Evaluation of Continuous Positive Airway Pressure Therapy on Renin–Angiotensin System Activity in Obstructive Sleep Apnea

Jul 18, 2014American journal of respiratory and critical care medicine

Continuous positive airway pressure therapy and its effects on blood pressure regulation in obstructive sleep apnea

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Abstract

Continuous positive airway pressure (CPAP) therapy significantly improved renal hemodynamics in patients with obstructive sleep apnea (OSA).

CPAP therapy corrected OSA and nocturnal hypoxemia, reducing the respiratory disturbance index from 42 ± 4 to 4 ± 1 h(-1).
Glomerular filtration rate (GFR) decreased from 124 ± 8 ml/min to 110 ± 6 ml/min after CPAP therapy.
Renal plasma flow (RPF) increased from 692 ± 36 ml/min to 749 ± 40 ml/min, although this was not statistically significant.
The filtration fraction (FF) decreased from 18.9 ± 1.6% to 15.3 ± 1.0%, indicating changes in intraglomerular pressure.
Post-CPAP, the GFR response to angiotensin II was blunted, while the RPF response was augmented.
CPAP therapy was also associated with reductions in mean arterial pressure, plasma aldosterone levels, and urinary protein excretion.

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RATIONALE: Obstructive sleep apnea (OSA) has been associated with kidney function loss, which may be related to changes in the renin-angiotensin system (RAS).

OBJECTIVES: We sought to determine the effect of continuous positive airway pressure (CPAP) of patients with OSA on renal hemodynamics at baseline and in response to angiotensin II (AngII), which reflects RAS activity.

METHODS: Twenty normotensive, nondiabetic, newly diagnosed OSA subjects (15 men, 5 women, 50 ± 2 yr, respiratory disturbance index [RDI] > 15 h(-1)) with nocturnal hypoxemia (SaO2 < 90% for >12% of the night) were studied in high-salt balance pre- and post-CPAP therapy (>4 h CPAP use/night for 1 mo). Glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) (a surrogate marker for intraglomerular pressure) were measured pre- and post-CPAP using inulin and para-aminohippurate clearance techniques at baseline and in response to graded AngII infusion (3 ng/kg/min × 30 min and 6 ng/kg/min × 30 min, respectively).

MEASUREMENTS AND MAIN RESULTS: CPAP corrected OSA and hypoxemia (RDI: 42 ± 4 vs. 4 ± 1 h(-1), P < 0.001; duration SaO2 < 90%: 36% ± 5% vs. 6 ± 2%, P < 0.001). CPAP reduced GFR (124 ± 8 ml/min vs. 110 ± 6 ml/min, P = 0.014), increased RPF (692 ± 36 ml/min vs. 749 ± 40 ml/min, P = 0.059), and reduced baseline FF (18.9 ± 1.6% vs. 15.3 ± 1.0%, P = 0.004). Post-CPAP demonstrated a blunted GFR response (-9 ± 3 ml/min vs. -2 ± 2 ml/min, P = 0.033) and augmented RPF response (-182 ± 22 ml/min vs. -219 ± 25 ml/min, P = 0.024) to AngII. FF response was maintained (P = 0.4). CPAP reduced baseline mean arterial pressure (94 ± 2 vs. 89 ± 2 mm Hg, P = 0.002), plasma aldosterone (149 ± 18 vs. 109 ± 10 pmol/L, P = 0.003), and urinary protein excretion (61 [39-341] mg/day vs. 56 [22-204] mg/d, P = 0.003).

CONCLUSIONS: CPAP therapy was associated with improved renal hemodynamics and down-regulation of renal RAS activity, suggesting a potential therapeutic benefit for kidney function.

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Evaluation of Continuous Positive Airway Pressure Therapy on Renin–Angiotensin System Activity in Obstructive Sleep Apnea

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