Renal fibrosis can be defined as the nonstandard accumulation of fibrotic material within the kidney. This condition obstructs kidney function and eventually, it might lead to renal failure. With the help of genetically altered mice, scientists from Duke University investigated the interaction methods between the AT1 (angiotensin receptors), macrophages, and T cells to comprehend their role in impeding renal fibrosis. A recent research report published in the American Journal of Pathology highlights that specifically activating AT1 receptors on T cells might assist treat renal fibrosis.
Steven D. Crowley, M.D., Division of Nephrology, Departments of Medicine, Duke University, proclaimed that the latest studies are important. He added this study suggests that rather than employing global angiotensin receptor blockers, ways of jamming AT1 receptors directly in the kidney should be discovered. While doing this, tasks of AT1 receptors on immune cells as well should be maintained.
On a similar note, researchers at the University of Virginia came into the news as they found that removal of kidney obstruction encourages repair and regeneration of developing kidneys. This research might lead to advanced treatment for adults as well as infants with severe kidney disease.
Maria Luisa S. Sequeira-Lopez, M.D., FAHA, Harrison Distinguished Professor in Pediatrics and Biology at University of Virginia, is the co-author of this research. She proclaimed that at present, most critical obstructions with decreased renal function and grade IV hydronephrosis can be surgically corrected. Additionally, she stated that babies with gentle to moderate obstructions are generally followed with ultrasound. Surgical intervention and renal function tests are indicated when renal function declines more or if the hydronephrosis develops. However, on the basis of Sequeira-Lopez’s studies in mice, early deletion of the obstruction may avoid further kidney damage. Sequeira-Lopez and associates employed a partial unilateral obstruction prototype in genetically altered neonatal mice.