Obstructive Sleep Apnea Dramatically Improves After Kidney Transplantation in End-Stage Renal Disease: A Case Report

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Sleep Med Res. 2025;16(4):261-264

Publication date (electronic) : 2025 December 31

doi : https://doi.org/10.17241/smr.2025.03139

Un-Chang Heo, MD, Jung-Hwan Oh, MD

Department of Neurology, College of Medicine, Jeju National University, Jeju, Korea

Corresponding Author: Jung-Hwan Oh, MD, Department of Neurology, Jeju National University Hospital, College of Medicine, Jeju National University, 15 Aran 13-gil, Jeju 63241, Korea, Tel +82-64-717-1620, Fax +82-64-717-1100, E-mail oh.junghwan77@gmail.com

Received 2025 September 18; Revised 2025 November 4; Accepted 2025 November 18.

Abstract

INTRODUCTION

Obstructive sleep apnea (OSA) is a common form of sleep-disordered breathing (SDB) marked by repeated episodes of partial or complete blockage of the upper airway during sleep. These episodes lead to intermittent hypoxia and fragmented sleep patterns. Clinically, OSA can cause daytime sleepiness, cognitive impairment, mood disturbances, and a reduced quality of life [1]. Recent studies increasingly acknowledge a bidirectional relationship between chronic kidney disease (CKD) and OSA. The mechanisms behind this connection include fluid overload, rostral fluid shifts when lying down, ventilatory control instability caused by uremia, and systemic inflammation, all of which are believed to enhance airway collapsibility in patients with end-stage renal disease (ESRD) [2]. Conversely, intermittent hypoxia and sympathetic overactivation due to OSA can cause glomerular injury, oxidative stress, and the progression of CKD. However, there are few clinical reports that demonstrate improvement in OSA severity following the reversal of uremia [3].

Here, we present a case of a patient with ESRD who was undergoing peritoneal dialysis and showed significant improvement in OSA after kidney transplantation. This case underscores the clinical importance of renal dysfunction in the development of OSA and suggests that restoring renal function may offer opportunities for modifying the disease.

CASE REPORT

A 51-year-old male with a history of ESRD due to diabetic nephropathy had been on continuous ambulatory peritoneal dialysis for over 3 years. He was referred to our sleep clinic for evaluation of persistent snoring, witnessed apneas, excessive daytime sleepiness, and fragmented sleep that affected his daily functioning. Five years prior, he had undergone uvulopalatopharyngoplasty and tonsillectomy, but this had not significantly improved his symptoms.

His baseline scores were an Epworth Sleepiness Scale (ESS) of 8 and a Sleep Apnea Score (SAS) of 47, and a Beck Depression Inventory (BDI) score was 17. An initial overnight polysomnography (PSG) revealed an apnea-hypopnea index (AHI) of 103.2 events per hour and an oxygen desaturation index (ODI) of 96, indicating OSA (Table 1).

Table 1

Sequential changes in clinical, laboratory, and polysomnographic profiles before and after renal transplantation in end-stage renal disease

He was initially prescribed an auto-titrating positive airway pressure (APAP) device. The patient used the device for 28 out of 30 days, averaging 4 hours and 53 minutes per night, but his AHI remained elevated at 58.6. With no improvement in his symptoms, a follow-up PSG for continuous positive airway pressure (PAP) titration was conducted 6 months later (Table 1). Consequently, he was placed on bi-level PAP with inspiratory and expiratory pressures of 14/5 cmH₂O. He used this device for 18 out of 19 days, averaging 6 hours and 4 minutes per night, yet his AHI was still 42.9.

Sixteen months after the second PSG, the patient received a deceased-donor kidney transplant. Post-transplant, he reported a dramatic improvement in daytime sleepiness and mood stability (Table 1). His immunosuppressive therapy included tacrolimus and methylprednisolone. A repeat PSG 3 months after the transplant showed an AHI of 8.9 and an ODI of 8.3, indicating significant improvement. Sixteen months after transplantation, he was maintained on low-pressure APAP (4–8 cmH₂O), using it for 13 out of 30 days with an average nightly duration of 2 hours and 35 minutes, and his AHI was 1.0.

This study adhered to the principles of the Declaration of Helsinki and received approval from the Jeju National University Hospital Institutional Review Board (JEJUNUHIRB#: 2025-08-011). The requirement for written informed consent was waived.

DISCUSSION

This case illustrates a significant improvement in OSA following successful kidney transplantation in a patient ESRD. In ESRD, OSA is influenced by systemic factors such as fluid overload, fluid shifts during recumbency, uremic neuromuscular dysfunction, and inflammation, in addition to anatomical airway collapse. These mechanisms compromise upper airway stability and ventilatory control, thereby limiting the effectiveness of standard PAP therapies [4].

The marked post-transplant reductions in AHI and ODI—despite prior PAP failure—suggest that renal dysfunction-related mechanisms were the predominant drivers of his OSA [5]. Kidney transplantation may reverse several pathophysiological drivers of OSA that do not respond to airway-targeted interventions alone by restoring normal fluid balance, enhancing metabolic clearance, and reducing inflammation. Our observations align with those of several prospective studies, which have shown varying degrees of improvement in OSA following kidney transplantation. Small cohort studies reported significant reductions in the AHI and oxygen desaturation indices within a few months post-transplant [6], while a larger study noted a more modest 20% decrease in AHI, which corresponded with reductions in extracellular fluid volume, supporting the notion of a fluid-normalization mechanism [3]. Conversely, one investigation found no significant change in the AHI despite improvements in sleep architecture. This suggests that the extent of OSA recovery may depend on factors such as baseline severity, post-transplant volume status, and individual physiological characteristics.

Although improvements were also observed in ESS and SAS scores following OSA resolution, the notable improvement in mood (BDI) highlights the importance of resolving uremia and stabilizing autonomic function for sleep recovery. However, the persistence of mild OSA indicates that some structural or neuromuscular changes may be only partially reversible. This underscores the necessity for post-transplant reassessment and the development of individualized long-term treatment plans. Despite the patient’s significant improvement, the ongoing mild OSA suggests that certain contributing factors—such as chronic airway remodeling or neuromuscular changes—may be independent of renal function. This emphasizes the need for posttransplant evaluations, including follow-up PSG and consideration of continued PAP therapy, even at lower pressures, when appropriate.

It is important to note that the improvement in OSA after kidney transplantation varies among individuals and is influenced by factors such as baseline body mass index, craniofacial anatomy, and weight changes after the transplant. Following kidney transplantation, the normalization of extracellular volume helps reduce pharyngeal wall edema and enhances upper airway patency. Additionally, early weight reduction after the transplant typically indicates the resolution of pretransplant fluid overload rather than a genuine loss of adipose tissue [7]. While transplantation addresses systemic contributors, it may also introduce new risks, such as weight gain or fluid shifts due to immunosuppressants [8]. Although our case did not provide detailed mechanistic insights, existing literature offers some context. In a cohort study of kidney transplant recipients, the use of various immunosuppressive agents—including steroids, calcineurin inhibitors (e.g., cyclosporine A, tacrolimus), mycophenolate mofetil, and mTOR inhibitors—showed no significant associations with the presence or severity of OSA [9]. Separately, anti-inflammatory and immunomodulatory drugs have varying effects on sleep. Corticosteroids often impair sleep quality by inducing insomnia or altering sleep architecture, while non-steroidal immunomodulators like azathioprine do not appear to significantly impact sleep according to current studies [10]. This indicates that while immunosuppressive regimens are important for transplant recipients, their direct impact on the severity of OSA may be limited or non-specific. The significant improvement in our patient’s OSA after transplantation is likely due to the restoration of renal function and the resolution of uremia rather than the effects of medication.

In conclusion, OSA in ESRD is not just a structural airway issue; it is closely linked to systemic physiology. Kidney transplantation can lead to substantial reductions in OSA severity by correcting these systemic disturbances. However, the variability in individual responses underscores the need for personalized evaluation and follow-up.

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