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Effect of continuous positive airway pressure on proteinuria in obstructive sleep apnea.

Masuda T, Honma S, Sasaki N, Hanawa-Yazawa S, Iwazu Y, Kusano E, Asano Y - Clin Kidney J (2012)

Bottom Line: However, the effect on proteinuria of OSA treatment with continuous positive airway pressure (CPAP) is unknown.We experienced a case of severe OSA, where proteinuria was clearly improved after CPAP initiation without any changes of medication or body weight.The remarkable reduction of repetitive apnea and hypopnea by CPAP might ameliorate proteinuria by lessening renal hypoxia and sympathetic nerve activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Japanese Red Cross Koga Hospital, Koga, Ibaraki, Japan ; Divisionsof Nephrology, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.

ABSTRACT
Obstructive sleep apnea (OSA) is common in patients with renal disease, and an association between OSA and proteinuria has been proposed. However, the effect on proteinuria of OSA treatment with continuous positive airway pressure (CPAP) is unknown. We experienced a case of severe OSA, where proteinuria was clearly improved after CPAP initiation without any changes of medication or body weight. The remarkable reduction of repetitive apnea and hypopnea by CPAP might ameliorate proteinuria by lessening renal hypoxia and sympathetic nerve activation. This case suggests that CPAP is a promising option for OSA with proteinuria.

No MeSH data available.


Related in: MedlinePlus

Representative records of PSG before and after CPAP initiation. PSG before CPAP initiation exhibits repetitive obstructive apnea, which was diagnosed by airflow absence with paradoxical thoracic and abdominal movements. Along with sustained apnea, oxygen saturation (SaO2) gradually decreased to <80%. In contrast, PSG after CPAP initiation shows a normal breathing pattern.
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fig2: Representative records of PSG before and after CPAP initiation. PSG before CPAP initiation exhibits repetitive obstructive apnea, which was diagnosed by airflow absence with paradoxical thoracic and abdominal movements. Along with sustained apnea, oxygen saturation (SaO2) gradually decreased to <80%. In contrast, PSG after CPAP initiation shows a normal breathing pattern.

Mentions: A 60-year-old man was referred to Japanese Red Cross Koga Hospital with the main complaint of proteinuria and hypertension in September 2008. At another clinic, proteinuria had been identified in 2003, and hypertension and hyperlipidemia had been diagnosed in 2007. A medication regimen of amlodipine (2.5 mg/day) and pitavastatin (2 mg/day) began in January 2008. The patient had no history of diabetes or other glomerular diseases. Physical findings at the first visit to our hospital were the following: height 157.6 cm, body weight 68.0 kg, body mass index (BMI) 27.4, blood pressure (BP) 148/91 mmHg, pulse rate 73 beats/min, body temperature 36.4°C and the tonsils were not enlarged. Blood examination showed blood urea nitrogen 3.89 mmol/L (10.9 mg/dL), serum creatinine 88.4 μmol/L (1.00 mg/dL), uric acid 39.2 μmol/L (6.6 mg/dL), serum albumin 43 g/L (4.3 g/dL), total cholesterol 4.87 mmol/L (188 mg/dL), immunoglobulin (Ig) G 13.49 g/L (1349 mg/dL), IgA 4.35 g/L (435 mg/dL) and IgM 0.83 g/L (83 mg/dL). Autoimmune serological findings and tumor markers such as CEA and CA19-9 were within normal ranges. Urine examination revealed proteinuria (protein and creatinine ratio) 0.67 g/g Cr and urinary red blood cells at 3 per high power field. Urinary protein was determined by Protein Assay Rapid Kit (Wako; Pure Chemical Industries Ltd, Tokyo, Japan). Renal biopsy was not performed because the patient refused it. We added candesartan (2 mg/day), an angiotensin II receptor antagonist, to decrease BP and proteinuria [7]. As a result, the BP decreased while in our hospital to within the normal range (120–130/80–85), but proteinuria increased gradually. In September 2010, he complained of repetitive apnea during sleep which his wife had noticed and pointed out to him. Therefore, we decided to screen for sleep apnea by first performing pulse oximetry (PULSOX-Me300; Teijin Pharma Ltd, Tokyo, Japan) and Epworth Sleepiness Scale (ESS), a questionnaire about daytime sleepiness [8]. In these tests, 3% oxygen desaturation index by pulse oximetry was 56.88 (normal range < 5) and ESS score was 10 (normal range ≤ 10). As these results indicated severe sleep apnea, polysomnography (PSG) was performed for a detailed examination (Sleep Watcher E; Teijin Pharma, Ltd and Compumedics Ltd, Victoria, Australia). We then diagnosed severe OSA based on the following data: total apnea–hypopnea index (AHI) 78.3 events per h, obstructive AHI 77.6 events per h, average oxygen saturation (SaO2) 94.0%, minimum SaO2 65.0% and cumulative time percentage of total sleep time when SaO2 was <90% (SaO2 <90%) 20.7% (Figure 2 and Table 1).


Effect of continuous positive airway pressure on proteinuria in obstructive sleep apnea.

Masuda T, Honma S, Sasaki N, Hanawa-Yazawa S, Iwazu Y, Kusano E, Asano Y - Clin Kidney J (2012)

Representative records of PSG before and after CPAP initiation. PSG before CPAP initiation exhibits repetitive obstructive apnea, which was diagnosed by airflow absence with paradoxical thoracic and abdominal movements. Along with sustained apnea, oxygen saturation (SaO2) gradually decreased to <80%. In contrast, PSG after CPAP initiation shows a normal breathing pattern.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400518&req=5

fig2: Representative records of PSG before and after CPAP initiation. PSG before CPAP initiation exhibits repetitive obstructive apnea, which was diagnosed by airflow absence with paradoxical thoracic and abdominal movements. Along with sustained apnea, oxygen saturation (SaO2) gradually decreased to <80%. In contrast, PSG after CPAP initiation shows a normal breathing pattern.
Mentions: A 60-year-old man was referred to Japanese Red Cross Koga Hospital with the main complaint of proteinuria and hypertension in September 2008. At another clinic, proteinuria had been identified in 2003, and hypertension and hyperlipidemia had been diagnosed in 2007. A medication regimen of amlodipine (2.5 mg/day) and pitavastatin (2 mg/day) began in January 2008. The patient had no history of diabetes or other glomerular diseases. Physical findings at the first visit to our hospital were the following: height 157.6 cm, body weight 68.0 kg, body mass index (BMI) 27.4, blood pressure (BP) 148/91 mmHg, pulse rate 73 beats/min, body temperature 36.4°C and the tonsils were not enlarged. Blood examination showed blood urea nitrogen 3.89 mmol/L (10.9 mg/dL), serum creatinine 88.4 μmol/L (1.00 mg/dL), uric acid 39.2 μmol/L (6.6 mg/dL), serum albumin 43 g/L (4.3 g/dL), total cholesterol 4.87 mmol/L (188 mg/dL), immunoglobulin (Ig) G 13.49 g/L (1349 mg/dL), IgA 4.35 g/L (435 mg/dL) and IgM 0.83 g/L (83 mg/dL). Autoimmune serological findings and tumor markers such as CEA and CA19-9 were within normal ranges. Urine examination revealed proteinuria (protein and creatinine ratio) 0.67 g/g Cr and urinary red blood cells at 3 per high power field. Urinary protein was determined by Protein Assay Rapid Kit (Wako; Pure Chemical Industries Ltd, Tokyo, Japan). Renal biopsy was not performed because the patient refused it. We added candesartan (2 mg/day), an angiotensin II receptor antagonist, to decrease BP and proteinuria [7]. As a result, the BP decreased while in our hospital to within the normal range (120–130/80–85), but proteinuria increased gradually. In September 2010, he complained of repetitive apnea during sleep which his wife had noticed and pointed out to him. Therefore, we decided to screen for sleep apnea by first performing pulse oximetry (PULSOX-Me300; Teijin Pharma Ltd, Tokyo, Japan) and Epworth Sleepiness Scale (ESS), a questionnaire about daytime sleepiness [8]. In these tests, 3% oxygen desaturation index by pulse oximetry was 56.88 (normal range < 5) and ESS score was 10 (normal range ≤ 10). As these results indicated severe sleep apnea, polysomnography (PSG) was performed for a detailed examination (Sleep Watcher E; Teijin Pharma, Ltd and Compumedics Ltd, Victoria, Australia). We then diagnosed severe OSA based on the following data: total apnea–hypopnea index (AHI) 78.3 events per h, obstructive AHI 77.6 events per h, average oxygen saturation (SaO2) 94.0%, minimum SaO2 65.0% and cumulative time percentage of total sleep time when SaO2 was <90% (SaO2 <90%) 20.7% (Figure 2 and Table 1).

Bottom Line: However, the effect on proteinuria of OSA treatment with continuous positive airway pressure (CPAP) is unknown.We experienced a case of severe OSA, where proteinuria was clearly improved after CPAP initiation without any changes of medication or body weight.The remarkable reduction of repetitive apnea and hypopnea by CPAP might ameliorate proteinuria by lessening renal hypoxia and sympathetic nerve activation.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Japanese Red Cross Koga Hospital, Koga, Ibaraki, Japan ; Divisionsof Nephrology, Department of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.

ABSTRACT
Obstructive sleep apnea (OSA) is common in patients with renal disease, and an association between OSA and proteinuria has been proposed. However, the effect on proteinuria of OSA treatment with continuous positive airway pressure (CPAP) is unknown. We experienced a case of severe OSA, where proteinuria was clearly improved after CPAP initiation without any changes of medication or body weight. The remarkable reduction of repetitive apnea and hypopnea by CPAP might ameliorate proteinuria by lessening renal hypoxia and sympathetic nerve activation. This case suggests that CPAP is a promising option for OSA with proteinuria.

No MeSH data available.


Related in: MedlinePlus