Atypical Gitelman syndrome with L623P mutation of the thiazide-sensitive Na-Cl cotransporter gene exhibiting lack of hypocalciuria and increased proximal tubule salt reabsorption.
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چکیده
prevent recurrent central line sepsis. J Infect 2004; 49: 20–22 5. Schwab SJ, Weiss MA, Rushton F et al.Multicenter clinical trial results with the LifeSite hemodialysis access system. Kidney Int 2002; 62: 1026–1033 6. Sissons CH, Wong L, Cutress TW. Inhibition by ethanol of the growth of biofilm and dispersed microcosm dental plaques. Arch Oral Biol 1996; 41: 27–34 7. Laird J, Soutar R, Butcher I. Complications of the ethanol-lock technique in the treatment of central venous catheter sepsis. J Infect 2005; 51: 338 8. Crnich CJ, Halfmann JA, Crone WC, Maki DG. The effects of prolonged ethanol exposure on the mechanical properties of polyurethane and silicone catheters used for intravascular access. Infect Control Hosp Epidemiol 2005; 26: 708–714
منابع مشابه
Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia.
Thiazide diuretics enhance renal Na+ excretion by blocking the Na+-Cl- cotransporter (NCC), and mutations in NCC result in Gitelman syndrome. The mechanisms underlying the accompanying hypocalciuria and hypomagnesemia remain debated. Here, we show that enhanced passive Ca2+ transport in the proximal tubule rather than active Ca2+ transport in distal convolution explains thiazide-induced hypocal...
متن کاملA novel initial codon mutation of the thiazide-sensitive Na-Cl cotransporter gene in a Japanese patient with Gitelman's syndrome.
We here report a novel mutation of the thiazide-sensitive Na-Cl cotransporter (TSC) (SLC12A3) gene in a Japanese patient with Gitelman's syndrome (GS). GS is characterized by a renal disorder and is associated with hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria arising from the defective tubular reabsorption of magnesium and potassium. This disease is reportedly caused by mu...
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1. Bettinelli A, Giovanni M, Bianchetti MG et al. Use of calcium excretion values to distinguish two forms of primary renal tubular hypokalemic alkalosis: Bartter and Gitelman syndrome. J Pediatr 1992; 120: 38–43 2. Lin S-H, Cheng N-L, Hsu Y-J, Halperin ML. Intrafamilial phenotype variability in patients with Gitelman syndrome having the same mutations in their thiazide-sensitive sodium/chlorid...
متن کاملAttenuated renal excretion in response to thiazide diuretics in Gitelman's syndrome: a case report.
Gitelman's syndrome is a variant of Bartter's syndrome characterized by hypocalciuria and hypomagnesemia. The administration of thiazide diuretics may induce a subnormal increase of urinary Na+ and Cl- excretion in patients with Gitelman's syndrome, consistent with the hypothesis that less Na+ and Cl- than normal is reabsorbed by the thiazide-inhibitable transporter in Gitelman's syndrome. Spec...
متن کاملEffect of thiazide on renal gene expression of apical calcium channels and calbindins.
Thiazide diuretics are specific inhibitors of the Na-Cl cotransporter in the distal convoluted tubule (DCT). In addition to producing diuresis and natriuresis, they have a hypocalciuric effect. Recently, two apical calcium channels have been identified, transient receptor potential vanilloid 5 (TRPV5) and TRPV6; both are expressed in the DCT. We studied the effects of thiazides on mouse renal c...
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ورودعنوان ژورنال:
- Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
دوره 21 11 شماره
صفحات -
تاریخ انتشار 2006