Renal Secondary Hyperparathyroidism Research Articles

Parathyroid Nodular Hyperplasia and Responsiveness to Drug Therapy in Renal Secondary Hyperparathyroidism: An Open Question.

The goal of the pharmacological therapy in secondary hyperparathyroidism (SHPT) is to reduce serum levels of parathyroid hormone and phosphorus, to correct those of calcium and vitamin D, to arrest or reverse the parathyroid hyperplasia. However, when nodular hyperplasia or an autonomous adenoma develops, surgery may be indicated. We reviewed the literature with the aim of defining if the echographic criteria predictive of unresponsiveness of SHPT to calcitriol therapy are valid also in the cinacalcet era and if drug therapy may reverse nodular hyperplasia of parathyroid gland (PTG). The responsiveness to therapy and regression of the nodular hyperplasia of PTG remains an open question in the calcimimetic era as well as the cutoff between medical and surgical therapy. Prospective studies are needed in order to clarify if an earlier use of cinacalcet in moderate SHPT might arrest the progression of parathyroid growth and stabilize SHPT.

Parathyroidectomy for children with chronic renal failure and secondary hyperparathyroidism; what is the best technique?

Introduction: Reducing serum parathyroid hormone (PTH) level in patients with chronic renal failure can be achieved either by medical treatment or by parathyroidectomy. However, the long-term outcome of parathyroidectomy is better. More than one surgical technique can be done and there is no consensus about the best technique. Objectives: In this study, we present our results in different techniques for parathyroidectomy for these children. Patients and Methods: Six patients of both sexes with chronic renal failure and secondary hyperparathyroidism were collected from pediatric surgery department, Ain Shams University in the period between October 2014 and October 2015. All these patients underwent parathyroidectomy (Subtotal with preservation of half a gland in three patients, Subtotal with preservation of a whole gland in two patients and total with auto-transplantation in one patient). Patients were followed up for serum PTH and calcium levels to detect recurrence of hyperparathyroidism. Results: Serum PTH and calcium levels dropped to normal levels after three months, in 3 of 6 patients (one with preservation of half of a gland, one with preservation of a whole gland and one with total parathyroidectomy and auto-transplantation). Two patients developed hypercalcemia and increased PTH level (one with preservation of half of a gland and the other with preservation of a whole gland). The sixth patient died one month postoperatively (the one with preservation of half of a gland). Conclusion: There is no consensus upon the preferred surgical technique of parathyroidectomy in children with chronic renal failure and secondary hyperparathyroidism.

Spontaneous bilateral femoral neck fracture in a man with end-stage renal disease and severe secondary hyperparathyroidism

Medical treatment is the primary recommended method for in the management of severe secondary hyperparathyroidism (SHPT) in pre-dialysis individuals. This paper reports a case of end-stage renal disease (ESRD) and severe SHPT with pathologic bilateral hip fractures. A 61-year-old man, as a known case of ESRD, with radial osteoporosis and persistent SHPT ( intact PTH >2000 pg/mL) and hypercalcemia with appropriate level of phosphorus and 25(OH) D who did not respond to medical treatment referred to hospital with multiple fractures. The patient referred for subtotal parathyroidectomy. One month after parathyroidectomy, parathyroid hormone (PTH) level significantly diminished from its preoperative values. Serum calcium and phosphorus returned to normal values and muscle weakness progressively improved until the patient became able to walk again. Parathyroidectomy in patients with severe secondary hyperparathyroidism (persistent serum levels of intact PTH>800 pg/mL) is suggested, particularly when is associated with severe hypercalcemia and/or hyperphosphatemia, and progressive and debilitating hyperparathyroidism bone disease, that are refractory and resistant to medical therapy.

Association of Vitamin D Metabolites with Parathyroid Hormone, Fibroblast Growth Factor-23, Calcium, and Phosphorus in Dogs with Various Stages of Chronic Kidney Disease.

BackgroundHypovitaminosis D is associated with progression of renal disease, development of renal secondary hyperparathyroidism (RHPT), chronic kidney disease‐mineral bone disorder (CKD‐MBD), and increased mortality in people with CKD. Despite what is known regarding vitamin D dysregulation in humans with CKD, little is known about vitamin D metabolism in dogs with CKD.ObjectivesThe purpose of our study was to further elucidate vitamin D status in dogs with different stages of CKD and to relate it to factors that affect the development of CKD‐MBD, including parathyroid hormone (PTH), fibroblast growth factor‐23 (FGF‐23), calcium, and phosphorus concentrations.MethodsThirty‐seven dogs with naturally occurring CKD were compared to 10 healthy dogs. Serum 25‐hydroxyvitamin D [25(OH)D], 1,25‐dihydroxyvitamin D [1,25(OH)2D], and 24,25‐dihydroxyvitamin D [24,25(OH)2D], and PTH and FGF‐23 concentrations were measured. Their association with serum calcium and phosphorus concentrations and IRIS stage was determined.ResultsCompared to healthy dogs, all vitamin D metabolite concentrations were significantly lower in dogs with International Renal Interest Society (IRIS) stages 3 and 4 CKD (r [creatinine]: −0.49 to −0.60; P < .05) but not different in dogs with stages 1 and 2 CKD. All vitamin D metabolites were negatively correlated with PTH, FGF‐23, and phosphorus concentrations (r: −0.39 to −0.64; P < .01).Conclusions and Clinical ImportanceCKD in dogs is associated with decreases in all vitamin D metabolites evaluated suggesting that multiple mechanisms, in addition to decreased renal mass, affect their metabolism. This information could have prognostic and therapeutic implications.

Fibrous osteodystrophy with facial hyperostosis associated with renal secondary hyperparathyroidism in dogs

Fibrous osteodystrophy with facial hyperostosis associated with renal secondary hyperparathyroidism in dogs

US-guided Microwave Ablation of Hyperplastic Parathyroid Glands: Safety and Efficacy in Patients with End-Stage Renal Disease—A Pilot Study

Purpose To evaluate the safety and efficacy of microwave ablation (MWA) in patients with end-stage renal disease and secondary hyperparathyroidism. Materials and Methods The study protocol was approved by the human ethics review committee. Between March 1, 2014, and June 30, 2015, 51 patients (25 men, 26 women; mean age ± standard deviation, 53.1 years ± 12.9) were enrolled. All patients had at least one enlarged parathyroid gland and secondary symptomatic hyperparathyroidism, which was treated with ultrasonographically (US) guided MWA. The levels of intact parathyroid hormone, serum calcium, phosphorus, and alkaline phosphatase were compared before and after MWA. Paired-sample t tests and paired-sample Wilcoxon signed-rank tests were used to compare treatment outcomes before and after MWA. Results Complete ablation was achieved in all 96 glands in 51 of 120 patients with severe secondary hyperparathyroidism. The mean follow-up time was 11.1 months ± 3.3. The maximum diameter of the glands ranged from 0.5 cm to 4.8 cm (mean, 1.5 cm ± 0.6). The ablation time for each gland was 216.1 seconds ± 130.1. The mean serum intact parathyroid hormone, calcium, and phosphorus levels after MWA (400 pg/mL [400 ng/L; range, 151.3-629.0 ng/L], 2.33 mmol/L ± 0.23, and 1.54 mmol/L ± 0.43, respectively) were significantly lower than those before MWA (1203 pg/mL [1203 ng/L; range, 854.7-1694.5 ng/L], 2.53 mmol/L ± 0.24, and 1.97 mmol/L ± 0.50, respectively; P < .01), while the alkaline phosphatase levels did not change with MWA (P > .05). Ipsilateral recurrent laryngeal nerve injury was seen in one patient (2%). A hematoma developed during one procedure in one patient (2%) and was treated successfully with injection of thrombin. Conclusion US-guided MWA is safe and effective for destroying parathyroid gland tissue in patients with end-stage renal disease and severe secondary hyperparathyroidism. Further experience with the technique is clearly necessary. © RSNA, 2016.

Subtotal parathyroidectomy for secondary renal hyperparathyroidism: a 20-year surgical outcome study.

AimThe aim of this study was to evaluate the outcomes of surgery for patients with secondary renal hyperparathyroidism (rHPT).MethodsThis is a retrospective cohort study. Our institutional database was searched for eligible patients treated in 1995–2014. The inclusion criterion was initial parathyroidectomy for rHPT. Clinical and follow-up data were analyzed to estimate the cure rate (primary outcome), and morbidity (secondary outcome).ResultsThe study group comprised 297 patients (154 females, age 44.5 ± 13.7 years, follow-up 24.6 ± 10.5 months), including 268 (90.2 %) patients who had underwent subtotal parathyroidectomy, and 29 (9.8 %) who had had incomplete parathyroidectomy. Intraoperative iPTH assay was utilized in 207 (69.7 %) explorations. Persistent rHPT occurred in 12/268 (4.5 %) patients after subtotal parathyroidectomy and 5/29 (17.2 %) subjects after incomplete parathyroidectomy (p = 0.005). The patients operated on with intraoperative iPTH assay had a higher cure rate than non-monitored individuals, 201/207 (97.1 %) vs. 79/90 (87.8 %), respectively (p = 0.001). In-hospital mortality occurred in 1/297 (0.3 %) patient. The hungry bone syndrome occurred in 84/268 (31.3 %) patients after subtotal parathyroidectomy and 2/29 (6.9 %) subjects after incomplete parathyroidectomy (p = 0.006). Transient recurrent laryngeal nerve paresis occurred in 14/594 (2.4 %) and permanent in 5/594 (0.8 %) nerves at risk.ConclusionsSubtotal parathyroidectomy is a safe and efficacious treatment for patients with rHPT. Utilization of intraoperative iPTH assay can guide surgical exploration and improve the cure rate.

Vitamin D in patients with chronic kidney disease: a position statement of the Working Group "Trace Elements and Mineral Metabolism" of the Italian Society of Nephrology.

In the late 1970s, calcitriol was introduced into clinical practice for the management of secondary renal hyperparathyroidism in chronic kidney disease (CKD). Since then, the use of calcifediol or other native forms of vitamin D was largely ignored until the publication of the 2009 Kidney Disease Improving Global Outcomes (KDIGO) recommendations. The guidelines suggested that measurement of circulating levels of 25(OH)D (calcifediol) and its supplementation were to be performed on the same basis as for the general population. This indication was based on the fact that the precursors of active vitamin D had provided to CKD patients considerable benefits in survival, mainly due to their pleiotropic effects on the cardiovascular system. However, despite the long-term use of various classes of vitamin D in CKD, a clear definition is still lacking concerning the most appropriate time for initiation of therapy, the best compound to prescribe (active metabolites or analogs), the proper dosage, and the most suitable duration of therapy. The aim of this position statement is to provide and critically appraise the current plentiful evidence on vitamin D in different clinical settings related to CKD, particularly focusing on outcomes, monitoring and treatment-associated risks. However, it should be taken in account that position statements are meant to provide guidance; therefore, they are not to be considered prescriptive for all patients and, importantly, they cannot replace the judgment of clinicians.

Intra-operative parathyroid hormone monitoring through central laboratory is accurate in renal secondary hyperparathyroidism

ObjectiveThe usefulness, the methods and the criteria of intra-operative monitoring of the parathyroid hormone (ioPTH) during parathyroidectomy (PTX) for renal secondary hyperparathyroidism (rSHPT) in patients on chronic hemodialysis remain still matter of debate. The present study aimed to evaluate the ability of a low cost central-laboratory second generation PTH assay to predict an incomplete resection of parathyroid glands (PTG). MethodsThe ioPTH decay was determined In 42 consecutive patients undergoing PTX (15 subtotal and 27 total without auto-transplant of PTG) for rSHPT. The ioPTH monitoring included five samples: pre-intubation, post-manipulation of PTG and at 10, 20 and 30min post-PTG excision. The patients with PTH exceeding the normal value (65pg/ml) at the first postoperative week, 6 and 12months were classified as persistent rSHPT. ResultsThe concentrations of ioPTH declined significantly over time in patients who received total or subtotal PTX; however, no difference was found between the two types of PTX. Irrespective of the type of PTX and the number of PTG removed, combining the absolute and percentage of ioPTH decay at 30min after PTG excision, we found high sensitivity (100%), specificity (92%), negative predictive value (100%) and accuracy (93%) in predicting the persistence of rSHPT. ConclusionsThe monitoring of the ioPTH decline by a low cost central-laboratory second generation assay is extremely accurate in predicting the persistence of disease in patients on maintenance hemodialysis undergoing surgery for rSHPT.

Autotransplantation of parathyroid grafts into the tibialis anterior muscle after parathyroidectomy: a novel autotransplantation site.

BackgroundSurgical management of renal secondary hyperparathyroidism (sHPT) is varying. Total parathyroidectomy with heterotopic autotransplantation (TPTX + AT) is one of the standard surgical procedures in sHPT, but there is no consensus about the optimal site for graft insertion. At the surgical department of the University Hospital of Heidelberg we prefer the autotransplantation into the tibialis anterior muscle. The aim of this study was to assess the long-term function of the auto-transplanted parathyroid tissue in this type of surgical procedure.MethodsThe function of the autograft of 42 patients was assessed 8.2 ± 2.5 years after surgery, using a modified Casanova-test of the leg bearing the parathyroid tissue. Ischemic blockage was induced by tourniquet and the levels of parathyroid hormone (PTH) were assessed during the test.ResultsAt the point of assessment, the ischemic blockage led to a significant reduction in the concentration of PTH (≥50 % of the baseline value) in 19 patients (45 %) indicating well-functioning autografts. In 11 patients (26 %), ischemic blockage did not cause any change in the concentration of PTH (≤20 % of the baseline value), indicating functioning residual parathyroid tissue from another site. The source of PTH production was classified as unidentifiable in five patients (12 %). Two patients had developed graft-dependent recurrent HPT (5 %) without therapeutic consequences and three patients suffered from persistent symptomatic hypoparathyroidism (7 %).ConclusionsThese results indicate that TPTX + AT into the tibialis anterior muscle is a successful surgical treatment for renal HPT and that the modified Casanova-test is a suitable diagnostic tool for autografts function.

Oral Manifestations of Chronic Kidney Disease and Renal Secondary Hyperparathyroidism: A Comparative Review.

Recent epidemiological studies have demonstrated that significant associations exist between oral disease and diseases involving non-oral tissues. Occasionally, the roles may be reversed and the oral cavity can be severely affected by systemic disease originating in another part of the body. Renal secondary hyperparathyroidism is a common endocrinopathy that occurs as a consequence of chronic azotemic kidney disease. Renal osteodystrophy, the most dramatic clinical consequence of renal secondary hyperparathyroidism is uncommon, but can result in demineralization of maxillofacial bones, loosening of teeth, and pathological jaw fractures. The purpose of this report is to update the current understanding of the pathophysiology of this endocrine disease and to compare the oral manifestations of renal secondary hyperparathyroidism in humans and companion animals. A 50-year review of the veterinary literature was undertaken to examine the clinical presentation of renal osteodystrophy in dogs, and to determine what clinical consequences of renal secondary hyperparathyroidism have been reported in domestic cats.

Chronic kidney disease induced by adenine: a suitable model of growth retardation in uremia.

Growth retardation is a major manifestation of chronic kidney disease (CKD) in pediatric patients. The involvement of the various pathogenic factors is difficult to evaluate in clinical studies. Here, we present an experimental model of adenine-induced CKD for the study of growth failure. Three groups (n = 10) of weaning female rats were studied: normal diet (control), 0.5% adenine diet (AD), and normal diet pair fed with AD (PF). After 21 days, serum urea nitrogen, creatinine, parathyroid hormone (PTH), weight and length gains, femur osseous front advance as an index of longitudinal growth rate, growth plate histomorphometry, chondrocyte proliferative activity, bone structure, aorta calcifications, and kidney histology were analyzed. Results are means ± SE. AD rats developed renal failure (serum urea nitrogen: 70 ± 6 mg/dl and creatinine: 0.6 ± 0.1 mg/dl) and secondary hyperparathyroidism (PTH: 480 ± 31 pg/ml). Growth retardation of AD rats was demonstrated by lower weight (AD rats: 63.3 ± 4.8 g, control rats: 112.6 ± 4.7 g, and PF rats: 60.0 ± 3.8 g) and length (AD rats: 7.2 ± 0.2 cm, control rats: 11.1 ± 0.3 cm, and PF rats: 8.1 ± 0.3 cm) gains as well as lower osseous front advances (AD rats: 141 ± 13 μm/day, control rats: 293 ± 16 μm/day, and PF rats: 251 ± 10 μm/day). The processes of chondrocyte maturation and proliferation were impaired in AD rats, as shown by lower growth plate terminal chondrocyte height (21.7 ± 2.3 vs. 26.2 ± 1.9 and 23.9 ± 1.3 μm in control and PF rats) and proliferative activity index (AD rats: 30 ± 2%, control rats: 38 ± 2%, and PF rats: 42 ± 3%). The bone primary spongiosa structure of AD rats was markedly disorganized. In conclusion, adenine-induced CKD in young rats is associated with growth retardation and disturbed endochondral ossification. This animal protocol may be a useful new experimental model to study growth in CKD.

Staging studies for evaluation of squamous cell carcinoma. Staging of left temporal squamous cell carcinoma with PET-CT.

Primary hyperoxaluria is a rare congenital disorder of abnormal glyoxylate metabolism with resultant over-accumulation of oxalate, which then binds with calcium and precipitates in the kidneys, resulting in nephrocalcinosis and nephrourolithiasis. As renal function worsens, patients develop systemic oxalosis with calcium oxalate deposition in the soft tissues, musculoskeletal system, cardiovascular system, central nervous system, and eyes [1–5]. There are three common types of primary hyperoxaluria (types I–III). Type I is the most common and severe and involves a mutation in the alanine glyoxylate aminotransferase (AGT) enzyme causing overproduction of oxalate glyoxylate [1]. Type II results from deficiency of glyoxylate reductase and hydroxypyruvate reductase (GRHPR), which results in overproduction of oxalate and L-glyceric aciduria [1, 5]. Type III results from mutation in 4-hydroxy-2oxoglutarate aldolase (HOGA) and is the least aggressive hyperoxaluria type, with most patients not progressing to end-stage renal disease (ESRD) [1]. Imaging findings in primary hyperoxaluria vary depending on patient age and renal function [2–6]. Prior to renal function impairment, imaging is frequently normal. As renal failure develops, cortical nephrocalcinosis and nephrourolithiasis will be seen (Fig. 1). Calcium oxalate subsequently deposits in soft tissues, tendons, and joint capsules, with joint effusions and nodular-appearing tumoral calcinosis (especially in periarticular regions, which can cause erosive arthropathy) [2–6]. As ESRD develops toward the late stage of the disease, musculoskeletal imaging manifestations typically associated with renal osteodystrophy and secondary hyperparathyroidism will develop, such as osteosclerosis, subperiosteal resorption, Brugger-jersey^ spine, and vascular/soft tissue calcifications (also seen in Fig. 1). Abnormal skeletal maturation and pathologic fractures with delayed healing can also be seen but are similarly nonspecific. Oxalate deposition in the subcutaneous and dermal tissues can cause skin necrosis/ulceration, and oxalate deposition in the myocardium, pericardium, ocular and vascular regions has also been described [4–9]. Skeletal findings more specific to primary hyperoxaluria may include irregular diametaphyseal transverse sclerotic bands and wide metaphyseal zones [5]. Lytic lesions can be seen in primary hyperoxaluria, which histopathologically represent foci of calcium oxalate deposition with a granulomatous foreign body histiocytic reaction, which appear essentially identical to brown tumors on The case presentation can be found at doi: 10.1007/s00256-015-2161-1.

Feline hyperparathyroidism: pathophysiology, diagnosis and treatment of primary and secondary disease.

Hyperparathyroidism exists in primary and secondary forms. Primary hyperparathyroidism has typically been considered a disease that uncommonly affects cats, but this condition is more prevalent than previous diagnoses would suggest. Secondary hyperparathyroidism may be caused by either nutritional influences (ie, nutritional secondary hyperparathyroidism) or chronic kidney disease (ie, renal secondary hyperparathyroidism). Tertiary hyperparathyroidism has yet to be documented in veterinary medicine, but it is possible that this condition occurs in some cats following longstanding renal secondary hyperparathyroidism. Diagnosis of this group of calcium metabolic disorders presents a number of challenges for the clinician. For example, clinical signs can be non-specific and, especially in the case of primary hyperparathyroidism, there is often a low index of suspicion for the disease; careful sample handling is required for testing of parathyroid hormone (PTH) and ionized calcium levels; and there is currently no feline-specific assay for PTH, which has implications for test sensitivity and interpretation of results. This article briefly outlines PTH and calcium physiology by way of introduction to a review of PTH measurement and interpretation. Various forms of feline hyperparathyroidism are then described, encompassing diagnosis and treatment options.

Two Years of Cinacalcet Hydrochloride Treatment Decreased Parathyroid Gland Volume and Serum Parathyroid Hormone Level in Hemodialysis Patients With Advanced Secondary Hyperparathyroidism

The long-term effect of cinacalcet hydrochloride treatment on parathyroid gland (PTG) volume has been scarcely investigated in patients with moderate to advanced secondary hyperparathyroidism (SHPT). The present study was a prospective observational study to determine the effect of cinacalcet treatment on PTG volume and serum biochemical parameters in 60 patients with renal SHPT, already treated with intravenous vitamin D receptor activator (VDRA). Measurement of biochemical parameters and PTG volumes were performed periodically, which were analyzed by stratification into tertiles across the baseline parathyroid hormone (PTH) level or PTG volume. We also determined the factors that can estimate the changes in PTG volume and the achievement of the target PTH range by multivariable analyses. Two years of cinacalcet treatment significantly decreased the serum levels of PTH, calcium, and phosphate, followed by the improvement of achieving the target ranges for these parameters recommended by the Japanese Society for Dialysis Therapy. Cinacalcet decreased the maximal and total PTG volume by about 30%, and also decreased the serum PTH level independent of the baseline serum PTH level and PTG volume. Ten out of 60 patients showed 30% increase in maximal PTG after 2 years. Multivariable analysis showed that patients with nodular PTG at baseline and patients with higher serum calcium and PTH levels at 1 year were likely to exceed the target range of PTH at two years. In conclusion, cinacalcet treatment with intravenous VDRA therapy decreased both PTG volume and serum intact PTH level, irrespective of the pretreatment PTG status and past treatment history.

A correlation between decreased parathyroid α-Klotho and fibroblast growth factor receptor 1 expression with pathological category and parathyroid gland volume in dialysis patients.

The objective of this study was to investigate α-Klotho and fibroblast growth factor receptor 1 (FGFR1) expression in hyperplastic parathyroid glands, as well as their role in the development of renal hyperparathyroidism. Hyperplastic parathyroid glands (n = 90) were obtained from 24 patients who received parathyroidectomy due to secondary renal hyperparathyroidism. Normal parathyroid tissue was obtained from glands (n = 6) that were inadvertently removed, in conjunction with thyroidectomy, from patients with thyroid carcinoma. The expression of α-Klotho and FGFR1 in the parathyroid tissue was detected using immunohistochemical staining. The expression of α-Klotho and FGFR1 was significantly reduced in the hyperplastic parathyroid tissue compared to that in the normal parathyroid tissue. The expression of α-Klotho decreased further with increasing parathyroid pathology. A significant positive correlation was observed between α-Klotho and FGFR1 (r = 0.38, P < 0.01). FGFR1 (r = -0.21, P < 0.05) and α-Klotho (r = -0.42, P < 0.01) were negatively correlated with the volume of the hyperplastic parathyroid tissue. The expression of α-Klotho and FGFR1 decreases in the parathyroid glands of dialysis patients with secondary hyperparathyroidism, and this decrease may play an important role in the pathogenesis of secondary renal hyperparathyroidism.

"Hungry Bone" Syndrome after Parathyroidectomy: Up-To-Date

The hungry bone syndrome is considered in literature as being a complication following parathyroidectomy and it refers to the rapidly installed, severe, prolonged, and in most cases clinically manifested hypocalcaemia, which is sometimes accompanied by hypophosphatemia and hypomagnesemia. It appears due to the rapid demineralization of the dystrophic bone as a result of the sudden drop in the seric level of the parathyroid hormone. The prevalence of this complication is reported in literature with different variations, the number reported ranging from 4-95% depending on the type of affection - i.e. primary hyperparathyroidism or renal secondary hyperparathyroidism, but also on the geographical areas where the respective reports have been filled. The high preoperatory level of calcaemia, seric parathyroid hormone and alkalyne phophatase correlate statistically with the risk of postoperatory hungry bone syndrome appearance; the elderly patients present a higher risk for this complication, increasingly because this category of patients is oftenly associated with D hypovitaminosis and insufficient intake of nutritional calcium. The syndrome semiology is one of a hypocalcaemia and the curative treatment is initially a symptomatic one of fighting the severe postparathyroidectomy hypocalcaemia and only later a patogenic one, aiming to remineralize the distrofic bone. The purpose of this review is to describe the main epidemiologic, physiopathologic and clinical aspects of hungry bone syndrome but also of presenting prevention and treatment methods for this complication of parathyroidectomy.

Simultaneous Bilateral Rupture of the Triceps Tendon in a Renal Transplant Patient.

The unilateral rupture of the triceps brachii tendon is a rare lesion representing 1% of all tendon injuries. The most common causes are the result of a contraction against resistance (especially weightlifters) and direct trauma. It has also been associated with systemic diseases such as diabetes mellitus, chronic renal failure, secondary hyperparathyroidism, and use of systemic corticosteroids. Simultaneous bilateral rupture of the triceps tendons is less frequent and has been described in association with chronic metabolic disorders, especially in those patients on hemodialysis. This paper presents a case of bilateral triceps tendon rupture of a 36-year-old woman with renal transplantation secondary to chronic renal failure. Early surgical repair was performed using a bone tunnel technique with a nonabsorbable suture. Clinically active extension with 135 degrees of range of motion was achieved.

Leontiasis Ossea Following Secondary Hyperparathyroidism and Hemodialysis

Leontiasis ossea is a rare medical condition which is characterized by an overgrowth of the facial and cranial bones secondary to chronic renal failure and secondary hyperparathyroidism. We reported a case of leontiasis ossea with history of secondary hyperparathyroidism due to end-stage renal disease on regular hemodialysis. A 37-year-old female with end-stage renal disease from lupus disease on regular hemodialysis complaining of progressive facial deformity for two years causing dyspnea, dental malocclusion and dysarthria with the final diagnosis of uremic leontiasis ossea. It is important to recognize features of leontiasis ossea, as it may result in life-threatening upper airway obstruction and compressive cranial neuropathy while after parathyroidectomy, facial changes can be stabilized or improved mildly.

Chronological Progress of Calcified Lesion in the Iliofemoral Vein in a Patient with Chronic Renal Failure

We report the case of a 64-year-old man refered to our department for edema and tiredness in legs, who had been followed up for chronic renal failure and secondary hyperparathyroidism. He had no history of medical treatment for deep venous thrombosis, however, computed tomography (CT) revealed extensive calcification in veins of the lower half of the body. Since peripheral venous calcification is a rare disease and advances slowly, imaging the chronological progress of calcification is difficult. This case suggests the usefulness of CT for diagnosing and treating peripheral venous calcification.