[Significance of the changes of urinary uric acid, ANP, renin and aldosterone in sleep apnea syndrome patients].

OBJECTIVES

To assess the utility of urinary uric acid excretion and urinary uric acid/creatinine ratio as the marker of nocturnal respiratory disturbance in patient with sleep apnea syndrome (SAS) before and after the institution of nasal continuous positive airway pressure (nCPAP). Another purpose is to explore the relationship between the nocturnal diuresis and atrial natriuretic peptide (ANP), renin-aldosterone in SAS.

METHODS

22 cases diagnosed as SAS by polysomnography (PSG) were selected as trial group, 11 cases excluded from SAS by PSG were as control group, and 13 severe SAS patients were treated by nCPAP and taken as nCPAP therapy group. The markers mentioned above were compared in these groups.

RESULTS

The overnight change in urinary uric acid/creatinine ratio in trial group is 0.47 +/- 0.31, which is significantly higher than that in control group (0.01 +/- 0.23), P < 0.05, and in nCPAP therapy group after therapy (0.01 +/- 0.19) significantly lower than that before nCPAP therapy (0.48 +/- 0.27), P < 0.001. The morning urinary uric acid excretion in trial group is (5.4 +/- 2.3) mg/L which is also significantly higher than that in control group (3.2 +/- 1.4) mg/L, P < 0.001, and in nCPAP therapy group (3.3 +/- 1.2) mg/L significantly lower than that before nCPAP (5.9 +/- 2.6) mg/L, P < 0.05. The mean morning blood ANP in trial group is (0.182 +/- 0.004) microgram/L, which is higher than that in control group (0.182 +/- 0.004) microgram/L, P < 0.05, and in nCPAP therapy group (0.122 +/- 0.001) microgram/L is much lower than that before nCPAP therapy (0.180 +/- 0.003) microgram/L, P < 0.001. However there are no statistic significant differences between these groups in blood renin-aldosterone.

CONCLUSIONS

The urinary uric acid excretion and overnight change in urinary uric acid/creatinine are good markers to determine the effects of nCPAP on SAS. The nocturnal diuresis in SAS patients is correlated with the increase of ANP in plasma.