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Renal contribution to cardiovascular dysfunction following preterm birth

A postgraduate research opportunity at the University of Otago.


Close date
Friday, 1 May 2020
Academic background
Sciences, Health Sciences
Host campus
PhD, Master’s, Honours
Paediatrics and Child Health (Wellington)
Dr Rebecca Dyson, Dr Max Berry, Dr Clint Gray


Under normal developmental conditions, nephrogenesis continues until the 36th week of gestation in utero, and no new nephrons develop following birth in full-term infants. Developmental programming in the kidney may result in a reduction in nephron number and thus a reduction in whole kidney glomerular surface area, which in turn may be a factor contributing to higher blood pressure (by limiting sodium excretory capacity) and increased risk of chronic kidney disease (through a reduced capacity to compensate for renal injury). Additionally, the renin angiotensin aldosterone system (RAAS) can be acutely altered during preterm birth and persistently activated in later life. Further, RAAS alterations may occur as consequence of kidney and heart immaturity to promote adaptive responses, suggesting a dual role of this system on fetal and neonatal organogenesis. The overall aim of this work is to characterise the sex-specific effects of preterm birth on renal function and establish if preterm-related renal dysfunction is also associated with dysfunction observed in central cardiovascular function in ex-preterm individuals.

This project will be run in collaboration with our colleagues at the Hudson Institute of Medical Research, Monash University, Australia. The project will utilise our established guinea pig model of preterm birth and involve non-invasive measures of renal and cardiovascular function, histological assessment of kidneys, and measurement of mediators, such as RAAS peptides and receptors, to assess the contribution of the kidneys to long-term cardiovascular dysfunction in the ex-preterm.


Becs Dyson
Tel   027 581 2969