Bidirectional association between chronic kidney disease and sleep apnea: a systematic review and meta-analysis

Hansrivijit, Panupong; Puthenpura, Max; Ghahramani, Nasrollah; Cheungpasitporn, Wisit

doi:10.1007/s11255-020-02699-1

Cited by 6 publications

(2 citation statements)

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“…Wang et al [ 24 ] demonstrated that disturbances of genioglossal mitophagy are related to IH-induced mitochondrial morphology and function impairment, and supplementation of adiponectin can relieve the impairment via enhancing mitophagy. A two-way relationship between OSA and renal dysfunction has been proven in recent years [ 1 , 2 ]. As a novel pathophysiological feature of OSA, IH was demonstrated to be closely associated with renal impairment in experimental studies [ 7 – 10 , 25 – 28 ].…”

Section: Discussionmentioning

confidence: 99%

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Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury

et al. 2022

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Background As a novel pathophysiological characteristic of obstructive sleep apnea, intermittent hypoxia (IH) contributes to human renal tubular epithelial cells impairment. The underlying pathological mechanisms remain unrevealed. The present study aimed to evaluate the influence of Bcl-2 19-kDa interacting protein 3 (BNIP3)-mediated mitophagy on IH-induced renal tubular epithelial cell impairment. Material/Methods Human kidney proximal tubular (HK-2) cells were exposed to IH condition. IH cycles were as follows: 21% oxygen for 25 min, 21% descended to 1% for 35 min, 1% oxygen sustaining for 35 min, and 1% ascended to 21% for 25 min. The IH exposure lasted 24 h with 12 cycles of hypoxia and re-oxygenation. Both the siBNIP3 and BNIP3 vector were transfected to cells. Cell viability and apoptosis, mitochondrial morphology and function, and mitophagy were detected by cell counting kit-8, flow cytometry and TUNEL staining, transmission electron microscopy, western blotting, and immunofluorescence, respectively. Results In the IH-induced HK-2 cells, inhibition of BNIP3 further aggravated mitochondrial structure damage, and decreased mitophagy level, leading to increased cell apoptosis and decreased cell viability. While overexpression of BNIP3 enhanced mitophagy, which protected mitochondrial structure, it can decrease cell death in HK-2 cells exposed to IH. Conclusions The present study showed that BNIP3-mediated mitophagy plays a protective role against IH-induced renal tubular epithelial cell impairment.

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Section: Discussionmentioning

confidence: 99%

“…The relationship between obstructive sleep apnea (OSA) and renal dysfunction was found in recent years [ 1 , 2 ]. Especially, OSA can aggravate renal dysfunction in chronic renal diseases and vice versa [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury

et al. 2022

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Prevalence of sleep disorders in children with chronic kidney disease: a meta-analysis

et al. 2022

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Sleep apnoea syndrome prevalence in chronic kidney disease and end-stage kidney disease patients: a systematic review and meta-analysis

Pisano,

Zoccali,

Bolignano

et al. 2023

Clinical Kidney Journal

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Background Several studies have examined the frequency of sleep apnoea (SA) in patients with chronic kidney disease (CKD), reporting different prevalence rates. Our systematic review and meta-analysis aimed to define the clinical penetrance of SA in CKD and end-stage kidney disease (ESKD) patients. Methods Ovid-MEDLINE and PubMed databases were explored up to 5 June 2023 to identify studies providing SA prevalence in CKD and ESKD patients assessed by different diagnostic methods, either sleep questionnaires or respiration monitoring equipment [such as polysomnography (PSG), type III portable monitors or other diagnostic tools]. Single-study data were pooled using the random-effects model. The Chi2 and Cochrane-I2 tests were used to assess the presence of heterogeneity, which was explored performing sensitivity and/or subgroup analyses. Results A cumulative analysis from 32 single-study data revealed a prevalence of SA of 57% [95% confidence interval (CI) 42%–71%] in the CKD population, whereas a prevalence of 49% (95% CI 47%–52%) was found pooling data from 91 studies in ESKD individuals. The prevalence of SA using instrumental sleep monitoring devices, including classical PSG and type III portable sleep monitors, was 62% (95% CI 52%–72%) and 56% (95% CI 42%–69%) in CKD and ESKD populations, respectively. Sleep questionnaires revealed a prevalence of 33% (95% CI 16%–49%) and 39% (95% CI 30%–49%). Conclusions SA is commonly seen in both non-dialysis CKD and ESKD patients. Sleep-related questionnaires underestimated the presence of SA in this population. This emphasizes the need to use objective diagnostic tools to identify such a syndrome in kidney disease.

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Bidirectional association between chronic kidney disease and sleep apnea: a systematic review and meta-analysis

Cited by 6 publications

References 55 publications

Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury

Bcl-2 19-kDa Interacting Protein 3 (BNIP3)-Mediated Mitophagy Attenuates Intermittent Hypoxia-Induced Human Renal Tubular Epithelial Cell Injury

Prevalence of sleep disorders in children with chronic kidney disease: a meta-analysis

Sleep apnoea syndrome prevalence in chronic kidney disease and end-stage kidney disease patients: a systematic review and meta-analysis

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