European Journal of Cardiovascular Medicine

Obstructive Sleep Apnoea (OSA) is a prevalent and often underrecognized disorder characterized by repeated episodes of upper airway obstruction during sleep, leading to reduced or completely halted airflow despite ongoing respiratory efforts. These events cause intermittent hypoxia, sleep fragmentation, and significant daytime somnolence, which collectively impact cardiovascular health and overall quality of life. OSA is known to affect approximately 9–38% of the general adult population, with higher rates observed in individuals with comorbid conditions such as obesity, hypertension, and diabetes mellitus [1].

Chronic Kidney Disease (CKD) is a progressive decline in renal function marked by the irreversible loss of nephrons and associated metabolic disturbances. The global burden of CKD is increasing, affecting millions worldwide and contributing substantially to morbidity and mortality [2]. Patients with CKD frequently exhibit metabolic and cardiovascular complications that increase mortality risk. Recently, attention has been drawn to the coexistence of OSA and CKD, as emerging evidence reveals a potentially detrimental interplay between these two conditions.

The pathophysiological mechanisms linking OSA and CKD are multifactorial and complex. OSA may accelerate kidney disease progression through repeated episodes of intermittent hypoxia leading to oxidative stress, systemic inflammation, endothelial dysfunction, and sympathetic nervous system overactivity. Additionally, nocturnal hypoxia and fragmented sleep may worsen hypertension and insulin resistance, which are established risk factors for CKD progression [3]. On the other hand, CKD itself predisposes patients to OSA due to fluid overload, uremic neuropathy affecting upper airway muscles, and altered airway anatomy [4].

Despite these interrelations, the true prevalence of OSA in patients with varying stages of CKD remains inadequately defined, especially in the Indian population. Understanding the prevalence and clinical profile of OSA among CKD patients is crucial for early identification and intervention, which may reduce cardiovascular risks, improve quality of life, and potentially slow renal function decline [5].

This study aims to assess the prevalence of obstructive sleep apnoea among CKD patients attending a tertiary care center and to examine the association of OSA with clinical factors such as BMI, hypertension, diabetes, and CKD stage.

Objective: To determine the prevalence of obstructive sleep apnoea in patients with chronic kidney disease and to assess its clinical correlates and associated risk factors.

This investigation was designed as a cross-sectional observational study and was conducted over a period of two years at the Department of Respiratory Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, Uttar Pradesh, India. The study adhered to ethical principles outlined in the Declaration of Helsinki and obtained approval from the institutional ethical committee prior to commencement.

Study Population and Sample Size

The study enrolled a total of 70 patients diagnosed with chronic kidney disease, attending the outpatient and inpatient services of the institute. Inclusion criteria mandated that participants be aged 18 years or older, have a confirmed diagnosis of CKD based on estimated glomerular filtration rate (eGFR) using the CKD-EPI formula, and clinical evaluation consistent with CKD stages 3, 4, or 5.

Patients were excluded if they had a history of respiratory disorders other than OSA, acute kidney injury, or were previously diagnosed and treated for OSA. Those unable to undergo overnight polysomnography due to clinical instability or refusal to consent were also excluded.

Data Collection

Upon enrollment, detailed demographic data including age, gender, height, weight, and body mass index (BMI) were recorded. Clinical history emphasizing hypertension, diabetes mellitus, smoking status, and duration and stage of CKD was collected. Relevant laboratory parameters, such as serum creatinine and eGFR, were documented.

Polysomnography (PSG)

Each patient underwent overnight attended polysomnography in a sleep laboratory according to standard protocols. Parameters recorded included airflow through nasal and oral sensors, respiratory effort via chest and abdominal bands, pulse oximetry for oxygen saturation, electroencephalography for sleep staging, and electromyography to detect muscle activity.

OSA diagnosis was established based on the apnea-hypopnea index (AHI), calculated as the average number of apneas and hypopneas per hour of sleep. An AHI ≥ 5 events per hour was considered diagnostic of OSA. Severity was classified as mild (5-15), moderate (16-30), or severe (>30) based on AHI.

Statistical Analysis

Data were entered into a statistical software package and analyzed. Continuous variables were expressed as mean ± standard deviation and categorical variables as percentages. The prevalence of OSA in the CKD cohort was calculated. Comparisons between groups with and without OSA were conducted using the chi-square test for categorical variables and the independent t-test for continuous variables. The association between OSA prevalence and CKD stages was evaluated using appropriate tests for trend. A p-value of less than 0.05 was considered statistically significant.

The study comprised 70 patients diagnosed with chronic kidney disease. The demographic profile revealed a mean age of 52.4 ± 11.3 years, with a male predominance of 60% (42 males) compared to 40% females (28 females). Distribution of patients according to CKD stages was 30% (21 patients) in Stage 3, 40% (28 patients) in Stage 4, and 30% (21 patients) in Stage 5 (end-stage renal disease).

Overnight polysomnography identified obstructive sleep apnoea (OSA) in 38 patients, yielding an overall prevalence of 54.3% in the CKD population. Among these, 15 patients (21.4%) exhibited mild OSA (AHI 5–15), 13 patients (18.6%) moderate OSA (AHI 16–30), and 10 patients (14.3%) severe OSA (AHI >30). The remaining 32 patients did not meet the criteria for OSA diagnosis.

A clear trend was observed demonstrating a rising prevalence of OSA with advancing CKD stage. Prevalence was 28.6% in Stage 3 CKD, increased to 57.1% in Stage 4, and reached 85.7% in Stage 5 patients. This association was statistically significant (p < 0.01), indicating a strong link between declining renal function and the presence of OSA.

The mean BMI of patients diagnosed with OSA was significantly higher at 27.2 ± 3.8 kg/m² compared to 24.6 ± 3.2 kg/m² in those without OSA (p = 0.02). Additionally, comorbidities including hypertension and diabetes mellitus were more prevalent among the OSA group, with hypertension affecting 76.3% versus 50% (p = 0.03) and diabetes present in 65.8% compared to 40% (p = 0.04) of the non-OSA cohort.

No statistically significant differences were observed in age (p = 0.56) or gender distribution (p = 0.57) between patients with and without OSA. Furthermore, patients with severe OSA demonstrated greater nocturnal hypoxia and higher oxygen desaturation indices than those with mild or moderate disease (p < 0.05).

Table: Prevalence of Obstructive Sleep Apnoea in Chronic Kidney Disease Patients

*Significant at p < 0.05; NS = Not significant

This study demonstrates that obstructive sleep apnoea (OSA) is highly prevalent in patients suffering from chronic kidney disease (CKD), with more than half (54.3%) of the enrolled cohort exhibiting the disorder. Our findings are consistent with prior reports emphasizing the strong relationship between OSA and CKD, and particularly highlight that the prevalence of OSA increases significantly as renal function deteriorates. The most advanced CKD patients (Stage 5) had an OSA prevalence as high as 85.7%, underscoring the close association between end-stage renal disease and sleep-disordered breathing.

The increased body mass index (BMI), hypertension, and diabetes mellitus observed in the OSA group align with established risk factors for both CKD and OSA. Obesity promotes upper airway narrowing and increased collapsibility during sleep, contributing to OSA development. Meanwhile, hypertension and diabetes are known to both precipitate and be exacerbated by OSA through mechanisms such as intermittent hypoxia and systemic inflammation, potentially creating a vicious cycle worsening kidney damage [6].

The pathophysiological link between OSA and CKD is supported by biological mechanisms involving intermittent hypoxia leading to oxidative stress, endothelial dysfunction, and activation of the sympathetic nervous system. These pathways contribute to systemic hypertension, a major driver of CKD progression. Furthermore, CKD patients may have altered upper airway anatomy due to fluid retention and uremic neuropathy, predisposing them to obstructive events during sleep. This bidirectional relationship amplifies the importance of early OSA detection and treatment in this population [7,8].

Several previous studies corroborate our findings. Hanly et al. identified OSA prevalence nearing 50% in CKD patients, associating the disorders with systemic inflammation and hypoxia-related injury [9]. Sharma et al. reported a markedly higher OSA frequency among dialysis patients, emphasizing the role of uremic factors in sleep apnea pathogenesis [10,11]. Our study expands upon these observations in an Indian cohort, demonstrating that OSA remains underdiagnosed and untreated in CKD populations despite its high prevalence and clinical significance.

Limitations of the study include its single-center design and relatively small sample size, which may restrict the generalizability of results. Polysomnography was performed only once per patient, which may not capture night-to-night variability in OSA severity. The study did not assess the impact of OSA treatment on kidney function or quality of life outcomes, which are critical clinical considerations.

Future multicenter longitudinal studies with larger cohorts are needed to validate these findings across diverse populations. Investigating the effects of continuous positive airway pressure (CPAP) and other OSA therapies on CKD progression and cardiovascular outcomes is an important area for further research. Additionally, elucidation of molecular and physiological pathways linking OSA and CKD may facilitate novel therapeutic approaches [12,13].

This study highlights that obstructive sleep apnoea is highly prevalent among patients with chronic kidney disease, particularly in advanced stages and in those with comorbidities such as diabetes mellitus and hypertension. Given the potential impact of OSA on cardiovascular risk and renal function deterioration, early screening and intervention for OSA in CKD patients should be considered an essential component of comprehensive renal care. Timely diagnosis and management of OSA could improve overall clinical outcomes, reduce cardiovascular morbidity, and potentially slow the progression of kidney disease in this vulnerable patient population.

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