Nowadays, obstructive sleep apnea syndrome (OSAS) has been established to promote both structural and functional changes in the kidneys. The basis for these changes is pathophysiological mechanisms, such as hyperproduction of free radicals and disruption of NO-mediated vasodilator responses, activation of the sympathetic autonomic nervous system and the renin-angiotensin-aldosterone system, endothelial dysfunction, development of renal venous hypertension, and stimulation of atrial natriuretic peptide production, which in turn results in increased intraglomerular pressure and glomerular hyperfiltration. In patients with OSAS, the kidneys may be damaged by OSAS-related abnormalities, such as hypertension, diabetes mellitus, metabolic syndrome, erythrocytosis, atherosclerosis, and cor pulmonale, which may also lead to kidney injury under isolated conditions and, when concurrent OSAS is present, may even aggravate the existing kidney injury.