Short-term use of continuous positive airway pressure ameliorates glomerular hyperfiltration in patients with obstructive sleep apnoea syndrome

Abstract

Patients with OSAS (obstructive sleep apnoea syndrome) demonstrate renal signs such as proteinuria, glomerular hypertrophy and focal glomerular sclerosis. We performed a clinical study to investigate the glomerular function in OSAS patients and the short-term effect of CPAP (continuous positive airway pressure) on it. OSAS patients underwent a sodium thiosulphate and p-aminohippurate double clearance test, polysomnography and ambulatory blood pressure monitoring before and a week after the induction of CPAP. Twenty-seven consecutive patients (24 males) with moderate-to-severe OSAS admitted to our hospital for the induction of CPAP, and 32 healthy donors for renal transplantation as controls participated in the study. Before treatment, the glomerular filtration rate, estimated by the sodium thiosulphate clearance test, was within normal range, and the renal plasma flow was significantly lower than normal in the OSAS patients, thus the FF (filtration fraction) value was much higher than normal. FF before CPAP was not significantly correlated with age, body mass index or blood pressure; however, indices of increased hypoxaemia correlated with increased FF values. Polysomnographic variables after CPAP showed significant improvements in all patients, and only the nocturnal blood pressures were slightly lower than before CPAP. In 21 patients who underwent the clearance test after CPAP, FF significantly decreased from 0.26 +/- 0.04 to 0.23 +/- 0.03 (P < 0.001). OSAS patients were generally in a glomerular-hyperfiltrating condition that appeared to cause the renal findings associated with OSAS. CPAP might prevent nephropathy by ameliorating the glomerular hyperfiltration in OSAS patients.

High Prevalence of Obstructive Sleep Apnea and Its Association with Renal Function among Nondialysis Chronic Kidney Disease Patients in Japan

“…It could be assumed that OSA has an adverse effect on renal function. The most direct mechanism may be chronic elevations in BP through heightened sympa- thetic nerve tone (4), which also activates the renin-angiotensin-aldosterone system, causing glomerular hyperfiltration (28). At the same time, OSA promotes systemic oxidative stress, microinflammation, and endothelial dysfunction (5-7), which are now believed to be the major pathogenic mechanisms of chronic renal ischemia and the progression of CKD.…”

Hypoxia: The Force that Drives Chronic Kidney Disease

“…81 This treatment also ameliorates glomerular hyperfiltration, improves endothelial function and survival, reduces the production of reactive oxygen species, C-reactive protein and interleukin 6, increases vasodilator levels, and decreases the levels of vasoconstrictors. 81,83,87,[317][318][319][320][321][322] That re-oxygenation has such a dramatic beneficial influence on renal function further underscores the intimate connection between renal hypoxia and the pathogenesis of CKD.…”

“…Systemic oxygenation strategies include the administration of erythropoietin to increase hematocrit levels, apparatus to effect continuous positive airway pressure, and whole-body chambers to produce an environment of 100% oxygen. 81,83,87,[110][111][112]377,378 Artery narrowing is already routinely counteracted by renal angioplasty with or without stenting and the administration of vasoconstriction inhibitors that target the renin-angiotensin-aldosterone system. 49,[379][380][381] The targeting of vasoconstriction pathways controlled through vasopressin, endothelin, and voltage dependent calcium channels are in their infancy, as is the use of vasodilators such as arginine and kallikrein.…”

Sleep Apnea and Cardiovascular Disease

“…295,296 OSA has also been linked to glomerular hyperfiltration. 297 Whether OSA is an independent predictor of proteinuria is controversial. 298,299 Importantly, coexisting OSA may increase the likelihood of cardiovascular complications, which are the principal cause of morbidity and mortality in ESRD patients.…”