Gene/Protein Disease Symptom Drug Enzyme Compound
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Both relative hypoparathyroidism and low turnover bone play crucial roles in the pathogenesis of adynamic bone disease (ABD), which is the most common form renal osteodystrophy (ROD). In addition to individual factors, including diabetes, elder age, and/or uremic toxins, dialysis therapy and treatment for ROD, administration of calcium-containing phosphorus binder or active vitamin D (VD) metabolite, are associated with the pathological processes. Recently it has been suggested a potential association ABD and VD receptor polymorphism, or malnutrition state.
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PMID:[Pathogenesis of adynamic bone disease]. 1577 6

Vitamin D3 is modified by vitamin D3-25-hydroxylase in the liver, and 25-hydroxyvitamin D3-1alpha-hydroxylase in the kidney, to form the active metabolite, 1,25-dihydroxyvitamin D3. Chronic kidney disease (CKD) is characterized by reduced synthesis of 1,25-dibydroxyvitamin D3, inadequate renal phosphate clearance and calcium imbalance, secondary hyperparathyroidism (SHPT) and bone disease. CKD patients encounter a much higher risk of cardiovascular disease (CVD) than the general public. The cardiovascular risk factors for CKD patients include conventional factors such as age, gender, hypertension, diabetes, dyslipidemia and smoking, and non-conventional factors, such as anemia, uremia, reduced vascular compliance, inflammation and various hormonal factors. Several vitamin D analogs are currently available for the treatment of SHPT, and recent clinical data show that these analogs provide survival benefit for CKD patients in the order of paricalcitol > calcitriol > no vitamin D analog, independent of parathyroid hormone and calcium. Moreover, the survival benefit seems to be associated with cardiovascular causes. The observations made from these clinical studies raised intriguing questions about the involvement of the vitamin D receptor locus (VDR) in the cardiovascular system. This review discusses recent data regarding the role of vitamin D and its analogs in the CVD associated with CKD.
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PMID:Cardiovascular disease in chronic kidney failure: is there a role for vitamin D analogs? 1581

Vitamin D is taken for granted and is not appreciated for its importance in overall health and well-being. Vitamin D, known as the sunshine vitamin, is appreciated as being important for the prevention of rickets in children. It is now recognized that vitamin D is important for not only the growing skeleton, but for the maintenance of a healthy musculoskeletal system throughout life. Vitamin D deficiency in adults precipitates and exacerbates osteoporosis and causes the painful bone disease osteomalacia. The revelation that vitamin D is biologically inactive and requires sequential hydroxylations in the liver and kidney to form 1,25-dihydroxyvitamin D helps explain why patients with renal failure are often resistant to vitamin D and suffer from secondary hyperparathyroidism and renal osteodystrophy. In addition to its role in maintaining calcium and phosphorus homeostasis, vitamin D is now being recognized as important for maintaining maximum muscle strength and for the prevention of many chronic diseases, including type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common cancers. Vitamin D status is best determined by the measurement of circulating levels of 25-hydroxyvitamin D. Vigilance for maintaining a 25-hydroxyvitamin D level of at least 20 ng/ml and preferably 30-50 ng/ml has important benefits for both healthy children and adults, as well as children and adults suffering from chronic kidney disease.
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PMID:Vitamin D for health and in chronic kidney disease. 1607 48

Renal osteodystrophy is an important complication of chronic kidney disease characterized by abnormal bone turnover with varied bone histologic changes. Etiology is multifactorial including abnormalities of serum calcium, phosphorus, and 1,25(OH)(2)-vitamin D deficiency; secondary hyperparathyroidism; age; cause of kidney disease; diet; renal replacement therapy; and drug therapy. In addition, there is evidence that there may be ethnic differences. Our study is a description of a case series of hormonal and biochemical abnormalities of bone disease in end-stage renal disease patients in South India. A total of 115 patients were studied; 86% were on hemodialysis and 14% were on peritoneal dialysis (age, 47.31 +/- 14.66 years). Sixty-eight percent were men. Diabetes was the cause of end-stage renal disease in 29.5%. Intact parathyroid hormone (PTH) level was 124.6 +/- 174.9 pg/mL and less than twice normal in 69.5% of patients. Hypocalcemia was present in 16.5% and hyperphosphatemia in 35.7% of patients. Empirical vitamin D was prescribed in 40% of patients. Age, sex, diabetic status, and vitamin D use were similar in patients with high PTH (130 pg/mL) and low PTH levels (< 130 pg/mL). Bone histologic studies were not performed owing to economic limitation. But the biochemical and hormonal results are suggestive of a mild form of osteodystrophy in Indian patients. Etiology remains uncertain but differences in dietary intake, tropical climate, vitamin D activation, vitamin D receptor polymorphism, parathyroid gland sensitivity, and PTH target organ sensitivity may account for the difference in pattern in bone disease.
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PMID:Parathyroid hormone and biochemical profile in chronic kidney disease patients in South India. 1619 Oct 55

Vitamin D deficiency is now recognized as an epidemic in the United States. The major source of vitamin D for both children and adults is from sensible sun exposure. In the absence of sun exposure 1000 IU of cholecalciferol is required daily for both children and adults. Vitamin D deficiency causes poor mineralization of the collagen matrix in young children's bones leading to growth retardation and bone deformities known as rickets. In adults, vitamin D deficiency induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures. In addition, the poor mineralization of newly laid down bone matrix in adult bone results in the painful bone disease of osteomalacia. Vitamin D deficiency causes muscle weakness, increasing the risk of falling and fractures. Vitamin D deficiency also has other serious consequences on overall health and well-being. There is mounting scientific evidence that implicates vitamin D deficiency with an increased risk of type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common deadly cancers. Vigilance of one's vitamin D status by the yearly measurement of 25-hydroxyvitamin D should be part of an annual physical examination.
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PMID:The vitamin D epidemic and its health consequences. 1625 41

The delayed wound healing of tooth extraction, the activation of alveolar absorption and the being hindered bone formation around the implants in diabetes are difficult to be solved for dentists. So, the aim of the study was to investigate the influences of hyperglycemia and insulin-like growth factor I (IGF-I) on osteoblasts. Osteoblasts were cultured in different conditions: normal glucose, mimic hyperglycemia, hyperglycemia with IGF-I, hyperglycemia with insulin. The proliferation and mineralization of osteoblasts were observed. As abnormal transport of glucose involved in the development of chronic complications in diabetes. The expression of glucose transporter 1 (GLUT1) was further evaluated by RT-PCR, immunofluorescence and Western blot in different groups. These results showed that hyperglycemia increased the proliferation and inhibited the mineralization of osteoblasts, while IGF-I seemed to reverse these effects. The levels of GLUT1 mRNA and protein in hyperglycemia were elevated by 51% and 35%, respectively, compared with that in normal glucose, while the levels in hyperglycemia with IGF-I were almost the same as that in normal glucose. In conclusion, the increased expression of GLUT1 may contribute to the delayed mineralization of osteoblasts in hyperglycemia. Also IGF-I may be a new drug for diabetic bone disease through normalizing the expression of GLUT1.
Diabetes Res Clin Pract 2006 Jul
PMID:Effects of insulin-like growth factor I on the development of osteoblasts in hyperglycemia. 1641 42

Patients with chronic kidney disease (CKD) have high rates of healthcare utilization, morbidity, and mortality. Increasing rates of obesity, diabetes, and hypertension suggest that the expected numbers of patients with CKD will rise. Managing the economic and clinical burden of CKD will be a significant challenge for the healthcare system. The burden of CKD can be considered in terms of both CKD-specific and CKD-related morbidity and mortality. CKD-specific complications include anemia and bone disease. CKD-related complications include obesity, diabetes and hypertension. CKD-specific complications tend to occur later in the course of disease and may be best treated by a nephrologist, while CKD-related complications may be most easily treated by primary care physicians. Coordinating patient care is essential to managing the burden of this growing disease.
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PMID:Managing the burden of chronic kidney disease. 1662 Jan 97

In patients with end stage renal disease, metabolic bone abnormalities are frequently seen. Diabetes may affect bone metabolism through various mechanisms, including hyperglycemia, insulin deficiency, and accumulation of advanced glycation end-products. Bone disease in hemodialysis patients with diabetes mellitus is characterized by low bone turnover, resulting from either impaired secretion of parathyroid hormone or osteoblast dysfunction. The prevalence rate of vertebral fractures in diabetic hemodialysis patients was 32%, which was greater than that of non-diabetic hemodialysis patients (13%). In non-diabetic hemodialysis patients, those with vertebral fracture showed significantly lower bone mineral density in either lumbar spine or distal one third of radius than the respective value in those without fracture. However, in diabetic hemodialysis patients, neither bone mineral density in lumbar spine nor distal one third of radius was significantly lower in those with vertebral fracture than in those without.
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PMID:[Bone abnormalities in diabetic hemodialysis patients]. 1688 43

A broad range of different factors aggravates renal osteodystrophy, which is present in virtually all patients with chronic kidney disease and after successful kidney transplantation. Altered hormonal status, including sex hormones and parathyroid hormone (PTH), a deficit of 1,25(OH)(2) vitamin D(3) (calcitriol), immunosuppressive therapy and post-operative immobilization contribute to a progressive loss of bone density and structure. The decrease of bone mass is particularly prominent during the first 6 months after kidney transplantation and is associated with an increased number of fractures, both compared with the normal population as well as with dialysis patients. At particular risk are patients with a history of diabetes, long duration of haemodialysis and post-menopausal women. To prevent post-transplant bone loss prescription of steroids should be minimized and withdrawn as early as possible. Additional intake of alpha-calcidol [25(OH) vitamin D(3)] or calcitriol, despite normal serum levels, reduces persistent hyperparathyroidism after kidney transplantation, improves intestinal calcium absorption and activates osteoblasts. Inhibition of osteoclasts by biphosphonate therapy seems to effectively reverse bone loss during the early and late course of kidney transplantation. However, as the majority of transplant recipients have a low-turnover bone disease, inhibition of osteoclasts, through which bone turnover is impaired, might further reduce osteoblast activity and promote osteoid synthesis. Most investigations were small-scale studies with 10-100 participants and a follow up of only 12 months. This makes conclusions on the effect of any intervention on the fracture rate impossible. Larger, randomized multicentre studies investigating bone-sparing therapy on hard end points are therefore advocated.
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PMID:Effect of kidney transplantation on bone. 1688 99

Although prevention of metabolic bone disease is a principal component of management of end-stage renal disease, the clinical epidemiology of long-bone fractures is not completely understood. Hospital discharge claims from 1994 through 1999 for 7159 subjects in the Dialysis Morbidity and Mortality Study were used to quantify incidence and risk factors of long-bone fractures and to test the hypothesis that long-bone fractures are associated with cardiovascular and infectious events and death in patients receiving hemodialysis. The incidence of long-bone fractures was 16.93 per 1000 patient-years, with the femoral neck being the most common site (59.8%); multivariate analysis revealed greater risk with older age, female gender, diabetes, more years receiving dialysis, and cardiovascular disease, and lower risk with African American race, increasing body mass index, parathyroid hormone values in the fourth quintile (227.1-538.0 pg/mL), and renal transplantation during followup. Postfracture mortality rates were 522.57 per 1000 patient years (versus 215.35 in the overall population). Time-dependent analysis suggested the adverse prognosis of long-bone fractures was related to subsequent congestive heart failure, stroke, pulmonary embolism, pneumonia, and septicemia. Long-bone fractures are common in patients receiving dialysis; their adverse prognostic implications may be linked to major cardiovascular and infectious events.
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PMID:Clinical epidemiology of long-bone fractures in patients receiving hemodialysis. 1719 13


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