Vanderbilt University researchers have come closer to solving a mystery that has puzzled scientists for more than a century: after the loss of one kidney, what causes the growth of the remaining kidney to take up the slack?

TGF-beta signaling in the kidney was thought to be a target for reducing renal fibrosis, but Vanderbilt researchers report that fibrosis still occurs in the absence of TGF-beta signaling.

Chronic kidney disease impairs the protective functions of HDL, Vanderbilt researchers report this month.

Diabetic nephropathy, or kidney disease caused by diabetes, is a major source of morbidity and mortality. In the United States, more than 30 percent of patients receiving either dialytic therapy or renal transplantation have end stage renal disease as a result of diabetic nephropathy.

In some cases, HDL, the "good cholesterol," may not function properly and may actually accelerate atherosclerosis.

Researchers in Vanderbilt’s Division of Nephrology conducted a Phase 3 clinical trial to test the safety and efficacy of a new drug to treat patients with end-stage renal disease.

A novel molecular “conversation” regulates kidney fibrosis – the final result of end-stage chronic kidney disease – suggesting new treatment options for this currently irreversible process.