Hypoparathyroidism is the most common complication after total thyroidectomy and may be particularly severe in pediatric Graves' disease. We report the case of a 14-year-old boy with Graves' disease who developed profound postoperative hypocalcemia after total thyroidectomy, with serum calcium 5.9 mg/dL, ionized calcium 0.83 mmol/L, and undetectable parathyroid hormone. Despite intravenous and high-dose oral calcium plus calcitriol, biochemical control remained poor, with persistent hypocalcemia, hyperphosphatemia, and ongoing treatment requirements after 16 days. Off-label subcutaneous palopegteriparatide, a long-acting PTH(1-34) prodrug, was started after multidisciplinary assessment and informed consent from the family. Serum calcium improved within 48 h, intravenous calcium was stopped after 5 days, and calcitriol, sevelamer, and calcium acetate were discontinued within 11 days. Treatment was well tolerated. This case suggests that early PTH replacement may be a useful rescue strategy in selected children with severe refractory post-thyroidectomy hypocalcemia.

Sevelamer carbonate, a non-calcium phosphate binder widely used in end-stage renal disease (ESRD), is an increasingly recognized but underdiagnosed cause of medication-induced colitis through gastrointestinal crystal deposition. We report a 56-year-old Palestinian male with ESRD on hemodialysis who presented with a one-month history of watery non-bloody diarrhea, vomiting, and diffuse abdominal pain. He had been repeatedly misdiagnosed with amebic colitis and treated with metronidazole without improvement. Colonoscopy revealed diffuse patchy erythema throughout the colon with right-sided predominance. Histopathology confirmed sevelamer-induced active colitis, demonstrating characteristic brownish fish scale-like crystals with active neutrophilic infiltrate. Sevelamer carbonate was discontinued with subsequent clinical improvement. This case highlights a clinically important diagnostic pitfall in resource-limited settings where amebic colitis is endemic and empiric metronidazole is commonly the first-line response to chronic diarrhea in dialysis patients.

Normophosphatemic familial tumoral calcinosis (NFTC) is characterized by cutaneous calcifications with no metabolic disorders; it manifests in the first years of life; associated with mutations in SAMD9 gene. Chronic trauma and transient hyperphosphatemia play a leading role in calcification formation.Surgical treatment can remove calcifications, but it does not prevent recurrence and can cause complications. Various conservative therapy is used. Lowering of blood phosphate levels is considered a promising pathogenetic treatment method.We present a clinical case of a patient with NFTC associated with the homozygous variant p.E1200K in SAMD9. A characteristic feature of our patient is the presence of multiple calcifications not only in the areas of injury (limbs), but also in areas of acne (face), as well as particularly active progression of the disease during puberty. A reduction in calcification size was observed after one year of continuous hypophosphatemic therapy (aluminum hydroxide and sevelamer 800 mg). The effectiveness of this therapy is debatable and limited by both poor patient tolerability of sevelamer and poor adherence.This is the first description of a patient with molecularly confirmed NFTC in Russia. A precise diagnosis allowed us to clarify the pathogenetic mechanism of calcification formation and propose treatment options.

Calcified amorphous tumors (CATs) are rare, non-neoplastic intracardiac masses first described by Reynolds et al. in 1997. Although increasingly reported, their pathogenesis remains poorly understood, and they are frequently misdiagnosed as vegetations, cardiac myxomas, or malignant tumors. Proposed mechanisms include abnormalities in calcium-phosphate metabolism and hypercoagulable states. We report a case of CAT formation in a patient receiving peritoneal dialysis with severe, refractory hyperphosphatemia. A 47-year-old woman with type 2 diabetes mellitus, hypertension, heart failure with reduced ejection fraction, and end-stage renal disease on peritoneal dialysis had unremitting hyperphosphatemia (>10 mg/dL). Phosphate control was limited despite having trialed sevelamer and calcium acetate and intolerance to tenapanor due to gastrointestinal adverse effects. She had mixed adherence to dietary recommendations. She presented with leg pain and imaging raised concern for a psoas abscess. As part of an infectious embolic evaluation, transthoracic echocardiography revealed mitral valve dysfunction caused by a mobile intracardiac mass. Surgical resection was performed, and histopathologic examination confirmed a CAT. CATs typically present with symptoms related to valvular obstruction or embolization. Imaging findings on echocardiography, computed tomography, or magnetic resonance imaging are nonspecific, making histopathology essential for definitive diagnosis. Surgical excision remains the treatment of choice, with recurrence reported rarely. Given the propensity for calcium-phosphate deposition in patients with chronic hyperphosphatemia, strict phosphate control may reduce the risk of CAT development in patients with end-stage renal disease, though further studies are needed to clarify preventive strategies.

Background: Patients with chronic kidney disease (CKD) undergoing hemodialysis commonly present multiple comorbidities and require complex medication regimens. Polypharmacy increases the risk of clinically relevant drug interactions that may compromise treatment safety and effectiveness. Objective: To estimate the prevalence of potential drug interactions among patients with CKD undergoing hemodialysis and classify these interactions according to clinical risk and mechanism of action. Methods: A cross-sectional study was conducted with patients undergoing hemodialysis at a dialysis clinic in Southern Santa Catarina, Brazil. Potential drug interactions were identified using the Medscape and Drugs.com databases and classified according to severity (major, moderate, or minor) and mechanism of action. Results: A total of 151 patients were included. Potential drug interactions were identified in all participants (973 interactions; mean 6.4 per patient). Of these, 234 (24.0%) were classified as major, 545 (56.0%) as moderate, and 194 (19.9%) as minor. The most frequent major interactions involved furosemide + losartan (n = 8) and acetylsalicylic acid + clopidogrel (n = 6). Among moderate interactions, the most common were sevelamer + calcium carbonate (n = 14) and losartan + amlodipine (n = 12). The most frequent minor interactions involved epoetin alfa + acetylsalicylic acid (n = 14) and epoetin alfa + calcium carbonate (n = 10). Pharmacodynamic interactions predominated, mainly involving additive effects of cardiovascular medications. Conclusions: Potential drug interactions were highly prevalent among patients undergoing hemodialysis, with moderate-severity interactions predominating. Routine screening for potential drug interactions may support safer prescribing, optimize pharmacotherapy, and strengthen multidisciplinary medication management in this high-risk population.

This study aimed to evaluate adverse events (AEs) associated with sevelamer through data mining of the US FDA Adverse Event Reporting System, identify potential drug-related AEs, and provide guidance for clinical medication safety. AE reports related to sevelamer from the first quarter of 2004 to the second quarter of 2025 were extracted from the US FDA Adverse Event Reporting System database, classified by preferred term (PT) and system organ class, and risk signals were analyzed. Among 6780 AE reports in which sevelamer was the primary suspect drug, 123 PTs spanning 24 system organ classes were identified. Male reports exceeded females (20.66% vs 18.07%), with highest proportion in 60 to 74 years (11.81%). Median AE occurrence time - medication date was 119.00 (interquartile range, 14.00, 476.50) days, with most events occurring more than 60 days after administration (n = 353, 30.46%) and within 7 days (n = 121, 10.44%). Among the positive risk signal PTs, "constipation, gastric or intestinal ulcer/hemorrhage/perforation/necrosis/ischemia, colitis ischemic, erosive esophagitis/gastritis, abdominal pain, dysphagia, nausea, vomiting, peritonitis and pruritus" exhibited high signal strength, consistent with the label. Additionally, new signals included aorto-esophageal fistula, diabetic gastroparesis, large intestinal stenosis, short-bowel syndrome, bezoar, diverticulum intestinal, gastric polyps, large intestine polyp, feces pale, diverticulum, hemorrhagic intestinal diverticulum, crystal deposit intestine, appendicitis (complicated or perforated), renal cyst infection, colonic or abdominal abscess, pseudomembranous colitis, diverticulitis, gangrene, pseudopolyp, mucosal ulceration or necrosis, skin fibrosis, and excessive granulation tissue. Therapeutic use of sevelamer remains associated with risks of diverse AEs. Therefore, clinical practice requires close monitoring of gastrointestinal disorders, metabolic, skin disorders and infections, particularly GI disorders. Prompt intervention is essential to prevent severe complications.

Background and Objectives: Hyperphosphatemia is a key component of chronic kidney disease-mineral and bone disorder and is associated with higher rates of cardiovascular events and mortality in patients undergoing dialysis. Phosphate binders are essential for phosphorus reduction, and their evaluation relies on several factors, such as chemical composition, binding capacity, and safety profile. Unfortunately, long-term management is hindered by high pill burden and poor adherence. Magnesium phosphate binders have proven effectiveness in reducing phosphate levels. Nevertheless, despite their efficacy, they are not widely used in clinical settings because of concerns related to their use. This study assessed the efficacy of low-dose magnesium carbonate as a phosphate binder in patients undergoing chronic dialysis, focusing on its biochemical control, tolerability, and cost-effectiveness. Materials and Methods: A prospective observational study was conducted on 54 hemodialysis patients with end-stage renal disease at a single dialysis center. Patients were taking either 250 mg magnesium carbonate or 2400 mg sevelamer carbonate for 3 months. Results: Both groups showed decreased phosphorus levels, with a 14.2% significant reduction in the magnesium carbonate group (p < 0.001) and a 5.1% reduction in the sevelamer carbonate group. At the end of the study, no significant differences were observed between the groups (p = 0.682). In the magnesium carbonate group at month 3, compared to baseline, no significant differences were detected in other laboratory parameters reflecting calcium-phosphorus metabolism (Ca-p = 0.681, PTH-p = 0.126). Simultaneously, good compliance without clinically relevant gastrointestinal side effects was observed, including the absence of clinically significant hypermagnesemia. Conclusions: The phosphorus-lowering potential of low-dose magnesium carbonate is non-inferior to that of low-dose sevelamer carbonate. However, its favorable safety profile, low incidence of adverse effects, and cost-effectiveness make it a promising option in clinical practice, further highlighting the need for better recognition by physicians.

Secondary hyperparathyroidism (sHPT) is a prevalent complication of end-stage renal disease, driven by phosphate retention, vitamin D deficiency, hypocalcemia, and calcium-sensing receptor dysregulation. Despite international guidelines, optimal biochemical control remains challenging in real-world practice. This narrative review synthesizes current evidence on the pharmacological management of sHPT in dialysis patients, with attention to the underrepresented Middle Eastern and Gulf Cooperation Council (GCC) context. A narrative review was conducted using PubMed and Scopus, identifying original clinical studies, randomized controlled trials, and observational cohorts examining calcimimetics, vitamin D analogs, and phosphate binders in dialysis patients with sHPT. In total, 22 studies were included. Calcimimetics, particularly cinacalcet, reduce parathyroid hormone (PTH) by approximately 43% in hemodialysis patients without raising serum calcium, though hypocalcemia and gastrointestinal adverse effects limit tolerability. Intravenous etelcalcetide offers superior PTH suppression with improved gastrointestinal tolerability and eliminates oral adherence challenges through supervised dialysis-circuit administration. A large trial demonstrated no mortality benefit despite sustained PTH lowering. Vitamin D analogs suppress PTH gene transcription but carry a narrow therapeutic window with risks of hypercalcemia and hyperphosphatemia. Phosphate binders address the primary upstream driver of sHPT; non-calcium-based agents such as sevelamer offer cardiovascular advantages but impose a pill burden contributing to nonadherence rates of 22-74%. Novel agents including tenapanor offer complementary phosphate-lowering mechanisms with substantially reduced pill burden. Combination therapy allows dose reduction of individual agents while optimizing biochemical outcomes. Evidence from Middle Eastern and GCC dialysis populations is virtually absent. Pharmacological management of sHPT requires individualized, guideline-informed combination therapy. A critical evidence gap exists in the GCC region, where diabetic nephropathy dominance, endemic vitamin D deficiency, and lower calcimimetic utilization may limit generalizability of existing trial data. Locally conducted research is urgently needed.

Calciphylaxis, also termed calcific uremic arteriolopathy, is a rare and devastating complication of end-stage renal disease (ESRD). Its occurrence in patients with HIV-associated ESRD is sparsely characterized in the literature. We report a 36-year-old African American woman with ESRD secondary to longstanding hypertension and virologically suppressed HIV infection (CD4 count 348 cells/μL) who developed three discrete presentations of recurrent calciphylaxis over 18 months, with histopathologic confirmation at initial diagnosis and at first recurrence. At initial presentation (T1), intact parathyroid hormone (iPTH) was 806.5 pg/mL; she was treated with paricalcitol, sevelamer carbonate, and intravenous sodium thiosulfate (STS) but remained intermittently nonadherent to hemodialysis and prescribed therapies, with a single-pool Kt/V of 0.29 documented at recurrence. At second presentation 12 months later (T2), iPTH was 308.4 pg/mL despite active cutaneous lesions; management included surgical debridement, broad-spectrum antibiotics for superimposed polymicrobial soft tissue infection, continued STS, and dialysis intensification. Six months after T2 (T3), the patient represented with lesion expansion and new ulcerations, and iPTH had risen to 1,764.9 pg/mL alongside hypocalcemia and hyperphosphatemia, consistent with progression toward tertiary hyperparathyroidism. Parathyroidectomy was deferred at T2 and T3 because of acute infectious burden and uncontrolled hyperkalemia, respectively. This case illustrates the diagnostic and management complexity of recurrent calciphylaxis in HIV-associated ESRD, demonstrates how intermittent treatment adherence may produce highly discordant iPTH measurements that complicate threshold-based monitoring, and underscores the importance of multidisciplinary planning before surgical and metabolic barriers to parathyroidectomy accumulate.