The relation and mechanism of kidney injury in obstructive sleep apnea: a literature review

Up to date, it is found that the presence of obstructive sleep apnea (OSA) contributes to the development of structural, ultra-structural, functional, and proteomics changes in the kidney. These changes are based on pathological processes, such as increased production of free radicals, disruption of mediated NO vasodilation reactions, activation of the sympathetic autonomic nervous system, the renin–angiotensin–aldosterone system, dysfunction of endothelium, the development of renal venous hypertension, and stimulation of atrial natriuretic peptide production. All this in turn contributes to an increase in intra-glomerular pressure, the occurrence of glomerular hyperfiltration, nocturnal polyuria, renal functional changes, proteinuria and renal tubular dysfunction. Kidney injury in OSA patients can also be caused by pathological conditions associated with OSA, such as cor pulmonale, erythrocytosis, diabetes mellitus, metabolic syndrome, hypertension, coronary heart diseases, and atherosclerosis, which in isolated conditions can lead to development of kidney damage, and co-occurring with OSA can even aggravate the course of the latter. There is a bidirectional relationship between kidney diseases and OSA through a number of potential pathological mechanisms, which suggests the possibility of both diseases to be a possible risk factor for each other. Moreover, kidney diseases may lead to OSA through a multifarious of mechanisms, including chemoreflex responsiveness, pharyngeal narrowing due to fluid overload, and accumulation of uremic toxins.