Enhanced chemo-responsiveness in patients with sleep apnoea and end-stage renal disease

Abstract

Although sleep apnoea is very common in patients with end-stage renal disease, the physiological mechanisms for this association have not yet been determined. The current authors hypothesised that altered respiratory chemo-responsiveness may play an important role.In total, 58 patients receiving treatment with chronic dialysis were recruited for overnight polysomnography. A modified Read rebreathing technique, which is used to assess basal ventilation, ventilatory sensitivity and threshold, was completed before and after overnight polysomnography. Patients were divided into apnoeic (n538; apnoea/hypopnoea index (AHI) 35¡22 events?h -1 ) and nonapnoeic (n520; AHI 3¡3 events?h -1 ) groups, with the presence of sleep apnoea defined as an AHI .10 events?h -1 . While basal ventilation and the ventilatory recruitment threshold were similar between groups, ventilatory sensitivity during isoxic hypoxia (partial pressure of oxygen (PO 2 ) 6.65 kPa) and hyperoxia (PO 2 19.95 kPa) was significantly greater in apnoeic patients. Overnight changes in chemoreflex responsiveness were similar between groups.In conclusion, these data indicate that the responsiveness of both the central and peripheral chemoreflexes is augmented in patients with sleep apnoea and end-stage renal disease. Since increased ventilatory sensitivity to hypercapnia destabilises respiratory control, the current authors suggest this contributes to the pathogenesis of sleep apnoea in this patient population.

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

“…Second, ventilation control is known to be instable in CKD patients. Because chemoreflex responsiveness has been reported to be augmented in patients with end-stage renal disease, possibly because of the accumulation of uremic molecules or metabolic acidosis, this destabilized respiratory control-as explained by a high "loop gain" theory-can contribute to the pathogenesis of OSA (27). Although these two mechanisms have been established in hemodialysis patients, it is plausible that they are also applicable to the nondialysis CKD population.…”

Sleep Disorders Associated with Chronic Kidney Disease

“…Displacement of fluids from the lower limbs increases neck circumference and pharyngeal resistance and reduces upper air way cross sectional area, contributing to the pathogenesis of obstructive sleep apnea (OSA). Pharyngeal cross sectional area in patients on CHD was smaller than the control, suggesting that this may predispose to upper airway occlusion during sleep (22). Conversion from CHD to NHD is associated with an increase in pharyngeal cross sectional area, possibly due to improve fluid removal (31).…”

“…Sleep apnea is caused by both impaired central ventilatory control and upper air way occlusion during sleep. Enhanced ventilatory sensitivity to hypercapnea correlates with apnea severity (22). Conversion from conventional Hemodialysis (CHD) to nocturnal Hemodialysis (NHD) has been associated with reduced severity of sleep apnea due to reduction in ventilatory sensitivity to hypercapnea (31).…”

Obstructive sleep apnea in non-dialysis chronic kidney disease patients

“…Chemoreflex responsiveness has been reported to be augmented in patients with CKD V, possibly because of the accumulation of uremic molecules or metabolic acidosis, explained by a high ''loop gain'' theory, which contributes to the pathogenesis of OSA in CKD. 21 Upper airway dilator muscle dysfunction secondary to neuropathy or myopathy associated with either chronic uratemia or the underlying cause of CKD, such as diabetes mellitus can attribute to OSA. 22 There is a paucity of data in the Indian population.…”

“…1,14,[17][18][19][20] Beecroft et al reported that the pharyngeal cross-sectional area measured by pharyngometry in ESRD patients was 12% less than that in the normal renal function control group matched for BMI. 21 Such pharyngeal narrowing was considered to occur because of upper airway edema due to systemic fluid overload and upper airway dilator muscle dysfunction due to neuropathy or myopathy associated with chronic uremia. Ventilation control is known to be unstable in CKD patients.…”