Comment on "Which Patients with Obesity Are at Risk for Renal Disease?"

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A CASE OF CARDIAC COMPRESSION BY HEPATIC CYST IN A WOMAN WITH POLYCYSTIC KIDNEY DISEASE.

Liver cysts are common extrarenal manifestations of autosomal dominant polycystic kidney disease (ADPKD). They occur more frequently in women, and are also more in number and larger in size, than in men. Liver cysts tend to develop slower than the kidney cysts; their number and size increases with the age (worsening kidney function), number of pregnancies, and estrogen assumption. Although most patients with ADPKD report no liver symptoms, sometimes, chronic manifestations related to progressive increase of the polycystic liver are experienced. The quality of life can be severely impaired with huge hepatomegaly causing abdominal distension, pain, dyspepsia, dyspnoea, fatigue, physical and even psychological handicap. In addition, few patients develop acute complications that follow a life-threatening course [1]

Glycaemic variability and inflammation in subjects with metabolic syndrome.

Subjects who develop diabetes have an increased cardiovascular risk even before the appearance of diabetes. The aim of this study was to investigate the glycaemic var- iability measured by continuous glucose monitoring (CGM CV%) in nondiabetic subjects with metabolic syndrome (MS) and to explore if glycaemic variability was associated with circulating levels of interleukin-6 (IL-6), a proinflam- matory cytokine, or with an anti-inflammatory factor like adiponectin. Three groups of obese subjects with (MS?: 6m, 8f; BMI 33.1 ± 1.4 mean ± SEM) or without metabolic syndrome (MS-: 2m, 4f; BMI 29.2 ± 2.2) and with MS associated with type 2 diabetes (MS/T2D: 3m, 5f; BMI 32.9 ± 1.4) were investigated. The glycaemic variability was measured in all subjects in terms of CV% of the gly- caemic values obtained every 3 min during the course of a 48 h CGM performed using a subcutaneous glucose sensor. The average CGM CV% increased from MS- group (21.1%) to the MS? group (23.9%) and to the MS?/T2D group (27.4%) but it was not correlated to the CGM mean glycaemia (r = 0.20; P = ns). In some instances, CGM CV% was found higher in MS? subjects than in some MS? T2D ones. Stepwise multiple correlation analysis showed that IL-6 predicted CGM CV% (R2 = 0.35, b = 0.13; P \ 0.05) independently from BMI, waist circumference, adiponectin and insulin concentrations. In conclusion, the CGM CV% may contribute to better describe the individual metabolic state and to understand the pathogenesis of endothelial dysfunction in non diabetic subjects with MS