Vitamin D deficiency and secondary hyperparathyroidism among patients with chronic kidney disease

BACKGROUND: Chronic kidney disease (CKD) is associated with morbid complications that lead to high mortality and costs. Vitamin D deficiency and secondary hyperparathyroidism (SHPT) are frequent complications of CKD. METHODS: We reviewed the current literature regarding the prevalence, diagnosis, complications, and management of vitamin D deficiency and SHPT among patients with CKD. RESULTS: There is a high prevalence of vitamin D deficiency among adolescents and adults in the United States (age and gender dependent). Patients with CKD or those who are dialysis-dependent are much more likely to have low levels of vitamin D in comparison to those without kidney disease. In order to avoid significant complications including SHPT and musculoskelatal diseases, vitamin D needs to be measured routinely by primary care physicians and nephrologists. In the majority of CKD patients, SHPT is not diagnosed until late, leading to advanced cardiovascular and bone diseases. CONCLUSIONS: In conclusion, current management of vitamin D deficiency and SHPT is suboptimal. Early diagnosis of vitamin D deficiency and SHPT are integral to optimal management of CKD, and additional research is needed in this area.     

Vitamin D in chronic kidney disease

In chronic kidney disease (CKD), abnormalities in vitamin D metabolism contribute to the development of mineral and skeletal disorders, elevations in parathyroid hormone (PTH), hypertension, systemic inflammation, renal and cardiovascular damage. CKD induces a progressive loss of the capacity of the kidney not only to convert 25-hydroxyvitamin D [25(OH)D] to circulating calcitriol, the vitamin D hormone, but also to maintain serum 25(OH)D levels for non-renal calcitriol synthesis. The resulting calcitriol and 25(OH)D deficiency associates directly with accelerated disease progression and death. This chapter presents our understanding of the pathophysiology behind 25(OH)D and calcitriol deficiency in CKD, of the adequacy of current recommendations for vitamin D supplementation and PTH suppression, and of potential markers of renal and cardiovascular lesions unrelated to PTH suppression, a knowledge required for the design of trials to obtain evidence-based recommendations for vitamin D and calcitriol replacement that improve outcomes at all stages of CKD.     

Vitamin D deficiency in chronic liver disease

Vitamin D is an important secosteroid hormone with known effect on calcium homeostasis, but recently there is increasing recognition that vitamin D also is involved in cell proliferation and differentiation, has immunomodulatory and anti-inflammatory properties. Vitamin D deficiency has been frequently reported in many causes of chronic liver disease and has been associated with the development and evolution of non-alcoholic fatty liver disease (NAFLD) and chronic hepatitis C (CHC) virus infection. The role of vitamin D in the pathogenesis of NAFLD and CHC is not completely known, but it seems that the involvement of vitamin D in the activation and regulation of both innate and adaptive immune systems and its antiproliferative effect may explain its importance in these liver diseases. Published studies provide evidence for routine screening for hypovitaminosis D in patients with liver disease. Further prospectives studies demonstrating the impact of vitamin D replacement in NAFLD and CHC are required.     

Vitamin D deficiency and chronic lung disease

Vitamin D deficiency is increasingly being recognized as a prevalent problem in the general population. Patients with chronic lung diseases such as asthma, cystic fibrosis, chronic obstructive lung disease and interstitial pneumonia appear to be at increased risk for vitamin D deficiency for reasons that are not clear.Several studies indicate that vitamin D possesses a range of anti-inflammatory properties and may be involved in processes other than the previously believed functions of calcium and phosphate homeostasis. Various cytokines, cellular elements, oxidative stress and protease/antiprotease levels appear to affect lung fibroproliferation, remodelling and function, which may be influenced by vitamin D levels. Chronic lung diseases such as asthma and chronic obstructive lung disease have also been linked to vitamin D on a genetic basis. This immune and genetic influence of vitamin D may influence the pathogenesis of chronic lung diseases. A recent observational study notes a significant association between vitamin D deficiency and decreased pulmonary function tests in a large ambulatory population.The present review will examine the current literature regarding vitamin D deficiency, its prevalence in patients with chronic lung disease, vitamin D anti-inflammatory properties and the role of vitamin D in pulmonary function.     

维生素D缺乏与慢性阻塞性肺疾病

维生素D对钙磷代谢具有调节作用,并对骨骼健康会产生影响。但是维生素D及其代谢物广泛的生理作用远不只是对骨骼的生物学效应,许多生理过程都直接或间接受维生素D调节。近年来,维生素D在骨质代谢和钙调节之外的作用越来越受到重视。慢性阻塞性肺疾病（COPD）是一种进行性呼吸功能减退的呼吸道疾病,在老年人群中发病率很高。有研究表明,COPD的严重程度与维生素D缺乏相关。本文的主要目的是提高医务工作者对维生素D与COPD相关性的认识,并评估补充维生素D对减轻COPD患者病情的潜在作用。     

维生素D与慢性肾脏病和肾移植

维生素D的主要作用是维持体内钙稳态.近期研究发现,除钙磷调节外,维生素D还对机体许多疾病的病理生理过程有重要影响.维生素D与慢性肾脏病的关系已为人们所熟识,其对肾移植受者移植肾的作用也被人们逐渐认识,本文将就此作一综述.     

Vitamin D therapy in chronic kidney disease and end stage renal disease

Vitamin D has garnered much research and debate about supplementation in recent years, not only as it pertains to patients with kidney disease but also to those in the general population. This review discusses observational and available clinical trial evidence about the effects of both calcitriol and vitamin D analogs (active) and ergocalciferol and cholecalciferol (nutritional) vitamin D in patients with CKD and ESRD.     

维生素D缺乏与慢性阻塞性肺疾病

维生素D除了调节钙磷代谢外,近年来大量证据表明它还通过调节炎症因子、氧化应激,以及气道重塑等影响COPD的发展过程。此外,维生素D还能加强呼吸道上皮抗菌肽的表达而产生重要的先天免疫,能够减少病原体负荷和阻塞性肺疾病急性加重的频度。COPD患者的维生素D缺乏经常发生,而且与疾病严重程度相关,因此,严重的COPD患者应该补充维生素D。     

Anemia treatment and left ventricular hypertrophy in non-dialysis chronic kidney disease

To this day, the target hemoglobin level that minimizes cardiovascular risk in chronic kidney disease (CKD) patients remains unclear. When one examines the many randomized trials of epoetin therapy in aggregate, enhanced quality of life provides the most cogent argument for hemoglobin levels above 110 g/L. It remains unclear whether treatment of anemia improves longevity, or even a surrogate marker (such as left ventricular [LV] mass index), especially when applied at earlier phases of CKD.……     

Erythropoietin therapy improves endothelial function in patients with non-dialysis chronic kidney disease and anemia (EARNEST-CKD): A clinical study

Background:This study investigated whether administering erythropoiesis-stimulating agents (ESAs) improves endothelial function in patients with non-dialysis chronic kidney disease (CKD) and anemia.Methods:This single-center, prospective, single-arm comparison study enrolled patients with non-dialysis CKD (stages 4-5) and hemoglobin levels <10 g/dL. ESA administration followed the Kidney Disease: Improving Global Outcomes guideline. The primary endpoint was the change in flow-mediated dilatation after ESA administration in individual patients. The secondary endpoints were changes in 6-minute walk test results, blood pressure, New York Heart Association class, and echocardiographic parameters. The echocardiographic parameters examined included chamber quantification, Doppler parameters, and systolic and diastolic function parameters.Results:Initially, 13 patients were screened, but 2 discontinued due to either heart failure or voluntary withdrawal. The mean flow-mediated dilatation values significantly increased by 10.59% (from 1.36% ± 1.91% to 11.95% ± 8.11%, P = .001). Echocardiographic findings showed that the left ventricular mass index decreased by 11.9 g/m² (from 105.8 ± 16.3 to 93.9 ± 19.5 g/m², P = .006), and the left atrial volume index decreased by 10.8 mL/m² (from 50.1 ± 11.3 to 39.3 ± 11.3 mL/m², P = .004) after 12 weeks of ESA administration. There were no significant differences between pre- and post-ESA treatment 6-minute walk test results. No significant side effects were observed during the study period.Conclusions:This is the first clinical study to demonstrate that an ESA improves endothelial dysfunction, left ventricular hypertrophy, and left atrial volume in patients with non-dialysis CKD. Thus, ESAs may be considered as adjunctive therapy for reducing cardiovascular risk in these patients.     

Microvascular disease and endothelial dysfunction in chronic kidney diseases: therapeutic implication

This paper was aimed to study biomarkers of endothelial injury in chronic kidney diseases. Fifty chronic kidney disease patients were subject to the following determinations: (i) circulating endothelial cells, (ii) soluble VCAM-1, (iii) transforming growth factor beta (TGFB), and (iv) intrarenal hemodynamics. Increased number of circulating endothelial cells was significantly observed. A significant depletion of vascular endothelial growth factor (VEGF) or a depleted VEGF/TGFB ratio was also documented. Results showed that sVCAM was not significantly different from normal control. Intrarenal hemodynamic alteration demonstrated a characteristic of hemodynamic maladjustment. Since increased number of circulating endothelial cells is a sensitive biomarker for endothelial cell injury in chronic kidney diseases, such injury is supported by the depletion of VEGF. The endothelial cell loss correlates with the glomerular endothelial dysfunction characterized by hemodynamic maladjustment at the efferent arteriole and reduction in peritubular capillary flow. In conclusion, correction of such hemodynamic maladjustment with multidrug vasodilators can effectively restore renal function in chronic kidney diseases.     

Vitamin D deficiency/insufficiency in patients with chronic kidney disease stage 3 and 4 -- current concept and its therapeutic strategy

Vitamin D deficiency/insufficiency, which is clinically represented by low 25(OH)D concentration, is frequently seen in patients with CKD stage 3 and 4. Although its cause is unknown, hypovitaminosis D is partly associated with low 1,25(OH)2D in these patients, possibly leading to advancement of renal osteodystrophy. Recently, in United States, K/DOQI (Kidney disease outcomes quality initiative) guideline indicated that vitamin D deficiency/insufficiency of 25(OH)D concentration less than 30 ng/mL should be treated by supplementation of ergocalciferol. A Japanese guideline to treat vitamin D deficiency/insufficiency should be urgently established.     

维生素D治疗慢性肾脏疾病继发性甲状旁腺功能亢进症的进展

继发性甲状旁腺功能亢进症(SHPT)是慢性肾脏疾病(CKD)最常见的并发症之一.维生素D及其类似物是治疗SHPT的常用药物,充分了解低维生素D状态对CKD患者的危害,维生素D制剂治疗SHPT的药理机制及治疗过程中应该注意的问题,有助于临床医师合理应用此类药物,延缓SHPT发展为三发性甲状旁腺功能亢进症.     

维生素D缺乏与慢性心力衰竭

慢性心力衰竭(CHF)目前仍是发病率、再住院率和死亡率均高的心血管疾病。尽管近年大量临床观察性和动物实验研究已证实低水平维生素D(vitamin D)与CHF的发病率和死亡率密切相关,但确切机制尚不确定。本文综述了近年维生素D与CHF的研究进展,以探讨维生素D在CHF发生发展讨程中的可能机制。