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10.1159/000013303 http://scihub22266oqcxt.onion/10.1159/000013303 9481438!ä!9481438 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=9481438&cmd=llinks): Failed to open stream: HTTP request failed! 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Studies on the pathogenesis of hypokalemia in Gitelman s syndrome: role of bicarbonaturia and hypomagnesemia |pdf=|usr=}}{{9481438}} gab.com Text Studies on the pathogenesis of hypokalemia in Gitelman s syndrome: role of bicarbonaturia and hypomagnesemia JO: Am J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=9481438 #FOAvip OBJECTIVE: Hypokalemia and renal potassium (K) wasting are hallmarks of the group of disorders called Bartter's syndrome. The presence of hypomagnesemia and a low rate of excretion of calcium are currently used to characterize a subgroup of these patients as having Gitelman's syndrome (GS) in which the molecular lesion is a defect in the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule. This study was undertaken to examine whether bicarbonaturia or hypomagnesemia exacerbates the kaliuresis in patients with GS. METHODS: Six patients with most of the diagnostic features of GS were examined. To examine the role of bicarbonaturia, the transtubular K concentration gradient (TTKG) was assessed before and after an oral load of NH4Cl which caused the urine pH to be < 6. To evaluate the role of hypomagnesemia, the TTKG was examined after an infusion of enough magnesium (Mg) to achieve normal levels of Mg in plasma for close to 24 h. RESULTS: The TTKG remained very high even when the pH of the urine was < 6.0. An infusion of Mg caused the TTKG to approach expected values for hypokalemia in 4 of 6 patients. The infusion of Mg was extended in 1 patient who had a sustained high TTKG for 24 h; the TTKG remained elevated for 96 h despite normal plasma Mg levels. CONCLUSIONS: Bicarbonaturia does not play a critical role in maintaining the very high TTKG in these patients. The K wasting in 4 of 6 of these patients could largely be attributed to hypomagnesemia and/or Mg depletion. The plasma aldosterone level tended to be higher in patients who did not respond to the infusion of Mg. Therefore, these patients may not represent a homogeneous group with regard to the pathophysiology of their renal K wasting. Twit Text FOAVip Studies on the pathogenesis of hypokalemia in Gitelman s syndrome: role of bicarbonaturia and hypomagnesemia ????Am J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=9481438 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=9481438 #FOAvip English Wikipedia <ref>{{Cite pmid|9481438}}</ref> Studies on the pathogenesis of hypokalemia in Gitelman s syndrome: role of bicarbonaturia and hypomagnesemia #MMPMID9481438 Kamel KS; Harvey E; Douek K; Parmar MS; Halperin ML Am J Nephrol 1998[]; 18 (1): 42-9 PMID9481438show ga OBJECTIVE: Hypokalemia and renal potassium (K) wasting are hallmarks of the group of disorders called Bartter's syndrome. The presence of hypomagnesemia and a low rate of excretion of calcium are currently used to characterize a subgroup of these patients as having Gitelman's syndrome (GS) in which the molecular lesion is a defect in the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule. This study was undertaken to examine whether bicarbonaturia or hypomagnesemia exacerbates the kaliuresis in patients with GS. METHODS: Six patients with most of the diagnostic features of GS were examined. To examine the role of bicarbonaturia, the transtubular K concentration gradient (TTKG) was assessed before and after an oral load of NH4Cl which caused the urine pH to be < 6. To evaluate the role of hypomagnesemia, the TTKG was examined after an infusion of enough magnesium (Mg) to achieve normal levels of Mg in plasma for close to 24 h. RESULTS: The TTKG remained very high even when the pH of the urine was < 6.0. An infusion of Mg caused the TTKG to approach expected values for hypokalemia in 4 of 6 patients. The infusion of Mg was extended in 1 patient who had a sustained high TTKG for 24 h; the TTKG remained elevated for 96 h despite normal plasma Mg levels. CONCLUSIONS: Bicarbonaturia does not play a critical role in maintaining the very high TTKG in these patients. The K wasting in 4 of 6 of these patients could largely be attributed to hypomagnesemia and/or Mg depletion. The plasma aldosterone level tended to be higher in patients who did not respond to the infusion of Mg. Therefore, these patients may not represent a homogeneous group with regard to the pathophysiology of their renal K wasting. |Adult[MESH] |Ammonium Chloride/pharmacology[MESH] |Bartter Syndrome/blood/*physiopathology/urine[MESH] |Bicarbonates/*urine[MESH] |Child, Preschool[MESH] |Female[MESH] |Humans[MESH] |Hydrogen-Ion Concentration[MESH] |Hypokalemia/*physiopathology[MESH] |Kidney Tubules/physiopathology[MESH] |Magnesium Sulfate/administration & dosage/pharmacology[MESH] |Magnesium/*blood[MESH] |Male[MESH] |Potassium/metabolism[MESH]Studies on the pathogenesis of hypokalemia in Gitelman s syndrome: rol(epmc).pdf DeepDyve Pubget Overpricing