Large kidneys predict poor renal outcome in subjects with diabetes and chronic kidney disease

<p>Abstract</p> <p>Background</p> <p>Renal hypertrophy occurs early in diabetic nephropathy, its later value is unknown. Do large kidneys still predict poor outcome in patients with diabetes and Chronic Kidney Disease (CKD)?</p> <p>Methods</p> <p>Seventy-five patients with diabetes and CKD according to a Glomerular Filtration Rate (GFR, by 51Cr-EDTA clearance) below 60 mL/min/1.73 m²or an Albumin Excretion Rate above 30 mg/24 H, had an ultrasound imaging of the kidneys and were cooperatively followed during five years by the Diabetology and Nephrology departments of the Centre Hospitalier Universitaire de Bordeaux.</p> <p>Results</p> <p>The patients were mainly men (44/75), aged 62 ± 13 yrs, with long-standing diabetes (duration:17 ± 9 yrs, 55/75 type 2), and CKD: initial GFR: 56.5 (8.5-209) mL/min/1.73 m², AER: 196 (20-2358) mg/24 H. Their mean kidney lenght (108 ± 13 mm, 67-147) was correlated to the GFR (r = 0.23, p < 0.05). During the follow-up, 9/11 of the patients who had to start dialysis came from the half with the largest kidneys (LogRank: p < 0.05), despite a 40% higher initial isotopic GFR. Serum creatinine were initially lower (Small kidneys: 125 (79-320) μmol/L, Large: 103 (50-371), p < 0.05), but significantly increased in the "large kidneys" group at the end of the follow-up (Small kidneys: 129 (69-283) μmol/L, Large: 140 (50-952), p < 0.005 vs initial). The difference persisted in the patients with severe renal failure (KDOQI stages 4,5).</p> <p>Conclusions</p> <p>Large kidneys still predict progression in advanced CKD complicating diabetes. In these patients, ultrasound imaging not only excludes obstructive renal disease, but also provides information on the progression of the renal disease.</p

Development of the blood-brain barrier: relationship to perinatal medicine

The blood-brain barrier maintains central nervous system homeostasis and limits the entry of blood-borne substances that could alter neuronal function and survival. The barrier exists predominantly at the endothelium of cerebral vascular microvessels. The cerebral vascular endothelium becomes highly specialized during the formation of the neurovascular unit early in embryonic development. The blood-brain barrier is present and functional early in fetal life. The tightness of the barrier gradually increases throughout gestation and in the newborn period. Alterations in the basolateral environment of the cerebral microvasculature can modify the blood-brain barrier properties by modulating the expression of the endothelial tight junctions and other biochemical properties of the cerebral vascular endothelium. Maturation of the blood-brain barrier late in gestation correlates with increases in endogenous corticosteroids and with exposure to exogenous corticosteroids. Several adverse fetal and neonatal conditions can alter the structure and function of the blood-brain barrier. Impairment of blood-brain barrier function in the perinatal period could increase the entry of bilirubin and other neurotoxic substances from the systemic circulation into the brain, thereby exacerbating and/or causing damage to the developing brain