Treatment Of Renal Bone Disease Research Articles

Micropetrosis in hemodialysis patients

Micropetrosis develops as a result of stagnation of calcium, phosphorus and bone fluid, which appears as highly mineralized bone area in the osteocytic perilacunar/canalicular system regardless of bone turnover of the patients. And microcracks are predisposed to increase in these areas, which leads to increased bone fragility. However, micropetrosis of hemodialysis (HD) patients has not been discussed at all. Micropetrosis area per bone area (Mp.Ar/B·Ar) and osteocyte number per micropetrosis area (Ot.N/Mp.Ar) were measured in nine HD patients with renal hyperparathyroidism (Group I), twelve patients with hypoparathyroidism within 1 year after the treatment of renal hyperparathyroidism (Group II) and seven patients suffering from hypoparathyroidism for over two years (Group III). And bone mineral density (BMD) and tissue mineral density (TMD) were calculated using μCT to evaluate bone mineral content of iliac bone of the patients. These parameters were compared among the three groups. Only Mp.Ar/B·Ar was statistically greater in Group II and III compared to Group I in the parameters of bone mineral content and micropetrosis. However, the other parameters were not statistically different among the three groups. In long-term HD patients, BMD and TMD may be modified by the causes of renal insufficiency and the treatment of renal bone disease. We concluded that Mp.Ar/B·Ar was greater in patients with long-term hypoparathyroidism than both those with short-term hypoparathyroidism and with renal hyperparathyroidism. Special attention should be paid to avoid long-term hypoparathyroidism of the patients from the view point of increased fracture risk caused by increased micropetrosis area.

Renal bone disease: a dietitian's perspective

Renal bone disease increases morbidity and mortality in patients with chronic kidney disease by increasing the risk for fractures, osteoporosis and other bone problems and its association with cardiovascular disease, including calcification and arterial stiffness. Treatment of renal bone disease is through a combination of three main methods to reduce phosphate levels: dietary restriction of high-phosphate foods; dialysis clearance; and the use of phosphate binders to prevent its absorption.

VITAMIN D IN HEALTH AND DISEASE: Role of Parathyroid Hormone and Therapy with Active Vitamin D Sterols in Renal Osteodystrophy

ABSTRACTRenal osteodystrophy (ROD) represents a spectrum of bone lesions ranging from a high‐turnover to a low‐turnover state. The expression of the histologic bone lesions is modulated by parathyroid hormone (PTH), vitamin D, calcium, phosphorus, and aluminum that act as major regulators of osteoblastic activity and bone formation rate. The availability of immunometric PTH assays has allowed reasonable prediction of the subtypes of bone lesions in patients with chronic kidney disease (CKD). PTH levels as measured by these assays, however, may not reflect the true bone turnover state during treatment with intermittent active vitamin D. Early diagnosis and appropriate treatment of renal bone disease are essential in preventing the debilitating consequences of ROD on the growing skeleton. Calcitriol and calcium‐containing phosphate binders have been the mainstay of treatment for secondary hyperparathyroidism. Complications such as hypercalcemia, vascular calcifications, and the development of adynamic bone may arise from aggressive treatment. New vitamin D analogs and calcium‐free phosphate binders are promising in terms of limiting these complications. The management of ROD should be tailored to maintain normal rates of bone formation and turnover with age‐appropriate serum calcium and phosphorus levels and with serum PTH levels that correspond to normal rates of skeletal remodeling. These treatment goals would maintain bone health, maximize growth potential, and prevent the development of soft tissue and vascular calcifications.

Use and indication of vitamin D and vitamin D analogues in patients with renal bone disease.

Vitamin D plays a pivotal role in the pathogenesis and treatment of renal bone disease. Vitamin D levels decline in the early phase of renal failure, however, through a compensatory mechanism parathyroid hormone (PTH) stimulates the production of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3), calcitriol) to return it to normal circulating concentrations. Nevertheless, resistance to calcitriol is observed and may be related to the decreased presence of the heterodimeric, DNA-binding partner for the vitamin D receptor protein. In end-stage kidney disease (ESKD) the circulating levels of calcitriol are invariably low. The indications of vitamin D therapy are the replacement of the missing hormone vs suppression of hyperparathyroidism (HPT) requiring daily low-dose oral vs intermittent 'pulse' or oral administration. However, this therapy must be accompanied by careful patient monitoring to avoid hypercalcaemia and low bone turnover. Low bone turnover is not merely a histologic entity, but a clinical condition associated with a high risk of extraosseous calcifications, in particular in the cardiovascular system, leading to increased morbidity. Thus, determination of bone turnover in patients with ESKD is essential. Bone biopsy is the gold standard to assess bone turnover, however, it is not always available and nephrologists rely on PTH levels. The intact PTH assay measures PTH(1-84) and large C-PTH fragments, which may antagonize the PTH(1-84) effects on bone. An assay that measures exclusively PTH(1-84) has recently become available and a calculated PTH(1-84)/C-PTH fragment ratio has been shown to be the best predictor of bone turnover in patients with ESKD not treated with vitamin D or with other medications known to affect bone metabolism. 1,25-dihydroxy-22-oxavitamin D(3) (22-oxacalcitriol, OCT) is a vitamin D analogue that could control serum PTH concentrations without deleterious effects on bone.

Use and indication of vitamin D and vitamin D analogues in patients with renal bone disease

Vitamin D plays a pivotal role in the pathogenesis and treatment of renal bone disease. Vitamin D levels decline in the early phase of renal failure; however, through a compensatory mechanism parathyroid hormone (PTH) stimulates the production of calcitriol to return it to normal circulating concentrations. Nevertheless, resistance to calcitriol is observed and may be related to the decreased presence of the heterodimeric, DNA-binding partner for the vitamin D receptor protein. In end-stage kidney disease (ESKD) the circulating levels of calcitriol are invariably low. The indications of vitamin D therapy are the replacement of the missing hormone versus suppression of hyperparathyroidism requiring daily low-dose oral versus intermittent pulse or oral administration. However, this therapy must be accompanied by careful patient monitoring to avoid hypercalcemia and low bone turnover. Low bone turnover is not merely a histologic entity, but a clinical condition associated with high risk of extraosseous calcifications, in particular in the cardiovascular system, leading to increased morbidity. Thus, determination of bone turnover in patients with ESKD is essential. Bone biopsy is the gold standard to assess bone turnover, however, it is not always available and nephrologists rely on PTH levels. The intact PTH assay measures PTH (1-84) and large C-PTH fragments, which may antagonize the PTH (1-84) effects on bone. An assay that measures exclusively PTH (1-84) has recently become available and a calculated PTH (1-84) /C-PTH fragment ratio has been shown to be the best predictor of bone turnover in patients with ESKD not treated with vitamin D or with other medications known to affect bone metabolism. 22-Oxacalcitriol is a vitamin D analogue that could control serum PTH concentrations without deleterious effects on bone.

Oral vitamin D or calcium carbonate in the prevention of renal bone disease?

It is well known that hyperparathyroidism begins early in renal failure and progresses, probably not linearly, throughout the natural course of renal diseases and dialysis therapy. Recent progress in basic medical science has improved our understanding of the mechanisms by which the classically known stimuli for parathyroid hormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3 metabolism disturbances. In the treatment of hyperparathyroidism, although some authors stress the benefit of treating one of these stimuli, it is probably more effective to combine the treatment of them all. There is conclusive recent work showing the efficacy of using both CaCO3 and vitamin D3, either in chronic renal failure or in dialysis patients at every stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3 and vitamin D3 derivatives may be used in the prevention and treatment of renal bone disease. The limits of this association are the increasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficial effect of vitamin D3 derivatives on hyperparathyroidism.

Vitamin, Mineral, and Hormone Interactions in Renal Bone Disease

<h2>Abstract</h2> As part of the patient care team, the renal dietitian should actively participate in the development of the care plan for the prevention and treatment of renal bone disease in the dialysis patient. the renal dietitian should be involved in the choice of appropriate vitamin or mineral preparations to ensure that the patient's nutritional needs are met. This article is a review of renal nutrition as it relates to the prevention and treatment of renal bone disease through understanding of vitamin, mineral and hormone interactions.

Renal bone disease 1990: An unmet challenge for the nephrologist

A rational approach to the treatment of renal bone disease requires a basic understanding of: (1) the anatomic physiology of bone; (2) the pathophysiologic effects of renal failure on mineral metabolism and bone; and, (3) careful assessment of the various available therapeutic modalities

Treatment of Renal Bone Disease

Treatment of Renal Bone Disease

Correlation of clinical, biochemical and skeletal responses to 1alpha-hydroxyvitamin D3 in renal bone disease.

Thirty-five patients with bone disease and chronic renal failure (twenty-four on maintenance haemodialysis) were treated for 7--39 months with 1alpha-hydroxyvitamin D3, 2--2.5 microgram daily by mouth. Symptoms (bone pain and muscle weakness) and radiographic appearances improved and plasma alkaline phosphatase returned to normal in the majority of patients (87, 76 and 75% respectively). In contrast, histological appearances in bone improved in only 46% twenty-three patients from whom paired biopsies were available, and this change was not greatly different from that seen in a comparable group of untreated patients. Significant correlations were noted in individual patients between the changes in symptoms, X-rays, plasma alkaline phosphatase and immunoreactive parathyroid hormone and these, in turn, were related to histological changes in bone, although these latter changes were often small. It is concluded that 1alpha-hydroxyvitamin D3 is a useful new drug in the treatment of renal bone disease, but that the evaluation of the response depends critically on the method of assessment used.

The investigation and treatment of renal bone disease

Neutron activation analysis of a hand has been used to monitor changes in skeletal calcium content of patients undergoing maintenance hemodialysis. Assessed by this technic supplementary magnesium therapy was of value in reducing the progressive losses of skeletal calcium in a proportion of the patients receiving maintenance hemodialysis. Oral calcium supplements produced a decrease in the skeletal calcium losses of all the patients studied. 1-alpha-hydroxycholecalciferol, a potent vitamin D analogue, caused a significant increase in the calcium content of bone in three patients receiving maintenance hemodialysis; it may prove to be a safe and effective form of therapy for azotemic osteodystrophy.

The investigation and treatment of renal bone disease: Catto GRD, MacLeod M: Am J Med 61: 64–73, 1976

The investigation and treatment of renal bone disease: Catto GRD, MacLeod M: Am J Med 61: 64–73, 1976

I alpha-hydroxycholecalciferol: a treatment of renal bone disease.

Three patients with chronic renal failure on maintenance haemodialysis have been treated with 1 alpha-hydroxycholecalciferol (1 alpha-OHCC), a synthetic vitamin D analogue. A daily dose of 2 mug by mouth produced a significant increase in both calcium absorption from the gastrointestinal tract and calcium content of bone. Treatment with 1 alpha-OHCC appears to be effective in cases of metabolic bone disease associated with chronic renal failure.

Metabolic bone disease in patients on maintenance hemodialysis.

Renal bone disease is the consequence of secondary hyperparathyroidism (P retention and PTH resistance) and of defective metabolism of vitamin D. The effects of these biochemical abnormalities in the skeleton are described. The value of various diagnostic procedures (bone biopsy, serum chemistry, x-rays) is analyzed. Current views on prevention and treatment of renal bone disease before and during maintenance hemodialysis are discussed.

Treatment of Renal Bone Disease

Treatment of Renal Bone Disease