ABSTRACT
OBJECTIVES: Recent studies have shown a high prevalence of hypovitaminosis D, defined as a serum 25-hydroxyvitamin D level less than 30 ng/ml, in both healthy populations and patients with chronic kidney disease. Patients undergoing kidney transplant are at an increased risk of skin cancer and are advised to avoid sunlight exposure. Therefore, these patients might share two major risk factors for hypovitaminosis D: chronic kidney disease and low sunlight exposure. This paper describes the prevalence and clinical characteristics of hypovitaminosis D among patients undergoing kidney transplant. METHODS: We evaluated 25-hydroxyvitamin D serum levels in a representative sample of patients undergoing kidney transplant. We sought to determine the prevalence of hypovitaminosis D, compare these patients with a control group, and identify factors associated with hypovitaminosis D (e.g., sunlight exposure and dietary habits). RESULTS: Hypovitaminosis D was found in 79% of patients undergoing kidney transplant, and the major associated factor was low sunlight exposure. These patients had higher creatinine and intact parathyroid hormone serum levels, with 25-hydroxyvitamin D being inversely correlated with intact parathyroid hormone serum levels. Compared with the control group, patients undergoing kidney transplant presented a higher prevalence of 25-hydroxyvitamin D deficiency and lower serum calcium, phosphate and albumin but higher creatinine and intact parathyroid hormone levels. CONCLUSIONS: Our results confirmed the high prevalence of hypovitaminosis D in patients undergoing kidney transplant. Therapeutic strategies such as moderate sunlight exposure and vitamin D supplementation should be seriously considered for this population.
Subject(s)
Humans , Male , Female , Adolescent , Adult , Middle Aged , Aged , Aged, 80 and over , Young Adult , Sunlight , Vitamin D Deficiency/etiology , Kidney Transplantation/adverse effects , Vitamin D/analogs & derivatives , Vitamin D/blood , Vitamin D Deficiency/diagnosis , Case-Control Studies , Risk Factors , Environmental ExposureABSTRACT
Os pacientes portadores de doença renal crônica (DRC) apresentam elevado risco de complicações cardiovasculares (DCV). Esta associação foi primeiramente reconhecida nos pacientes em diálise, nos quais a incidência de morte por DCV é elevada. Nesses pacientes, fatores de risco nãotradicionais aliam-se aos tradicionais na promoção da DCV. Os distúrbios do metabolismo mineral são fatores de risco modificáveis, relacionados com calcificação vascular, mortalidade geral e cardiovascular. O mecanismo da calcificação vascular consiste em um processo ativo de precipitação de cálcio e fósforo e na presença de um desequilíbrio entre fatores estimuladores e inibidores da calcificação. A associação quer da remodelação óssea quer dosníveis séricos do PTH com a calcificação vascular não é clara. O efeito do PTH sobre o sistema cardiovascular não é explicado somente pela potencialização dos estados de hipercalcemia e hiperfosfatemia, ele atua na remodelação cardíaca e, portanto, sobre a morfologia e a função deste órgão.São necessários mais estudos para compreender o mecanismo fisiopatológico da DCV nos pacientes com DRC.
Adverse cardiovascular events are frequent complications of renal disease. This association was initially reported in end-stage renal disease patients inwhom cardiovascular death has a high frequency. In dialysis patients, non-traditional risk factors may act in concert with the traditional ones to the development of cardiovascular disease (CVD). Disorders of mineral metabolism are potentially modifiable and have been linked with cardiovascular outcomes indialysis population. Mechanisms involved in vascular calcification in CKD include active precipitation of calcium and phosphorus in the presence of markedly elevated extracellular concentrations, effect of calcification inducers or deficiency of inhibitors. The relationship between bone turnover and intact PTH concentration with vascular calcification were inconclusive. The adverse cardiovascular outcome in patients with high PTH concentrations is presumably not only explained by the association between PTH and high serum calcium and phosphorus concentrations. It also reflects direct adverse effects of PTH oncardiac function and morphology. The intrinsic effects of CKD on CVD risk profile are still unknown.