Renal Secondary Hyperparathyroidism Research Articles

Case Report on Brown Tumor: An Unusual Expression of Renal Osteodystrophy and Secondary Hyperparathyroidism

The new term of ‘Chronic Kidney Disease- Mineral and Bone Disorders’ has been introduced to encompass a wide-ranging syndrome, capturing various abnormalities in bone and mineral metabolism seen in patients with chronic kidney disease. Multifactorial disorders affecting mineral metabolism and bone structure emerge early in the progression of Chronic Kidney Disease. Brown tumors, an uncommon type of bone lesion are distinctive manifestations of high-turnover bone disease. In this case, a patient with chronic kidney disease (dialysis dependent) with IgA nephropathy that presented with multiple osseous lesions of bilateral ribs, sternum, scapula, clavicle, mandible and vertebral bodies. The case highlights the significance of considering brown tumors in the differential diagnosis and management of patients with both an osseous mass and chronic kidney disease. Failing to establish an accurate diagnosis may result in unnecessary additional diagnostic procedures and extensive surgery, ultimately increasing patient morbidity. Through this case report, the importance of preventing, early diagnosing, and treating secondary hyperparathyroidism to reduce the prevalence of high-turnover bone disease and associated complications such as brown tumors is emphasized.

Predictive analysis of severe hypocalcemia following total parathyroidectomy for renal secondary hyperparathyroidism.

This study aimed to evaluate the incidence and identify risk factors for severe hypocalcemia following total parathyroidectomy (TPTX) in patients with renal secondary hyperparathyroidism (SHPT). We included patients undergoing maintenance hemodialysis or peritoneal dialysis who underwent TPTX from January 1, 2018, to April 30, 2023. Participants were categorized into groups based on postoperative corrected serum calcium levels: severe hypocalcemia (<1.8 mmol/L) and non-severe hypocalcemia (≥1.8 mmol/L). We conducted univariate analyses of demographic and laboratory data to identify potential risk factors, which were further analyzed using a binary logistic regression model. Significant associations were observed with age, dialysis duration exceeding five years, type of dialysis (peritoneal dialysis), lower preoperative corrected serum calcium, elevated preoperative intact parathyroid hormone (iPTH), and increased preoperative alkaline phosphatase (ALP) levels (all p<0.05). Age, preoperative iPTH, and ALP levels were identified as independent risk factors for severe hypocalcemia post-TPTX. Younger patients with renal SHPT who have elevated preoperative iPTH and ALP levels are at an increased risk of experiencing severe hypocalcemia following TPTX. These findings underscore the importance of careful preoperative assessment and monitoring to mitigate the risk of this complication.

Juvenile primary acquired hypothyroidism in a dog with suspected renal dysplasia

AbstractA 1‐year 3‐month‐old, female, neutered crossbreed dog presented for investigation of polyuria, polydipsia and azotaemia. Subsequent biochemistry, endocrine testing and abdominal ultrasound identified hypercholesterolaemia, thyroglobulin autoantibody‐positive hypothyroidism, and IRIS stage II non‐hypertensive, non‐proteinuric suspected renal dysplasia, with a concurrent Escherichia coli urinary tract infection. The patient responded well clinically to levothyroxine treatment, with improvement in hypercholesterolaemia, azotaemia and demeanour at home. At follow‐up biochemistry assessment, hyperphosphataemia and hypercalcaemia (total and ionised) were documented, presumed to be driven by renal insufficiency and renal secondary hyperparathyroidism, although this aetiology was not definitively proven. Normalisation of these values was noted following renal diet implementation and addition of phosphate binders. This case highlights acquired primary hypothyroidism with evidence of thyroiditis in a juvenile dog with suspected congenital renal dysplasia.

Impact of Successful Secondary Hyperparathyroidism Treatment on Cardiovascular Morbidity in Patients with Chronic Kidney Disease Stage IIIB-V

Abstract Background Chronic kidney disease (CKD) patients grade III B(GFR 30-44ml/min), IV (GFR 15-29ml/min) and grade V (GFR &amp;lt;15ml/min) are patients with a severe chronic Kidney disease that are shortly before or in need of dialysis. 61.7% of patients on hemodialysis have been found to have secondary hyperparathyroidism. It has been associated with high cardiovascular morbidity by calcification of tissue leading to lung fibrosis and right heart insufficiency. Aims To assess the effect of treatment success of secondary renal hyperparathyroidism (SHPT) on cardiovascular morbidity. Methods Retrospective single-center analysis. 211 patients chronic kidney disease (CKD) stages IIIB-V undergoing computed tomography for coronary artery calcium (CAC) scoring at the University Hospital of Zurich between 2015 and 2019. Presence of and control of SHPT was assessed at the timepoint of CAC scoring, and 6-12 months prior. Information on left ventricular ejection fraction (LVEF), and left ventricular hypertrophy (LVH) were obtained from echocardiography at the timepoint of CAC scoring. Independent predictive factors for ACS and LVH were assessed by multivariable analysis. Results 34% (n=72) of the patients had uncontrolled SHPT, whereas 66% (n=139) had either no-(n=98) or a controlled SHPT(n=41). Patients with uncontrolled SHPT had a significantly lower LVEF (p=0.028), significantly more pronounced LVH (p=0.003), a higher left ventricular myocardial mass index (LVMMI) (p=0.002) than the group with no SHPT or well controlled SHPT. Uncontrolled SHPT had a significant higher risk for developing ACS (p=0.011) compared to no-or controlled SHPT patients (41.7% vs 31.7%). Conclusions Insufficient control of SHPT has a negative impact on cardiovascular morbidity with lower LVEF, increased LVH and a higher incidence of ACS. Increased focus on SHPT control in CKD patients is important and may have a beneficial impact on cardiovascular outcomes. If all conservative measures do not lead to a sufficient alignement of the secondary hyperparathyroidism parathyroidectomy may be indicated.

18F-fluorocholine PET/CT detects parathyroid gland hyperplasia as well as adenoma: 401 PET/CTs in one center.

During the past decade, 18F-fluorocholine (FCH) PET/CT has been continuously performed at Tenon Hospital (Paris, France) for the detection of hyperfunctioning parathyroid glands (PT). A cohort of 401 patients, deliberately referred for HPT since September 2012, has been analyzed. The aim of this real-life retrospective study was to determine the diagnostic utility of FCH in this setting, overall and in subgroups according to the type of hyperparathyroidism (HPT), the context of FCH in the imaging work-up and in the patient's history: initial imaging or persistence or recurrence after previous parathyroidectomy (PTX). The influence of the histologic type of resected PTs, hyperplasia or adenoma, on the preoperatory detection on FCH PET/CT has been studied as well. Four hundred one FCH PET/CTs were included in the cohort, performed in 323 patients with primary HPT (pHPT), including 18 with familial HPT (fHPT), and in 78 patients with secondary renal HPT (rHPT). The overall positivity rate in the 401 FCH PET/CTs was 73%. The PTX rate was twice greater in patients whose FCH PET/CT was positive than negative (73% vs. 35%). Abnormal PT(s) were pathology proven in 214 patients: only hyperplastic gland(s) in 75 cases and at least one adenoma in 136 cases; FCH PET/CT sensitivity was 89% and 92%, respectively. Similarly, there was no significant difference in patient-based sensitivity whether FCH PET/CT was performed as 1st line or later in the imaging work-up, or indicated for initial imaging or for suspicion of persistent or recurrent HPT. Gland-based sensitivity was significantly lower for hyperplasia than for adenoma (72% and 86%, respectively). The lowest gland-based sensitivity value was 65%, observed in case of hyperplasia and when FCH was performed late in the imaging work-up. FCH PET/CT correctly showed multiglandular HPT (MGD) in 36/61 proven cases, 59%. Results of ultrasonography (US) and 99mTc-sestaMIBI (MIBI) imaging were available in 346 and 178 patients, respectively. For both modalities, the corresponding sensitivity values were significantly less than those of FCH PET/CT (e.g., overall gland-based sensitivity 78% for FCH, 45% for US, 30% for MIBI) and MGD was detected in 32% of cases by US and 15% by MIBI. Although FCH PET/CT has been performed since 2017 as 1st line imaging for HPT at Tenon Hospital (Paris, France), a large majority of patients underwent prior US and/or MIBI in their preoperative work-up. Therefore, a selection bias is very likely, as most patients referred to FCH PET/CT had non-conclusive or discordant results of US and MIBI, explaining the low performance of those modalities in the present cohort compared to published results. Nevertheless, the superiority of FCH PET/CT over US and MIBI in detecting abnormal PTs reported in various comparative studies is definitely confirmed in this larger real-life cohort. The detection with FCH PET/CT of hyperplastic PTs was somewhat lower than that of adenomas but was better than using US or MIBI. The present results lead to recommend FCH PET/CT as the first line imaging modality in HPT when it is widely available or, if less available, at least in HPT with predominance of hyperplasia and/or MGD.

Residual risks of comorbidities after parathyroidectomy in a nationwide cohort of patients with primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT) is a common endocrine disorder with increasing incidence, while epidemiologic data in Asian population has been lacking. Therefore, we aimed to identify the incidence, prognosis, and prognostic factors of PHPT patients who underwent parathyroidectomy in Korea. In this retrospective nationwide cohort, patients with PHPT were defined as those with diagnostic codes of PHPT and procedural codes for parathyroidectomy, excluding chronic renal failure or secondary hyperparathyroidism based on National Health Insurance Services database in Korea in 2002-2018. Main primary outcomes were all-cause mortality, cardiovascular, and cerebrovascular events. A total of 5561 patients were diagnosed with PHPT and had parathyroidectomy. The mean age was 54.5 years, and 71.8% were women. The age-standardized incidence was 10.1/100,000 person-year in 2018, rising from 1.7/100,000 person-year in 2002. During a mean of 5.9 years, history of cardiovascular disease, mood disorder, and genitourinary stone had increased risks of mortality with hazard ratios (HRs) of 1.59 (95% confidence interval [CI] 1.10-2.29), 1.43 (CI 1.14-1.80), and 1.40 (CI 1.09-1.80), respectively. History of hypertension, cerebrovascular disease, diabetes mellitus, and mood disorder were risk factors for cardiovascular events with HRs of 1.42 (CI 1.22-1.66), 1.29 (CI 1.05-1.58), 1.22 (CI 1.07-1.40), and 1.14 (CI 1.00-1.29), respectively. Mood disorder was a significant risk factor for cerebrovascular events (HR 1.30, CI 1.11-1.52). The incidence of PHPT patients who underwent parathyroidectomy has been rising in Korea as reported in other countries. Patients with complications, especially mood disorder, had increased cardiovascular and cerebrovascular events and mortality risks.

Immune disorders in dogs with chronic kidney disease: Review

The aim of this literature review was to identify the stages of chronic kidney disease in dogs that have greater immune dysfunction and which cellular components of the innate and humoral immune system are most affected by the retention of uremic toxins. Chronic kidney disease is characterized by being a serious and irreversible disease, but common in the practice of medical clinic for dogs and cats and usually affects those of advanced age. The consequences of chronic kidney disease can expand to other systems as the disease progresses; systemic arterial hypertension, hypertensive retinopathies and secondary renal hyperparathyroidism are examples of extra-renal impairment caused by chronic kidney disease. The Interest Renal Society (IRIS), established degrees of progression of renal impairment according to serum concentrations of symmetrical creatinine and dimethylarginine, biomarkers of kidney injury, which allows aid in diagnosis, classification of the degree of nephrological and systemic impairment and treatment affected patient. Studies in human patients demonstrate that, in the terminal stages of kidney disease, there is an impairment of the immune function of these patients, which contributes to the increase in the rate of deaths related to secondary infections, cancers caused by viruses and low responsiveness to vaccines. In Veterinary Medicine, despite the scarcity of research on immunosuppression in dogs with chronic kidney disease, some have observed, in vitro and in vivo environments, dysfunction in the innate and humoral immune system of dogs with advanced chronic kidney disease, due to the proinflammatory environment resulting from the retention of uremic toxins that had their clearance affected by impaired kidney excretory function. Stage III of chronic kidney disease in dogs requires greater care, not only to prevent the disease from progressing to stage IV, but also to prevent immune disorders that may result in death. The adoption of intervention criteria and measures aimed at preventing and / or minimizing these immunological disorders depends on the expansion of research on this topic to establish better clinical management for dogs with nephrological disorder.

Renal secondary hyperparathyroidism should be considered a differential diagnosis in forensic cases where animal abuse is suspected

This case description reports an adult dog with multiple rib fractures that was initially suspected to be the victim of non-accidental trauma, but eventually was diagnosed with severe chronic interstitial nephritis and renal secondary hyperparathyroidism leading to fibrous osteodystrophy and multiple pathological fractures. The importance of the specific expertise of a dedicated expert panel on animal abuse is discussed. This case illustrates the significance of the identification of normal, pathological, and breed-related variations within an animal in addition to forensic expertise, emphasizing that the presence of multidisciplinary teams in an expert panel on animal abuse is crucial.

The American Association of Endocrine Surgeons Guidelines for the Definitive Surgical Management of Secondary and Tertiary Renal Hyperparathyroidism.

To develop evidence-based recommendations for safe, effective, and appropriate treatment of secondary (SHPT) and tertiary (THPT) renal hyperparathyroidism. Hyperparathyroidism is common among patients with chronic kidney disease, end-stage kidney disease, and kidney transplant. The surgical management of SHPT and THPT is nuanced and requires a multidisciplinary approach. There are currently no clinical practice guidelines that address the surgical treatment of SHPT and THPT. Medical literature was reviewed from January 1, 1985 to present January 1, 2021 by a panel of 10 experts in SHPT and THPT. Recommendations using the best available evidence was constructed. The American College of Physicians grading system was used to determine levels of evidence. Recommendations were discussed to consensus. The American Association of Endocrine Surgeons membership reviewed and commented on preliminary drafts of the content. These clinical guidelines present the epidemiology and pathophysiology of SHPT and THPT and provide recommendations for work-up and management of SHPT and THPT for all involved clinicians. It outlines the preoperative, intraoperative, and postoperative management of SHPT and THPT, as well as related definitions, operative techniques, morbidity, and outcomes. Specific topics include Pathogenesis and Epidemiology, Initial Evaluation, Imaging, Preoperative and Perioperative Care, Surgical Planning and Parathyroidectomy, Adjuncts and Approaches, Outcomes, and Reoperation. Evidence-based guidelines were created to assist clinicians in the optimal management of secondary and tertiary renal hyperparathyroidism.

Exuberant Scleral Calcification from Secondary Hyperparathyroidism

A 38-year-old man with chronic end-stage renal disease and secondary hyperparathyroidism presented with bilateral ocular inflammation. Visual acuity was 20/40 in the right eye and 20/60 in the left eye with normal intraocular pressure and full extraocular motility in both eyes. Examination was notable for keratoconjunctivitis and proptosis in both eyes. Testing revealed normal thyroid function and stimulating immunoglobulin levels, but elevated phosphate (12.4 mg/ml). Computed tomography was unremarkable for orbital inflammation yet demonstrated diffuse scleral calcification (Fig A-B) confirmed on ultrasonography (Fig C).

POS-198 CLINICAL EFFECT OF PARATHYROIDECTOMY AND AUTOLOGOUS HOMOGENATE TRANSPLANTATION IN THE TREATMENT OF SECONDARY HYPERPARATHYROIDISM

To explore the clinical effect of total parathyroidectomy combined with forearm autologous homogenate transplantation in the treatment of renal secondary hyperparathyroidism. Patients with CKD-MBD and secondary hyperparathyroidism were randomly divided into two groups. The granule embedding group was treated with total parathyroidectomy and autologous forearm granule embedding transplantation, and the homogenate injection group was treated with total parathyroidectomy and autologous forearm homogenate transplantation. The levels of serum calcium, phosphorus, iPTH and bone metabolism were compared between the two groups before and after treatment. The occurrence and improvement of vascular calcification, soft tissue calcification, skin pruritus, bone pain, pathological fracture, myasthenia, cardiovascular events and withdrawal after operation intervention. Analysis and comparison of postoperative recurrence between the two groups. The changes of blood calcium, phosphorus, iPTH, AKP and other indicators in the two groups before and after operation were compared. The improvement and changes of the above indicators in the homogenate injection group were significantly better than those in the granule embedding group, and the difference was statistically significant (P < 0.05). The incidence and improvement of complications such as vascular calcification, soft tissue calcification, skin pruritus, bone pain, pathological fracture, myasthenia, cardiovascular events and withdrawal in the homogenate injection group were better than those in the granule embedding group (P < 0.05). The recurrence rate in the homogenate injection group was significantly lower than that in the granule embedding group (P < 0.05). Total parathyroidectomy combined with autologous forearm homogenate injection transplantation can effectively treat CKD complicated with refractory secondary hyperparathyroidism, and has the advantages of high success rate, small trauma and simple operation, which can be widely used in clinic.

O15 Tumour-induced osteomalacia: a diagnostic challenge

Case report - IntroductionTumor-induced osteomalacia is a rare acquired metabolic bone disorder characterised by isolated renal phosphate wasting due to abnormal tumour production of fibroblast growth factor 23 (FGF23). Bloods show hypophosphatemia. However, given the lack of awareness of this disease, and the non-specific nature of the presenting symptoms, diagnosis is often delayed for years or even missed.With this case report, we want to shed light on this rare bone disorder and highlight the importance of not ignoring a low phosphate level.Case report - Case descriptionWe report the case of a 63-year-old gentleman who presented to us with a history of progressive bone pain, marked muscle weakness and fatigue. He had a persistently raised parathyroid hormone and very high alkaline phosphatase. Calcium was low normal, but vitamin D was normal. Phosphate was noted to be low and had been so since 6 years prior to being referred. X-ray pelvis showed sclerotic-looking iliac bones, but an isotope bone scan showed no evidence of metastatic disease.We referred him to our endocrinology colleagues to investigate for possible primary hyperparathyroidism. However, ultrasound scan of neck showed no abnormal parathyroid gland. PET and CT scan of the chest, abdomen and pelvis did not show any significant pathology. MIBI scan of parathyroid glands showed diffuse thyroid uptake. The SPECT-CT images showed a well-defined focal area of increased activity, posterior to the mid/lower pole of the right thyroid lobe, possibly indicative of hyperfunctioning parathyroid tissue. The radiologist questioned the possibility of renal osteodystrophy and resultant secondary hyperparathyroidism. However, there was no evidence for renal dysfunction with a creatinine of 80 umol/L.We referred this gentleman to the Oxfordshire Osteoporosis and Metabolic Bone Service. Bloods showed a raised P1NP. This was felt to be consistent with tumour-induced osteomalacia. Oversecretion of FGF23 was confirmed and DOTATATE scan revealed two areas of uptake: one in the right hip and one in the skull.Meanwhile, the patient had been started on Sandoz Phosphate and alfacalcidol, and his bone aches improved on this combination therapy.He had radio-ablation of the hip lesion this year and has now stopped all his medication. His fatigue and muscle strength has improved dramatically. The skull lesion is being monitored for now with yearly imaging and follow-up in the metabolic bone clinic.Case report - DiscussionTumour-induced or oncogenic osteomalacia is extremely rare. Symptoms include chronic muscle and bone pain, weakness, and fatigue and can result in fragility fractures due to osteomalacia. Lack of awareness of these clinical manifestations and relevance of low phosphate levels often leads to a diagnostic delay or misdiagnosis. As seen in our case, it took multiple investigations and almost 2 years before this gentleman had a confirmation of his diagnosis.The pathogenesis of tumour-induced osteomalacia involves tumour expression of fibroblast growth factor 23. This hormone inhibits reabsorption of phosphate in the proximal renal tubule and down-regulates renal conversion of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D. Replacing phosphate on its own paradoxically increases PTH levels. The metabolic abnormalities may be partially or completely corrected with phosphate supplementation and calcitriol. In our patient, his PTH levels remained elevated, but alkaline phosphatase improved, as did calcium and phosphate levels.Unlike many other causes of osteomalacia, tumour-induced osteomalacia is curable by resection of the offending tumour. However, finding the responsible FGF23-secreting tumour can be incredibly challenging. There is ongoing research into medical treatment for this condition, especially if the tumour is not found or is unresectable, or the patient is not a surgical candidate.Case report - Key learning pointsLow phosphate levels can be easily overseen, with significant consequences. This case emphasises the need to recognise hypophosphatemia and to look for its cause. Conversely, it also illustrates the need to investigate all patients with persistent musculoskeletal symptoms for hypophosphatemia.Our case underscores the importance of being aware of the rare condition of tumour-induced osteomalacia. This will enable early recognition and treatment of the metabolic abnormality, before the development of any deleterious effects of osteomalacia on the skeleton.

Vitamin D Metabolism and Its Role in Mineral and Bone Disorders in Chronic Kidney Disease in Humans, Dogs and Cats.

Some differences regarding Vitamin D metabolism are described in dogs and cats in comparison with humans, which may be explained by an evolutionary drive among these species. Similarly, vitamin D is one of the most important regulators of mineral metabolism in dogs and cats, as well as in humans. Mineral metabolism is intrinsically related to bone metabolism, thus disturbances in vitamin D have been implicated in the development of chronic kidney disease mineral and bone disorders (CKD-MBD) in people, in addition to dogs and cats. Vitamin D deficiency may be associated with Renal Secondary Hyperparathyroidism (RSHPT), which is the most common mineral disorder in later stages of CKD in dogs and cats. Herein, we review the peculiarities of vitamin D metabolism in these species in comparison with humans, and the role of vitamin D disturbances in the development of CKD-MBD among dogs, cats, and people. Comparative studies may offer some evidence to help further research about vitamin D metabolism and bone disorders in CKD.

Hibernation in hominins from Atapuerca, Spain half a million years ago

Both animal hibernation and human renal osteodystrophy are characterized by high levels of serum parathyroid hormone. To test the hypothesis of hibernation in an extinct human species, we examined the hominin skeletal collection from Sima de los Huesos, Cave Mayor, Atapuerca, Spain, for evidence of hyperparathyroidism after a thorough review of the literature. We studied the morphology of the fossilized bones by using macrophotography, microscopy, histology and CT scanning. We found trabecular tunneling and osteitis fibrosa, subperiosteal resorption, ‘rotten fence post’ signs, brown tumours, subperiosteal new bone, chondrocalcinosis, rachitic osteoplaques and empty gaps between them, craniotabes, and beading of ribs mostly in the adolescent population of these hominins. Since many of the above lesions are pathognomonic, these extinct hominins suffered annually from renal rickets, secondary hyperparathyroidism, and renal osteodystrophy associated with Chronic Kidney Disease - Mineral and Bone Disorder (CKD-MBD). We suggest these diseases were caused by poorly tolerated hibernation in dark cavernous hibernacula. This is particularly evidenced by the rachitic osteoplaques and the gaps between them in some of the adolescent individuals along with the evidence of healing mainly in the adults. The sublayers in the rachitic osteoplaques indicate bouts of arousal from hibernation. The strong projection of the external lip of the femoral trochlea, the rachitic osteoplaques with the empty gaps between them, the “rotten fence post" sign, and the evidence of annual healing also point to the presence of annually intermittent puberty in this extinct human species. The hypothesis of hibernation is consistent with the genetic evidence and the fact that the SH hominins lived during an extreme glaciation. Alternative hypotheses are examined. The present work will provide a new insight into the physiological mechanism of early human metabolism which could help in determining the life histories and physiologies of extinct human species.

Rare Surgical Lung Biopsy Findings of Metastatic Pulmonary Calcification Associated with Chronic Renal Failure

Abstract Introduction/Objective Metastatic pulmonary calcification is a metabolic lung disease characterized by depositions of calcium in lung parenchyma. Depositions of calcium salts are usually caused by hypercalcemia and are associated with end-stage renal disease, primary and secondary hyperparathyroidism, and hemodialysis. It is mostly asymptomatic and clinically silent but can lead to life-threatening respiratory failure. Methods We present a case of a 53-year-old woman, with a failed renal transplant and on hemodialysis, admitted with cough and shortness of breath. Computed tomography showed extensive diffuse bilateral groundglass and nodular opacities. Bronchoscopy was unremarkable. BAL results were negative for infection. The initial differential diagnosis included pneumonitis, interstitial lung disease, and chronic obstructive pulmonary disease. VATS lung wedge resection was performed. Results Microscopically there were numerous interstitial, peribronchial and perivascular calcifications highlighted by Van Kossa stain. Calcifications were associated with a marked interstitial fibrosis confirmed by trichrome stain. There was no evidence of significant acute and chronic inflammation, granulomas, fibroblastic foci and vasculitis. Conclusion Metastatic pulmonary calcification is found in 60–80% of autopsies of patients undergoing dialysis treatment. It is rarely diagnosed during their lifetime, because patients are usually asymptomatic, or the imaging findings are negative. The diagnosis of metastatic pulmonary calcification in our patient prompt further evaluation for repeat kidney transplant and the patient is being considered for parathyroidectomy for her tertiary hyperparathyroidism.

Intraoperative 99mTc-MIBI-Guided Parathyroidectomy Improves Curative Effect of Parathyroidectomy, Bone Metabolism, and Bone Mineral Density.

This study aimed to compare the postoperative effects of total parathyroidectomy plus forearm transplantation and radioguided parathyroidectomy on bone metabolism and bone mineral density (BMD). From June 2013 to October 2017, 67 patients with renal secondary hyperparathyroidism (SHPT) received surgical treatment. The control group included 30 cases of classical total parathyroidectomy plus forearm transplantation for SHPT. In the experimental group, 37 patients underwent 99mTc-MIBI-guided parathyroidectomy. Demographics, parathyroid hormone (PTH) level, blood calcium level, and pathological results were compared between the 2 groups. The curative effect of parathyroidectomy and its effect on BMD were also compared. The BMDs in the L1-L4 segments and femoral neck in both groups were significantly improved after operation (all P < .05). The T scores of the L1-L4 segments and femoral neck in both groups were significantly improved after operation (all P < .05). The improvement in the T score of the L4 in the experimental group was significantly higher than that in the control group (P < .05). No significant differences in the improvement in the L1-L3 segments and femoral neck were found between the 2 groups. Both traditional total parathyroidectomy plus forearm transplantation and 99mTc-MIBI-guided parathyroidectomy can improve PTH level, blood calcium level, phosphorus level, bone metabolism, and BMD to varying degrees in patients with SHPT. Compared with the traditional surgery, 99mTc-MIBI-guided parathyroidectomy can improve blood calcium and phosphorus metabolisms, reduce PTH level, and improve the T scores of L4 to a greater extent.

Cálcio, fósforo, fração de excreção urinária de fósforo e paratormônio em cães com leishmaniose visceral

The kidneys perform an essential role in the regulation of serum phosphorus concentration. In visceral leishmaniasis (VL), the decline of the glomerular filtration rate leads to hyperphosphatemia, whose primary consequence is the development of secondary renal hyperparathyroidism. This study aimed to determine the concentration of serum phosphorus, ionized calcium (Cai), urinary fractional excretion of phosphorus (uFEP), and parathormone (PTH) in azotemic and non-azotemic dogs with VL and evaluate the uFEP as a marker of secondary renal hyperparathyroidism. The study comprised 31 dogs, divided into 24 sick animals and 07 healthy animals used as a control group (GC). The sick animals were classified into groups as azotemic (GA) and non-azotemic (GNA). The serum levels of phosphorus, creatinine, Cai, and the plasma levels of PTH were measured and compared between groups. The uFEP was calculated using values of serum and urinary levels of phosphorus and creatinine. The Kruskal-Wallis test with a 0.05 significance level was used, followed by the Mann-Whitney test as a post hoc test, with a 0.016 significance level. The levels of serum phosphorus were higher in the GA group, whereas for the PTH, the GNA and GA groups demonstrated high values compared to the GC. The uFEP was significantly higher in the GA when compared to the GNA, although there was no statistical difference between the GC and the GNA. The uFEP showed to be a late marker of chronic kidney disease and secondary hyperparathyroidism in dogs with visceral leishmaniasis.

Clinical, CT and ultrasonographic features of renal secondary hyperparathyroidism in a juvenile dog

A nine-month-old female entire Rottweiler was presented for further investigation of progressive, symmetric facial swelling over the maxilla of four weeks duration. Biochemistry revealed severe azotaemia with hyperphosphataemia. CT revealed...

Risk Factors for Prolonged Length of Stay and Readmission After Parathyroidectomy for Renal Secondary Hyperparathyroidism.

Population-based analyses of 30-day outcomes after parathyroidectomy for renal secondary hyperparathyroidism are limited. We sought to identify risk factors associated with prolonged length of stay (LOS) and readmission in this patient population. Patients with secondary hyperparathyroidism who underwent parathyroidectomy were reviewed in the ACS-NSQIP database (2011-2016). Patients were identified by ICD codes specific to secondary hyperparathyroidism of renal origin and the ACS-NSQIP variable for current preoperative dialysis. Multivariable logistic regression was used to identify independent factors associated with prolonged LOS and 30-day readmission after parathyroidectomy. The cohort included 1846 patients with secondary hyperparathyroidism on dialysis who underwent parathyroidectomy. There were 416 (22.5%) patients classified under the prolonged LOS group. On multivariable analysis, factors associated with prolonged LOS included elevated preoperative alkaline phosphatase [OR 3.13 (95%-CI 2.09-4.70), p < 0.001], decreased preoperative hematocrit [OR 1.83 (95%-CI 1.25-2.68), p = 0.002], unplanned reoperation (OR 5.02 [95%-CI 2.22-11.3], p < 0.001) and any postoperative complication [OR 6.12 (95%-CI 3.31-11.3), p < 0.001]. The overall 30-day readmission rate was 15.0%. Hypocalcemia and hungry bone syndrome accounted for 47.0% (n = 93/198) of readmissions. On multivariable analysis, patients with a history of hypertension and those undergoing unplanned reoperation were at risk of readmission [2.16 (95%-CI 1.21-3.87), p = 0.009, and 2.40 (95%-CI 1.15-5.02), p = 0.020, respectively], whereas reoperative parathyroidectomy was inversely associated with readmission (OR 0.24, 95%-CI 0.07-0.80, p = 0.021). In patients undergoing parathyroidectomy for renal secondary hyperparathyroidism, several readily available preoperative biochemical markers, including those of increased bone turnover and anemia, are associated with prolonged postoperative LOS. Unplanned reoperation was predictive of both increased LOS and readmission.

Effects of ferric carboxymaltose on markers of mineral and bone metabolism: A single-center prospective observational study of women with iron deficiency.

Two weekly infusions of ferric carboxymaltose (FCM) are commonly prescribed for treatment of iron-deficiency anemia. However, administration of FCM increases intact levels of fibroblast growth factor 23 (FGF23), which causes hypophosphatemia due to renal phosphate wasting, calcitriol deficiency and secondary hyperparathyroidism. The adverse effects of FCM on mineral metabolism and bone health emerged from case reports and secondary analyses of trials. Data on these safety signals with FCM in clinical practice are limited because markers of mineral and bone metabolism are not routinely checked. To obtain real-world experience with effects of FCM on mineral and bone metabolism, we conducted a prospective observational study of 16 women who were managed at a single-center hematology clinic for iron-deficiency anemia. From October 2016 to February 2018, all participants received two weekly infusions of FCM at a hematology infusion clinic. We hypothesized that FCM would decrease phosphate, increase intact FGF23 (iFGF23), and decrease c-terminal FGF23 (cFGF23). Secondary outcomes were changes in hemoglobin, iron indices, urine fractional excretion of phosphate (FePi), parathyroid hormone (PTH), calcitriol, calcium, osteocalcin, and bone-specific alkaline phosphatase (BAP). FCM was administered at weeks zero and one, and we measured laboratory values at weeks zero, one, two, and five of the study. We used linear mixed models to analyze the significance of the changes in laboratory values over time. After two FCM infusions, nearly all (14 of 16) participants developed hypophosphatemia. iFGF23 increased, cFGF23 decreased, and phosphate decreased significantly from week zero to week two (iFGF23 increased by +134.0% [40.6, 305.8], p<0.001; cFGF23 decreased by -516.3% [-1332.7, -142.7], p=0.002; phosphate decreased by -49.8±15.4%, p<0.001). There was also a significant increase in FePi, PTH, and BAP and a significant decrease in calcitriol and calcium from week zero to week two. There was no significant change in osteocalcin during this time period. iFGF23, but not PTH, was independently associated with decreased phosphate. iFGF23 was also significantly associated with decrease in calcitriol from week zero to week two. Elevation in BAP suggests disordered bone mineralization in response to FCM therapy. In this prospective observational study of women with iron deficiency anemia, two FCM infusions significantly altered markers of bone mineralization and mineral metabolism. The results suggest that FCM should be used cautiously in the treatment of iron-deficiency anemia.