Abstract

Chronic kidney disease (CKD) is a growing health problem. Data from the US Renal Data System Reports show that the number of patients enrolled in end-stage renal disease (ESRD) Medicare-funded programs increased to a staggering 60-fold during the last 4 decades1–4 and now consumes a significant portion of the healthcare budget. Despite the magnitude of resources dedicated to treatment of chronic renal disease and the substantial improvements in the quality of dialysis and coadjuvant therapeutic strategies, these patients experience significant reductions in their quality of life, increased morbidity, and higher mortality. Furthermore, a recent projection shows that the incidence and prevalence of CKD may continue to increase in coming decades.5 This somber scenario emphasizes the need for a better understanding of underlying mechanisms of renal injury and the development of novel interventions and strategies to slow the onset and progression of CKD. Microvascular networks are dynamic anatomic units that are tightly balanced to provide nutrition and remove waste products to meet the metabolic and functional demands of each tissue. In the kidney, the glomerular and peritubular capillaries also command glomerular filtration, tubular reabsorption, and recirculation of body fluids, nutrients, hormones, and other substances to the body.6,7 Endothelial dysfunction as well as functional and structural rarefaction8 of the renal microvessels play a prominent role in inducing renal injury associated with major cardiovascular risk factors, such as hypertension, dyslipidemia, diabetes mellitus, and atherosclerosis. Furthermore, a defective renal microcirculation is a universal pathological feature in CKD that progresses as CKD evolves and compromise both the renal nutrition and renal function.6,7 The current review will focus on the role of microvascular disease in the progression of renal injury. It will discuss the involvement of microvascular disease as both cause and consequence of pathological …

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