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• W1962684563 abstract "We evaluated 27 adult patients with chronic hypokalaemia (K+=2.9±0.2 mmol/1), documented over at least 5 years, in whom the cause of the hypokalaemia had not been clarified in spite of previous testing. In 15 patients it was possible to establish a diagnosis by a thorough outpatient workup (diuretic abuse (n=5), surreptitious vomiting (n=8), laxative abuse (n=l), renal tubular acidosis (n=1)). Commonly utilized tests such as measurements of plasma renin activity, plasma aldosterone, and urinary potassium concentration proved not to be useful in the differential diagnosis of these patients. In contrast the following were diagnostically important: in surreptitious vomiting the hypochloraemia, the mild renal insufficiency, and the extremely low urinary chloride concentration; in diuretic abuse the high urinary concentration of chloride together with repeatedly positive toxicology screens for diuretics; in laxative abuse the high stool weight and extremely low urinary sodium concentration. In the remaining 12 patients none of these diagnoses applied and further tests for suspected Bartter's syndrome were done in the hospital. The patients showed hyperreninaemic hyperaldosteronism (plasma renin activity≡14.4±5 ng AI/ml h, normal≡0.2−2; aldosterone 16.2±6 ng/dl, normal=2−10), mild metabolic alkalosis, and inappropriately high urinary excretion of potassium (88±15 mmol/1) and magnesium for the degrees of their corresponding hypokalaemia (K+=2.8±0.08 mmol/1) and hypomagnesaemia (Mg2+=0.56±0.03 mmol/1). However, the following were normal or close to normal: the urinary excretion of PGE2 (0.47±0.23 μg/24 h), the platelet aggregation, the distal fractional chloride reabsorption coefficient (Q=0.79±0.02, classical Bartter's syndrome=0.49±0.08), the minimal urinary osmolality (Uosm min 85±3 mOsm/kg H2O, classical Bartter's syndrome=157±10), the maximal urinary concentration during a water deprivation test (Uosm=882±30 mOsm/kg H2O) and the urinary acidification (pH=5.3±0.23) in response to oral loading with (NH4Cl. The patients were also noted to be hypocalciuric (0.9±0.28 mmol/24h; normal: 2.5−8.0 mmol/24 h). Hypocalciuria is a hallmark of Gitelman's syndrome. Additional studies of potassium handling were done. Potassium channels of erythrocyte cell membranes were tested with the patch—clamp technique and showed normal conductances. The K+ concentration in stimulated sweat, however, was 8.2±0.3 in patients versus 6.9±0.3 mmol/1 in healthy controls (P<0.05). On the basis of our data we suggest that Gitelman's syndrome is a common cause of chronic severe hypokalaemia in adults, whereas classical Bartter's syndrome is very rare. In addition the Gitelman's syndrome was associated with increased sweat potassium concentration. This may indicate a defect of potassium transport by sweat-gland epithelium, which may also exist in the nephron of such patients." @default.
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• W1962684563 date "1995-09-01" @default.
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• W1962684563 title "Chronic hypokalaemia of adults: Gitelman's syndrome is frequent but classical Bartter's syndrome is rare" @default.
• W1962684563 doi "https://doi.org/10.1093/ndt/10.9.1607" @default.
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