Insulin Resistance is Associated with Subclinical Vascular Injury in Patients with a Kidney Disease.

Patients with kidney disease have a strikingly high cardiovascular risk in the absence of conventional cardiovascular risk factors, including smoking or elevation of cholesterol associated with low-density lipoprotein. Kidney failure remains independently associated with increased cardiovascular risk in patients with diabetes, underlining the specific adverse influence of kidney disease on cardiovascular risk. Vascular injury develops in asymptomatic patients with kidney failure early in the course of the disease. Defective arterial vasodilation, increased arterial stiffness, increased intima-media thickness, and vascular calcification develop in patients with kidney disease long before clinical evidence of cardiovascular events. Even mildly reduced kidney function is associated with a subclinical vascular disease, which is a predictor of worse cardiovascular outcome in patients with kidney failure, similar to the general population and patients with diabetes. Insulin resistance is a typical feature of kidney disease that occurs during the entire span of the disorder, from mild dysfunction to the dialysis phase. Insulin resistance (or its clinical manifestations, the metabolic syndrome or its components) is independently associated with a subclinical vascular injury in patients with kidney disease. Additionally, the risk of developing incident kidney disease and the rapid decline in kidney function is higher in patients with insulin resistance. Animal protein consumption increases dietary acid load and intensifies insulin resistance. Consistently, meat intake promotes diabetes, cardiovascular disease, and kidney failure, while the consumption of plant-based food is protective against the development of the vascular disease. Insulin resistance is a robust cardiovascular risk factor in the general population, patients with diabetes, and patients with kidney disease. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.