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INTRODUCTION: 25-OH vitamin D deficiency is associated with increased cardiovascular mortality in general population and in chronic kidney disease. The aim of this study was to evaluate 25-OH-Vitamin D (25-D) serum levels in chronic hemodialysis (HD) patients and its relationship with cardiovascular and non-cardiovascular risk factors. MATERIAL AND METHODS: We performed a cross-sectional study with 187 prevalent HD patients (106 M/ 81 F) in chronic hemodialysis. 25-D were measured in January and blood samples were collected for analysis before a midweek HD session. RESULTS AND CONCLUSIONS: The mean age of patients was 67 15 years with the mean HD time of 73 68 months. Forty-six patients (25%) were diabetics. 31% of the patients were taking i.v. paricalcitol and 22% were taking calciomimetics. None of patients were receiving native vitamin D. Serum levels of 25-OH-Vitamin D were low (11,77,5 ng/ml). Only 4% of patients had values of 25- OH-Vitamin D considered normal by the guidelines KDOQI. Levels of 25-D were deficient and insufficient respectively in 73% and 23% of the patients. In univariate analysis, serum levels of 25-D were negatively correlated with female sex and diabetes and positively correlated with albumin. In multivariate analysis dialysis vintage, lower serum calcium, hypoalbuminemia, higher BMI and treatment with paricalcitol were independently associated with lower levels of 25-OH-Vitamin D. Deficiency of 25-D is extremely common in chronic hemodialysis. It is still to be investigated by randomized prospective studies if native vitamin D supplementation is able to improve clinical outcomes in dialysis.

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PURPOSE: Arterial media calcification (AMC) is often the only vascular calcification (VC) present in young patients with chronic renal failure and its presence is associated with higher mortality rates. Currently, X-ray imaging (as a standard approach) is able to show AMC in areas without diffuse overlapping arterial intimal calcification (AIC), but X-ray imaging only allows us to identify this lesion when the vessel is widely calcified. The aim of this study was to evaluate the possibility of using ultrasonography as opposed to X-rays to visualize AMC in patients with chronic renal failure. Patients and Methods: In this cross-sectional study, we examined 105 patients (chronic kidney disease stage IV: 19 patients, hemodialysis: 48 patients, renal transplant: 26 patients; mean age: 54 ± 14 years; 65 males and 40 females); B-mode ultrasonography was performed to detect AMC or AIC on the superficial femoral artery (SFA). As a control, plain radiography of the thigh was performed in all patients. RESULTS: Upon ultrasonography investigation, 12 subjects were excluded due to diffuse VC on the SFA that did not permit a distinction between AMC and AIC. In the remaining 93 patients, AMC was detected on the SFA in 43 patients using ultrasonography and in 20 patients using the standard approach. The sensitivity and specificity of the standard approach for the detection of AMC on the SFA were 47 and 100%, respectively. The positive and negative predictive values of the standard approach were 1 and 0.68, respectively. CONCLUSION: Ultrasonography is able to detect AMC better than the X-ray approach, focusing on individuals at higher risk.

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Patients with chronic kidneyl disease (CKD) have a higher cardiovascular mortality than the general population, in partly due to the development of arterial media calcification (AMC). It is still a matter of discussion as to whether arterial intimal calcification (AIC) and AMC should be considered as distinct entities with different pathogenesis or as a single nosological entity. The pathogenesis of mediocalcinosis is multifactorial. It consists of several stages which overlap; oxidative stress, endothelial dysfunction, shear stress, neoangiogenesis, degradation of the extracellular matrix. Endothelial cells stimulate angiogenesis both by passage of inflammatory cytokines and by migration of osteoprogenitor cells through the tunica media. VSMCs and pericytes are transformed into osteoclast-like cells with production of calcifying matrix vesicles through an active process regulated by promoters and inhibitors factors. Currently, radiology modalities are the only imaging methods that can be used to detect AMC in non-overlapping areas of vessels but X-ray imaging only allows us to identify this lesion when the vessel is widely calcified. Recently, ultrasonography and RX mammography has also been used as an alternative tool for the diagnosis of AMC in patients affected by CKD and they can be used to recognize it earlier than X-ray imaging, which will aid in the treatment of high-risk patients Calcium-sensing receptor (CaSR) and vitamin D receptor (VDR) have been identified in vascular smooth muscle cells (VSMC). Considering the essential role of VSMC in the pathogenesis of AMC, it could be important to identify in an early stage patients who develop this shape of arterial calcification to start drugs as cinacalcet or paricalcitol when possible.

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A 53-year-old man with end-stage renal disease received a cadaver kidney after 15 months of peritoneal dialysis. Within one year of transplantation he developed hypertension and erythrocytosis. Percutaneous transluminal angioplasty was performed but 13 months later magnetic resonance angiography showed an anastomotic stenosis of the renal artery in the graft. In the meantime, he was submitted to venesections while the hypertension proved resistant to a multiple-drug combination. After two years, color Doppler sonography performed at our unit showed a noncritical stenosis, so we decided to start the patient on ACE inhibitors followed by angiotensin receptor blockers. A reduction of hematocrit to < 50% and partial control of blood pressure with stable renal function was obtained. Later we added minoxidil at low dosage, which resulted in excellent blood pressure control. The diagnosis of hemodynamically significant stenosis is not always easy to make; in this case a correct diagnosis was helpful for the treatment of erythrocytosis.

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