Left ventricular hypertrophy (LVH) is a cardiovascular complication highly
prevalent in patients with chronic kidney disease (CKD) and end-stage renal
disease. LVH in CKD patients has generally a negative prognostic value, because
it represents an independent risk factor for the development of arrhythmias,
sudden death, heart failure and ischemic heart disease. LVH in CKD patients is
secondary to both pressure and volume overload. Pressure overload is secondary to
preexisting hypertension, but also to a loss of elasticity of the vessels and to
vascular calcifications, leading to augmented pulse pressure. Anemia and the
retention of sodium and water secondary to decreased renal function are
responsible for volume overload, determining a hyperdynamic state. In particular,
the correction of anemia with erythropoietin in CKD patients is advantageous,
since it determines LVH reduction. Other risk factors for LVH in CKD patients are
documented: some are specific to CKD, as mineral metabolism disorders
(hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary
hyperparathyroidism), others are non-traditional, such as increased asymmetric
dimethylarginine, oxidative stress, hyperhomocysteinemia and endothelial
dysfunction that, in turn, accelerates the process of atherogenesis, triggers the
inflammation and pro-thrombotic state of the glomerular and the vascular
endothelium and aggravates the process of both CKD and LVH
