Professor Eberhard Ritz is a professor of internal medicine at the Ruperto Carola University, in Heidelberg, Germany. He studied medicine in the medical schools of Heidelberg, Munich and Montpellier and then worked at the Department of Internal Medicine Zürich, Switzerland and subsequently as an NIH postdoctoral fellow at the Department of Biochemistry, Washington University School of Medicine in St. Louis. He became Professor of Internal Medicine in 1974 then Chief of Division of Nephrology in 1977. He has been Professor Emeritus since 2003. He has held senior positions at numerous internationally recognized scientific bodies, and has earned many distinguished awards and medals. He is editor-in-chief emeritus of the journal Nephrology Dialysis Transplantation and is past-associate editor of the Journal of the American Society of Nephrology. Professor Ritz focuses his research on calcium metabolism in renal failure, hypertension and the kidney, diabetic nephropathy, and cardiac disorders in renal failure.
Abstract 1: Uric acid - a threat to the kidney beyond gout
For century it is known that kidney disease is associated with gout. Gout is mainly the result of genetic alterations of renal urate transport. Recently, there has been an epidemic of hyperuricemia mainly as a result of high fructose corn syrup and in some patients still the result of lead intoxication, but currently the main problem is the recent observation that hyperuricemia per se causes renal damage. This has been documented in animal experiments, but increasing evidence in humans also shows that high uric acid is also associated with greater rate of loss of renal function in patients with primary kidney disease even in the absence of gout. In addition it is also a predictor of both type 2 diabetes and a predictor of diabetic nephropathy. Paradoxically, however, high serum uric acid concentrations are associated with better outcomes in hemodialysed patients. <span style="\"line-height:" 1.5;\"="">In a controlled trial lowering of the serum uric acid concentration by administering Allopurinol has significantly lowered the progression in a small cohort of patients with advanced CKD. Because allopurinol is associated with the risk of “Stevens Johnsons syndrome”,a dangerous allergic reaction, the novel xanthine oxidase inhibitor Febuxostat has recently been studied intensively in gout and in CKD. In several studies Febuxostat was highly effective not only against gout, but also against progressive loss of renal function in hyperuricemic patients with CKD. In addition, lowering of uric acid has been shown to lower blood pressure as well as cardiovascular events in individuals with borderline or elevated uric acid concentrations presenting with borderline or elevated blood pressure.
Abstract 2: Obesity and the kidney
Obesity has become an ever more serious problem in the developed world. Its genesis is multifactorial. A body mass index (BMI) at young age is a predictor of CKD at adult age. In adults the prevalence of CKD increases with increasing BMI. The distribution of body fat is important for the risk of obesity associated complications. A predictor better than BMI is waist circumference (102 cm in males, 88 cm in females) which is linked to insulin sensitivity, albuminuria, diabetes risk. Waist circumference (a better predictor than body mass index) predicts microalbuminuria, CKD and even AKI. Obesity may cause in the kidney (i) non-parenchymal disease (carcinoma, nephrothiasis);(ii) a specific form of focal segmental glomerulosclerosis (FSGS) related to obesity; (iii) for all primary kidney diseases the outcome is worse in the presence of obesity. Obese individuals have markedly salt sensitive blood pressure. Aldosterone is increased via visceral fat produced secretagogues. Weight loss reduces GFR, RPF and albuminuria. This is particularly impressive after bariatric surgery. Paradoxically although BMI >25 kg/m2 is associated with a higher risk of CV events, individuals undergoing a CV event have a better prognosis if they are overweight.