Enhanced conductive body heat loss during sleep increases slow-wave sleep and calms the heart.

Substantial evidence suggests that the circadian decline of core body temperature (CBT) triggers the initiation of human sleep, with CBT continuing to decrease during sleep. Although the connection between habitual sleep and CBT patterns is established, the impact of external body cooling on sleep remains poorly understood. The main aim of the present study is to show whether a decline in body temperatures during sleep can be related to an increase in slow wave sleep (N3). This three-center study on 72 individuals of varying age, sex, and BMI used an identical type of a high-heat capacity mattress as a reproducible, non-disturbing way of body cooling, accompanied by measurements of CBT and proximal back skin temperatures, heart rate and sleep (polysomnography). The main findings were an increase in nocturnal sleep stage N3 (7.5 ± 21.6 min/7.5 h, mean ± SD; p = 0.0038) and a decrease in heart rate (- 2.36 ± 1.08 bpm, mean ± SD; p < 0.0001); sleep stage REM did not change (p = 0.3564). Subjects with a greater degree of body cooling exhibited a significant increase in nocturnal N3 and a decrease in REM sleep, mainly in the second part of the night. In addition, these subjects showed a phase advance in the NREM-REM sleep cycle distribution of N3 and REM. Both effects were significantly associated with increased conductive inner heat transfer, indicated by an increased CBT- proximal back skin temperature -gradient, rather than with changes in CBT itself. Our findings reveal a previously far disregarded mechanism in sleep research that has potential therapeutic implications: Conductive body cooling during sleep is a reliable method for promoting N3 and reducing heart rate.

Impact of sleep disruption on cognitive function in patients with postacute sequelae of SARS-CoV-2 infection: initial findings from a Neuro-COVID-19 clinic.

Introduction: Fatigue, brain fog, and sleep disturbance are among the most common symptoms of postacute sequelae of SARS-CoV-2 infection (PASC). We sought to determine the impact of sleep disruption on cognition and quality of life in patients with neurologic manifestations of PASC (Neuro-PASC). Methods: Thirty-nine patients were recruited from Neuro-COVID-19 clinic. Mean age was 48.1 years, 71.8% were female, and 82% were never hospitalized for COVID-19. Patients were evaluated via clinical assessment, quality-of-life measures in domains of cognitive function, fatigue, sleep disturbance, anxiety, and depression, NIH Toolbox cognitive tests, and 7 days of wrist actigraphy. Results: The median number of neurologic symptoms attributed to PASC was 6, with brain fog being the most common in 89.7%. Regarding non-neurologic symptoms, 94.9% complained of fatigue and 74.4% of insomnia. Patients reported significant impairment in all quality-of-life domains and performed worse in a task of attention compared to a normative US population. Actigraphy showed Neuro-PASC patients had lower sleep efficiency, longer sleep latency (both p < 0.001), and later sleep midpoint (p = 0.039) compared to 71 age-matched healthy controls with no PASC history. Self-reported cognitive symptoms correlated with the severity of fatigue (p < 0.001), anxiety (p = 0.05), and depression (p < 0.01). Objective evidence of sleep disruption measured by wakefulness after sleep onset, sleep efficiency, and latency were associated with decreased performance in attention and processing speed. Conclusion: Prospective studies including larger populations of patients are needed to fully determine the interplay of sleep disruption on the cognitive function and quality of life of patients with PASC.

Light exposure during sleep impairs cardiometabolic function.

SignificanceAmbient nighttime light exposure is implicated as a risk factor for adverse health outcomes, including cardiometabolic disease. However, the effects of nighttime light exposure during sleep on cardiometabolic outcomes and the related mechanisms are unclear. This laboratory study shows that, in healthy adults, one night of moderate (100 lx) light exposure during sleep increases nighttime heart rate, decreases heart rate variability (higher sympathovagal balance), and increases next-morning insulin resistance when compared to sleep in a dimly lit (<3 lx) environment. Moreover, a positive relationship between higher sympathovagal balance and insulin levels suggests that sympathetic activation may play a role in the observed light-induced changes in insulin sensitivity.

Does memory reactivation during sleep support generalization at the cost of memory specifics?

Sleep is important for memory, but does it favor consolidation of specific details or extraction of generalized information? Both may occur together when memories are reactivated during sleep, or a loss of certain memory details may facilitate generalization. To examine these issues, we tested memory in participants who viewed landscape paintings by six artists. Paintings were cropped to show only a section of the scene. During a learning phase, each painting section was presented with the artist's name and with a nonverbal sound that had been uniquely associated with that artist. In a test of memory for specifics, participants were shown arrays of six painting sections, all by the same artist. Participants attempted to select the one that was seen in the learning phase. Generalization was tested by asking participants to view new paintings and, for each one, decide which of the six artists created it. After this testing, participants had a 90-minute sleep opportunity with polysomnographic monitoring. When slow-wave sleep was detected, three of the sound cues associated with the artists were repeatedly presented without waking the participants. After sleep, participants were again tested for memory specifics and generalization. Memory reactivation during sleep due to the sound cues led to a relative decline in accuracy on the specifics test, which could indicate the transition to a loss of detail that facilitates generalization, particularly details such as the borders. Generalization performance showed very little change after sleep and was unaffected by the sound cues. Although results tentatively implicate sleep in memory transformation, further research is needed to examine memory change across longer time periods.

Effects of manipulating body temperature on sleep in postmenopausal women.

STUDY OBJECTIVES: A decline in sleep quality, slow wave sleep (SWS) and slow wave activity (SWA) are common in older adults. Prior studies have shown that manipulating body temperature during sleep can increase SWS/SWA. The aim of this study was to determine the effects of manipulation of body temperatures during sleep, using a high heat capacity mattress, on SWS/SWA and heart rate in post-menopausal women. METHODS: Twenty-four healthy postmenopausal women between 40 and 75 years of age (mean age 62.4 ± 8.2 years, mean BMI 25.4 ± 3.5 kg/m2) were randomized in a single-blind, counterbalanced, cross-over manner to sleep on either a high heat capacity mattress (HHCM) or a low heat capacity mattress (LHCM) a week apart. Sleep was recorded using polysomnography during an 8-h sleep opportunity. Core and peripheral temperature were recorded using an ingestible capsule and thermochron respectively. RESULTS: In comparison to the LHCM, sleep on HHCM exhibited a selective increase in SWS (average increase in Stage N3 of 9.6 min (2.1%), p = 0.04) and in slow oscillatory (SO) activity (0.5-1 Hz) in the first NREM/REM cycle (p = 0.04). In addition, the HHCM induced a greater reduction in core body temperature (p = 0.002). The reduction in core body temperature (first 180 min after lights out) from LHCM to HHCM was associated (r = 0.5, p = 0.012) with the increase in SO activity (SO cycle 1 and 2/cycle 3 and 4). Average heart rate was 1.6 beats/minute lower across the night on the HHCM compared to the LHCM (p = 0.001). CONCLUSIONS: The results of this study indicate that manipulation of body temperature during sleep may be a useful approach to enhance SWS sleep in postmenopausal women.

Autonomic dysregulation and sleep homeostasis in insomnia.

STUDY OBJECTIVES: Insomnia is common in older adults, and is associated with poor health, including cognitive impairment and cardio-metabolic disease. Although the mechanisms linking insomnia with these comorbidities remain unclear, age-related changes in sleep and autonomic nervous system (ANS) regulation might represent a shared mechanistic pathway. In this study, we assessed the relationship between ANS activity with indices of objective and subjective sleep quality in older adults with insomnia. METHODS: Forty-three adults with chronic insomnia and 16 age-matched healthy sleeper controls were studied. Subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), objective sleep quality by electroencephalogram spectral components derived from polysomnography, and ANS activity by measuring 24-h plasma cortisol and norepinephrine (NE). RESULTS: Sleep cycle analysis displayed lower slow oscillatory (SO: 0.5-1.25 Hz) activity in the first cycle in insomnia compared to controls. In insomnia, 24-h cortisol levels were higher and 24-h NE levels were lower than controls. In controls, but not in insomnia, there was a significant interaction between NE level during wake and SO activity levels across the sleep cycles, such that in controls but not in insomnia, NE level during wake was positively associated with the amount of SO activity in the first cycle. In insomnia, lower 24-h NE level and SO activity in the first sleep cycle were associated with poorer subjective sleep quality. CONCLUSION: Dysregulation of autonomic activity may be an underlying mechanism that links objective and subjective measures of sleep quality in older adults with insomnia, and potentially contribute to adverse health outcomes.

Neurostimulation techniques to enhance sleep and improve cognition in aging.

Sleep plays a critical role in the process of memory consolidation. In particular, during non-rapid eye movement (NREM) slow wave sleep, slow-oscillations, spindles, hippocampal sharp wave ripples, and their phase coupling are involved in the process of transferring and consolidating information recently encoded and temporarily stored in the hippocampus into long-term memory stored in the neocortex. There is evidence that aging and neurodegenerative conditions, in particular Alzheimer's disease, are associated with changes to this transient grouping of NREM oscillations. Therefore, methods to enhance sleep, particularly slow wave sleep, have the potential to improve cognitive performance. Transcranial electrical and magnetic stimulation have been shown useful to enhance sleep slow-waves and sleep-dependent memory consolidation, however there is need for more information regarding proper protocols of application and applicability and efficacy in patients with neurodegenerative conditions. Acoustic stimulation during sleep has been proven particularly effective in enhancing sleep slow-waves and spindles with associated improvement in overnight memory consolidation. More importantly, preliminary data indicate that similar results can be achieved in healthy older adults and those with amnestic mild cognitive impairment. Studies are needed to optimize the modalities of acoustic stimulation during sleep, which may vary based on age group or clinical disorder. Overall, non-invasive techniques of neurostimulation may represent a valid approach to mitigate cognitive decline associated with aging and neurodegeneration. Furthermore, they offer the unique opportunity to improve our understanding of the physiology behind sleep-dependent memory consolidation.

What volume to choose to assess online Kt/V?

INTRODUCTION: Urea distribution volume (V) can be assessed in different ways, among them the anthropometric Watson Volume (VW). However, many studies have shown that VW does not coincide with V and that the latter can be more accurately estimated with other methods. The present multicentre study was designed to answer the question: what V to choose to assess online Kt/V? MATERIALS AND METHODS: Pre- and postdialysis blood urea nitrogen concentrations and the usual input data set for urea kinetic modelling were obtained for a single dialysis session in 201 Caucasian patients treated in 9 Italian dialysis units. Only dialysis machines measuring ionic dialysance (ID) were utilized. ID reflects very accurately the mean effective dialyser urea clearance (Kd). Six different V values were obtained: the first one was VW; the second one was computed from the equation established by the HEMO Study to predict the single pool-adjusted modelled V from VW (VH) (Daugirdas JT et al. KI 64: 1108, 2003); the others were estimated kinetically as: 1. V_ID, in which ID is direct input in the in the double pool variable volume (dpVV) calculation by means of the Solute-solver software; 2. V_Kd, in which the estimated Kd is direct input in the dpVV calculation by means of the Solute-solver software; 3. V_KTV, in which V is calculated by means of the second generation Daugirdas equation; 4. V_SPEEDY, in which ID is direct input in the dpVV calculation by means of the SPEEDY software able to provide results quite similar to those provided by Solute-solver. RESULTS: Mean± SD of the main data are reported: measured ID was 190.6 ± 29.6 mL/min, estimated Kd was 211.6 ± 29.0 mL/min. The relationship between paired data was poor (R2 = 0.34) and their difference at the Bland-Altman plot was large (21 ± 27 mL/min). VW was 35.3 ± 6.3 L, VH 29.5 ± 5.5, V_ID 28.99 ± 7.6 L, V_SPEEDY 29.4 ± 7.6 L, V_KTV 29.7 ± 7.0 L. The mean ratio VW/V_ID was 1.22, (i.e. VW overestimated V_ID by about 22%). The mean ratio VH/V_ID was 1.02 (i.e. VH overestimated V_ID by only 2%). The relationship between paired data of V_ID and VW was poor (R2 = 0.48) and their mean difference at the Bland-Altman plot was very large (- 6.39 ± 5.59 L). The relationship between paired data of V_ID and VH was poor (R2 = 47) and their mean difference was small but with a large SD (- 0.59 ± 5.53 L). The relationship between paired data of V_ID and V_SPEEDY was excellent (R2 = 0.993) and their mean difference at the Bland-Altman plot was very small (- 0.54 ± 0.64 L). The relationship between paired data of V_ID and V_KTV was excellent (R2 = 0.985) and their mean difference at the Bland-Altman plot was small (- 0.85 ± 1.06 L). CONCLUSIONS: V_ID can be considered the reference method to estimate the modelled V and then the first choice to assess Kt/V. V_SPEEDY is a valuable alternative to V_ID. V_KTV can be utilized in the daily practice, taking also into account its simple way of calculation. VW is not advisable because it leads to underestimation of Kt/V by about 20%.

Sleep and Limb Movement Characteristics of Children With Atopic Dermatitis Coincidentally Undergoing Clinical Polysomnography.

STUDY OBJECTIVES: Atopic dermatitis (AD) is a prevalent, chronic, itchy skin condition. Children undergoing polysomnography (PSG) may coincidentally have AD. Many children with AD have sleep disturbances. Our study aimed to characterize limb movements in children with AD and their effect on sleep. METHODS: A retrospective chart review was conducted for children who underwent comprehensive attended PSG and had AD. PSG sleep parameters were compared to published normative data. A subset of patients with markedly elevated total limb movements was further compared to a matched group of patients with a diagnosis of periodic limb movement disorder (PLMD) and no history of AD. RESULTS: There were 34 children with AD 6.36 ± 3.21 years (mean ± standard deviation), 50% female and with mild to moderate AD. There was increased wake after sleep onset (WASO = 46.0 ± 37.8 minutes), sleep onset latency (46.5 ± 53.0 minutes) and total limb movement index (13.9 ± 7.5 events/h) compared to normative values. Although our cohort was mostly mild AD, 7 of the 34 children with AD (20%) had a total limb movement index during sleep > 15 events/h. Increased total limb movements in PLMD versus patients with AD was most notable during stage N2 sleep (38 ± 17 versus 22 ± 7, P = .01, respectively). CONCLUSIONS: We found altered PSG parameters in children with AD, suggesting that clinicians should consider the diagnosis when affected children undergo PSG. Although our AD cohort was mild, we still determined a need to consider AD when diagnosing PLMD given the presence of elevated total limb movements in children with AD. CITATION: Treister AD, Stefek H, Grimaldi D, Rupani N, Zee P, Yob J, Sheldon S, Fishbein AB. Sleep and limb movement characteristics of children with atopic dermatitis coincidentally undergoing clinical polysomnography. J Clin Sleep Med. 2019;15(8):1107-1113.

Insomnia and cardiovascular autonomic control.

Insomnia is the most prevalent sleep disorder, particularly among middle and older aged adults, and is associated with a variety of negative health consequences, including higher risk for cardiovascular disease. Unfortunately, the mechanisms linking insomnia with cardiovascular risk remain largely unknown, thus limiting targeted therapeutic interventions. The hyperarousal hypothesis has attracted the most support, positing that insomnia is a result of multisystem over-activation, including sympathetic hyperactivity, which promotes wakefulness and blocks the occurrence of sleep at the desired time. The results from literature in support of this hypothesis are inconclusive and mainly relay on studies that used methods to assess sympathetic activity lacking in specificity and reproducibility. The present review aims at summarizing the primary findings on autonomic nervous system regulation in insomnia while highlighting the advantages and limitations of the methods mainly used to support the increase in sympathetic function in insomnia. Collectively, this review aims to provide novel perspectives on conceptualizing insomnia and suggest innovative approaches to help elucidate the relationship between insomnia and autonomic nervous system activity.

Acoustic enhancement of sleep slow oscillations in mild cognitive impairment.

OBJECTIVE: Slow-wave activity (SWA) during sleep is reduced in people with amnestic mild cognitive impairment (aMCI) and is related to sleep-dependent memory consolidation. Acoustic stimulation of slow oscillations has proven effective in enhancing SWA and memory in younger and older adults. In this study we aimed to determine whether acoustic stimulation during sleep boosts SWA and improves memory performance in people with aMCI. METHODS: Nine adults with aMCI (72 ± 8.7 years) completed one night of acoustic stimulation (stim) and one night of sham stimulation (sham) in a blinded, randomized crossover study. Acoustic stimuli were delivered phase-locked to the upstate of the endogenous sleep slow-waves. Participants completed a declarative recall task with 44 word-pairs before and after sleep. RESULTS: During intervals of acoustic stimulation, SWA increased by >10% over sham intervals (P < 0.01), but memory recall increased in only five of the nine patients. The increase in SWA with stimulation was associated with improved morning word recall (r = 0.78, P = 0.012). INTERPRETATION: Acoustic stimulation delivered during slow-wave sleep over one night was effective for enhancing SWA in individuals with aMCI. Given established relationships between SWA and memory, a larger or more prolonged enhancement may be needed to consistently improve memory in aMCI.

Admission Heart Rate Variability is Associated with Fever Development in Patients with Intracerebral Hemorrhage.

BACKGROUND: Fever is associated with worse outcome after intracerebral hemorrhage (ICH). Autonomic dysfunction, commonly seen after brain injury, results in reduced heart rate variability (HRV). We sought to investigate whether HRV was associated with the development of fever in patients with ICH. METHODS: We prospectively enrolled consecutive patients with spontaneous ICH in a single-center observational study. We included patients who presented directly to our emergency department after symptom onset, had a 10-second electrocardiogram (EKG) performed within 24 h of admission, and were in sinus rhythm. Patient temperature was recorded every 1-4 h. We defined being febrile as having a temperature of ≥ 38 °C within the first 14 days, and fever burden as the number of febrile days. HRV was defined by the standard deviation of the R-R interval (SDNN) measured on the admission EKG. Univariate associations were determined by Fisher's exact, Mann-Whitney U, or Spearman's rho correlation tests. Variables associated with fever at p ≤ 0.2 were entered in a logistic regression model of being febrile within 14 days. RESULTS: There were 248 patients (median age 63 [54-74] years, 125 [50.4%] female, median ICH Score 1 [0-2]) who met the inclusion criteria. Febrile patients had lower HRV (median SDNN: 1.72 [1.08-3.60] vs. 2.55 [1.58-5.72] msec, p = 0.001). Lower HRV was associated with more febrile days (R = - 0.22, p < 0.001). After adjustment, lower HRV was independently associated with greater odds of fever occurrence (OR 0.92 [95% CI 0.87-0.97] with each msec increase in SDNN, p = 0.002). CONCLUSIONS: HRV measured on 10-second EKGs is a potential early marker of parasympathetic nervous system dysfunction and is associated with subsequent fever occurrence after ICH. Detecting early parasympathetic dysfunction may afford opportunities to improve ICH outcome by targeting therapies at fever prevention.

Strengthening sleep-autonomic interaction via acoustic enhancement of slow oscillations.

Slow-wave sleep (SWS) is important for overall health since it affects many physiological processes including cardio-metabolic function. Sleep and autonomic nervous system (ANS) activity are closely coupled at anatomical and physiological levels. Sleep-related changes in autonomic function are likely the main pathway through which SWS affects many systems within the body. There are characteristic changes in ANS activity across sleep stages. Notably, in non-rapid eye-movement sleep, the progression into SWS is characterized by increased parasympathetic activity, an important measure of cardiovascular health. Experimental manipulations that enhance slow-wave activity (SWA, 0.5-4 Hz) can improve sleep-mediated memory and immune function. However, effects of SWA enhancement on autonomic regulation have not been investigated. Here, we employed an adaptive algorithm to deliver 50 ms sounds phase-locked to slow-waves, with regular pauses in stimulation (~5 s ON/~5 s OFF), in healthy young adults. We sought to determine whether acoustic enhancement of SWA altered parasympathetic activity during SWS assessed with heart rate variability (HRV), and evening-to-morning changes in HRV, plasma cortisol, and blood pressure. Stimulation, compared with a sham condition, increased SWA during ON versus OFF intervals. This ON/OFF SWA enhancement was associated with a reduction in evening-to-morning change of cortisol levels and indices of sympathetic activity. Furthermore, the enhancement of SWA in ON intervals during sleep cycles 2-3 was accompanied by an increase in parasympathetic activity (high-frequency, HRV). Together these findings suggest that acoustic enhancement of SWA has a positive effect on autonomic function in sleep. Approaches to strengthen brain-heart interaction during sleep could have important implications for cardiovascular health.

[FSGS collapsing variant during anabolic steroid abuse: Case Report].

Anabolic Androgenic Steroids (AAS) is an hormone family whose use has considerably increased among body-builders during the last decades. The AAS abuse, especially associated with other drugs or nutritional supplements and protein loads, may cause a variety of pathologies to several organs with a mechanism related to dosage, timing and substance. The kidney is the main metabolizer of these drugs and it can be acutely or chronically damaged with ESKD. The literature reports some cases of Focal Segmental Glomerulosclerosis (FSGS) in body-builders who abused of AAS. However, the link is not well understood and limited to some case-studies. In this paper, we report the case of a young body-builder who developed a FSGS collapsing variant with ESKD after prolonged abuse of AAS and a strongly hyperproteic diet and other dietary supplements. The patient underwent a genetic test because of the rapid and irreversibile onset of ESKD. The test showed a gene mutation of ACTN4, predisposing and causal of some genetic forms of FSGS. It was a very complex case, caused by several factors. The mutant protein of ACTN4 gene makes most vulnerable the cytoskeleton of the podocytes to external disturbances. That would explain why in those patients where the mutation has occurred, only those patients subject to "unfavorable environmental conditions", like the abuse of AAS, can develop a disease.

Assessment of sympathetic neural activity in chronic insomnia: evidence for elevated cardiovascular risk.

Study Objectives: Chronic insomnia affects up to 15 per cent of adults. Recent cross-sectional and prospective epidemiological studies report an association between insomnia and hypertension, including incident hypertension, yet mechanisms underlying the association remain unknown. We hypothesized that participants with chronic insomnia would have elevated sympathetic neural outflow, blunted baroreflex sensitivity, and augmented sympathetic neural and cardiovascular reactivity to stress when compared with good-sleeper controls. Methods: Twelve participants with chronic insomnia (11 women, 1 man) and 12 controls (8 women, 4 men) underwent one night of laboratory polysomnography, two weeks of at-home wrist actigraphy, and one night of controlled laboratory sleep prior to a comprehensive morning autonomic function test. The autonomic function test consisted of simultaneous recordings of muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat blood pressure (finger plethysmography), and heart rate (electrocardiogram) during a 10 min supine baseline and a 2 min cold pressor test. Results: Baseline blood pressure, heart rate, and MSNA were not different between groups, but sympathetic baroreflex sensitivity was significantly blunted in participants with insomnia (-2.1 ± 1.0 vs. -4.3 ± 1.3 bursts/100 heartbeats/mm Hg; p < 0.001). During the cold pressor test, systolic arterial pressure reactivity (Δ21 ± 11 vs. Δ14 ± 8 mm Hg; time × group = 0.04) and total MSNA reactivity (Δ127%, 54%-208% vs. Δ52%, 30%-81%; time × group = 0.02) were augmented in chronic insomnia. Conclusions: Participants with chronic insomnia demonstrated impaired sympathetic baroreflex function and augmented neural cardiovascular responsiveness to stress, when compared with controls. These findings support growing evidence of cardiovascular risk and physiological hyperarousal in chronic insomnia. Clinical Trial Registration: NCT02048878. https://clinicaltrials.gov/ct2/show/NCT02048878.

Different renal phenotypes in related adult males with Fabry disease with the same classic genotype.

BACKGROUND: Fabry disease related patients with classical mutation usually exhibit similar severe phenotype especially concerning renal manifestation. METHODS: A dry blood spot screening (DBS) and the DNA analysis has been performed in a 48-year-old man (Patient 1) because of paresthesia. RESULTS: The DBS revealed absent leukocyte α-Gal A enzyme activity while DNA analysis identified the I354K mutation. Serum creatinine and e-GFR were in normal range and also albuminuria and proteinuria were absent. The brain MRI showed ischemic lesions and a diffuse focus of gliosis in the white matter, while the echocardiogram showed a left ventricular hypertrophy. The renal biopsy performed in the case index showed a massive deposition of zebra bodies. By a familiar investigation, it was recognized that his brother (Patient 2) died 2 years before from sudden death syndrome at the age of 49. He had suffered sporadic and undiagnosed pain at the extremities, a prior cataract, bilateral neurosensorial hearing loss and left ventricular hypertrophy on Echocardiogram. His previous laboratory examinations revealed a normal serum creatinine and the absence of proteinuria. Pedigree analysis of the brothers revealed a high disease burden among family members, with an affected cousin (Patient 3) who progressed early to end-stage renal disease (ESRD) that required renal transplantation. CONCLUSIONS: Here we describe the clinical history of three adult male members of the same family with the same genotype who manifested different presentation and progression of the disease, particularly concerning the renal involvement.

Effect of one week of CPAP treatment of obstructive sleep apnoea on 24-hour profiles of glucose, insulin and counter-regulatory hormones in type 2 diabetes.

Studies examining the impact of CPAP treatment on glycaemic control have yielded conflicting results, partly because of insufficient nightly CPAP use. We examined the 24-hour profiles of glucose, insulin and counter-regulatory hormones in 12 subjects with type 2 diabetes and OSA before and after 1 week of effective in-laboratory CPAP therapy over an entire 8-hour night thus ensuring optimal CPAP compliance. Blood samples were collected every 15 to 30 minutes for 24 hours under controlled conditions. The 24-hour mean glucose decreased from 153.2 ± 33.0 to 139.7 ± 24.2 mg/dL with CPAP (-13.5 ± 13.5 mg/dL; P = .005) without change in insulin levels. Morning fasting glucose levels decreased by 14.6 ± 3 mg/dL (P = .001) and the dawn phenomenon decreased by 7.8 ± 9.8 mg/dL (P = .019). CPAP treatment decreased norepinephrine levels while the 24-hour profiles of growth hormone and cortisol remained unchanged. In conclusion, 1 week of effective treatment of OSA over an entire 8-hour night results in a clinically significant improvement in glycaemic control via an amelioration of evening fasting glucose metabolism and a reduction in the dawn phenomenon, a late-night glucose increase that is not adequately treated by oral medications. Clinical Trials Information: ClinicalTrials.gov Identifier: NCT01136785.