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Hypocalcemia secondary to hypomagnesemia in a patient on liraglutide.

ABSTRACT: A 73-year-old man with type 2 diabetes on Liraglutide with a history of coronary artery disease. Admitted to emergency for abdominal pain, severe diarrhea and episodes of tetany attacks. Laboratory workup reveals hypomagnesemia, hypocalcemia and normal parathormone (PTH). After intravenous administration of magnesium and calcium, the blood ionogram quickly normalized. In addition, plasma levels of intact parathyroid hormone increased immediately after magnesium administration. Strongly suggests that hypocalcemia resulted from a disruption of adequate parathyroid hormone secretion caused by hypomagnesemia which in turn was caused by severe diarrhea under treatment with Liraglutide.

SUBMITTER: Habnouny JEL

PROVIDER: S-EPMC7662844 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Hypocalcemia secondary to hypomagnesemia in a patient on liraglutide.

Habnouny J E L JEL Jandou I I Latrech H H Bourgon C C

Annals of medicine and surgery (2012) 20201029

A 73-year-old man with type 2 diabetes on Liraglutide with a history of coronary artery disease. Admitted to emergency for abdominal pain, severe diarrhea and episodes of tetany attacks. Laboratory workup reveals hypomagnesemia, hypocalcemia and normal parathormone (PTH). After intravenous administration of magnesium and calcium, the blood ionogram quickly normalized. In addition, plasma levels of intact parathyroid hormone increased immediately after magnesium administration. Strongly suggests ...[more]

PMID: 33224484

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Project description:BackgroundChronic hypomagnesemia is commonly due to diarrhea, alcoholism, and drugs. More rarely, it is caused by genetic defects in the effectors of renal magnesium reabsorption.MethodsIn an adult patient with acquired severe hypomagnesemia, hypocalcemia, tubulointerstitial nephropathy, and rapidly progressing kidney injury, similarities between the patient's presentation and features of genetic disorders of renal magnesium transport prompted us to investigate whether the patient had an acquired autoimmune cause of renal magnesium wasting. To determine if the patient's condition might be explained by autoantibodies directed against claudin-16 or claudin-19, transmembrane paracellular proteins involved in renal magnesium absorption, we conducted experiments with claudin knockout mice and transfected mouse kidney cells expressing human claudin-16 or claudin-19. We also examined effects on renal magnesium handling in rats given intravenous injections of IgG purified from sera from the patient or controls.ResultsExperiments with the knockout mice and in vitro transfected cells demonstrated that hypomagnesemia in the patient was causally linked to autoantibodies directed against claudin-16, which controls paracellular magnesium reabsorption in the thick ascending limb of Henle's loop. Intravenous injection of IgG purified from the patient's serum induced a marked urinary waste of magnesium in rats. Immunosuppressive treatment combining plasma exchange and rituximab was associated with improvement in the patient's GFR, but hypomagnesemia persisted. The patient was subsequently diagnosed with a renal carcinoma that expressed a high level of claudin-16 mRNA.ConclusionsPathogenic claudin-16 autoantibodies represent a novel autoimmune cause of specific renal tubular transport disturbances and tubulointerstitial nephropathy. Screening for autoantibodies targeting claudin-16, and potentially other magnesium transporters or channels in the kidney, may be warranted in patients with acquired unexplained hypomagnesemia.

Dataset Information

Hypocalcemia secondary to hypomagnesemia in a patient on liraglutide.

Publications

Hypocalcemia secondary to hypomagnesemia in a patient on liraglutide.

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