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Abnormal bone metabolism is a recognized complication of end-stage renal disease, but fracture risk following renal transplantation has not been well quantified. We followed the 86 Olmsted County, Minnesota, residents who underwent initial renal transplantation in 1965-1995 for 911 person-years (median, 10.6 years per subject) in a retrospective cohort study. Fractures, and possible risk factors, were assessed through review of each subject's complete community medical records. Altogether, 117 fractures were observed during follow-up extending to 33 years. The cumulative incidence of any fracture at 15 years was 60% versus 20% expected ( P<0.001). There was a significantly increased risk of fractures generally [standardized incidence ratio (SIR), 4.8; 95% CI, 3.6-6.4] and vertebral (SIR, 23.1; 95% CI, 12.3-39.6) and foot fractures (SIR, 8.4; 95% CI, 5.1-12.9) especially. Age at first transplantation, renal failure due to diabetes, pancreas transplantation, peripheral neuropathy, peripheral vascular disease and blindness were all associated with overall fracture risk. In a multivariate analysis, however, only age and diabetic nephropathy were independent predictors of fracture risk generally, while higher activity status was protective. Diabetes was the only independent predictor of lower limb fractures, whereas age and osteoporosis history predicted vertebral fractures. Cumulative corticosteroid dosage was not associated with increased fracture risk in this analysis. Despite the fact that our patients had few risk factors for preexisting bone disease attendant to postmenopausal osteoporosis, prior corticosteroid use or renal osteodystrophy, these data indicate that renal transplantation is associated with a significant increase in fracture risk among unselected patients in the community. Diabetic patients, particularly, experience excess lower limb fractures. Patients and their care providers should be aware of this elevated fracture risk, which continues long-term.
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PMID:Long-term fracture risk following renal transplantation: a population-based study. 1466

Kidney transplantation is the optimal form of renal replacement therapy for many with end-stage kidney disease. However, kidney transplantation comes with a unique set of medical complications, important among them is bone disease. Posttransplant bone disorders are manifestations of pathologic processes occurring posttransplant that are superimposed on preexisting disorders of bone and mineral metabolism secondary to kidney failure and/or diabetes mellitus. As a consequence of early rapid bone loss, which is seen commonly within the first 3 to 6 months of transplant, the fracture risk posttransplant increases and has been reported as high as 5% to 44%. Posttransplant fractures occur more commonly at peripheral than central sites. Patients with a history of diabetes mellitus are at particular risk for fracture. Parathyroid hormone (PTH) and osteocalcin levels generally decrease after transplantation. Alkaline phosphatase and urinary collagen cross-links are unpredictable. Bone histology varies. No single biomarker unequivocally distinguishes between the various bone disorders found on biopsy examination. Immunosuppression is a major cause of posttransplant bone disorders. Glucocorticoids lead to decreased bone formation whereas the calcineurin inhibitors appear to cause increased bone turnover. Evaluating and managing posttransplant bone disease is an integral part of posttransplant medical care.
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PMID:Bone disease after kidney transplantation. 1473 May 14

Post-transplant diabetes mellitus (PTDM) is a frequent and serious complication after kidney transplantation. Its ethiopathogenesis is multifactorial and includes the immunosuppressive regimen, the ethnicity, older age and the body mass index. Among these, calcineurine inhibitor and steroid use seems to have outstanding relevance. Both patient and graft survival is significantly reduced in recipients affected by PTDM. The main clinical aspects of transplant recipients with PTDM are patient and graft survival rate, infections, cardiovascular complications and late complications of diabetes that include nephropathy, neuropathy, retinopathy, micro-macroangiopathy and bone disease. The main stages of PTDM prophylaxis and treatment are: to identify patients at risk pre-transplantation; to control modifiable risk factors post-transplantation; to control hypertension and lipid profiles and a strict metabolic control. Insulin treatment is indicated mainly in thin patients and oral hypoglycemic agents should be reserved for overweight patients. Transplant centers are currently accepting higher risk candidates for post-transplant complications; therefore, attention needs to shift to the prevention and the control of complications, such as PTDM, because they can lead to a poor quality of life and an increased mortality in patients with functioning grafts.
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PMID:Post-transplant diabetes mellitus. 1473 7

The Pituitary Society in conjunction with the European Neuroendocrine Association held a consensus workshop to develop guidelines for diagnosis and treatment of the co-morbid complications of acromegaly. Fifty nine pituitary specialists (endocrinologists, neurosurgeons and cardiologists) assessed the current published literature on acromegaly complications in light of recent advances in maintaining tight therapeutic control of GH hypersecretion. The impact of elevated GH levels on cardiovascular disease, hypertension, diabetes, sleep apnea, colon polyps, bone disease, reproductive disorders, and neuropsychologic complications were considered. Guidelines are proposed for effective management of these complications in the context of overall acromegaly control. When appropriate, requirements for prospective evidence-based studies and surveillance database development are enunciated. Effective management of co-morbid acromegaly complications will lead to improved morbidity and mortality in acromegaly.
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PMID:Diagnosis and treatment of acromegaly complications. 1505 79

In the early stages of renal failure, hyperparathyroidism develops as a compensatory mechanism to control serum levels of calcium, phosphorus and calcitriol. As kidney disease progresses, this ability to maintain mineral homeostasis is lost, leading to the development of renal osteodystrophy (ROD). Over the past decade, the pattern of ROD seen in patients with chronic kidney disease (CKD) has changed. Previously, the majority of patients had mixed uraemic osteodystrophy or aluminium-related osteomalacia. The decreased use of aluminium-based phosphate binders, coupled with improvements in the management of hyperphosphataemia, led to a reduction in the prevalence of these types of ROD. Since the mid-1990s, there has been an increase in the prevalence of adynamic bone disease as a result of increased suppression of parathyroid hormone through the use of calcium-based phosphate binders and calcitriol therapy. Adynamic bone disease is also associated with several clinical factors, such as older age, use of continuous ambulatory peritoneal dialysis and the presence of diabetes mellitus, as well as the use of calcitriol therapy. Studies of calcium metabolism in patients with CKD have shown that adynamic bone disease is a distinct clinical condition that leads to hypercalcaemia via mechanisms different from that seen in high-turnover bone disease. As high calcium x phosphorus product has been associated with soft tissue and vascular calcifications, and increased mortality, optimizing bone health may be an important way of reducing cardiovascular risk in patients with CKD. To do this, novel, effective, non-calcium, non-aluminium phosphate binders will be necessary.
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PMID:The importance of bone health in end-stage renal disease: out of the frying pan, into the fire? 1512 48

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

Osteoprotegerin is a circulating osteoclastogenesis inhibitory factor and serum osteoprotegerin levels are elevated in hemodialysis patients. This study investigated whether osteoprotegerin levels correlated with various clinical parameters in hemodialysis patients. The subjects were 45 men and 37 women aged from 27 to 94 years (mean = 60.4 +/- 13.9 years), and the duration of dialysis was 9-277 months (mean = 89.5 +/- 64.7 months). Serum osteoprotegerin levels were measured by enzyme-linked immunosorbent assay. Data were analyzed by stepwise multiple regression analysis. The mean osteoprotegerin level of the hemodialysis patients was 303 +/- 210 pg/mL, which was higher than in age-matched healthy controls. Osteoprotegerin levels increased with age, a longer duration of dialysis, and the presence of diabetes. Skeletal resistance to parathyroid hormone might be increased by aging, a long dialysis period, and diabetes, perhaps explaining why adynamic bone disease is more common in older or diabetic patients.
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PMID:Increased serum osteoprotegerin level in older and diabetic hemodialysis patients. 1527 86

Hyperinduced oxidant stress may have a role in the pathogenesis of diabetes and its micro- and macrovascular complications. Attaining euglycemia and the use of antioxidant vitamins could reduce oxidant stress and complications. In general, evidence does not support the use of supplements, and supplements are not recommended unless patients are deficient. Use of vitamins in excess may have adverse effects. Vitamin supplements are indicated in patients deficient in vitamins due to inadequate dietary intake or intestinal disease. Treatment with proper amounts of vitamins and antioxidants is best accomplished with a balanced diet including 3 servings of vegetables and 2 servings of fruits. Regarding supplementation of specific vitamins: carotene cannot be recommended in view of the possible harm and lack of benefit in clinical studies. Vitamin A (retinol) and Vitamin D should be repleted if deficient by laboratory assay. Excesses should be avoided. Vitamin A supplements, particularly in pregnancy, should not exceed 10,000 IU daily or a supplement should not exceed 25,000 units weekly. Vitamin E (alpha-tocopherol) alone in doses of 400 units is of questionable value, and larger doses may cause intracranial hemorrhage or interact negatively with lipid-lowering drugs. Vitamin E should not be used in patients who have bleeding disorders or patients on anticoagulants or acetylsalicylic acid (ASA). Vitamin C (ascorbic acid) losses in urine may be excessive in diabetic patients and may require repletion to 200 mg in nonsmokers and 250 mg in smokers. Further studies are needed testing: (1) vitamin supplementation in subgroups of patients at high risk for specific complications using tissue-specific indicators of oxidative stress; (2) the role of oxidative stress in nephropathy, diabetic myocardiopathy, dermopathy, joint limitation syndromes, peripheral edema, metabolic bone disease, and pregnancy; (3) the impact of renal failure on oxidative stress; and (4) the effects of diabetes and dietary vitamins on the relative amounts of retinoids, carotenoids, and vitamin E in the chylomicron and lipoproteins, and how this affects assimilation, oxidation of lipids, and atherosclerotic plaque formation.
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PMID:Advances in diabetes for the millennium: vitamins and oxidant stress in diabetes and its complications. 1564 9

Dialysis, in its routine 3 x week manifestation, undoubtedly is life saving. The therapy is limited by a number of factors that persist despite the development of safe machines and highly efficient dialyzers. The turnover of known, and very likely, many unknown uremic toxins, is rapid so that 3 x week dialysis is accompanied by relatively high levels of these substances. Only the lower part of the range of molecular weights of those putative uremic toxins, which are small proteins, are removed by current therapies. For substances such as phosphorus, long dialysis is successful in removing the excess retained dietary phosphorus, perhaps the only proven uremic toxin. The difficulty of achieving a normal extracellular volume is probably a major factor in the progression and poor outcomes of cardiovascular disease despite the potential improvement with management of hyperlipidemia, inflammation, potential arrhythmias, and cardiac failure due to other pathogenetic mechanisms. New developments in understanding of Vitamin D metabolism, Ca receptor inhibitor drugs, and control of hyperphosphatemia may reduce the problems of kidney bone disease and the adverse cardiovascular effect of calcium phosphorus disposition. Dialysis more frequent than 3 x week is already routinely, if only infrequently, used to deal with the very large volume or overhydrated patient. However, daily dialysis--whether short or long-is now beginning as a therapy with a large randomized NIH trial in the offing. Currently, the net growth of dialysis is approximately 4% a year, but it would not be surprising if there were a gradual increase in growth rates as CKD patients live longer due to control of cardiac disease. Eventually, the treatment of early kidney disease should reduce the dialysis population, particularly if diabetes can be better controlled or even prevented. The dialysis aspect of nephrology as a profession for physicians, nurses, and technicians appears to be on a long course with increasing demand and the need for applying what is already known, while awaiting new technical developments. Wearable artificial kidneys, involving the application of technology and use of new materials, are currently being investigated. The presence of nephrologists during the actual dialysis treatment is certainly not as evident as it was in the past. Reimbursement methodology has ensured at least a minimum of documented visits by nephrologists or nurse practitioners to the dialysis patient during treatment. It is controversial as to the value of this, but evidence has been presented that certain outcomes, such as use of appropriate dialysis dose and blood chemistries, are improved by more frequent visits. The present is over.
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PMID:Technology: kidneys--the present of dialysis. 1567 76

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


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