Early introduction of oral paricalcitol in renal transplant recipients. An open-label randomized study.

In stable renal transplant recipients with hyperparathyroidism, previous studies have indicated that vitamin D agonist treatment might have anti-proteinuric effects. Animal studies indicate possible anti-fibrotic and anti-inflammatory effects. Early introduction of paricalcitol in de novo renal transplant recipients might reduce proteinuria and prevent progressive allograft fibrosis. We performed a single-center, prospective, randomized, open-label trial investigating effects of paricalcitol 2 µg/day added to standard care. Participants were included 8 weeks after engraftment and followed for 44 weeks. Primary end point was change in spot urine albumin/creatinine ratio. Exploratory microarray analyses of kidney biopsies at study end investigated potential effects on gene expression. Secondary end points included change in glomerular filtration rate (GFR), pulse wave velocity (PWV), and endothelial function measured by peripheral arterial tonometry as reactive hyperemia index (RHI). Seventy-seven de novo transplanted kidney allograft recipients were included, 37 receiving paricalcitol. Paricalcitol treatment lowered PTH levels (P = 0.01) but did not significantly reduce albuminuria (P = 0.76), change vascular parameters (PWV; P = 0.98, RHI; P = 0.33), or influence GFR (P = 0.57). Allograft gene expression was not influenced. To summarize, in newly transplanted renal allograft recipients, paricalcitol reduced PTH and was well tolerated without negatively affecting kidney function. Paricalcitol did not significantly reduce/prevent albuminuria, improve parameters of vascular health, or influence allograft gene expression.

Management of mineral and bone disorders in renal transplant recipients.

The management of post-transplantation bone disease is a complex problem that remains under-appreciated in clinical practice. In these patients, pre-existing metabolic bone disorder is further impacted by the use of immunosuppressive medications (glucocorticoids and calcineurin-inhibitors), variable post-transplantation renal allograft function and post-transplantation diabetes mellitus. The treatment of post-transplantation bone loss should begin pre-transplantation. All patients active on transplant waiting lists should be screened for bone disease. Patients should also be encouraged to take preventative measures against osteoporosis such as regular weight-bearing exercise, smoking cessation and reducing alcohol consumption. Biochemical abnormalities of disordered mineral metabolism should be corrected prior to transplantation wherever possible, and because these abnormalities commonly persist, post transplant hypophosphatemia, persistent hyperparathyroidism and low vitamin D levels should be regularly monitored and treated. Bone loss is greatest in the first 6-12 months post-transplantation, during which period any intervention is likely to be of greatest benefit. There is strong evidence that bisphosphonates prevent post-transplantation bone loss; however, data are lacking that this clearly extends to a reduction in fracture incidence. Denosumab is a potential alternative to vitamin D receptor agonists and bisphosphonates in reducing post-transplantation bone loss; however, further studies are needed to demonstrate its safety in patients with a significantly reduced estimated glomerular filtration rate. Clinical judgement remains the cornerstone of this complex clinical problem, providing a strong rationale for the formation of combined endocrinology and nephrology clinics to treat patients with Chronic Kidney Disease-Mineral and Bone Disorder, before and after transplantation.

Effect of cholecalciferol on parathyroid hormone and vitamin D levels in chronic kidney disease.

AIM: We aimed to determine the effect of a monthly oral vitamin D on the serum 25-hydroxyvitamin D levels and iPTH levels in patients with CKD. METHODS: This was a prospective controlled trial of 48 patients with CKD stage 3-4. Patients were divided into two groups Group1 the cholecalciferol treatment group, Group 2, the control group. One patient in Group 1, and 3 patients in Group2 were excluded after the baseline 25(OH)D levels were determined to be greater than 30ng/ml. Two patients in Group1, and one patient in Group 2 were excluded after the baseline iPTH was determined to be less than 70 pg/ml and greater than 300 pg/ml. Five patients in both groups were lost to follow-up. Thus, a total of 16 patients in Group 1 and 15 patients in Group2 completed the three month study. Group1 patients received 300,000 IU month oral cholecalciferol. RESULTS: The mean serum 25(OH)D concentration of the group1 was significantly higher at baseline (P=0.039). At the end of the three months; serum 25 (OH) D level increased significantly in Group1 (P=0.001). iPTH level of Group1 was significantly lower at baseline (P=0.034). The values of the group1 before and end of third month was compared, serum Ca (P=0.011), P (P=0.013) level showed significant increase, but no significant increase in the Group 2 (P>0.05). The groups had not a clinically significant change in serum Ca and P level (P>0.05). CONCLUSION: Oral cholecalciferol supplementation can be used safely and effective in reducing iPTH levels and correcting vitamin D insufficiency/deficiency in patients with CKD.

How should the patient with multiple endocrine neoplasia type 1 (MEN 1) be followed?

Multiple endocrine neoplasia type 1 (MEN 1) is a complex multi-system disease manifesting a diverse range of primary and secondary metabolic and neoplastic disorders. It is possible to improve patient prognosis by early disease detection and treatment. Regular biochemical and radiological screening for parathyroid, gastro-enteropancreatic, pituitary, intrathorasic and adrenal lesions forms the basis of surveillance. The likelihood of adverse sequelea such as renal and bone disease resulting from hyperparathyroidism, severe peptic ulceration and gastric carcinoidosis secondary to hypergastrinaemia can be ameliorated by early detection and management.

Calcimimetic inhibits late-stage cyst growth in ADPKD.

In polycystic kidney disease (PKD), genetic mutations in polycystin 1 and 2 lead to defective intracellular trafficking of calcium, thereby decreasing intracellular calcium and altering cAMP signaling to favor proliferation. We hypothesized that calcimimetics, allosteric modulators of the calcium-sensing receptor, would reduce cyst growth by increasing intracellular calcium. We randomly assigned 20-wk-old male rats with a form of autosomal dominant PKD (heterozygote Cy/+) to one of four groups for 14 to 18 wk of treatment: (group 1) no treatment; (group 2) calcimimetic R-568 formulated in the diet; (group 3) R-568 plus calcium-supplemented drinking water (R-568 plus Ca); or (group 4) Ca-supplemented drinking water with a normal diet (Ca). Severity of PKD did not progress in any of the three treatment groups between 34 and 38 wk. Compared with no treatment, cyst growth was unaffected at 34 wk by all treatments, but cyst volume and fibrosis were lower at 38 wk, with both R-568-treated groups demonstrating a greater reduction than calcium alone. Between 34 and 38 wk, the total kidney weight increased by 78% in the control group (P < 0.001) and by 19% in the Ca group (P < 0.01), but did not increase in the R-568 or R-568 plus Ca groups, suggesting inhibition of disease progression despite equivalent suppression of parathyroid hormone. In summary, treatment of hyperparathyroidism halts late-stage progression of rodent cystic kidney disease. The benefit of R-568 alone suggests calcium-sensing receptor modulation may have additional inhibitory effects on late-stage cyst growth resulting from a direct modulation of intracellular calcium.

Management of X-linked hypophosphatemia in adults.

X-linked hypophosphatemia (XLH) is caused by mutations in the PHEX gene which result in Fibroblast Growth Factor-23 (FG-F23) excess and phosphate wasting. Clinically, XLH children present with rickets, bone deformities and short stature. In adulthood, patients may still be symptomatic with bone and joint pain, osteomalacia-related fractures or pseudofractures, precocious osteoarthrosis, enthesopathy, muscle weakness and severe dental anomalies. Besides these musculoskeletal and dental manifestations, adult XLH patients are also prone to secondary and tertiary hyperparathyroidism, cardiovascular and metabolic disorders. Pathophysiology of hyperparathyroidism is only partially understood but FGF23 excess and deficient production of calcitriol likely contributes to its development. Similarly, the pathophysiological mechanisms of potential cardiovascular and metabolic involvements are not clear, but FGF-23 excess may play an essential role. Treatment should be considered in symptomatic patients, patients undergoing orthopedic or dental surgery and women during pregnancy and lactation. Treatment with oral phosphate salts and active vitamin D analogs has incomplete efficacy and potential risks. Burosumab, a recombinant human monoclonal antibody against FGF-23, has proven its efficacy in phase 2 and phase 3 clinical trials in adult patients with XLH, but currently its position as first line or second line treatment differ among the countries.

Efficacy and safety of paricalcitol in patients undergoing hemodialysis: a meta-analysis.

BACKGROUND: The elevated calcium and phosphorus levels in patients undergoing hemodialysis may increase the risk of all-cause mortality. Paricalcitol, as a new vitamin D receptor activator (VDRA), seemed to be effective in reducing the calcium and phosphorus levels. OBJECTIVES: The aim of this study was to compare the efficacy and safety of paricalcitol with other VDRAs in patients undergoing hemodialysis. METHODS: PubMed, Embase, and Web of Science database were systematically reviewed. SELECTION CRITERIA: Studies that focused on the use of paricalcitol for hemodialysis patients were eligible for inclusion. DATA COLLECTION AND ANALYSIS: Two independent investigators performed the literature search, data extraction, and assessment of methodological quality. The outcomes were expressed with standard mean difference (SMD), HR, or risk ratio (RR) with 95% CI. RESULTS: Thirteen studies involving 112,695 patients were included in this meta-analysis. Among these studies, four studies were cohort studies and nine studies were randomized controlled trials (RCTs). For cohort studies, they were regarded as being of high quality; for RCTs, only one was classified as being at low risk of bias; and the remaining eight studies were at being unclear risk of bias. Compared with other VDRAs, paricalcitol significantly improved the overall survival (HR =0.86, 95% CI: 0.80, 0.92; P<0.001) and reduced the intact parathyroid hormone (iPTH) (SMD =-0.53, 95% CI: -0.90, -0.17; P=0.004). Paricalcitol offered similar effect with other VDRAs in the control of calcium (SMD =0.32, 95% CI: -0.04, 0.67; P=0.078) and phosphorus (SMD =0.06, 95% CI: -0.26, 0.37; P=0.727) levels. However, the serum change in calcium phosphate product was greater in the paricalcitol group than in the other VDRA group (SMD =2.13, 95% CI: 0.19, 4.07; P=0.031). There was no significant difference in the incidence of adverse events between the two groups (RR =1.02, 95% CI: 0.93, 1.12; P=0.674). CONCLUSION: Paricalcitol was crucial in reducing the mortality in patients undergoing hemodialysis. Moreover, both paricalcitol and other VDRAs were effective in control of the serum iPTH, calcium, and phosphorus levels. Given the potential limitations in this study, more prospective large-scale, well-conducted RCTs are needed to confirm these findings.

Management of Post-transplant Hyperparathyroidism and Bone Disease.

Significant advances in immunosuppressive therapies have been made in renal transplantation, leading to increased allograft and patient survival. Despite improvement in overall patient survival, patients continue to require management of persistent post-transplant hyperparathyroidism. Medications that treat persistent hyperparathyroidism include vitamin D, vitamin D analogues, and calcimimetics. Medication side effects such as hypocalcemia or hypercalcemia, and adynamic bone disease, may lead to a decrease in the drugs. When medical management fails to control persistent post-transplant hyperparathyroidism, treatment is a parathyroidectomy. Surgical techniques are not uniform between centers and surgeons. Undergoing the surgery may include a subtotal technique or a technique including total parathyroid gland resection with partial heterotopic gland reimplantation. In addition, there are possible post-surgical complications. The ideal treatment for persistent post-transplant hyperparathyroidism is the treatment and prevention of the condition while patients are being managed for their late-stage chronic kidney disease and end-stage renal disease.

Nuclear imaging and minimally invasive surgery in the management of hyperparathyroidism.

Primary hyperparathyroidism is the most common cause of hypercalcemia, and the treatment is primarily surgical. Because of biochemical screening, more patients now present with asymptomatic primary hyperparathyroidism, and consensus guidelines have been developed for the treatment of these patients. There is now considerable interest in minimally invasive approaches to the treatment of hyperparathyroidism. Sestamibi scanning as a localizing study, used in combination with anatomic imaging and intraoperative rapid parathyroid hormone assays, has enabled focused surgical approaches. Patients with localizing studies that indicate a single parathyroid adenoma are candidates for such approaches, including unilateral neck exploration, minimally invasive single-gland exploration, or endoscopic exploration instead of the traditional approach of bilateral neck exploration. Nuclear imaging is also critical to the successful management of patients with persistent or recurrent hyperparathyroidism.

Effects of calcimimetics on extraskeletal calcifications in chronic kidney disease.

While the precise mechanisms of vascular calcification (VC) in chronic kidney disease (CKD) remain to be elucidated, there is a close association between VC and secondary hyperparathyroidism (HPT). The elevations in calcium, phosphorus, the Ca x P product, and parathyroid hormone (PTH) observed in patients with CKD and secondary HPT have been associated with VC and increased risk of cardiovascular morbidity and mortality. We have investigated the development of extraskeletal calcification in uremic rats with secondary HPT treated with vitamin D derivatives (calcitriol or paricalcitol), calcimimetics (R-568 or AMG 641), or the combination of both types drugs. Treatment with calcitriol resulted in a significant increase in the extraosseous calcium and phosphorus content and high mortality. By contrast, treatment with calcimimetics, which provided a better control of plasma PTH levels, did not result in extraskeletal mineral accumulation and did not cause mortality. More important, when added to calcitriol, calcimimetics prevented the development of VC and reduced mortality. Paricalcitol administration to uremic rats resulted in calcification levels and mortality rates that were lower than in rats treated with calcitriol but higher than in rats treated with calcimimetics. The mechanism(s) of action responsible for the anticalcification effect of calcimimetics are likely related to the fact that these drugs can control PTH levels without increasing the plasma Ca x P product. In addition calcimimetic activation of vascular calcium-sensing receptor may also modulate the expression of proteins that prevent the development of VC, like matrix Gla protein.

Metabolic control and growth during exclusive growth hormone treatment in X-linked hypophosphatemic rickets.

BACKGROUND: GH may improve phosphate balance and height in X-linked hypophosphatemic rickets (XLH). This study evaluated the impact of exclusive rhGH therapy on phosphate homeostasis and growth. METHODS: Ten children (median age 12.2 years) with XLH were included in a 12-month trial with GH. Conventional treatment was discontinued 1 month prior GH (0.033 mg/kg/day); 1alpha-hydroxyvitamin D was added at 6 months and oral phosphate at 12 months, when GH was discontinued. Patients were followed 1-3 monthly until 18 months for clinical, biochemical and radiographic parameters. RESULTS: Serum phosphate Z-score increased significantly from baseline at 6 months (p = 0.005) and 9 months (p = 0.009) but returned to baseline by 12 months. Serum 1,25-dihydroxyvitamin D also increased significantly. Parathyroid function normalized. The median height Z-score was -2.2 (-2.7 to +0.4) at GH onset and -1.7 (-2.3 to +0.3) at 12 months. One patient showed a significant increase in radiographic rickets activity and 3 patients aggravation of lower limb deformity; the others showed no changes or improvement in these parameters. CONCLUSIONS: GH treatment improved serum phosphate and 1,25-dihydroxyvitamin D, normalized parathyroid function and improved longitudinal growth in XLH. It may however aggravate pre-existing skeletal deformities.

Long-term effects of low calcium dialysates on the serum calcium levels during maintenance hemodialysis treatments: A systematic review and meta-analysis.

Hypercalcemia and hyperparathyroidism in patients receiving maintenance hemodialysis (MHD) can cause the progression of cardiovascular diseases (CVD) and mineral bone disorders (MBD). The KDIGO recommends the dialysates with a calcium (Ca) concentration of 1.25-1.5 mmol/L for MHD treatments, but the optimal concentration remains controversial. Here, we conducted a systematic review and a meta-analysis of seven randomized controlled trials examining a total of 622 patients to investigate the optimal concentration for MHD for 6 months or longer. The dialysates with a low Ca concentration (1.125 or 1.25 mmol/L) significantly lowered the serum Ca and raised the intact parathyroid hormone levels by 0.52 mg/dL (95% confidence interval, 0.20-0.85) and 39.59 pg/mL (14.80-64.38), respectively, compared with a high Ca concentration (1.50 or 1.75 mmol/L). Three studies showed that a low concentration was preferred for lowering arterial calcifications or atherosclerosis in different arteries, but one study showed that coronary arterial calcifications increased with a low concentration. Two studies showed contradictory outcomes in terms of MBD. Our meta-analysis showed that a dialysate with a low Ca concentration lowered the serum Ca levels in patients receiving long-term MHD, but further studies are needed to determine the optimal Ca concentration in terms of CVD and MBD.

Effects of lowering dialysate calcium concentration on mineral metabolism and parathyroid hormone secretion: a multicentric study.

This prospective study was conducted with the aim of examining the efficacy of lowering dialysate calcium (dCa) in order to: (i) stimulate bone turnover in hemodialysis patients with biochemical signs of adynamic bone disease (ABD) (hypercalcemia, normal alkaline phosphatase and intact parathyroid hormone (iPTH) <150 pg/mL); and (ii) diminish hypercalcemia in patients with secondary hyperparathyroidism (sHPT) (hypercalcemia, high alkaline phosphatase and iPTH > 400 pg/mL), thus permitting the use of calcium-containing phosphorus binders and vitamin D metabolites. Patients were divided into: an ABD-treated group (24 patients), a sHPT-treated group (18 patients), an ABD-control group (12 patients) and a sHPT-control group (11 patients). For the ABD- and sHPT-treated patients, hemodialysis was conducted with dCa 1.5 mmol/L for three months and then with dCa 1.25 mmol/L for an additional three months, while in the control groups hemodialysis was conducted with dCa 1.75 mmol/L during the entire study. Reduction of dCa in patients with ABD caused a slight but insignificant decrease of Ca, but a significant and permanent increase of bone-specific alkaline phosphatase and intact parathyroid hormone level serum levels. Reduction of dCa in patients with sHPT slightly but insignificantly decreased Ca and intact parathyroid hormone level values. Nevertheless, this enabled the calcium-based phosphate binder dose to be raised and vitamin D3 metabolites to be introduced. Logistic regression analysis indicated that milder bone disease (both ABD and sHPT) was associated with more the favorable effect of dCa reduction. Thus, low dCa stimulated parathyroid glands and increased bone turnover in ABD patients, and enabled better control of mineral metabolism in sHPT patients.

Tertiary hyperparathyroidism attributable to long-term oral phosphate therapy.

OBJECTIVE: To report a rare case of tertiary hyperparathyroidism (HPT) as a result of long-term oral phosphate therapy. METHODS: We present a case report, with a focus on clinical manifestations and biochemical findings during the course of tertiary HPT, and discuss the pathophysiologic features of this disorder and the therapeutic strategies. RESULTS: A 35-year-old woman, 22 years after the initial diagnosis of familial hypophosphatemic rickets and initiation of treatment with phosphate and vitamin D, underwent assessment for recurrent symptomatic kidney stones, bone pain, and fatigue. Laboratory studies performed 10 months before this presentation showed findings consistent with secondary HPT. Examination was notable for short stature, and pertinent laboratory results were as follows: intact parathyroid hormone 602 pg/mL, calcium 10.9 mg/dL, and phosphorus 3.6 mg/dL. Tertiary HPT was diagnosed, and she underwent subtotal parathyroidectomy and transcervical thymectomy. Postoperatively, she had hypocalcemia and was treated with calcitriol, phosphate, and calcium carbonate; the last agent was discontinued when the serum calcium normalized. Despite multiple dosage alterations in the phosphate and calcitriol therapy, the patient had recurrent tertiary HPT and another kidney stone (treated by lithotripsy). Three years after the subtotal parathyroidectomy, treatment consisted of cinacalcet, calcitriol, and elemental phosphate. CONCLUSION: Long-term follow-up of patients with tertiary HPT is critical, with careful dosage adjustments in phosphate and vitamin D therapy and monitoring of serum levels of phosphorus, calcium, and parathyroid hormone.

1,25-dihydroxyvitamin D(3) therapy is protective for renal function and prevents hyperparathyroidism in renal allograft recipients.

1,25-Dihydroxyvitamin D(3) (calcitriol) therapy has been extensively used for posttransplant osteoporosis. Beside its effect on bone metabolism, calcitriol has an important immunomodulatory effect. We evaluated the effects of oral calcitriol therapy on allograft function and parathyroid hormone levels after renal transplantation. The patients were retrospectively selected from a renal transplant patient population who received calcitriol (group 1, n = 59, 36 male/23 female, follow-up: 52.8 +/- 12.2 months) compared with group (group 2, n = 52, 42 male/9 female, follow-up: 62.0 +/- 24.4 months) without calcitriol therapy after renal transplantation. Calcitriol therapy was started 24.0 +/- 19.1 months posttransplantation. All patients were under three-drug immunosuppression. The pretransplant and posttransplant data were studied retrospectively. Additionally, creatinine levels before and after the initiation of calcitriol therapy were recorded at 6 months intervals for 3 successive years. Our results were analyzed according to the first and third year on therapy data. According to the first year data, there were no differences in patient groups in terms of creatinine and iPTH levels. In the third year, the patients in group 1 showed significantly lower creatinine (P = .01) and iPTH (P < .04) levels and needed lower pulse steroid doses (P < .04). According to a Friedman repeated measures variance test, the creatinine level was significantly lower among group I (P < .04) at 3-year follow-up. In conclusion, even a delayed start of calcitriol therapy after renal transplantation exerts a protective effect on renal allograft function and prevents the development of hyperparathyroidism.

Effect of gastric bypass surgery on vitamin D nutritional status.

BACKGROUND: We previously reported a 60% prevalence of vitamin D (VitD) depletion, defined as a 25-hydroxyvitamin D (25-OHD) level of < or =20 ng/mL, in morbidly obese patients preoperatively. We now report the effect of gastric bypass (GB) on the VitD nutritional status in these patients. METHODS: We prospectively studied 108 morbidly obese patients who had undergone GB. Routine postoperative supplementation consisted of 800 IU VitD and 1500 mg calcium daily. Serum calcium, parathyroid hormone, and 25-OHD were measured before and 1 year after GB. RESULTS: The mean patient age was 46 +/- 9 years, 93% were women, and 72% were white. Preoperatively and at 1 year postoperatively, the prevalence of VitD depletion and hyperparathyroidism (HPT) and the mean 25-OHD level was 53% and 44%, 47% and 39%, and 20 and 24 ng/mL, respectively. One year after GB, the percentage of excess weight loss was 67% and demonstrated significant correlations both positively with 25-OHD and inversely with parathyroid hormone. At both intervals, blacks had a greater incidence of VitD depletion than did whites, and, at 1 year after GB, HPT was more common in patients with VitD depletion (55% versus 26%, P = .002). CONCLUSION: With customary supplementation, VitD nutrition is improved after GB, but VitD depletion persists in almost one half of patients, and blacks are at a significantly greater risk than whites. HPT did not improve, and those with VitD depletion had a significantly greater rate of HPT. Additional prospective studies are needed to determine how to optimize VitD nutrition and avoid potential long-term skeletal complications after GB.

[What are the major parameters to follow for the management anaemia in dialysis patients? What is the frequency of survey and what are the guidelines?]. / Quels sont les principaux paramètres a surveiller pour optimiser le traitement de l'anémie chez le dialysé? Quelle est la fréquence de surveillance et queues sont les recommandations?

Anaemia treatment in dialysis population is a permanent preoccupation for nephrologists. The erythropoiesis stimulating agents have disrupted its management. The international guidelines define the different parameters to follow and the periodicity of survey. It allows us to harmonize our practice and guaranty an optimization of anaemia treatment in the dialysis population.

25(OH)D Serum levels decline with age earlier in women than in men and less efficiently prevent compensatory hyperparathyroidism in older adults.

BACKGROUND: Although a host of factors are known to influence 25-hydroxyvitamin D [25(OH)D] serum levels, few studies addressed the distinctive sex-specific influence of aging, and the age-specific relationship of parathyroid hormone (PTH) with 25(OH)D. The aims of this research were to evaluate changes of 25(OH)D and PTH levels with age in a large population-based sample of men and women and to test the hypothesis that 25(OH)D serum concentrations needed to offset age-associated hyperparathyroidism are significantly higher in older than in younger persons. METHODS: In 1107 participants of the InCHIANTI (Invecchiare in Chianti, i.e., Aging in the Chianti area) study, we collected information on dietary intake, daylight exposure, and disability, and measured renal function and serum 25(OH)D and PTH. RESULTS: In women, the age-related decline of 25(OH)D was already evident shortly after age 50, whereas in men it started only after age 70 and was substantially less steep. Age, daylight exposure, winter season, and disability were independent predictors of low 25(OH)D levels. For any given level of 25(OH)D, PTH levels were progressively and consistently higher in older than in younger participants. CONCLUSIONS: These findings suggest that the age-associated fall of serum 25(OH)D starts earlier in women than in men and that higher levels of 25(OH)D are required in older compared to younger persons to avoid the age-associated compensatory hyperparathyroidism.

Intrathyroidal parathyroid adenoma.

A 54-year-old woman was referred for imaging studies after presentation for palpitations and a palpable thyroid nodule. The patient underwent a dual-phase single-agent Tc-99m sestamibi scan followed later by a thyroid ultrasound at an outside hospital. The Tc-99m sestamibi scan showed a marked focus of activity separate from the thyroid bed in the inferior left neck. Thyroid ultrasound showed a dominant calcified nodule in the left lobe of the thyroid, measuring 1.3 cm, as well as 3-mm cystic lesions in both lobes of the thyroid. Also, an iodine-123 scan was performed showing a cold nodule in the left inferior thyroid. During surgery, the patient underwent a left thyroid lobectomy for an intrathyroidal parathyroid adenoma.

Bone disease in post-transplant patients.

PURPOSE OF REVIEW: Mineral and bone disorders are common problems in organ transplant recipients. Successful transplantation solves many aspects of abnormal mineral and bone metabolism, but the degree of improvement is frequently incomplete. Posttransplant bone disease can affect long-term outcomes as well as increase the likelihood of fracture. In this article, we reviewed the major posttransplant bone diseases and recent advances in treatment strategies. RECENT FINDINGS: Pretransplant bone disease and immunosuppressants are important risk factors for posttransplant bone disease. Corticosteroid withdrawal may result in minimal or no protection against fractures, with increased risk for acute rejection. Vitamin D analogue and bisphosphonate are frequently used to prevent and treat posttransplant osteoporosis. Posttransplant hyperparathyroidism increases the risk for all-cause mortality and graft loss, but not major cardiovascular events. Cinacalcet was well tolerated and effectively controlled hypercalcemic hyperparathyroidism; however, it did not improve bone mineral density and discontinuation led to parathyroid hormone rebound. Six-month paricalcitol supplementation reduced parathyroid hormone levels and attenuated bone remodeling and mineral loss in case of posttransplant hyperparathyroidism. SUMMARY: Posttransplant bone diseases present in various forms, including osteoporosis, hyperparathyroidism, adynamic bone disease, and osteonecrosis. Prophylactic and therapeutic approaches to both pretransplant and posttransplant periods should be considered.