No abstract

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Abstract:: Patients with kidney disease experience strikingly high cardiovascular risk in the absence of conventional cardiovascular risk factors, including smoking or elevation of cholesterol associated to 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 subclinical vascular disease which is a predictor of worse cardiovascular outcome in patients with kidney failure, similarly 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 subclinical vascular injury in patients with kidney disease. Additionally, the risk for developing incident kidney disease and for rapid decline of 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 consumption of plant-based food is protective against the development of vascular disease. Insulin resistance is a robust cardiovascular risk factor in the general population, patients with diabetes and patients with kidney disease.