Oxidative stress has been implicated in the pathophysiology of diabetic nephropathy. Studies in experimental animal models of diabetes strongly implicate oxidant species as a major determinant in the pathophysiology of diabetic kidney disease. The translation, in the clinical setting, of these concepts have been quite disappointing, and new theories have challenged the concepts that oxidative stress per se plays a role in the pathophysiology of diabetic kidney disease. The concept of mitochondrial hormesis has been introduced to explain this apparent disconnect. Hormesis is intended as any cellular process that exhibits a biphasic response to exposure to increasing amounts of a substance or condition: specifically, in diabetic kidney disease, oxidant species may represent, at determined concentration, an essential and potentially protective factor. It could be postulated that excessive production or inhibition of oxidant species formation might result in an adverse phenotype. This review discusses the evidence underlying these two apparent contradicting concepts, with the aim to propose and speculate on potential mechanisms underlying the role of oxidant species in the pathophysiology of diabetic nephropathy and possibly open future more efficient therapies to be tested in the clinical settings.

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Sleep medicine remains an exciting and fast-evolving field of medicine with insomnia, hypersomnia, parasomnia, sleepdisordered breathing and circadian rhythm disorders affecting significant proportions of the population. This update provides a selected overview about recent publications in the field. Sleep-disordered breathing and comorbidities The high prevalence of obstructive sleep apnoea (OSA) differs between genders, with male patients being more affected (1). In a US-nationwide study of 1,704,905 patients who had a diagnosis of OSA and 1,704,417 controls matched for age, sex and state of residence, the prevalence of co-morbidities [OR (95% CI)], such as type 2 diabetes [2.29 (2.28-2.31)], cardiac arrhythmia [3.26 (3.20-3.32)], ischaemic heart disease [2.54 (2.51-2.56)], stroke [3.51 (3.42-3.60)], hypertension [2.14 (2.13-2.15)], depression [4.99 (4.91-5.07)] and congestive heart failure [4.30 (4.21-4.39)] was increased (2). Non-communicable disease is important (3) and its link with comorbidities, predominantly its association with obesity (1), make OSA an important confounding factor that impacts on physical, social and mental health (4). Diagnostic criteria for sleep apnoea There have been ongoing discussions about the classification and diagnostic parameters of OSA. Study outcomes investigating OSA are dependent on accurate description, definition and comparisons of their patient groups. Heinzer et al. argue that the present International Classification of Sleep Disorders (ICSD-3) definition of sleep apnoea yields an unrealistically high prevalence of OSA (5), in part related to a low apnoea-hypopnoea index (AHI) threshold for normal subjects (5/h) and a high prevalence of coexisting symptoms and conditions such as fatigue, insomnia and hypertension which may not be related to the underlying OSA (6). In a group of 2,121 patients who underwent full home polysomnography (PSG) ['HypnoLaus' cohort; 48% male, median age 57, (interquartile range, IQR 49-68) years, mean body mass index (BMI) 25.6 kg/m 2 , standard deviation (SD) 4.1 kg/m 2 ], they applied the 2013 American Academy of Sleep Medicine (AASM) criteria for OSA: An apnoea was defined as ≥90% reduction in airflow from baseline, lasting for ≥10 seconds; a hypopnea was defined as ≥30% reduction in airflow from baseline, lasting for ≥10 seconds with either a ≥3% drop in oxygen saturation or an arousal (7,8). These criteria led to a diagnosis of moderate-to-severe OSA (sOSA) (AHI ≥15/h) in 23.4% (95% CI: 20.9-26.0) of women and 49.7% (95% CI: 46.6-52.8) of men (9). However, analysing the same cohort in 2016, but using the ICSD-3 criteria which are defined by an AHI ≥15/hour, or an AHI ≥5/hour associated with one or more symptoms of OSA or cardiovascular and metabolic comorbidities, the prevalence of OSA increased to 74.7% of men, and 52.1% of women (5,6,10). The authors suggested that a better definition of OSA should be sought using prospective and large cohort follow-up studies. Screening for OSA in a bariatric population OSA and obesity commonly co-exi...

ObjectivesThe aims of the authors’ case series were to outline the clinical features of prepubertal nocturnal vulval pain syndrome and to look at management and outcomes.MethodsClinical details of prepubertal girls experiencing episodes of nocturnal vulval pain with no identifiable cause were recorded and analyzed. Parents completed a questionnaire to look at outcomes.ResultsEight girls with age at onset of symptoms between 3.5 and 8 years (mean 4.4 years) were included. Each patient described intermittent episodes of vulval pain lasting between 20 minutes and 5 hours, starting 1–4 hours after falling asleep. They were crying and rubbing or holding the vulva with no obvious cause seen. Many were not fully awake and 75% had no recollection of the events. Management focused on reassurance alone. The questionnaire showed that 83% had full resolution of symptoms with a mean duration of 5.7 years.ConclusionsPrepubertal nocturnal vulval pain syndrome may be a subset of vulvodynia (generalized, spontaneous, intermittent) to be included in the clinical spectrum of night terrors. Recognizing the clinical key features should aid prompt diagnosis and reassurance of the parents.