Markers of potassium homeostasis in salt losing tubulopathies- associations with hyperaldosteronism and hypomagnesemia.

BACKGROUND: Renal loss of potassium (K+) and magnesium (Mg2+) in salt losing tubulopathies (SLT) leads to significantly reduced Quality of Life (QoL) and higher risks of cardiac arrhythmia. The normalization of K+ is currently the most widely accepted treatment target, however in even excellently designed RCTs the increase of K+ was only mild and rarely normalized. These findings question the role of K+ as the ideal marker of potassium homeostasis in SLT. Aim of this hypothesis-generating study was to define surrogate endpoints for future treatment trials in SLT in terms of their usefulness to determine QoL and important clinical outcomes. METHODS: Within this prospective cross-sectional study including 11 patients with SLTs we assessed the biochemical, clinical and cardiological parameters and their relationship with QoL (RAND SF-36). The primary hypothesis was that QoL would be more dependent of higher aldosterone concentration, assessed by the transtubular-potassium-gradient (TTKG). Correlations were evaluated using Pearson's correlation coefficient. RESULTS: Included patients were mainly female (82%, mean age 34 ± 12 years). Serum K+ and Mg2+ was 3.3 ± 0.6 mmol/l and 0.7 ± 0.1 mmol/l (mean ± SD). TTKG was 9.5/3.4-20.2 (median/range). While dimensions of mental health mostly correlated with serum Mg2+ (r = 0.68, p = 0.04) and K+ (r = 0.55, p = 0.08), better physical health was associated with lower aldosterone levels (r = -0.61, p = 0.06). TTKG was neither associated with aldosterone levels nor with QoL parameters. No relevant abnormalities were observed in neither 24 h-ECG nor echocardiography. CONCLUSIONS: Hyperaldosteronism, K+ and Mg2+ were the most important parameters of QoL. TTKG was no suitable marker for hyperaldosteronism or QoL. Future confirmatory studies in SLT should assess QoL as well as aldosterone, K+ and Mg2+.

The psychosis of metabolic alkalosis.

Metabolic alkalosis as an additional etiology for organic psychosis is presented and covered, with theoretical and clinical considerations, including treatment. Illustrative case histories are cited and certain parameters of acid-base equilibrium are described as favorable to the normal awake state, while substantial deviation towards metabolic alkalosis is seen as conducive to psychotic aberration.

[Development of tetany in siblings suffered from Bartter's syndrome].

The present authors observed and treated a siblings case of normocalcemic tetany, which is considered as belonging to Bartter's syndrome. As far as we know, there are a number of familial cases of tetany in literature, but none of them spreads over more than two generations, so that the tetany appears to be recessive in hereditary characters including our patients. Both of them presented tetanic seizures in the course of Bartter's syndrome and they were regarded as one of various manifestations of the syndrome. In other words, the Bartter's syndrome or the hypopotassemia should be one of the fundamental disorders for developing tetanic symptom. The tetanic symptoms became extinct during the treatment with spironolactone against hypopotassemia. Of the two patients, younger sister had shown an agitated depression developed on her childish and over-sensitive personality, but the depression was improved in parallel to the recovery from tetany and hypopotassemia. Therefore, it appears to be certain that the patients would have some premorbid deviation of personality traits, where symptomatic psychoses could be attributed, in the case of Bartter's syndrome. Generally speaking the psychic disorders, such as personality deviation and psychotic episode, seem to by very important symptoms in patient with Bartter's syndrome as well as in patient with hypocalcemia or hypoparathyroidism.