The impact of obstructive sleep apnea on chronic kidney disease

Abstract

Obstructive sleep apnea (OSA) is an important clinical problem in the chronic kidney disease (CKD) population. OSA is associated with hypoxemia and sleep fragmentation, which activates the sympathetic nervous system, the renin-angiotensin-aldosterone system, alters cardiovascular hemodynamics, and results in free radical generation. In turn, a variety of deleterious processes such as endothelial dysfunction, inflammation, platelet aggregation, atherosclerosis, and fibrosis are triggered, predisposing individuals to adverse cardiovascular events and likely renal damage. Independent of obesity, OSA is associated with glomerular hyperfiltration and may be an independent predictor of proteinuria, a risk factor for CKD progression. OSA is also associated with hypertension, another important risk factor for CKD progression, particularly proteinuric CKD. OSA may mediate renal damage via several mechanisms, and there is a need to better elucidate the impact of OSA on incident renal disease and CKD progression.

Fig. 1

Pathophysiologic links between obstructive sleep apnea (OSA) and chronic kidney disease (CKD). The most direct mechanism by which long-standing OSA might contribute to CKD progression is by inducing chronic elevations in blood pressure. OSA could further contribute to the CKD progression by increasing sympathetic nerve discharge directed at the kidney and other vascular beds, raising blood pressure during episodes of upper airway occlusion, and chronically accelerating the progression of renal damage, with sustained elevations in blood pressure during the awake state [47, 48]. OSA has also been linked to glomerular hyperfiltration [19]. Whether OSA is an independent predictor of proteinuria is controversial [49, 50]. eGFR—estimated glomerular filtration rate; RAAS—renin-angiotensin-aldosterone system