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Secondary hyperparathyroidism (SHPT) is common in patients with end-stage kidney disease (ESKD) on kidney replacement therapy, which leads to abnormalities of bone and mineral metabolism. Patients conceiving on kidney replacement therapy add a further layer of complexity to the management of their SHPT. Existing literature in cases of primary hyperparathyroidism (PHPT) has linked untreated hyperparathyroidism to increased maternal and fetal morbidity, including hypertensive disorders of pregnancy, fetal growth restriction and neonatal hypocalcaemia.

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BACKGROUND Although hypomagnesemia is common in type 2 diabetes, clinical presentations with severe hypomagnesemia are rare. A number of oral blood glucose-lowering medications can reduce serum magnesium concentrations, and several severe cases have been reported in the presence of marked glucagon-like peptide-1 receptor agonist (GLP-1RA)-associated gastrointestinal adverse effects. In the present case, an acute presentation with severe hypomagnesemia was likely due to polypharmacy including semaglutide, albeit with a delayed relationship to discontinuation of this GLP-1RA, due to nausea and vomiting.

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Calcium Homeostasis in the human body is regulated by hormones, including parathyroid hormone and vitamin D3. Dysfunction in the form of hypoparathyroidism causes hypocalcaemia. In patients treated for primary hypoparathyroidism with activated vitamin D replacement, iatrogenic hypercalcaemia can occur.

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Vitamin D-dependent rickets type 2A (VDDR2A) is a rare cause of infantile-onset alopecia, characterized by severe hypotrichosis, small cutaneous cysts, early-onset treatment-resistant rickets, and hypocalcemia. Alopecia, often starting a few weeks to months after birth, may be the presenting feature. We present three cases of VDDR2A with genetic variants in the vitamin D receptor (VDR) gene, their clinical features and biochemical parameters.

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Plasmapheresis for extracorporeal membrane oxygenation (ECMO)-induced hemolysis in infants.

J Extra Corpor Technol

December 2024

Division of Pediatric Nephrology, Joe DiMaggio Children's Hospital, 1131 N35th Ave, Hollywood, FL 33021, USA - Charles E. Schmidt College of Medicine at Florida Atlantic University, 777 Glades Rd BC-71, Boca Raton, FL 33431, USA.

Background: Intravascular hemolysis is a known complication of extracorporeal membrane oxygenation (ECMO). Characterized by elevated plasma-free hemoglobin (PFH), intravascular hemolysis is associated with cytotoxic effects leading to renal replacement therapy (RRT), longer ECMO runs, and mortality. Therapeutic plasma exchange (TPE) in tandem with ECMO was described as a therapy for various pathologic conditions, but there are no Extracorporeal Life Support Organization (ELSO) guidelines for the treatment of ECMO-induced hemolysis.

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