[Severe obstructive sleep apnea-hypopnea syndrome with latent renal dysfunction: analysis of 238 cases].

OBJECTIVE

To evaluate the association between severity of obstructive sleep apnea hypopnea syndrome (OSAHS) without chronic kidney disease (CKD) and serum cystatin C.

METHODS

A total of 238 patients with snoring during sleep admitted between January 2012 and June 2015 underwent full-night polysomnography for diagnosis of OSAHS. The patients were divided according to the apnea-hypopnea index (AHI) scores into simple snoring group (AHI<5) and mild (AHI, 5-15), moderate (AHI, 15-30), and severe OSAHS (AHI>30) groups. The medical history, baseline demographic characteristics, blood glucose, blood lipids, peripheral blood cell count and serum cystatin C were measured, and the correlation between polysomnographic parameters and serum cystatin C were analyzed in different groups.

RESULTS

The simple snoring, mild, moderate, and severe OSAHS groups consisted of 41, 49, 56, and 92 cases, respectively. Serum cystatin C, WBC and its subtype counts, RBC count, and superoxide dismutase (SOD) were all significantly higher in severe OSAHS group than in the other 3 groups (P<0.05), but serum creatinine and estimated glomerular filtration rate were comparable among the groups (P>0.05). Linear correlation analysis revealed that serum cystatin C was positively correlated with gender, BMI, neck circumference, abdominal circumference, SBP, AHI, and WBC (P<0.01) and inversely correlated with the average pulse oxygen saturation (ASpO2), minimum pulse oxygen saturation (MSpO(2)), and SOD (P<0.01). Multiple regression analysis identified AHI and SOD as independent factors that were positively and inversely correlated with serum cystatin C (β=0.218, P<0.010; β=-0.217, P<0.009), respectively.

CONCLUSION

Severe OSAHS is closely correlated with serum cystatin C, WBC, and SOD, suggesting that severe OSAHS may initiate the pathological process of early renal damage possibly in association with chronic intermittent hypoxia-induced oxidative stress and the initiation of the inflammatory cascade.