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Patients on renal replacement therapy (RRT) infected with the human immunodeficiency virus (HIV) are a special group with growing interest. In order to study the epidemiological data of HIV+ patients on RRT in Spain, we collected individual information from 2004-2011 (period of use of highly active antiretroviral therapy [HAART] in the Autonomous Communities of Andalusia, Aragon, Asturias, Catalonia, Valencia, Castilla la Mancha, Castilla León, Galicia, Madrid, La Rioja and the Basque Country, comprising 85% of the Spanish population. A total of 271 incident and 209 prevalent patients were analysed. They were compared with the remaining patients on RRT during the same period. The annual incidence was 0.8 patients per one million inhabitants, with a significant increase during the follow-up period. The proportion of prevalent HIV+ patients was 5.1 per 1,000 patients on RRT (95% confidence interval [CI] 4.4-5.8. Although glomerular diseases constituted the majority of cases (42%), diabetic nephropathy was the cause in 14% of patients. The nation-wide totals for these percentages were 13 and 25%, respectively. Compared to the total of patients in treatment, the risk of death was significantly higher in the HIV+ group: hazard ratio (HR) adjusted for age, sex and diabetes was 2.26 (95% CI 1.74 - 2.91). Hepatitis C coinfection increased the risk of death in the HIV+ group (HR 1.77; 95% CI 1.10 - 2.85). The probability of kidney transplantation in HIV+ was only 17% after 7 years, comparing with total RTT patients (HR 0.15; 95% CI: 0.10-0.24). Despite the use of HAART, the incidence of HIV+ patients on dialysis has increased; their mortality still exceeds non-HIV patients, and they have a very low rate of transplantation. It is necessary to further our knowledge of this disease in order to improve results., (Copyright © 2015 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Secondary hyperparathyrodism (SH) is an early manifestation of chronic renal failure (CRF), which has serious complications. Moreover, treating SH is not a risk-free process. Once in its advanced state, it is extremely difficult to reverse and therefore it is critical an early intervention and prevention. An excess of phosphorus and a deficit of calcium and calcitriol are key factors in the evolution of SH. Despite the fact that plasma phosphorus levels remain normal until an extremely advanced stage of CRF, and even apparent hyperphosphatemia in mild CRF, it has been shown that restricting dietary levels of protein and phosphorus impedes the progression of SH. A decrease of protein in the diet also decreases the amount of calcium, thus the calcium levels must be supplemented in order to prevent their deficit. In addition to that slightly diminished levels of calcitriol can be observed in the early stages of CRF, thus it is logical to provide this hormone. However, administering calcitriol may induce hypercalcemia and hyperphosphatemia, which in turn risks the onset of cardiovascular calcifications and complications. Therefore, the calcitriol dosage should be small and then adjusted according to the degree of SH. Neither the PTH levels nor alterations in the phospho-calcium metabolism follow a linear increase appropriate to the decrease in renal function, therefore we propose a treatment strategy which adapts to the different degrees of renal failure.

Background: BsmI vitamin D receptor (VDR) gene polymorphism has been associated with the severity of hyperparathyroidism in patients on hemodialysis. The aim of this study was to analyze the influence of this polymorphism on parathyroid function and serum calcitriol levels in patients with different degrees of chronic renal failure (CRF) before dialysis., Methods: A total of 248 CRF patients, divided into three groups according to creatinine clearance (CCr; mild CRF group> 60 to 35 to 10 to 2.5 mmol/liter and serum phosphorus levels of> 1.6 mmol/liter or who needed phosphorus binding agents were excluded. The statistical analysis was done with the general factorial analysis of variance entering first PTH and then calcitriol as the dependent variable; the genotype (BB, Bb and bb), sex and CCr group were defined as factors; and covariables included serum calcium, serum phosphorus, 1/creatinine versus time slope, PTH when calcitriol was the dependent variable, and calcitriol when PTH was the dependent variable., Results: When serum PTH levels were entered as the dependent variable, serum calcium, CCr group, and the interaction of genotype with the CCr group were found to be significant factors (P = 0.025, P <0.001 and P = 0.039, respectively). When serum calcitriol levels were entered as the dependent variable, genotype, the interaction of genotype with CCr, the CCr group, and the 1/creatine versus time slope were found to be significant (P = 0.027, P = 0.028, P <0.001 and P = 0.044, respectively). The marginal means of PTH, adjusted with the general factorial analysis of variance across the three groups were: (a) mild CRF group, BB 5.3 pmol/liter (CI 0 to 13.8), Bb 5.5 pmol/liter (CI 2 to 9), bb 5.4 pmol/liter (CI 0.6 to 10.2); (b) moderate CRF group, BB 6.2 pmol/liter (CI 1.5 to 10.9), Bb 7.8 pmol/liter (CI 5.3 to 10.3), bb 7.5 pmol/liter (CI 4.8 to 10.1); (c) severe CRF group, BB 9.3 pmol/liter (CI 4.2 to 14.3), Bb 17.1 pmol/liter (CI 13.9 to 20.2), bb 21.9 pmol/liter (CI 18.7 to 25.2). The marginal means of calcitriol adjusted with the general factorial analysis of variance across the three groups were: (a) mild CRF group, BB 47 pg/ml (CI 37 to 57), Bb 40.9 pg/ml (CI 37 to 44.8), bb 32.6 pg/ml (CI 26.8 to 38. 4); (b) moderate CRF group, BB 24.1 pg/ml (CI 18.3 to 29.8), Bb 26.6 pg/ml (CI 23.5 to 29.7), bb 25.3 pg/ml (CI 22 to 28.6); (c) severe CRF group, BB 27.4 pg/ml (CI 21.3 to 33.5), Bb 19.4 pg/ml (CI 15.5 to 23.2), bb 20.4 pg/ml (CI 16.1 to 24.7)., Conclusion: The progression of hyperparathyroidism is slower in predialysis patients with BB genotypes than in the other genotypes. Also, calcitriol levels are less reduced in the BB genotype, which may act to lessen the severity of secondary hyperparathyroidism.