{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T01:08:31Z","timestamp":1788916111227,"version":"build-2803163510"},"reference-count":54,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2019,12,1]]},"abstract":"<jats:p>The present study tested the hypotheses that nephrotic syndrome (NS) leads to renal K<jats:sup>+<\/jats:sup>loss because of augmented epithelial Na<jats:sup>+<\/jats:sup>channel (ENaC) activity followed by downregulation of renal K<jats:sup>+<\/jats:sup>secretory pathways by suppressed aldosterone. The hypotheses were addressed by determining K<jats:sup>+<\/jats:sup>balance and kidney abundance of K<jats:sup>+<\/jats:sup>and Na<jats:sup>+<\/jats:sup>transporter proteins in puromycin aminonucleoside (PAN)-induced rat nephrosis. The effects of amiloride and angiotensin II type 1 receptor and mineralocorticoid receptor (MR) antagonists were tested. Glucocorticoid-dependent MR activation was tested by suppression of endogenous glucocorticoid with dexamethasone. Urine and plasma samples were obtained from pediatric patients with NS in acute and remission phases. PAN-induced nephrotic rats had ENaC-dependent Na<jats:sup>+<\/jats:sup>retention and displayed lower renal K<jats:sup>+<\/jats:sup>excretion but elevated intestinal K<jats:sup>+<\/jats:sup>secretion that resulted in less cumulated K<jats:sup>+<\/jats:sup>in NS. Aldosterone was suppressed at day 8. The NS-associated changes in intestinal, but not renal, K<jats:sup>+<\/jats:sup>handling responded to suppression of corticosterone, whereas angiotensin II type 1 receptor and MR blockers and amiloride had no effect on urine K<jats:sup>+<\/jats:sup>excretion during NS. In PAN-induced nephrosis, kidney protein abundance of the renal outer medullary K<jats:sup>+<\/jats:sup>channel and \u03b3-ENaC were unchanged, whereas the Na<jats:sup>+<\/jats:sup>-Cl<jats:sup>\u2212<\/jats:sup>cotransporter was suppressed and Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-ATPase increased. Pediatric patients with acute NS displayed suppressed urine Na<jats:sup>+<\/jats:sup>-to-K<jats:sup>+<\/jats:sup>ratios compared with remission and elevated plasma K<jats:sup>+<\/jats:sup>concentration, whereas fractional K<jats:sup>+<\/jats:sup>excretion did not differ. Acute NS is associated with less cumulated K<jats:sup>+<\/jats:sup>in a rat model, whereas patients with acute NS have elevated plasma K<jats:sup>+<\/jats:sup>and normal renal fractional K<jats:sup>+<\/jats:sup>excretion. In NS rats, K<jats:sup>+<\/jats:sup>balance is not coupled to ENaC activity but results from opposite changes in renal and fecal K<jats:sup>+<\/jats:sup>excretion with a contribution from corticosteroid MR-driven colonic secretion.<\/jats:p>","DOI":"10.1152\/ajprenal.00179.2019","type":"journal-article","created":{"date-parts":[[2019,9,30]],"date-time":"2019-09-30T14:24:06Z","timestamp":1569853446000},"page":"F1549-F1562","source":"Crossref","is-referenced-by-count":6,"title":["Nephrotic syndrome is associated with increased plasma K<sup>+<\/sup>concentration, intestinal K<sup>+<\/sup>losses, and attenuated urinary K<sup>+<\/sup>excretion: a study in rats and humans"],"prefix":"10.1152","volume":"317","author":[{"given":"Rikke","family":"Ydegaard","sequence":"first","affiliation":[{"name":"Department of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, 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