96 ± 0 21 The atherosclerotic plaques in the common carotid arte

96 ± 0.21. The atherosclerotic plaques in the common carotid arteries were visualized in 38 patients (80.1%), the mean thickness of the atherosclerotic plaque was 1.61 ± 0.8 mm. We found a significant positive correlation between CAC and CCA-IMT (r = 0.70, P < 0.001). The thickness of atherosclerosis plaque positively correlated with CAC as well as with CCA-IMT (r = 0.60, P < 0.001 and r = 0.7, P < 0.003, respectively). Conclusion:  The study revealed close relationships between CAC, intima media thickness and the thickness of atherosclerotic plaques in dialysis patients. It may indicate that both vascular calcification and atherosclerotic lesions frequently coexist in patients with

ESRD and that the intima media thickness could serve as a surrogate marker of vascular calcification. “
“Low birthweight reflects the congenital Alectinib defects of organs, which is associated with chronic kidney disease through its direct influence on nephron number and function, also through related metabolic disease-induced kidney damage. We reviewed the current evidence regarding the role of low birthweight in the pathogenesis

of chronic kidney disease. Barker put forward the ‘foetal origins hypothesis’ in 1989, that was the higher risk of many chronic disease in adulthood was associated with low birthweight (LBW),1 and the underlying mechanism was the intrauterine reprogramming of certain organs in order for the embryo to survive in a malnutrition condition. LBW as one easily measured index of malnutrition in uterine was used to assess the degree of undergrowth of organs. In 1993, Brenner further adopted the LY294002 Barker hypothesis to nephrology.2 He speculated that lower nephron number of LBW infants resulted in the higher blood pressure and progressive renal injury in their adulthood. After that, more and more animal experiment and epidemiological studies provided plentiful evidence for the correlation between LBW and chronic kidney disease (CKD). Animal models3 showed that LBW animals have a significantly lower nephron Clomifene number (decreased by 20–50%). Human studies also revealed the low nephron number in

both infants and adults, approximately a 1 kg increase in birthweight correlated to a 257 000 increase in nephron number.4 The examination of the kidneys of infants who died from non-renal causes showed that the nephron number of LBW infants maintained at a low level even after 1 year of their birth.5 Most human studies and animal experiments showed that the kidney underdevelopment was mainly compensated by the augmentation of nephrons.6,7 In animal experiments, low nephron number was compensated by an increasing single nephron glomerular filtration rate,8 therefore resulting in a higher risk of proteinuria. Human epidemiological studies also confirmed the close correlation between LBW and proteinuria, with every 1 kg decrease of birthweight associated with a 1.

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