TRANSMEMBRANE and immunoglobulin domain-containing 1 (TMIGD1), a previously unknown protein involved in protecting kidney epithelial cells from damage, may comprise a novel target for replenishing kidney function following various forms of kidney disease. The discovery by researchers from Boston University School of Medicine (BUSM), Boston, Massachusetts, USA, could change the way kidney disease is treated in the future. TMIGD1 belongs to a new class of proteins involved in cell–cell recognition, with the first member (IGPR-1) being identified by the same research team in early 2012; IGPR-1 is involved in tumour angiogenesis and the development of new blood vessels.
The research team from Boston were able to decrease the expression of TMIGD1 in kidney epithelial cells and showed that they became susceptible to injury, while increasing the expression of TMIGD1 protected the cells from injury. “This study demonstrates that by altering the function of TMIGD1, it is possible to reduce kidney epithelial cell death and possibly avoid the high incidence of kidney failure and morbidity associated with kidney injury,” explained corresponding author Dr Nader Rahimi, Associate Professor of Pathology and Laboratory Medicine, BUSM.
Kidneys may fail over a period of days in acute kidney failure, or may fail over a period of years in chronic kidney disease. Both types of kidney failure are prevalent and constitute a substantial healthcare burden. Furthermore, kidney failure amongst inpatients not only extends hospital stays but also suggests a poor prognosis overall. “While dialysis and transplantation are considered the cornerstone of therapy for both forms of renal failure, none of these strategies directly targets the kidney proximal epithelial cells. Therapeutic agents that could protect these cells from death can prevent and retard renal damage, thus postponing dialysis or need for transplantation,” added co-author Dr Vipul Chitalia, Assistant Professor of Medicine at BUSM and a nephrologist at Boston Medical Center, Boston.