Cases reported "Hyperaldosteronism"

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11/14. Familial Bartter's syndrome.

    Two sisters were found to have Bartter's syndrome. Both had hypokalemia, hyperreninemia, normal BPs, and decreased pressor responses to angiotensin ii. During a water diuresis, patient 1 had an abnormally low distal tubular fractional reabsorption of chloride initially, but this normalized after hypokalemia was corrected for one year. Patient 2 had no demonstrable defect in chloride transport. hypokalemia in Bartter's syndrome may be caused by some hereditary mechanisms other than defective reabsorption of chloride in the distal tubules.
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12/14. Asymptomatic Bartter's syndrome.

    A 63-year-old man had asymptomatic Bartter's syndrome, discovered during evaluation for hypokalemia. Elevated plasma renin and aldosterone levels, angiotension resistance, and elevated urinary prostaglandin excretion were noted. Tubular function studies implicated the proximal tubule as the site of a mild sodium reabsorption defect, and renal wasting of potassium and magnesium were also noted. indomethacin therapy lowered the urinary prostaglandin excretion and the renin and aldosterone levels but did not correct the hypokalemia. spironolactone therapy resulted in normalization of serum potassium but not serum magnesium levels. Bartter's syndrome may result from various causes but renal wasting of sodium, potassium and/or magnesium probably exist in all cases. Unexplained, asymptomatic hypokalemia in any age group may be due to Bartter's syndrome.
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13/14. The renal tubular defect of Bartter's syndrome.

    The site of reduced electrolyte transport in Bartter's syndrome (BS) was studied with a new technique whereby resorption can be separately measured as equivalent volumes of free water generated along the ascending limb of Henle's loop (CH2O-HL) and cortical distal tubule (CH2O-DT): the fractional proximal resorption (FPR) and the volume of free water dissipated along collecting ducts (CD) by back diffusion (CH2O-BD) in the absence of ADH are also measured during maximal water diuresis. Data are expressed as ml . min-1 GFR-1 . 100. The studies were performed on 2 brothers with all clinical and laboratory features of BS. They achieved external Na balance within 3 days when placed on either 10, 100, or 230 mEq Na daily. With the 100-mEq-Na diet indomethacin caused a stable 1.5 kg weight gain. FPR was 0.69 in normal controls (NC), 0.77 in BS; CH2O-HL 16.7 vs. 16.4; CH2O-DT 9.7 vs. 3.9; CH2O-BD 13.8 vs. 13.8; CH2O (free water excretion) 12.5 vs. 6.1; urine flow rate (V) 17.6 vs. 9.9. Thus, BS is characterized by a slight fall in proximal delivery, normal HLNa transport, a striking impairment of DTNa transport and preserved interstitial hypertonicity which drives a normal osmotic flow of CH2O-BD. aspirin injected intravenously during water load affected CH2O and V in proportion to the change in GFR, which fell from 145 /- 19 to 114 /- 12 ml . min-1, p less than 0.01). Thus, the primary abnormality of BS is impaired Na transport along the early portion of the distal tubule. This is compensated by volume contraction attended by reduced proximal delivery and full activation of renin-angiotensin-aldosterone system. Consequently, more distal cation exchange sites reclaim Na at the expenses of excessive K and H losses, trapping NH4Cl within tubular lumen and generating hypokalemic metabolic alkalosis. The excess angiotensin is counterbalanced by increased prostaglandin (PG) secretion, which brings renal vascular resistances toward normal and causes tachyphylaxis to angiotensin. Inhibition of PG synthesis leads to a fall in GFR and proximal delivery: this causes distal delivery to fall below reabsorptive capacity for Na: therefore both Na and K retention ensues causing partial volume reexpansion till a new balance is established. PGs do not affect either Na or Cl resorption in BS except by a purely hemodynamic action.
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14/14. A case of secondary aldosteronism similar to Bartter's syndrome with no abnormality in renal chloride reabsorption.

    We had a 20-year-old male patient of secondary aldosteronism similar to Bartter's syndrome, which had proved to be evident after the remission of nephrotic syndrome. In the patient, hypokalemic alkalosis and hyperreninemic hyperaldosteronemia were observed, although the blood pressure was normal. hyperplasia of juxtaglomerular cells was observed and no abnormalities indicating either glomerulonephritis or renal artery stenosis were found; the pressor response to intravenously infused angiotensin (ang) II was markedly decreased; urinary prostaglandin (PG) E2, kallikrein and kinin excretion were elevated. The inhibition of PG synthesis with indomethacin decreased renal PG production and partially corrected both hypokalemia and pressor responsiveness to ang II. Thus, this case is considered to be a case of Bartter's syndrome. Contrary to the previously reported observations, the effective fractional chloride reabsorption rate in the renal distal tubules was normal (> 80%) and not changed by PG inhibition. plasma atrial natriuretic peptide level was normal. An interaction between renin-angiotensin and PG systems appears to play a prior role in this case. To explain the pathophysiology, we have hypothesized an abnormal function of ang II receptor signal transduction which excessively stimulates PLA2, resulting in overproduction of PG synthesis in tissues.
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