Gitelman syndrome is a rare inherited renal tubular disorder with features that resemble thiazide use, including a hypokalemic metabolic alkalosis, hypomagnesemia, hypocalciuria and a low or normal blood pressure, hyperreninemia and hyperaldosteronism. Treatment is primarily correction of the potassium and magnesium levels. The diagnosis is confirmed with genetic testing but Gitelman syndrome is often not suspected. However, the association with ectopic calcification in the retina, blood vessels and chondrocalcinosis in the joints is a useful pointer to this diagnosis. Bilateral symmetrical whitish deposits of calcium pyrophosphate are visible superotemporally on ophthalmoscopy and retinal photography but are actually located beneath the retina in the sclerochoroid. Optical coherence tomography is even more sensitive for their detection. These deposits increase in size with time, but the rate of progression slows with long-term correction of the hypomagnesemia. Calcification may be complicated by atrophy of the overlying retina and visual loss. The deposits often correlate with ectopic calcification in the aorta and coronary and cerebral vessels. Chondrocalcinosis occurs in the large joints such as the knees. Ectopic calcification in Gitelman syndrome indicates the need for more aggressive management of Mg levels. Calcification is much less common in Bartter syndrome, which itself is rarer and associated less often with hypomagnesemia.
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http://dx.doi.org/10.1093/ckj/sfab034 | DOI Listing |
Medicine (Baltimore)
January 2025
The Department of Clinical Laboratory, Zhejiang Hospital, Hangzhou, China.
Rationale: Gitelman syndrome (GS) is a rare hereditary electrolyte disorder caused by mutations in the SLC12A3 gene. There is limited literature on the role of hydrochlorothiazide (HCT) testing and the SLC12A3 single heterozygous mutation in the diagnosis and management of patients with GS. In addition, cases of GS with concomitant kidney stones are rare.
View Article and Find Full Text PDFJ Am Soc Nephrol
January 2025
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Cité, F-75006 Paris, France.
The renal tubule and collecting duct express a large number of proteins, all having putative immunoreactive motives. Therefore, all can be the target of pathogenic autoantibodies. However, autoimmune tubulopathies seem to be rare and we hypothesize that they are underdiagnosed.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Molecular Physiology Unit, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, and Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, Mexico City, 14080 Mexico.
The field of the with no lysine kinases (WNKs) regulation of the thiazide-sensitive NaCl cotransporter (NCC) began at the start of the century with the discovery that mutations in two members of the family, WNK1 and WNK4, resulted in a condition known as Familiar Hyperkalemic Hypertension (FHHt). Since FHHt is the mirror image of Gitelman's syndrome that is caused by inactivating mutations of the SLC12A3 gene encoding NCC, it was expected that WNKs modulated NCC activity and that the increased function of the cotransporter is the pathophysiological mechanism of FFHt. This turned out to be the case.
View Article and Find Full Text PDFBMC Nephrol
November 2024
Nephrology Division, Department of Internal Medicine, University of Utah Health, Salt Lake City, USA.
Am J Case Rep
November 2024
Department of Endocrinology, Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
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