Modelling Autoregulation in the Kidney - Research Groups -The Centre for Bioengineering - University of Canterbury - New Zealand

Modelling Autoregulation in the Kidney

Corrosion cast of an adult human kidney (AO Foundation). The anterior and posterior branches of the renal artery and the ureter have been injected with red, white, and yellow acrylic resin respectively.

Chronic kidney disease includes conditions that damage the kidneys and decrease their ability to maintain homeostasis in the body. As kidney disease progresses, waste products can rise to high levels in the blood and cause illness and complications like high blood pressure, anemia, weak bones, poor nutritional health, and nerve damage. Also, kidney disease increases the risk of developing heart and blood vessel disease, deterioration which can occur over a long period of time. Chronic kidney disease may be caused by diabetes, high blood pressure and other disorders. When kidney disease progresses, it may eventually lead to kidney failure, which requires dialysis or a kidney transplant to survive. There is therefore great emphasis placed on the understanding of factors that increase the risk of kidney disease and how blood is distributed and autoregulated throughout the kidney, enabling proper filtration.

Current Research

The current research is focused on modelling the kidney on multiple levels, from the functionality of the whole organ down to autoregulation in the nephron, the filtration unit of the kidney. There are approximately one million nephrons in each human kidney, each being an independent entity capable of producing urine via plasma filtration.

The filtration and excretion of metabolic waste is a major function of the kidney that is closely related to its' other important task, maintaining desired concentrations of key constituents in bodily fluids, namely sodium. The filtration, reabsorption, and excretion process of the nephron is elaborate, and there is a large amount of evidence that suggests chaotic interactions between neighboring nephrons, which adds another degree of complexity to the model. In gaining a greater understanding of the mechanisms governing this balance, we hope to develop novel diagnostic and treatment approaches that are more effective than current medical practices.

The Quantitative Kidney Database is a project that has the full support of our group, and it is a rapidly growing resource of experimental data and modeling parameters.


Side view of renal venous tree, with color as an indicator of vessel order via Strahler ordering scheme (Nordsletten et al 2006)


Illustration (not-to-scale) of the nephron, where blood flows in through the afferent arteriole (red), is filtered as plasma through the glomerulus, the complex capillary bed leading to the tubule system, where the majority of reabsorption takes place, and finally exiting as urine through the collecting duct (grey)

People Contributing

This project is under the supervision of Professor Tim David. Postgraduate students working on the project include Nicole Kleinstreuer and Scott Graybill. This work is being conducted in cooperation with Dr. Mike Plank and Dr. Alex James of the Mathematics department and Professor Zoltan Endre, a nephrologist from the Christchurch School of Medicine and Health Sciences.

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