The department of Pediatric Nephrology at Children's Health℠ and physicians at UT Southwestern provide care for children with kidney disease and hypertension. Led by Michel Baum, M.D., the department is among the largest pediatric nephrology programs in the U.S. and is consistently ranked among top pediatric hospitals by U.S. News & World Report. The team is not only devoted to providing excellent patient care but also to improving the lives of children with renal disease by performing cutting-edge research.
Clinical Research Highlights
The department performs clinical research to study the pathogenesis and therapy for children with chronic kidney disease, end-stage renal disease, hypertension and transplantation. Patients with end-stage renal disease are at risk for developing metabolic bone disease and opportunistic infections. The department has made significant contributions examining therapy for these complications. We also care for a large number of children with metabolic bone disease. We have made significant strides in improving the care and outcome for patients with X-linked hypophosphatemic rickets.
Education & Training Highlights
The department of Pediatric Nephrology is one of a handful of nephrology programs to be funded by an NIH T32 grant. This grant has funded the training of some of the most successful and productive pediatric nephrologists in the country. We have six trainees in our ACGME training program. Fellows spend a total of 12 months on inpatient clinical service during the three years of training. They spend one day a week seeing outpatients in our nephrology clinic and also spend time in the metabolic bone clinic at Texas Scottish Rite Hospital. The rest of their training is devoted to clinical or basic research. Trainees may go into one of our basic science laboratories or another laboratory of others on campus that studies renal disease. Some of our trainees have elected to spend a fourth year of training in renal transplantation.
Led by Michel Baum, M.D., the laboratory has published over 140 research papers and 60 reviews in chapters in areas related to the understanding of how ions are transported across the renal epithelia in both children and adults. The Baum laboratory has been funded by the NIH for over 25 years and investigated the regulation of salt transport by the neonatal and adult kidney as well as the transporters involved in salt transport. The laboratory has shown that some of the mechanisms involved in both active and passive salt transport are different in neonates than adults. Recently, the laboratory has focused on the mechanism of hypertension with prenatal programming.
Gestational age infants who are small and very premature infants may develop hypertension and chronic kidney disease. The Baum laboratory uses a rat model to explore the pathophysiology for the increase in blood pressure and kidney injury with programming. Most recently, they have made significant discoveries that have shown that hypertension and kidney injury can be prevented by changes in the postnatal environment.
FGF23 is a phosphaturic hormone that is elevated in many metabolic bone diseases. It is the first hormone to increase in the blood stream in patients with chronic kidney disease and the levels increase progressively as renal disease worsens. Led by Jyothsna Gattineni, M.D., the laboratory has characterized the receptors for this hormone and in so doing has generated a mouse that has a 50-fold increase in FGF23 levels. Dr. Gattineni is using this mouse to determine if FGF23 contributes to the bone, vascular and cardiac disease seen in patients with chronic kidney disease.
Led by Matthias Wolf, M.D., the laboratory studies the mechanism and regulation of magnesium and calcium transport. Calcium and magnesium are transported in the distal tubule by channels. The Wolf laboratory has made seminal contributions showing how these channels get to and stay in the membrane. Several diseases including diabetes have dysregulated magnesium transport that can make the disease much worse. The Wolf laboratory is examining why there is dysregulation of magnesium transport in diabetes and if there are factors that can normalize magnesium transport and improve the outcome of patients with diabetes.