, renin-angiotensin system, and renal nerves.
Main Results:
- Compensatory kidney growth in SFK involves tubular and glomerular hypertrophy and increased SNGFR.
- These adaptive mechanisms can promote kidney injury and hypertension later in life.
- Studies implicate the renal nitric oxide system, renin-angiotensin system, and renal nerves in SFK-associated kidney disease and hypertension.
Conclusions:
- Compensatory mechanisms in SFK, while initially beneficial, pose long-term risks for kidney injury and hypertension.
- Understanding the roles of the nitric oxide and renin-angiotensin systems, as well as renal nerves, is key to mitigating these risks.
- Development of next-generation prognostic factors is needed to identify high-risk SFK individuals for targeted interventions.
Abstract:
Children born with a solitary functioning kidney (SFK) have an increased risk of hypertension and kidney disease from early in adulthood. In response to a reduction in kidney mass, the remaining kidney undergoes compensatory kidney growth. This is associated with both an increase in size of the kidney tubules and the glomeruli and an increase in single nephron glomerular filtration rate (SNGFR). The compensatory hypertrophy and increase in filtration at the level of the individual nephron results in normalization of total glomerular filtration rate (GFR). However, over time these same compensatory mechanisms may contribute to kidney injury and hypertension. Indeed, approximately 50% of children born with a SFK develop hypertension by the age of 18 and 20-40% require dialysis by the age of 30. The mechanisms that result in kidney injury are only partly understood, and early biomarkers that distinguish those at an elevated risk of kidney injury are needed. This review will outline the compensatory adaptations to a SFK, and outline how these adaptations may contribute to kidney injury and hypertension later in life. These will be based largely on the mechanisms we have identified from our studies in an ovine model of SFK, that implicate the renal nitric oxide system, the renin angiotensin system and the renal nerves to kidney disease and hypertension associated with SFK. This discussion will also evaluate current, and speculate on next generation, prognostic factors that may predict those children at a higher risk of future kidney disease and hypertension.
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