Finding a new treatment for end-stage renal disease is one of the primary research interests of Cascia. Over 450 thousand people in the United States are on some form of renal replacement therapy, and most often this consists of visits to a renal dialysis center every two days. Worldwide the number of people on dialysis therapy exceeds 2 million, and the numbers continue to grow.
The only other alternative to dialysis is a kidney transplant, but donor organs are exceedingly scarce. In the United States, about 25,000 kidney transplants are performed anually, and a significant percentage of those are repeat procedures for patients who have already received a transplant that are in need of a replacement due to rejection.
Approximately 60% of patients on dialysis have Type II diabetes, 25% have hypertension, 20% have cardiac disease, and 20% suffer from other diseases, many of which are genetic. The percentages total to more than 100% because many patients have multiple conditions.
Cascia is focused on providing a cellular alternative to transplant, but we also seek to reduce the impact of comorbid syndromes. Many patients suffer from one of the cardiorenal syndromes in which a decline in kidney function is accompanied by a decline in heart function, and vice versa. As the functionality of each organ deteriorates, it creates a self-reinforcing downward spiral that eventually ends in death of the patient. Cascia believes that early intervention, long before dialysis is required, will maintain and improve kidney function obviating the need for other interventions and, by mitigating the effects of cardiorenal syndrome, improve the patient's cardiac profile as well.
Patients with chronic kidney disease (CKD) consume a disproportionate amount of healthcare resources. In the Medicare population, those without CKD, heart failure (HF), or diabetes (DM) comprise roughly two-thirds of the population, but account for less than 50% of spending. Those with CKD and another comorbid condition have the most disproportionate spending.
It is well-known that when patients experience a case of acute kidney failure, the functional parameters, such as the filtration rate, often improve once the proximate cause of the acute failure has been addressed. More than twenty years ago, researchers determined that the kidney maintains a quiescent population of renal progenitor cells that, when activated, initiate self-repair of the kidney. That discovery raised the obvious question: If the kidney can self-repair after an episode of acute injury, why can't the kidney self-repair in patients with chronic disease?
Our research set out to understand the underlying mechanisms that cause this disparity, and to design a process that would allow us to initiate these inherent self-repair mechanisms. This led us to develop a protocol in tandem with nephrologists at several leading research universities for treating patients with our cellular therapies. Our next step is to initiate testing in human subjects.