Kidney Function

Diabetic nephropathy is the leading cause of end-stage renal disease, and both the incidence and prevalence of diabetic nephropathy continue to increase. Currently, various treatment regimens and combinations of therapies provide only partial renoprotection. It is obvious that new approaches are desperately needed to retard the progression of diabetic nephropathy. Recently, a number of new agents have been described that have the potential to delay the progression of diabetic kidney disease and minimize the growing burden of end-stage renal disease. These include inhibitors and breakers of advanced glycation end products, receptor antagonists for advanced glycation end products, protein kinase C inhibitors, NADPH (reduced nicotinamide adenine dinucleotide phosphate) oxidase inhibitors, glycosaminoglycans, endothelin receptor antagonists, antifibrotic agents, and growth factor inhibitors. This review addresses these promising new therapeutic agents for delaying the progression of diabetic kidney disease.

Racial differences in the cause, natural history, and effects of chronic kidney disease have long been the subject of investigation. Dialysis-dependent kidney failure occurs nearly 4 times more often in African Americans than European Americans. Despite this observation, studies repeatedly show that African Americans have a significant survival advantage after initiating dialysis therapy. Although this phenomenon has been attributed to environmental and socioeconomic factors, recent studies show that inherited factors strongly influence racial differences in the development of diverse kidney diseases and may affect the risk of nephropathy-associated cardiovascular disease. We review relevant studies and propose the hypothesis that inherited factors leading to organ-limited kidney diseases and a lower burden of systemic atherosclerosis contribute in part to the improved survival rates in African American patients on dialysis therapy.

Membranous nephropathy (MN) is a pathologic entity characterized by a spectrum of changes in the glomerular basement membrane (GBM). Diagnostic features include subepithelial immune deposits and thickening of the GBM. In 1968, Ehrenreich and Churg proposed a morphologic classification of MN using electron microscopic findings. This classification was based on immune deposits in the GBM, GBM reaction to the deposits, and resolution of glomerular injury with resorption of the deposits. However, some biopsy specimens with features of MN also show spherical microparticles and podocyte microvillous entrapment in thickened GBM on electron microscopy. The presence of such features has been the source of considerable confusion. In this report, we describe an adult patient with the membranous pattern of injury using light microscopy and atypical electron microscopy findings. It is likely that this represents a distinct pathologic entity unrelated to classic membranous nephropathy.