Analyses of Subjects with Hypokalemic Metabolic Alkolosis, Gitelman's and Bartter's Syndrome

Önem, Yalçın; Küçükardalı, Yaşar; Şahan, Burak; Atasoyu, Enes Murat; İpçioğlu, Osman Metin; Terekeci, Hakan; Solmazgül, Emrullah; Top, Cihan; Öktenli, Çağatay

doi:10.1080/08860220802212718

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…[26] The presentation of our patient (metabolic alkalosis, refractory hypokalemia, hypocalcemia hypomagnesemia, and hypercalceuria) was suggestive of BS while other close differential diagnosis, Gitelman syndrome was ruled out by the the presence of low serum Ca level and documentation of hypercalciuria. [7] Our case represents characterization of a rare and potential danger of gentamicin therapy.…”

Section: Discussionmentioning

confidence: 99%

Acquired Bartter syndrome following gentamicin therapy

et al. 2016

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Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS), or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

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Section: Discussionmentioning

confidence: 99%

Acquired Bartter syndrome following gentamicin therapy

et al. 2016

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“…Patients with Bartter's syndrome present in early childhood with severe clinical course, showing edema, growth retardation, polyuria and hearing loss (Onem et al 2008;Fremont and Chan 2012). Gitelman's syndrome usually manifests itself in adults, and patients can sustain normal life with excellent long-term prognosis (Cruz et al 2001;Knoers 2006;Knoers and Levtchenko 2008).…”

Section: Introductionmentioning

confidence: 99%

Gitelman’s Syndrome with Vomiting Manifested by Severe Metabolic Alkalosis and Progressive Renal Insufficiency

Lee

Han

2013

Tohoku J. Exp. Med.

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Gitelman's syndrome is an autosomal recessive salt-losing tubulopathy showing hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis and hyperreninemic hyperaldosteronism. This syndrome is caused by mutations in the SLC12A3 gene that encodes sodium-chloride cotransporter expressed at the apical membrane of renal distal convoluted tubule. Symptoms and renal outcomes of Gitelman's syndrome are, in general, mild and benign, and renal insufficiency from Gitelman's syndrome associated with long-standing hypokalemia and volume depletion is extremely rare. Herein, we report a 27-year-old male patient with Gitelman's syndrome who manifested renal failure, hypokalemia, severe metabolic alkalosis and altered mentality. About one year ago, the patient had been transferred to Seoul National University Hospital, because of unsolved hypokalemia, and was diagnosed as Gitelman's syndrome by clinical features and genetic analysis of the SLC12A3 gene. The patient carries a missense mutation at one allele of SLC12A3 gene (c.781C>T, p.Arg261Cys). His mother is also heterozygous for the same mutation and she had a history of hypokalemia. On this admission, the patient had recurrent bouts of vomiting induced by psychiatric eating disorder and showed severe volume depletion with hypotension, azotemia and metabolic alkalosis. Intense hydration therapy and emergency hemodialysis transiently improved his fluid-electrolyte imbalance and renal function. However, renal dysfunction progressively deteriorated despite the medical treatment. Our findings suggest that even in Gitelman's syndrome, constant monitoring for volume status and other comorbid conditions should be employed to prevent progressive renal injury.

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“…The clinical use of fractional excretions only became popular three decades ago when the fractional excretion of sodium (FeNa) was first employed to help solve the common dilemma for the clinician; namely, the need to distinguish pre-renal azotemia (PRA) from intrinsic renal pathology (ATN) in patients with oliguric azotemia. 1 Since that time, the fractional excretions of other solutes such as magnesium, potassium, bicarbonate, chloride, calcium, and phosphorus have been occasionally used to diagnose cyclosporine toxicity, 2 distal acidification 2 and proximal bicarbonate wasting, 3 tubular transport errors, 4 bullemia, 5 and familial hypocalciuric hypercalcemia 6 and to differentiate hyperparathyroidism 7 from vitamin D toxicity; 8 however, none of these calculations have achieved the clinical utility of the FeNa in the differentiation of PRA from ATN in oliguric azotemia which remains commonly recommended. 9 As assessment of hydration can be difficult 10 and classical clinical signs are often lacking, 11 the FeNa remains an extremely valuable tool; however, many drugs and medical conditions interfere with the accuracy of the FeNa (Table 1).…”

Section: Introductionmentioning

confidence: 99%

Toward the optimal clinical use of the fraction excretion of solutes in oliguric azotemia

et al. 2010

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While the fractional excretion of solutes have long been considered excellent research tools to investigate tubular physiology, their clinical use has become common over the last 40 years in the diagnoses of many disorders; however, none have reached the clinical utility of the fractional excretion of sodium in the ability to distinguish pre-renal azotemia from acute tubular necrosis. Nevertheless, there are many drugs and medical conditions that interfere with that utility and recently other solutes, including urea, uric acid and lithium, have been recently investigated to improve the diagnostic ability in clinical situations where the fractional excretion of sodium is known to be unreliable. We review the tubular physiology of these solutes and show how the differences in tubular physiology might be exploited to develop a strategy for their optimal clinical use.

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Analyses of Subjects with Hypokalemic Metabolic Alkolosis, Gitelman's and Bartter's Syndrome

Cited by 4 publications

References 16 publications

Acquired Bartter syndrome following gentamicin therapy

Acquired Bartter syndrome following gentamicin therapy

Gitelman’s Syndrome with Vomiting Manifested by Severe Metabolic Alkalosis and Progressive Renal Insufficiency

Toward the optimal clinical use of the fraction excretion of solutes in oliguric azotemia

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