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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal osteodystrophy is a universal complication of uremia. Renal failure patients are at risk for low bone mineral density (BMD) and fractures. Parathyroid hormone (PTH) plays a pivotal role in the pathophysiology of uremic bone disease. Histomorphometric studies suggest that the maintenance of PTH levels between two and four times the upper limit of normal is associated with the lowest prevalence of two common forms of osteodystrophy: osteitis fibrosa cystica and adynamic bone disease. The purpose of this study was to investigate whether the above recommendation for PTH levels in dialysis patients corresponds to a more optimal BMD with a special emphasis on diabetic versus nondiabetic subjects. Twenty-eight patients with chronic renal failure on hemodialysis underwent measurement of PTH levels, as well as BMD at the lumbar spine, hip, and forearm. They were divided into three groups based on the mean PTH level over the 5 years prior to having BMD measured. Osteoporosis was diagnosed in 55% of men and 87% of women on dialysis. Predictors of BMD were gender, duration on hemodialysis, and diabetes. Our study supports the histomorphometry-based studies suggesting that the maintenance of intact PTH levels two to four times the upper limit of normal may be associated with better skeletal health in uremic patients on hemodialysis, and that the diabetic subgroup is at particular risk for low BMD.
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PMID:Predictors of bone mineral density in patients on hemodialysis. 1525 16

Secondary hyperparathyroidism (SHPT) is a common occurrence in patients with chronic renal failure and is characterized by excessive serum parathyroid hormone (PTH) levels, parathyroid hyperplasia and imbalances in calcium and phosphorus metabolism. PTH acts as a uraemic toxin and it may be responsible for the following long-term consequences: renal osteodystrophy; non-skeletal abnormalities, including severe vascular and heart valve calcification; alterations in cardiovascular structure and function; immune dysfunction; and renal anaemia. The risk of developing SHPT is not the same for all uraemic patients. Black patients appear to have a higher risk of developing SHPT than Caucasian patients, and patients with diabetes have a lower risk than non-diabetic patients. Current treatments include dietary phosphate restriction, oral phosphate binders, vitamin D and its analogues, and, in severe cases, parathyroidectomy. These treatments do not provide optimal treatment for many patients, and compounds that directly inhibit PTH secretion may prove a major step forward in the treatment of SHPT.
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PMID:The clinical consequences of secondary hyperparathyroidism: focus on clinical outcomes. 1528 53

An increasing number of patients are developing chronic kidney disease (CKD). Appropriate care for patients with CKD must occur in the earliest stages, preferably before CKD progresses to more severe stages. Therefore, recognition and treatment of CKD and its associated complications must occur in primary care settings. Patients with CKD often have comorbid conditions such as diabetes mellitus, hypertension, and dyslipidemia, creating specific considerations when treating these diseases. Also, these patients have CKD-related conditions, including anemia and renal osteodystrophy, that are not traditionally evaluated and monitored by the primary care practitioner. Collectively, many opportunities exist for pharmacists who practice in the primary care setting to improve the care of patients with CKD.
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PMID:Caring for patients with chronic kidney disease: a joint opinion of the ambulatory care and the nephrology practice and research networks of the American College of Clinical Pharmacy. 1576 29

Renal osteodystrophy (ROD) in chronic renal failure (CRF) patients with diabetes mellitus (DM) is characterized by lower degree of secondary hyperparathyroidism and higher prevalence of low turnover bone disorders than that in non-DM CRF patients. Particularly, aplastic bone disease is frequently observed (30 - 40 %). Compared to non-DM CRF patients, serum levels of osteocalcin are significantly decreased, and bone mineral density of trabecular bones is significantly decreased in DM CRF patients. Dietary calcium intake is often less than daily requirement, and hypovitaminosis D is frequently observed. Although persistent hyperglycemic state and impairment of insulin action are major contributors to diabetic osteodystrophy, many factors complicate the feature of DM-CRF. Control of blood glucose levels is the most important to alleviate abnormal bone metabolism in DM-CRF patients, and dietary calcium intake should be normalized. Further, therapeutic strategy of appropriate vitamin D administration should be established, in addition to appropriate exercise therapy, in order to prevent the progression of ROD in DM CRF patients.
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PMID:[Renal osteodystrophy with diabetic bone disease]. 1577 95

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 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

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

Renal osteodystrophy encompasses several histologic subtypes, all of which can undergo change over time. In peritoneal dialysis (PD) patients, we studied bone histology and the factors influencing any changes over 1 year In 44 PD patients, we collected two paired bone biopsies (at baseline and after 12 months) and biochemical and treatment data (at baseline and every 3 months). Of the 44 original patients, 24 completed the study. Of these 24 patients, 19 were initially diagnosed with adynamic bone lesion (ABL). After 1 year, 12 still had ABL; the other 7 had changed to high turnover bone lesion (HTBL). Another 5 patients were initially diagnosed with HTBL. Among these, 4 still had HTBL at 1 year; 1 had changed to ABL. In patients who changed to HTBL from ABL, serum albumin had increased to 4.2 +/- 0.3 g/dL at month 12 from 3.7 +/- 0.4 g/dL at baseline (p < 0.05). In patients who still had ABL, serum albumin did not change. Additionally, the percentage increase in serum albumin over the study was higher in HTBL patients than in ABL patients (0.1408 +/- 0.139 g/dL vs. -0.0076 +/- 0.113 g/dL, p = 0.009). A lower likelihood of diabetes (p = 0.033) and a higher serum albumin [area under the curve: 0.822; 95% confidence interval (CI): 0.651 to 0.993] identified a HTBL diagnosis at 12 months. Older age increased the probability of changing to ABL (OR: 1.2935; 95% CI: 1.03 to 1.67; p= 0.02). Bone lesions can change over time, and this change is associated with age, diabetes, and serum albumin. A change to HTBL was associated with improvement in serum albumin. Protein status is possibly a factor influencing bone lesion outcome.
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PMID:Serum albumin levels, an additional factor implicated in hyperparathyroidism outcome in peritoneal dialysis: a prospective study with paired bone biopsies. 1698 69

Renal osteodystrophy is a complication of chronic kidney disease (CKD) that present in low and high turnover patterns. This disorder has a key role in the disability of CKD patients in whom early diagnosis and treatment can result in better outcome. We studied hyperparathyroidism prevalence and its relationship with renal osteodystrophy in our advanced CKD population. We included 80 patients (of whom 44 (55%) were diabetic) during 6 months period. The patients answered a questionnaire about symptoms related to bone disease and blood levels of parathormone (PTH), calcium, phosphorus, and alkaline phosphatase were obtained, in addition to hand and skull radiographs in all the study patients. Prevalence of clinically evident hyperparathyroidism in our patients was 45%. Hyperparathyroidism had significant relationship with alkaline phosphatase and radiological findings, but did not have a significant relationship with dialysis duration, age, sex, familial history, diabetes mellitus, or hypertension. We conclude that secondary hyperparathyroidism is prevalent in our dialysis population and has high correlation with serum alkaline phosphatase levels and radiological changes.
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PMID:Evaluation of secondary hyperparathyroidism in patients undergoing hemodialysis. 1808 40


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