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Diabetes mellitus (DM) is associated with an increased risk of fractures due to deterioration of bone quality, which can be referred to as "diabetic osteodystrophy." Furthermore, the risk of fracture is increased in DM, even if bone mineral density is normal or high and is associated with increased morbidity if a fracture develops. In addition to the pathophysiological mechanisms of DM, diabetesrelated complications and drugs used in the treatment of DM may also affect bone health. Moreover, the increased risk of falling due to microvascular complications, hypoglycemia, and postural hypotension also contributes to the development of fractures. Individuals with DM should be screened for osteoporosis with recommendations similar to those of the general population. When diagnosing osteoporosis and deciding on treatment, it should be kept in mind that DM may be an important risk factor, and lower threshold values of the T score should be used. [ABSTRACT FROM AUTHOR]

Pyrethroid insecticides are currently a widely used class of pesticides. It is therefore important to determine the mechanism of disorders in some mammalian systems due to prolonged exposure to these pesticides and to justify means to prevent poisoning com- plications. The study was conducted on 30 female rats aged 3 months for 120 days. Intoxication was modeled using α-cypermethrin at a dose of 10 mg/kg. The prevention of intoxication complications was carried out with an adaptogenic complex consisting of the flavonoid quercetin, vitamins C and D3, and minerals (Ca, Mn, Zn, Cu, Se, Mg) at a dose of 500 mg/kg. Assessment of intoxication and preventive efficacy of the adaptogen was performed by determining the duration of the estrous cycle, ovarian organ index, degree of atrophy of the alveolar process in the jaws, as well as density, content of mineral and organic components in the bones. Hepatotoxicity markers were determined in the blood serum, osteoresorption markers in the alveolar bone homogenate, inflammation indicators in the liver, and antioxidant system status in all tissues. Prolonged exposure to α-cypermethrin was associated with a prolongation of the estrous cycle due to a reduction in the diestrus stage and a decrease in the ovarian organ index along with a significant increase in blood estradiol levels. In intoxicated animals, the degree of atrophy of the alveolar process increased and the density of femurs and vertebrae decreased due to a decrease in the weight fraction of the mineral component in the bones. In the bone tissue of the alveolar process, an increase in the activity of elastase and markers of oxidative stress (an increase in the content of malondialdehyde and a decrease in catalase activity), as well as a compensatory increase in the alkaline phosphatase activity were found. In the rat liver, an increase in the acid phosphatase activity and the inhibition of antioxidant defense were observed. An increase in the elastase activity and a decrease in the catalase activity with an increase in the malondialdehyde content were found in the serum of the animals. The use of an adaptogen under conditions of α-cypermethrin intoxication contributed to the normalization of the estrous cycle, ovarian organ index and blood estradiol levels. In the tissue of the femur and vertebrae of rats, the treatment by the prophylactic complex led to an increase in bone density due to an increase in the content of the mineral component, and a decrease in the degree of atrophy of the jaws, in the tissue of which the activation of the enzymatic link of antioxidant defense and a decrease in the activity of destructive elastase too were found. The developed adaptogen prevented the development of oxidative stress and inflammation in the blood serum and liver in the animals. The results of the research indicate a negative effect of α-cypermethrin on the sexual function in female rats, on the state of bone tissue along with the hepatotoxic effect of the pesticide. The proposed agent for the prevention of α-cypermethrin intoxication effectively prevented endocrine disruption in the ovaries, bone destruction and inflammation in the liver. [ABSTRACT FROM AUTHOR]

Objective To investigate the changes of OAT expression in bone cells in chronic renal failure (CRF) and involved mechanism, and to explore the effect of OAT expression on bone metabolism. Methods Randomly divide the rats into a control group (n=6) and a model group (n=6) .The model group established a rat chronic renal failure model using "single nephrectomy+adenine gavage" method, and the red blood cell ( RBC) and hemoglobin ( HGB) of the rat body were measured using a blood routine analyzer; Measure indicators such as creatinine (Cr), urea nitrogen (BUN), uric acid (UA), blood calcium (Ca2+), and blood phosphorus (P3+) using a fully automated biochemical analyzer; Pathological examination of rat kidneys; X-ray examination of rat tibia; Immunohistochemical examination of bone tissue OAT1 level. Results The bone density of the model group rats is lower than that of the control group; The calcium and phosphorus metabolism of rats in the model group was in metabolic disorder, and the OAT1 value of bone tissue binding was much lower than that of the control group (P= 0.001 8), which was statistically significant. (P=0.001 8) Conclusion Chronic renal failure affected the binding ability of OAT1 in bone tissue, leading to the metabolic disorder for calcium absorption and phosphorus metabolism, thus aggravating renal osteodystrophy (P<0.05). [ABSTRACT FROM AUTHOR]

Simple Summary: Mineral and bone disorder (MBD) is usually prevalent in pediatric patients with chronic kidney disease (CKD) and is correlated with meaningful morbidity. CKD may cause disorders in bone remodeling/modeling, which are more evident in the growing skeleton, expressing as short stature, bone pain and deformities, fractures, slipped epiphyses and ectopic calcifications. Although evaluation of bone health is a crucial part in the clinical care of children with CKD, it persists as a significant challenge for pediatricians. Intense changes in mineral and bone metabolism are frequent in chronic kidney disease (CKD) and represent an important cause of morbidity and reduced quality of life. These disorders have conventionally been defined as renal osteodystrophy and classified based on bone biopsy, but due to a lack of bone biopsy data and validated radiological methods to evaluate bone morphology in children, it has been challenging to effectively assess renal osteodystrophy in pediatric CKD; the consequence has been the suboptimal management of bone disorders in children. CKD–mineral and bone disorder (CKD-MBD) is a new expression used to describe a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is a triad of biochemical imbalances in calcium, phosphate, parathyroid hormone, and vitamin D; bone deformities and soft tissue calcification. This literature review aims to explore the pathogenesis, diagnostic approach, and treatment of CKD-MBD in children and the effects of renal osteodystrophy on growing skeleton, with a specific focus on the biological basis of this peculiar condition. [ABSTRACT FROM AUTHOR]

The health and productivity of animals, as well as farmers' financial well-being, can be significantly impacted by cattle illnesses. Accurate and timely diagnosis is therefore essential for effective disease management and control. In this study, we consider the development of models and algorithms for diagnosing diseases in cattle based on Sugeno's fuzzy inference. To achieve this goal, an analytical review of mathematical methods for diagnosing animal diseases and soft computing methods for solving classification problems was performed. Based on the clinical signs of diseases, an algorithm was proposed to build a knowledge base to diagnose diseases in cattle. This algorithm serves to increase the reliability of informative features. Based on the proposed algorithm, a program for diagnosing diseases in cattle was developed. Afterward, a computational experiment was performed. The results of the computational experiment are additional tools for decision-making on the diagnosis of a disease in cattle. Using the developed program, a Sugeno fuzzy logic model was built for diagnosing diseases in cattle. The analysis of the adequacy of the results obtained from the Sugeno fuzzy logic model was performed. The processes of solving several existing (model) classification and evaluation problems and comparing the results with several existing algorithms are considered. The results obtained enable it to be possible to promptly diagnose and perform certain therapeutic measures as well as reduce the time of data analysis and increase the efficiency of diagnosing cattle. The scientific novelty of this study is the creation of an algorithm for building a knowledge base and improving the algorithm for constructing the Sugeno fuzzy logic model for diagnosing diseases in cattle. The findings of this study can be widely used in veterinary medicine in solving the problems of diagnosing diseases in cattle and substantiating decision-making in intelligent systems. [ABSTRACT FROM AUTHOR]

Patients with CKD have a 4–fivefold higher rate of fractures. The incidence of fractures increases with deterioration of kidney function. The process of skeletal changes in CKD patients is characterized by compromised bone strength because of deterioration of bone quantity and/or quality. The fractures lead to a deleterious effect on the quality of life and higher mortality in patients with CKD. The pathogenesis of bone loss and fracture is complex and multi-factorial. Renal osteodystrophy, uremic milieu, drugs, and systemic diseases that lead to renal failure all contribute to bone damage in CKD patients. There is no consensus on the optimal diagnostic method of compromised bone assessment in patients with CKD. Bone quantity and mass can be assessed by dual-energy x-ray absorptiometry (DXA) or quantitative computed tomography (QCT). Bone quality on the other side can be assessed by non-invasive methods such as trabecular bone score (TBS), high-resolution bone imaging methods, and invasive bone biopsy. Bone turnover markers can reflect bone remodeling, but some of them are retained by kidneys. Understanding the mechanism of bone loss is pivotal in preventing fracture in patients with CKD. Several non-pharmacological and therapeutic interventions have been reported to improve bone health. Controlling laboratory abnormalities of CKD-MBD is crucial. Anti-resorptive therapies are effective in improving BMD and reducing fracture risk, but there are uncertainties about safety and efficacy especially in advanced CKD patients. Accepting the prevalent of low bone turnover in patients with advanced CKD, the osteo-anabolics are possibly promising. Parathyroidectomy should be considered a last resort for intractable cases of renal hyperparathyroidism. There is a wide unacceptable gap in osteoporosis management in patients with CKD. This article is focusing on the updated management of CKD-MBD and osteoporosis in CKD patients. Chronic kidney disease deteriorates bone quality and quantity. The mechanism of bone loss mainly determines pharmacological treatment. DXA and QCT provide information about bone quantity, but assessing bone quality, by TBS, high-resolution bone imaging, invasive bone biopsy, and bone turnover markers, can guide us about the mechanism of bone loss. [ABSTRACT FROM AUTHOR]

Hormonal changes and hepatic osteodystrophy are less often studied complications of cirrhosis. This study describes the variance in hormones and osteodystrophy between Frail and Not frail patients with cirrhosis. 116 outpatients with cirrhosis were prospectively enrolled in this study. Frailty assessment was done using Liver Frailty Index (LFI). Sociodemographic assessment, anthropometry, nutritional assessment, hormone profile, and dual-energy X-ray absorptiometry scan were done in all patients. 116 patients, predominantly males (100 (86.2%) with mean age of 50.16 years (95% CI, 48.43–51.89) were included. Malnutrition was more common in Frail group as compared to Not frail group. Subjective global assessment (SGA) class-B patients were significantly more in Frail group (37 (74%) vs 3 (4.5%), P = 0.001). The prevalence of lower parathyroid hormone (PTH) (14 (28%) vs 2 (3%)), testosterone (33 (66%) vs 15 (22.7%)), vitamin D3 (44 (88%) vs 39 (59.1%)), and cortisol (37 (74%) vs 37 (56.1) levels was higher in Frail group (P < 0.05). The number of patients diagnosed with osteodystrophy (34 (68%) vs 21 (31.8%), P = 0.001) was significantly higher in Frail group. The marker of osteoclastic activity, β-cross laps, was significantly elevated in the Frail group both in males (736 (655–818) vs 380 (329–432), P = 0.001) and (females 619 (479–758) vs 313 (83–543), P = 0.02). Bone mineral density (BMD) at lumbar spine (LS) and neck of femur (NF) had significant correlation with LFI (ρ = 0.60, P = 0.001 for LS and ρ = 0.59, P = 0.001 for NF), serum testosterone (ρ = 0.58, P = 0.001 for LS and ρ = 0.53, P = 0.001 for NF), β-cross laps (ρ = 0.38, P = 0.001for LS and ρ = 0.35, P = 0.000 for NF), vitamin D3 (ρ = 0.23, P = 0.04 for LS and ρ = 0.25, P = 0.01 for NF), PTH (ρ = 0.52, P = 0.001 for LS and ρ = 0.48. P = 0.001 for NF), and cortisol (ρ = 0.50, P = 0.001 for LS and ρ = 0.45, P = 0.001 for NF) levels. This is the first study that highlights the high prevalence of hormonal changes and hepatic osteodystrophy in frail patients with cirrhosis and opens a new dimension for research and target of therapy in this field. [ABSTRACT FROM AUTHOR]

Hyperphosphatemia is common in chronic kidney disease (CKD). Often seen as the "silent killer" because of its dramatic effect on vascular calcifications, hyperphosphatemia explains, at least partly, the onset of the complex mineral and bone disorders associated with CKD (CKD-MBD), together with hypocalcemia and decreased 1-25(OH)2 vitamin D levels. The impact of CKD-MBD may be immediate with abnormalities of bone and mineral metabolism with secondary hyperparathyroidism and increased FGF23 levels, or delayed with poor growth, bone deformities, fractures, and vascular calcifications, leading to increased morbidity and mortality. The global management of CKD-MBD has been detailed in international guidelines for adults and children, however, with difficulties to obtain an agreement on the ideal PTH targets. The clinical management of hyperphosphatemia is a daily challenge for nephrologists and pediatric nephrologists, notably because of the phosphate overload in occidental diets that is mainly due to the phosphate "hidden" in food additives. The management begins with a dietary restriction of phosphate intake, and is followed by the use of calcium-based and non-calcium-based phosphate binders, and/or the intensification of dialysis. The objective of this review is to provide an overview of the pathophysiology of hyperphosphatemia in CKD, with a focus on its deleterious effects and a description of the clinical management of hyperphosphatemia in a more global setting of CKD-MBD. [ABSTRACT FROM AUTHOR]

Chronic kidney disease affects patients of all ages and, as it progresses, it greatly affects their lives, especially with the complications it causes. One major complication is renal osteodystrophy (ROD) which starts to develop from the early stages of the disease, but becomes most apparent in patients in need of renal replacement therapy. Diagnosing ROD in the early stages remains a challenge, which brings up the need to find novel biomarkers. Studies are focusing on the role of fibroblast growth factor 23 and Klotho in the bone and mineral homeostasis, but the results are conflicting. ROD remains a major complication in CKD patients, therefore we need to gain a better understanding from the pathophysiological point of view, in order to be able to adjust the medical therapy. [ABSTRACT FROM AUTHOR]

Background: From 1980s to the new millennium, the number of patients surviving with end stage renal disease (ESRD) has increased by 3 fold. This is driven by early detection of primordial and primary risk factors, state of the art renal replacement therapy and ease of public access to healthcare. Renal osteodystrophy (RO) is a metabolic bone disease causing significant morbidity in patients with ESRD, in particular fragility fractures. In this case series, we present the surgical management of 3 ESRD patients with pathological fractures of the neck of femur (NOF) and surgical treatment (parathyroidectomy) of tertiary hyperparathyroidism of ESRD patients in the same surgical setting. Up to date there has been no reports on bipolar hemiarthroplasty and total parathyroidectomy implemented in the same operative setting. Methods: We present 3 cases, 2 males and a female with an average age of 48 years. All patients presented with no trauma or minimal trauma. With high index of suspicion and after confirming the diagnosis with advanced imaging, the patients underwent cemented modular hemiarthroplasty with posterior approach. Parathyroidectomy was sequentially performed to address the tertiary hyperparathyroidism at the same setting. We followed them for 48 months. Results: At 48-month follow up, all the patients were at their pre-morbid ambulatory status and there were no major complications. They did not need any revision surgery or re-operation either for the hemiarthroplasty surgery or the parathyroidectomy during the follow up period. Conclusion: To avoid diagnostic pitfalls in this group of patients we recommend MRIs of both hips in patients complaining of unilateral hip pain even when the roentgenograms are clear of fractures. Total parathyroidectomy at the same setting with the bipolar hemi-arthroplasty is a safe combination. This reduces the anaesthesia risk, the recovery time as well as the equilibrium time for calcium homeostasis. [ABSTRACT FROM AUTHOR]

A female German Shepherd dog aged 10 years was presented to the Referral Veterinary Polyclinic, Indian Veterinary Research Institute, Bareilly, with the chief complaint of facial swelling for the last 7 days. Physical examination revealed a painless, soft swelling of the maxilla and mandible. Radiographic examination showed fibrous osteodystrophy. Serum biochemistry revealed hypocalcemia, hyperphosphatemia and azotemia. Based on the clinical, laboratory and imaging studies, the case was diagnosed as renal osteodystrophy. [ABSTRACT FROM AUTHOR]

Pseudopseudohypoparathyroidism is a rare clinical entity of autosomal dominant inheritance, which shows phenotypic similarity to pseudohypoparathyroidism. However, the main difference lies in their biochemical profiles. The former disease is characterized by normal serum calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) level, whereas the latter shows features suggestive of PTH resistance. Our patient presented after post blunt trauma of head with diabetes insipidus and short stature. Investigations revealed multiple pituitary hormone deficiency. Further examination was conducted for pseudohypoparathyroidism, keeping in mind short metacarpals, knuckle knuckle dimple dimple sign, and short stature, but normal calcium, phosphorus, vitamin D and PTH value led to the diagnosis of pseudopseudohypoparathyroidism. GNAS mutation analysis is necessary to confirm the diagnosis, which could not be performed in this patient due to the high cost. This case shows that pseudopseudohypoparathyroidism, although a rare disease, should be appropriately investigated in such patients if they present with peculiar skeletal features of pseudohypoparathyroidism. [ABSTRACT FROM AUTHOR]

L'ostéodystrophie hépatique peut compliquer les hépatites virales chroniques. En Tunisie, l'étude des anomalies du métabolisme osseux dans ces cas est rare. Les objectifs de ce travail étaient d'évaluer l'atteinte osseuse et l'intérêt des marqueurs biologiques de remodelage osseux dans l'ostéodystrophie des hépatopathies chroniques virales B et C. Il s'agit d'une étude rétrospective, descriptive et analytique. Nous avons inclus des patients atteints d'hépatopathies virales chroniques B et C compensées indemnes d'autres pathologies affectant le métabolisme osseux. Le bilan biologique a comporté la calcémie, la phosphorémie, les phosphatases alcalines, la parathormone, la vitamine D, l'ostéocalcine et le CTX urinaire. La densitométrie était mesurée au niveau du rachis et du fémur. L'étude statistique a été faite par SPSS 20.0. Quarante et un patients et 33 témoins ont été colligés (âge médian respectif : 51 et 44 ans). Une vitamine D basse était trouvée chez 97,6 % des patients (médiane = 8,6 ng/mL). Une hyperparathyroïdie a été notée chez neuf patients (22 %). L'ostéocalcine était basse chez 21 % des patients (médiane = 21,7 ng/mL). Le taux médian de CTX urinaire était de 204 μg/mmol de créatinine. Une masse osseuse basse était notée dans 70,7 % des cas (ostéoporose = 9,7 %, ostéopénie = 61 %). Aucune corrélation n'a été trouvée entre les paramètres de remodelage osseux et la densitométrie osseuse ainsi que l'activité de l'hépatopathie ou la fibrose. L'ostéodystrophie est très fréquente et doit être dépistée au cours des hépatopathies virales chroniques compensées indépendamment de l'activité ou de la fibrose. Le seul examen qui serait recommandé dans ce cas est l'ostéodensitométrie. Hepatic osteodystrophy may be a complication of chronic viral hepatitis. In Tunisia, there is a scarcity of studies that focused on bone metabolism abnormalities in these populations. The aim of this work was to evaluate the bone status and the usefulness of bone turn over markers in osteodystrophy associated to chronic viral hepatitis B and C. It is a retrospective, descriptive and analytic study. We included patients suffering from chronic viral hepatitis B and C, non cirrhotic. Any disease which could interfere with bone metabolism was an exclusion criteria. The biological tests performed were: calcémia, phosphorémia, alcalin phosphatases, parathormon, vitamine D, osteocalcin and urinary CTX. Bone mineral density was measured at the rachis and the femoral bone. Statistical analysis was done by SPSS 20.0. Forty-one patients and 33 controls were enrolled. The median ages were respectively 51 and 44 years. Vitamine D was low in 97.6% of the patients (median = 8.6 ng/mL). hyperparathyroïdism was noted in nine patients (22%). Osteocalcin was low in 21% of cases (median = 21.7 ng/mL). The median rate of urinary CTX was 204 μg/mmol of creatinine. Low bone mineral density was observed based on 70.7% of cases (osteoporosis = 9.7%, osteopenia = 61%). We did not found any correlation between bone turn over markers and mineral density neither activity nor fibrosis. Hepatic osteodystrophy is very frequent independently of activity or fibrosis and patients with chronic viral hepatitis should be screened for. The only investigation recommended in these patients is measurement of bone mineral density. [ABSTRACT FROM AUTHOR]

The control of secondary hyperparathyroidism (SHPT) in pediatric chronic kidney disease is of utmost importance. Even though parathyroid hormone (PTH) is an important biomarker of mineral and bone disorders associated to CKD (CKD-MBD), calcium, phosphate, alkaline phosphatase, and vitamin D are also crucial and should be assessed together. In pediatric dialysis, high PTH levels have been associated with impaired longitudinal growth, bone disease, cardiovascular comorbidities, left ventricular hypertrophy, anemia, and even mortality (when PTH levels were above 500 pg/mL, i.e., 8.3-fold the upper normal limit (UNL)). As such, high PTH levels are for sure deleterious, but too low PTH levels have also been shown to impair growth and to promote vascular calcifications because of the underlying adynamic bone. This manuscript is part of a pros and cons debate for keeping PTH levels within the normal range in pediatric CKD, focusing on the pros. High bone turnover lesions can occur at lower PTH levels than "current" guidelines would suggest; thus, PTH alone is not a good predictor of the underlying osteodystrophy. PTH results can vary locally depending on the assay. Existing guidelines for PTH targets are conflicting and based on a very little evidence. However, the 120–180 pg/mL (2- to 3-fold the UNL) range is common to most of the guidelines; it seems to be a reasonable target in children undergoing dialysis, even though it does not correspond to "normal" PTH levels. As always, the philosophy of PTH levels in pediatric dialysis may be balanced, i.e., "not too low, not too high, and keep phosphate under control." [ABSTRACT FROM AUTHOR]

Background: Disordered metabolism of bone and minerals is a problem frequently encountered in patients with chronic kidney disease. Early biochemical changes include altered calcium and phosphate balance, while advanced disease produces reduced bone strength and extraskeletal calcification. The syndrome describing this constellation of findings is termed chronic kidney disease mineral and bone disorder. Case Report: This report details a rare and extrememanifestation of chronic kidney disease mineral and bone disorder in a patient on long-term hemodialysis for end-stage renal failure. Progressive abnormalities of the thoracic skeleton were ultimately severe enough to produce restrictive lung physiology and symptomatic respiratory failure. Conclusion: Cases of chronic kidney disease mineral and bone disorder with pronounced clinical sequelae occur uncommonly in contemporary practice because of early detection and effective therapies. To our knowledge, this report is the first case in the literature of severe thoracic involvement manifesting as respiratory failure. [ABSTRACT FROM AUTHOR]

Renal osteodystrophy develops as a result of phosphocalcium metabolism imbalance in patients with advanced chronic kidney disease. The aspects of renal osteodystrophy pathomechanism are still incompletely elucidated; however, recent findings regarding the importance and action of fibroblast growth factor 23 have led to changes in recommendations for monitoring disease activity. Despite the availability of international monitoring guidelines and the recent findings on the pathomechanism of this condition, the therapeutic options remain limited and the prognosis is discouraging. [ABSTRACT FROM AUTHOR]

Background Nutritional fibrous osteodystrophy may be developed due to dietary deficiency of calcium or dietary excess of phosphorus. Fibrous osteodystrophy (FOD) provokes hyperostotic distortion of cancellous bones, connective tissue proliferation, and poor mineralization of bone. The objectives of this study were to report the clinical characteristics and therapeutic management of FOD in goats. Materials and methods Four out of 8 Jamnapari goats developed fibrous osteodystrophy in a small scale intensive household farm in Chittagong. The age range of the affected goats was 4-5 months. The feeding history of goats was primarily wheat bran, gram and pea husk. Blood sample from all affected and non-affected animals and feed sample from household farm were collected for laboratory analysis. Fibrous osteodystrophy was primarily diagnosed by observing clinical signs of mandibular and maxillary enlargement, pain on pressure at the enlarged bone, protruded tongue and dyspnea, which was then confirmed by high level of phosphorus in serum evaluation. Results The calcium and phosphorus contents in the sampled gram, pea husk and bran were 0.5%, 0.3% and 0.5%, and 0.71%, 0.49% and 0.61%, respectively. Most of the affected animals had increased serum levels of phosphorus, glucose and alkaline phosphatase and decreased level of calcium. Based on the clinical findings and the laboratory report, the cases were diagnosed as fibrous osteodystrophy due to nutritional imbalance in diet. The owner was advised strictly to stop providing any bran to animals (affected and healthy). Affected animals were additionally treated with calcium preparation, vitamin ADE, ketoprofen, protein, and penicillin-streptomycin combination. Conclusion Treatment of fibrous osteodystrophy required a long time recovery along with balanced ration. A combined therapy of calcium and vitamin D and protein preparation is effective for treatment along with adequate green grass and balanced rations. [ABSTRACT FROM AUTHOR]

25-hydroxyvitamin D [25(OH)D] may not optimally indicate vitamin D receptor activity. Higher concentrations of its catabolic product 24,25-dihydroxyvitmin D [24,25(OH) 2 D] and a higher ratio of 24,25(OH) 2 D to 25(OH)D (the vitamin D metabolite ratio [VMR]) may provide additional information on receptor activity. We compared the strength of associations of these markers with serum PTH concentrations, hip bone mineral density (BMD), and risk of incident hip fracture in community-living older participants in the Cardiovascular Health Study. Among 890 participants, the mean age was 78 years, 60% were women, and the mean 25(OH)D was 28 ± 11 ng/ml. In cross-sectional analysis, the strength of association of each vitamin D measure with PTH was similar; a 1% higher 25(OH)D, 24,25(OH) 2 D, and VMR were associated with 0.32%, 0.25%, and 0.26% lower PTH, respectively ( p < 0.05 for all). Among 358 participants with available BMD data, we found no associations of 25(OH)D or VMR with BMD, whereas higher 24,25(OH) 2 D was modestly associated with greater hip BMD (1% higher 24,25(OH) 2 D associated with 0.04% [95% CI 0.01–0.08%] higher BMD). Risk of incident hip fracture risk was evaluated using a case-cohort design. There were 289 hip fractures during a mean follow up time of 8.4 years. Both higher 24,25(OH) 2 D and VMR were associated with lower risk of hip fracture (HR per SD higher, 0.73 [0.61, 0.87] and 0.74 [0.61, 0.88], respectively) whereas 25(OH)D was not associated with hip fracture (HR 0.93 [0.79, 1.10]). We conclude that evaluating vitamin D status by incorporating assessment of 24,25(OH)D and the VMR provides information on bone health above and beyond 25(OH)D alone. [ABSTRACT FROM AUTHOR]

The aim of this study was to establish the indicators of protein and lipid metabolism in Saanen goats in different physiological periods and with osteodystrophy. Fifteen goats were studied in the spring (postpartum period), in summer (lactation period), in autumn (initial fetal period of gestation), in winter (ending fetal period of gestation) for determine the influence of the physiological state of animals on the level of biochemical parameters in the blood serum. Two groups of goats were formed for 10 head in each: the first group - clinically healthy, the second - with clinical signs of osteodystrophy for establish the biochemical parameters of osteodystrophy. The content of total protein, protein fractions, β-lipoproteins, cholesterol, triglycerides and activity of the enzymes AlAT and AsAT were determined in the blood serum of goat's. It was established that the level of biochemical parameters varied in goats of the Saanen breed in different physiological periods. In goats with osteodystrophy there were significant changes in the parameters of protein and lipid metabolism: decrease levels of albumins; increase levels of β- and γ-globulin the activity of transaminases and concentration of ß-lipoproteins. [ABSTRACT FROM AUTHOR]

The purpose of this study was to research comparative analysis of data that have been obtained after clinical examination of goats and analysis of biochemical research of the level of metabolites of bone tissue metabolism in blood serum and urine for determination of criteria at diagnostics of osteodystrophy. The material of the study consisted of 20 adult goats. Diagnosis of was made according to physical examination of goats and analysis of biochemical research of the level of metabolites of bone tissue metabolism in blood serum and urine. Activity of aminotransferase (alanine aminotransferase, aspartate aminotransferase) and alkaline phosphatase and also concentration of glycoproteins (GP), chondroitin sulfate, fractional content of glucosaminoglycans, content of total and ionized calcium were assessed in blood serum. The content of hydroxyproline and total uronic acid were analyzed in urine. Comparative analysis of total clinical status of goats and level of biochemical components in blood serum and urine that characterize the state of connective tissue at diagnostics of osteodystrophy was conducted. The intergroup significant differences of some biochemical parameters (aspartate aminotransferase, alkaline phosphatase, chondroitin sulfate, fraction II mucopolysaccharides, sum of fractions glucosaminoglycans) were determined. Further investigation must be conducted to determine the biochemical parameters in goat with subclinical signs of osteodystrophy. [ABSTRACT FROM AUTHOR]

Objectives. Hepatic osteodystrophy represents the impairment of bone structure in patients with chronic liver disease. It is characterized by reduced bone mineral density, defined as osteoporosis/osteopenia. It is an important complication of viral liver disease, frequently underdiagnosed and, therefore, untreated. The objectives of this study were to determine the prevalence of osteodystrophy in patients with chronic viral hepatitis C and to identify the factors correlated with its severity. Material and methods. We performed a cohort study on 40 patients with chronic viral hepatitis C in order to assess global and segmental bone mineral density using osteodensitometry (DEXA, Dual Energy X-ray Absorptiometry) and to correlate bone mineral density changes with anthropometric parameters, biochemical, virological markers, non-invasive liver fibrosis assessment and treatment. Results. The overall prevalence of demineralization was high, 52.5% (n=21). In patients aged <50 years, the prevalence of low bone mineral density (BMD) was 23.07% (n=3), and in patients aged ≥50 years old or more, the demineralization prevalence was 18% (n=5) for osteoporosis and 48.14% (n= 3) for osteopenia. Furthermore, the data support a greater decrease in BMD in certain lumbar vertebrae (L1 and L3) and hip specific areas (area of the Ward triangle). Decreased bone mineral density significantly correlated with age, smoking, low body mass index (BMI), presence of liver cytolysis. Conclusions. It is necessary to assess early bone changes in chronic hepatitis C patients and start timely the antiosteoporotic treatment, in order to decrease fracture risk. [ABSTRACT FROM AUTHOR]

Objective Assess the effect of intensive nutrition education by trained dedicated dietitians on osteodystrophy management among hemodialysis patients. Methods Randomized controlled trial in 12 hospital-based hemodialysis units equally distributed over clusters 1 and 2. Cluster 1 patients were either assigned to usual care ( n = 96) or to individualized intensive staged-based nutrition education by a dedicated renal dietitian ( n = 88). Cluster 2 patients ( n = 210) received nutrition education from general hospital dietitians, educating their patients at their spare time from hospital duties. Main outcomes were: (1) dietary knowledge(%), (2) behavioral change, (3) serum phosphorus (mmol/L), each measured at T0 (baseline), T1 (post 6 month intervention) and T2 (post 6 month follow up). Results Significant improvement was found only among patients receiving intensive education from a dedicated dietitian at T1; the change regressed at T2 without statistical significance: knowledge (T0: 40.3; T1: 64; T2: 63) and serum phosphorus (T0: 1.79; T1: 1.65; T2: 1.70); behavioral stages changed significantly throughout the study (T0: Preparation, T1: Action, T2: Preparation). Conclusion The intensive protocol showed to be the most effective. Practice implications Integrating dedicated dietitians and stage-based education in hemodialysis units may improve the nutritional management of patients in Lebanon and countries with similar health care systems. [ABSTRACT FROM AUTHOR]

Whether chronic hepatitis C virus (HCV) infection is a risk factor for the development of bone disease has long been controversial. For this reason, chronic HCV-infected participants ( n = 69) were recruited into a prospective cohort study and underwent dual-energy X-ray absorptiometry for determination of bone mineral density (BMD). Fibrosis staging was evaluated according to the noninvasive index FIB-4. T scores at the femoral neck and lumbar spine were used as the primary outcome variables to assess the association between degree of liver disease and BMD. The study cohort was 41 % male with a mean age of 53.6 years. The mean BMD, Z score, and T score values of lumbar spine in chronic hepatitis C (CHC) patients were significantly lower than those in healthy controls ( p < 0.001). The rate of osteoporosis for CHC patients aged 45-54 years was significantly higher than that of the control group ( p = 0.011). Bone alkaline phosphatase and C-terminal cross-linking telopeptide of type I collagen levels were also significantly higher in CHC patients with reduced BMD. Patients with more advanced liver fibrosis had significantly lower BMD. In conclusion, reduced BMD is common in this population of chronic HCV-infected patients and associated with liver disease severity. This extrahepatic manifestation is probably secondary to increased bone turnover in osteodystrophy pathogenesis. [ABSTRACT FROM AUTHOR]

Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a complex interplay of risk factors, diseases and outcomes. In the last two decades, there has been a steady drift towards definitions depending ever more closely on laboratory abnormalities, which only represent at best possible risk factors for downstream pathology. In the early years of nephrology, especially when the therapeutic agents we had available to combat CKD-MBD were modest, bone and muscle problems were often advanced, and symptomatic, with bone and muscle pain, fractures and myopathy. This 'old style' hyperparathyroidism paradigm has become substantially less common now, and we can forget how symptomatic, and how draining of life-quality, CKD-MBD can be. In this chapter, we explore in the main the most feared complication of all, that of a fracture, which not only are dramatically more common in CKD patients, but also have a much heightened mortality over similar fractures but not in a CKD setting. [ABSTRACT FROM AUTHOR]

Abstract: In the course of chronic kidney disease, bone metabolism disturbances occur and become aggravated simultaneously with the progression of renal disorder, worsening patients’ quality of life. We conducted a 4-year follow-up to assess phalangeal quantitative ultrasound (QUS) measurements in 32 patients undergoing chronic hemodialysis (17 males and 15 females) whose mean ages were 56.3 ± 15.2 years. The QUSs of hand phalanges were performed using DBM 1200 (IGEA, Carpi, Italy) and are expressed as amplitude-dependent speed of sound (Ad-SoS), Z-scores, and T-scores. In comparison with the age-, sex-, and body mass index–adjusted control group, QUS parameters were significantly decreased in all patients undergoing dialysis. During the 4-year follow-up, Ad-SoS and T-scores in all study groups sloped significantly with time. The significant negative relationships between follow-up Ad-SoS results and both baseline and follow-up parathormone values were demonstrated. Our results confirm a high prevalence of bone disturbances in patients undergoing chronic hemodialysis, and they do not improve during renal replacement therapy. The parathormone level seems to be an important agent in influencing bone status, but further studies are needed to understand the other risk factors in kidney-related bone disease. [Copyright &y& Elsevier]

Bone is a dynamic tissue. Skeletal bone integrity is maintained through bone modeling and remodeling. The mechanisms underlying this bone mass regulation are complex and interrelated. An imbalance in the regulation of bone remodeling through bone resorption and bone formation results in bone loss. Chronic inflammation influences bone mass regulation. Inflammation-related bone disorders share many common mechanisms of bone loss. These mechanisms are ultimately mediated through the uncoupling of bone remodeling. Cachexia, physical inactivity, pro-inflammatory cytokines, as well as iatrogenic factors related to effects of immunosuppression are some of the common mechanisms. Recently, cytokine signaling through the central nervous system has been investigated for its potential role in bone mass dysregulation in inflammatory conditions. Growing research on the molecular mechanisms involved in inflammation-induced bone loss may lead to more selective therapeutic targeting of these pathological signaling pathways. [ABSTRACT FROM AUTHOR]

Background. Fibroblast growth factor-23 (FGF-23) is associated with mortality in dialysis patients, and concentrations are elevated in moderate chronic kidney disease (CKD). The threshold of CKD or albuminuria at which FGF-23 begins to change is unknown. [ABSTRACT FROM PUBLISHER]

Childhood and adolescence are crucial times for the development of a healthy skeletal and cardiovascular system. Disordered mineral and bone metabolism accompany chronic kidney disease (CKD) and present significant obstacles to optimal bone strength, final adult height, and cardiovascular health. Decreased activity of renal 1 alpha hydroxylase results in decreased intestinal calcium absorption, increased serum parathyroid hormone levels, and high-turnover renal osteodystrophy, with subsequent growth failure. Simultaneously, phosphorus retention exacerbates secondary hyperparathyroidism, and elevated levels contribute to cardiovascular disease. Treatment of hyperphosphatemia and secondary hyperparathyroidism improves growth and high-turnover bone disease. However, target ranges for serum calcium, phosphorus, and parathyroid hormone (PTH) levels vary according to stage of CKD. Since over-treatment may result in adynamic bone disease, growth failure, hypercalcemia, and progression of cardiovascular calcifications, therapy must be carefully adjusted to maintain optimal serum biochemical parameters according to stage of CKD. Newer therapeutic agents, including calcium-free phosphate binding agents and new vitamin D analogues, effectively suppress serum PTH levels while limiting intestinal calcium absorption and may provide future therapeutic alternatives for children with CKD. [ABSTRACT FROM AUTHOR]

Abstract: Normal bone homeostasis involves a balance between osteoblast and osteoclast action, regulated by hormones and cytokine stimuli. Hemodialysis patients appear to have increased production of interleukin-1 (IL-1), interleukin-6 (IL-6) and glycosaminoglycans (GAG) in serum. IL-1 plays a role in the synthesis, degradation and degree of sulphatation of ECM components such as glycosaminoglycans. Also, continuous changes in the ECM involve enzymes such as β-N-acetyl-d-glucosaminidase (β-NAG) and β-d-glucuronidase (β-GLU) which act on different GAG classes and collagen fibers. We examined the effects of IL-1α on ECM synthesis and the related enzymes in human uremic osteoblast cultures. We also measured the levels of IL-1β, and IL-6 and alkaline phosphatase activity. In biopsies of uremic bone there was less ECM deposition than resorption associated with changes in osteoblast morphology. In vitro osteoblast proliferation was higher (P ≤0.01), and extracellular GAG lower (P ≤0.01) than in controls. The enzyme β-NAG was high (P ≤0.05) but there were no noteworthy changes in β-GLU. ELISA of the medium indicated spontaneous production of IL-1β and IL-6, which significantly increased after IL-1α treatment compared to controls. IL-1α reduced alkaline phosphatase activity (P ≤0.01) in uremic osteoblast cultures. IL-1 acts on osteoblasts with decreases in GAG synthesis and alkaline phosphatase activity, while β-NAG increases. This lead to a reduction in the organic component in ECM and its mineralization, and to changes in the regulation of cytokine activity by GAG. The enzymatic breakdown might be facilitated by metabolic acidosis and failed osteoblast differentiation; these factors could be correlated with different degrees of osteodystrophy. [Copyright &y& Elsevier]

Amelogenesis imperfecta (AI) is a collective term for a number of developmental conditions characterized by abnormal enamel formation. AI is usually not associated with generalized findings; however, a few cases of AI associated with syndromes and metabolic disorders have been reported in the literature. We report two cases of AI presenting with renal disease and thereby highlight the importance of recognizing this possible association at an early stage, as AI in some cases, may be a marker of renal disease. [ABSTRACT FROM AUTHOR]

Background: Abnormal mineral metabolism is not uncommon after renal transplant (TXP). In dialysis patients, elevated serum phosphorous (P), calcium (Ca), CaP product, and parathyroid hormone (PTH) are associated with increased morbidity and mortality. The effect of these abnormalities on recipient and graft survival after renal transplantation is unknown. Methods: We retrospectively analyzed 422 kidney-only transplants performed between June 1996 and June 2003. Cases with graft or recipient survival less than three months, pre-TXP parathyroidectomy (PTX), cinacalcet therapy and incomplete records were excluded, leaving 303 cases for analysis using Cox models that included post-TXP PTX, levels of albumin-adjusted Ca(Caadj), P, CaadjP product and PTH. Results: There was an 11–25% prevalence of abnormal serum Caadj, P or CaadjP product within the first year post-TXP. At least 24% of recipients not undergoing PTX with an equation estimated GFR of 40–60 mL/min had PTH levels >130 pg/mL at one yr post-TXP. This is above levels recommended by the U.S National Kidney Foundation kidney disease quality initiative for patients with stages I–IV chronic kidney disease. Adjusted Ca > 10.5 mg/dL at three months post-TXP was an independent risk for recipient death (OR 3.0; 95% CI: 1.2–7.4). A CaadjP product >35 mg2/dL2 at six months (OR 4.0; 95% CI: 1.2–13.1), and Ca >10.5 mg/dL at 12 months post-TXP (OR 4.0; 95% CI: 1.2–14) were independent risks for death-censored graft loss. Twenty-two recipients underwent PTX for severe hyperparathyroidism. Conclusion: Abnormalities of mineral metabolism are common early after renal TXP. An elevated serum Caadj at three months post-TXP increases the risk for recipient death, while an elevated CaadjP and Caadj later in the first post-TXP year increases the risk of long-term death-censored graft loss. [ABSTRACT FROM AUTHOR]

Background: Pregnancy-associated plasma protein A (PAPP-A) was recently described as a new marker of cardiovascular events and of inflammation in uremic patients. The aim of this study was to determine levels of PAPP-A in chronic dialysis patients and its possible relationships with renal osteodystrophy. Methods: A total of 99 adult chronic hemodialysis patients, 14 peritoneal dialysis patients and 41 control subjects were included in the study. Serum PAPP-A, intact parathormone (iPTH), calcium, phosphorus and alkaline phosphatase (ALP) were measured. The correlations between PAPP-A and iPTH, calcium, phosphorus and ALP were determined. Results: PAPP-A levels were significantly higher in peritoneal dialysis [4.5 (3.2–6.7) mU/L, median (interquartile range)], and hemodialysis patients [4.7 (3.8–6.5) mU/L] in comparison to control subjects [3.4 (3.0–5.0) mU/L] (p<0.05). In hemodialysis patients, post-dialysis PAPP-A levels [6.2 (4.7–9.4) mU/L] were significantly higher than pre-dialysis levels [4.7 (3.8–6.5) mU/L] (p<0.05). There was a weak but statistically significant positive correlation between serum PAPP-A and iPTH (r=0.216; p=0.041) and ALP (r=0.205; p=0.044) in the hemodialysis group. Correlation between the duration of dialysis therapy and PAPP-A levels was also significant (r=0.267; p=0.008) in the hemodialysis group. Conclusions: PAPP-A levels are elevated in acute coronary syndromes and are closely related to inflammation and oxidative stress. We conclude that PAPP-A levels are increased in dialysis patients and may reflect a greater degree of chronic inflammation than osteodystrophy in uremic patients. Clin Chem Lab Med 2007;45:63–6. [ABSTRACT FROM AUTHOR]

With the introduction of the calcimimetic cinacalcet HCl, some patients who would previously have undergone parathyroidectomy are likely to remain on medical therapy. Data is available on complication rates and some important outcome measures of parathyroidectomy, but the efficacy of calcimimetics to influence patient-based endpoints such as cardiovascular mortality and renal osteodystrophy has not been established. Nevertheless, cinacalcet HCl has been demonstrated to improve levels of calcium, phosphate, the calcium phosphate product and parathyroid hormone (PTH). Based on available data, parathyroidectomy is proposed as the preferred treatment option when averaged levels of intact PTH (iPTH) exceed 85–95 pmol/L despite optimal therapy. When iPTH levels exceed 50 pmol/L, parathyroidectomy should be considered if levels of serum calcium, phosphate or the calcium phosphate product are above established target ranges or when patients with established osteoporosis have progressive loss of bone mineral density. Because the currently-recommended biochemical targets are difficult to achieve and maintain for many patients on dialysis, parathyroidectomy rates are likely to increase if these management proposals are followed. This highlights the need for prospective studies with ‘hard’ endpoints, to establish evidence-based roles for parathyroidectomy and calcimimetic therapy. [ABSTRACT FROM AUTHOR]

The last decade has been a remarkably productive one in the field of bone biology. New insights into the maintenance of a normal bone microenvironment have led to significant advances in our understanding of many important skeletal disorders, including renal osteodystrophy. Novel targets for therapeutic manipulation have been exposed and encouraging progress made towards new treatments. In addition, just as clinical studies have alerted us to the potential hazards of vascular calcification, basic science has unearthed the intimate nature of the relationship between the previously separate disciplines of bone and vascular biology. The clinical nephrologist, however, may be forgiven a little cynicism at this point. If such progress has been made, why do the same proverbial difficulties confront us in day-to-day practice? Control of phosphate remains inadequate, despite a literature which constantly reaffirms its crucial importance, and parathyroid hyperplasia seems inevitable in many patients. Furthermore, even the satisfaction of successful control of serum parathyroid hormone concentration must now be tempered by disquiet regarding the skeletal and cardiovascular consequences of oversuppression. This review aims to provide an update of the latest developments in relevant skeletal research and to assess how recently acquired knowledge may improve clinical nephrological practice over the next five years. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

A multicenter study on the affects of lanthanum carbonate (Fosrenol™) and calcium carbonate on renal bone disease in dialysis patients. Background. Lanthanum carbonate (LC) (Fosrenol™) is a novel new treatment for hyperphosphatemia. In this phase III, open-label study, we compared the effects of LC and calcium carbonate (CC) on the evolution of renal osteodystrophy (ROD) in dialysis patients. Methods. Ninety-eight patients were randomized to LC (N = 49) or CC (N = 49). Bone biopsies were taken at baseline and after one year of treatment. Acceptable paired biopsies were available for static and dynamic histomorphometry studies in 33 LC and 30 CC patients. Blood samples were taken at regular intervals for biochemical analysis and adverse events were monitored. Results. LC was well tolerated and serum phosphate levels were well controlled in both treatment groups. The incidence of hypercalcemia was lower in the LC group (6% vs. 49% for CC). At baseline, subtypes of ROD were similarly distributed in both groups, with mixed ROD being most common. At one-year follow-up in the LC group, 5 of 7 patients with baseline low bone turnover (either adynamic bone or osteomalacia), and 4 of 5 patients with baseline hyperparathyroidism, had evolved toward a normalization of their bone turnover. Only one lanthanum-treated patient evolved toward adynamic bone compared with 6 patients in the CC group. In the LC group, the number of patients having either adynamic bone, osteomalacia, or hyperpara decreased overall from 12 (36%) at baseline to 6 (18%), while in the calcium group, the number of patients with these types of ROD increased from 13 (43%) to 16 (53%). Conclusion. LC is a poorly absorbed, well-tolerated, and efficient phosphate binder. LC-treated dialysis patients show almost no evolution toward low bone turnover over one year (unlike CC-treated patients), nor do they experience any aluminum-like effects on bone. [ABSTRACT FROM AUTHOR]

The use of bone biopsy for histomorphometric analysis is a quantitative histological examination aimed at obtaining quantitative information on bone remodeling, structure and microarchitecture. The labeling with tetracycline before the procedure also allows for a dynamic analysis of the osteoblastic activity and mineralization process. In the nephrological setting, bone biopsy is indicated to confirm the diagnosis of subclinical or focal osteomalacia and to characterize the different forms of renal osteodystrophy (ROD). Even if bone biopsy is the gold standard for the diagnosis and specific classification of ROD, the use of this approach is very limited. The main reasons for this are the lack of widespread expertise in performing or interpreting bone biopsy results and the cost, invasiveness and potential pain associated with the procedure. In this regard, the sedation, in addition to local anesthesia routinely applied in Italian protocol, significantly reduces pain and ameliorates the pain perception of patients. Concerning the lack of widespread expertise, in Italy a Hub/Spokes model is proposed to standardize the analyses, optimizing the approach to CKD patients and reducing the costs of the procedure. In addition, new tools offer the possibility to evaluate the osteogenic potential or the ability to form bone under normal and pathological conditions, analyzing mesenchymal stem cells and their ability to differentiate in the osteogenic lineage. In the same way, circulating microRNAs are suggested as a tool for exploring osteogenic potential. The combination of different diagnostic approaches and the optimization of the bioptic procedure represent a concrete solution to spread the use of bone biopsy and optimize CKD patient management. [ABSTRACT FROM AUTHOR]

Strontium causes osteomalacia in chronic renal failure rats. Background . We recently reported an association between increased bone strontium (Sr) levels and osteomalacia in dialysis patients. Methods . To delineate whether or not Sr acts as a causal factor in the development of osteomalacia, we devised the following study: four groups of chronic renal failure (CRF) rats were given Sr, aluminum (Al), both of these compounds or none of the elements (controls). Results . Administration of Sr and/or Al resulted in increased bone levels of the respective elements. Histological examination revealed impairment of mineralization in the Sr group and to a lesser extent in the Al group as compared to the control group. There was also a significant increase in osteoid area in the Sr group, but not in the Al group. No differences in bone surface or erodic perimeter were noted between the various study groups. Histochemically, Sr could be localized in calcified bone, mainly in new bone close to the osteoid/calcification front, a critical site of bone mineralization. Histochemical findings were confirmed by electron probe X-ray microanalysis. Conclusions . These findings indicate that Sr accumulation in chronic renal failure rats resulted in the development of osteomalacic lesions, in contrast to the Al group where adynamic bone disease was induced in the present set-up. Further studies are required to define the mechanism by which way Sr causes osteomalacia in chronic renal failure rats. [ABSTRACT FROM AUTHOR]

The article discusses how the most immediate consequence or side effect of current therapy for secondary hyperparathyroidism is the increase in soft tissue calcification. Soft tissue calcifications may be contributing to conduction abnormalities and arrhythmias, left ventricular dysfunction, aortic and mitral stenosis, ischemia, congestive heart failure, and death.

A multicenter study on the affects of lanthanum carbonate (Fosrenol™) and calcium carbonate on renal bone disease in dialysis patients. Background Lanthanum carbonate (LC) (Fosrenol™) is a novel new treatment for hyperphosphatemia. In this phase III, open-label study, we compared the effects of LC and calcium carbonate (CC) on the evolution of renal osteodystrophy (ROD) in dialysis patients. Methods Ninety-eight patients were randomized to LC ( N = 49) or CC ( N = 49). Bone biopsies were taken at baseline and after one year of treatment. Acceptable paired biopsies were available for static and dynamic histomorphometry studies in 33 LC and 30 CC patients. Blood samples were taken at regular intervals for biochemical analysis and adverse events were monitored. Results LC was well tolerated and serum phosphate levels were well controlled in both treatment groups. The incidence of hypercalcemia was lower in the LC group (6% vs. 49% for CC). At baseline, subtypes of ROD were similarly distributed in both groups, with mixed ROD being most common. At one-year follow-up in the LC group, 5 of 7 patients with baseline low bone turnover (either adynamic bone or osteomalacia), and 4 of 5 patients with baseline hyperparathyroidism, had evolved toward a normalization of their bone turnover. Only one lanthanum-treated patient evolved toward adynamic bone compared with 6 patients in the CC group. In the LC group, the number of patients having either adynamic bone, osteomalacia, or hyperpara decreased overall from 12 (36%) at baseline to 6 (18%), while in the calcium group, the number of patients with these types of ROD increased from 13 (43%) to 16 (53%). Conclusion LC is a poorly absorbed, well-tolerated, and efficient phosphate binder. LC-treated dialysis patients show almost no evolution toward low bone turnover over one year (unlike CC-treated patients), nor do they experience any aluminum-like effects on bone. [ABSTRACT FROM AUTHOR]