Introduction: Sleep apnoea syndrome (OSAS) may induce albuminuria during sleep which could reflect one of the possible pathogenetic mechanisms regarding cardiovascular risk.
Materials and methods: We studied 224 patients with newly diagnosed OSAS, free of any chronic disease, and any regular drug therapy. The levels of urine albumin/creatinine ratio (ACR) before (ACR-bsleep) and immediately after (ACR-asleep) a sleep study were determined. The same procedure was repeated during the first night on CPAP treatment (n = 121) and in 46 reevaluated patients, after 3 months, on CPAP therapy. Ambulatory blood pressure was monitored in 133 of the patients.
Results: ACR-asleep was significantly higher in patients (17.82 ± 31.10 mg/g) compared with controls (6.54 ± 6.53 mg/g, p < 0.001). The mean percent change in ACR levels between after and before sleep (%dACR) was increased by 8.82% ± 61.06 in OSAS patients and reduced by 26.87% ± 18.95 in controls (p < 0.001). During the first sleep study on CPAP, the %dACR was reduced by 21.40% ± 24.59, in contrast to the increase observed during the initial study (10.73% ± 69.93, p < 0.001). This beneficial effect of CPAP treatment was preserved in the reevaluated patients. The %dACR was +29.33% ± 57.67 in nondippers (44% of the patients) and -5.57% ± 40.81 in dippers (p < 0.001). It was negatively correlated to the percent change of systolic (rho = -0.284, p = 0.003) and diastolic (rho = -0.341, p < 0.001) blood pressure between wakefulness and sleep. Contrary to normal people, ACR is increased in OSAS patients during sleep, at least partially, related to the nondipping phenomenon observed in these patients. Following CPAP treatment, urinary albumin excretion is reduced.