Awarded Grants

NCKRF funding is vital for renal research and allows investigators to generate preliminary scientific data to allow highly competitive funding proposals to be submitted to larger funders. This is often known as 'pump priming'. Without this initial funding, many projects which go on to provide treatments in the future, would not be possible.

Awarded grants will be posted upon receipt of committee approval. Details of previously awarded grants can be found in the files below.


The role of FHR4 in renal disease associated with complement C3 deposition
Professor Claire Harris

Membranoproliferative glomerulonephritis (MPGN) defines a group of devastating diseases in which the immune system causes inflammation in the kidney, this can lead to damaged tissue and failing kidney function.

The part of the immune system that can inappropriately attack the kidney is called ‘complement’. The normal role of complement is to prevent infection by destroying bacteria and viruses and to remove old cells and debris from the body, but in some people control of this system goes wrong and distinction between ‘self’ and ‘foreign’ becomes blurred and both healthy and old cells are destroyed.

We recently carried out a study of blood samples from a large group of patients with MPGN and we noted that one protein of the complement system was present in particularly high amounts, this protein is called factor H-related protein 4 (FHR4). Independently from our study, another team of researchers recently published a landmark study that strongly linked this same protein to the devastating blinding disease, age-related macular degeneration (AMD). AMD and MPGN are diseases where the complement system incorrectly attacks cells in the tissue.

Given these remarkable similarities, we will seek specific signals in patient DNA to provide further evidence supporting a key role for FHR4 in complement attack on the kidney. These data will form the essential groundwork for us to apply to national funders for large scale funding to translate this project into a drug development phase to help patients where complement causes their kidney to fail.

Real time assessment of the alternative pathway regulatory complexes in atypical haemolytic uraemic syndrome
Dr John Kavanagh

Genetic research undertaken in the National Renal Complement Therapeutics Centre ( in Newcastle and funded by the Northern Counties Kidney Research Fund identified the complement system as a cause of the rare kidney disease, atypical haemolytic uraemic syndrome. This ultimately led to a cure for this cause of kidney failure.

Genetic results allow us to give patients the best treatment for this condition. The latest genetic technologies allow rapid and affordable sequencing of the whole human genome (the blueprints for all proteins in the body) for individual patients.  This allows detection of mutations in DNA.

A mutation can be thought of as a spelling mistake in the DNA blueprint. The human genome is made of 4 letters (A,T,G,C) arranged in various orders to tell the body how to make proteins. Sometimes a spelling mistake in the DNA can radically alter the meaning e.g. Desert (an area, often covered with sand) and Dessert (pudding) while in others a spelling mistake does not alter the meaning at all (e.g.Disc/disk). It is frequently difficult to determine from the DNA if a mutation will result in a radical change in the protein. Thus although sequencing results may be available rapidly, their interpretation may be more challenging.

We have devised a revolutionary new assay that will allow interpretation of the significance of mutations in the complement system to allow personalised management of this rare kidney disease.

Transdermal measurement of GFR in mouse models of complement mediated renal disease
Kate Jackson-Smith

Developing kidney disease is a heavy burden of illness for patients; particularly if their kidneys fail and they require dialysis to maintain their health. Some kidney diseases develop in patients as their immune system does not work properly and their kidneys come under attack from their own immune system. This can lead to kidney failure. The complement system is a part of our immune system which has been shown to play a role in the developing of certain kidney diseases. Currently, treatment options are limited and many patients progress to kidney failure. One drug which targets the immune system and prevents it from attacking the kidneys is called Eculizumab and this drug has dramatically transformed patients’ lives who develop the disease atypical haemolytic uraemic syndrome.

However, there are other complement-related kidney diseases which currently do not have any specific treatment. Our group works on pre-clinical models of these kidney diseases and we are currently testing new treatments with the hope of one day translating this into a treatment for patients. In order to assess how well the treatment is working we need to be able to monitor the kidney function in our pre-clinical models. This grant will allow me to measure the kidney function accurately; enabling us to determine which treatment provides benefits and to ensure the treatment does not cause any harm to the kidneys.

We are in a unique position to test therapies in both our acute and chronic pre-clinical models of complement mediated renal diseases. Our current focus is targeting the alternative and terminal pathway.  In order to accurately assess the benefit of treatments we need a robust, reproducible and accurate measurement of kidney function. The transdermal monitor to measure Glomerular Filtration Rate (GFR), will complement our daily measurements of proteinuria, haematuria and blood pressure, which collectively provide us with an accurate assessment of kidney function. This sophisticated device measures GFR.
The benefits of enabling serial monitoring of kidney function over time during therapeutic studies will enable translational research to assess the efficacy of complement inhibiting therapy.
Thanks to Northern Counties Kidney Research fund for supporting our ongoing work.

Using urine derived kidney cells for diagnostics, disease mechanisms and discovery
Professor John Sayer

Disorders of the cilium, an important cell organelle, often cause cystic kidney disease and result in complete renal failure. Beyond dialysis and transplantation, there is no treatment.  We will use patient-specific cells, obtained from urine, to understand how genes that are involved in cilia lead to kidney disease and to test treatments, including gene editing we have developed. We will also explore in greater detail the types of cell found in the urine and ways of preserving them to allow transportation from abroad to further our work and allow sharing of these resources with other researchers. The proposed investigation represents a non-invasive and incredibly useful research tool for studying kidney diseases. This work is jointly funded by the MRC Discovery Medicine North programme.


For the details of grants awarded in 2018 please open the attached document. 
For the details of grants awarded in 2016 - 2017 please open the attached document. 
For the details of grants awarded in 2015 please open the attached document. 
For the details of grants awarded in 2014 please open the attached document.