The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
Pathogenic Dendritic Cells In Human Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$370,983.00
Summary
The cost of treating end stage kidney disease in Australia is more than a billion dollars per year. Kidney disease is associated with an influx of inflammatory cells. However, current therapeutics fail to target this process due to our poor understanding of inflammatory immune cells in disease progression. This project will investigate the biology of immune cells in human kidney disease. I believe that this study will inform more accurate diagnoses and improved treatments for patients.
Understanding The Mechanistic Basis Of Microalbuminuria In Diabetic Nephropathy
Funder
National Health and Medical Research Council
Funding Amount
$613,757.00
Summary
The appearance of small amounts of albumin in the urine (microalbuminuria) in people with diabetes is a marker of progressive kidney disease, while microalbuminuria in the general population is a major risk factor for cardiovascular disease. The reason why microalbuminuria develops is poorly understood. This project will investigate dysfunction of kidney tubular cells as the mechanistic basis of microalbuminuria. If proven, this will provide a new link between kidney and cardiovascular disease.
A Central Role For Carbonic Anhydrase In Renal Hypertrophy And Interstitial Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$414,888.00
Summary
1 in 3 Australians are at risk of developing kidney disease. Renal replacement therapies (dialysis and transplantation) currently cost over $1.2 billion per year. These therapies do not address the underlying cause of the disease. Much research has focused on novel strategies to reverse kidney damage with mixed success. In this project we examine a novel preventative strategy based on currently available therapeutics that may slow the progression of kidney disease.
Kidney Injury As A Determinant Of Macrophage Phenotype And Efficacy For Treating Chronic Kidney Disease (CKD)
Funder
National Health and Medical Research Council
Funding Amount
$548,341.00
Summary
Chronic kidney disease (CKD) is a major cause of death and disability in the Australian population. Current treatments for CKD are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or tranplantation to remain alive. Every year more than 1700 Australians require kidney replacement therapy for this reason and many more die of kidney failure or its complications. Macrophage infiltration of kidneys is characteristic of C ....Chronic kidney disease (CKD) is a major cause of death and disability in the Australian population. Current treatments for CKD are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or tranplantation to remain alive. Every year more than 1700 Australians require kidney replacement therapy for this reason and many more die of kidney failure or its complications. Macrophage infiltration of kidneys is characteristic of CKD, and it has been assumed that macrophages cause damage. However, we have shown that certain types of macrophages can reduce kidney damage. This project will explore whether macrophage type can be switched from that causing damage to that reducing injury, with the aim of using this approach to treat CKD.Read moreRead less
SGLT2 inhibitors are new glucose-lowering agents for type 2 diabetes. They promote glucose loss into urine, which lowers blood glucose levels. However, little is known regarding the changes to kidney physiology when this system is manipulated with these drugs. There is evidence that SGLT2 inhibitors do not protect against kidney disease in diabetic mice, despite being an effective blood glucose-lowering agent. I aim to characterise the changes to kidney function upon SGLT2 blockade in diabetes.
Two-photon Microscopy Of Albumin Handling By The Intact Kidney
Funder
National Health and Medical Research Council
Funding Amount
$346,602.00
Summary
The clinical association between protein loss in the urine and retention of salt, resulting in high blood pressure and progressive decline in kidney function, is well known. Under normal conditions, the kidneys filter 180 litres of water and reabsorb 1.7 kg of salt per day, a function which is principally performed by the kidney tubules in the kidney. Similarly the kidney tubule cells reabsorb and break down up to 3 grams of albumin per day. In the past, it has been considered that excessive pro ....The clinical association between protein loss in the urine and retention of salt, resulting in high blood pressure and progressive decline in kidney function, is well known. Under normal conditions, the kidneys filter 180 litres of water and reabsorb 1.7 kg of salt per day, a function which is principally performed by the kidney tubules in the kidney. Similarly the kidney tubule cells reabsorb and break down up to 3 grams of albumin per day. In the past, it has been considered that excessive protein loss in the urine is primarily due to problems in the filtering units of the kidneys, rather than due to abnormalities in the reabsorption of protein in the kidney tubules. However, we consider that common abnormalities in the processes within the kidney tubules that regulate both the reabsorption of salt and the excretion of acid may result in concomitant high blood pressure and increased protein loss in the kidney. Thus the overall aim of the project is to investigate the mechanisms by which the complex responsible for protein uptake determines the interrelationship between protein reabsorption and catabolism and the ion transporting proteins in the membrane of the proximal tubule. This project will use cutting-edge microscopic imaging technology to investigate the mechanisms of protein uptake in the intact kidney. This information will be integrated with data obtained from our molecular physiology experiments to define how the kidney handles protein. As persistent proteinuria is the most important predictor of tubulointerstitial pathology and progressive decline in renal function in almost all renal disease, the understanding of the precise mechanism by which this occurs is essential in the design of renoprotective therapies.Read moreRead less
Treatment Of Diverse Renal Diseases With Regulatory Cells
Funder
National Health and Medical Research Council
Funding Amount
$566,946.00
Summary
Chronic kidney disease (CKD) is a major cause of death and disability in the Australian population. Current treatments for CKD are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or tranplantation to remain alive. Every year more than 1700 Australians require kidney replacement therapy for this reason and many more die of kidney failure or its complications. Some forms of kidney disease are self-limited whereas oth ....Chronic kidney disease (CKD) is a major cause of death and disability in the Australian population. Current treatments for CKD are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or tranplantation to remain alive. Every year more than 1700 Australians require kidney replacement therapy for this reason and many more die of kidney failure or its complications. Some forms of kidney disease are self-limited whereas others are characterised by chronic kidney scarring and the eventual development of endstage disease. This project will explore whether natural protective cells (regulatory T cells) can be used to treat differing types of CKD, including those characterised predominantly by inflammation or by fibrosis. In addition, the protective mechanisms of regulatory T cells (including their interaction with resident kidney cells) will be explored, as will ways of increasing the efficacy of regulatory T cell therapy.Read moreRead less
DNA Vaccination Using Chemokine And Costimulatory Pathways As A Treatment For Chronic Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$450,390.00
Summary
Chronic kidney disease (CKD) is a great burden on Australia. Treatments are mostly ineffective. Our DNA vaccination against mediators of inflammation can protect against CKD. On the basis of ongoing studies we have identified 5 candidate molecules involved in recruitment and activation of inflammatory cells. We outline studies to generate DNA vaccines to these molecules, enhance their efficacy, and test them in models that represent the 3 most important causes of human CKD.