Bromocriptine effect on left ventricular hypertrophy in patients with diabetic nephropathy

Left ventricular hypertrophy (LVH) is a major cardiovascular risk factor in patients with diabetic nephropathy and chronic kidney disease (CKD), it predicts myocardial infarction, stroke and cardiovascular death. The prevalence of LVH increases as the renal function declines. High blood pressure, obesity and abnormal lipid profile which often coexist with diabetes have an important role in its development. The mechanism by which LVH develops includes activation of the renin-angiotensin system, aldosterone secretion, and sympathetic over activity. Bromocriptine a DA2 receptor agonist inhibits norepinephrine release and decrease blood pressure acting at the presynaptic receptors. In the kidney it mediates vasodilatation and decreases tubular sodium reabsorption, it also decreases the expression of type-1 angiotensin II receptors in renal proximal tubule and inhibits aldosterone secretion. All of these actions could exert an antiproliferative effect on LVH and modulate kidney function. The objective of this study was to analyze the effect of bromocriptine on left ventricular hypertrophy and its influence in residual renal function in patients with diabetic nephropathy, LVH and stage IV of CKD.