{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T19:55:49Z","timestamp":1787774149280,"version":"build-2784847793"},"reference-count":54,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2022,11,24]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Potassium chloride intake induced a reduction in sodium-chloride cotransporter (NCC) and phosphorylated NCC in urinary extracellular vesicles from patients with primary aldosteronism during a significantly raised level of endogenous aldosterone.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Low plasma potassium (secondary to aldosterone excess) may dominate in terms of NCC regulation in the setting of primary aldosteronism.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Elevated abundance of sodium-chloride cotransporter (NCC) and phosphorylated NCC (pNCC) are potential markers of primary aldosteronism (PA), but these effects may be driven by hypokalemia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We measured plasma potassium in patients with PA. If potassium was &lt;4.0 mmol\/L, patients were given sufficient oral potassium chloride (KCl) over 24 hours to achieve as close to 4.0 mmol\/L as possible. Clinical chemistries were assessed, and urinary extracellular vesicles (uEVs) were examined to investigate effects on NCC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 21 patients with PA who received a median total dose of 6.0 g (2.4\u201316.8 g) of KCl, increases were observed in plasma potassium (from 3.4 to 4.0 mmol\/L;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), aldosterone (from 305 to 558 pmol\/L;\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.01), and renin (from 1.2 to 2.5 mIU\/L;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001), whereas decreases were detected in uEV levels of NCC (median fold change\n                      <jats:sub>(post\/basal)<\/jats:sub>\n                      [FC]=0.71 [0.09\u20131.99];\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.02), pT60-NCC (FC=0.84 [0.06\u20131.66];\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.05), and pT55\/60-NCC (FC=0.67 [0.08\u20132.42];\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.02). By contrast, in 10 patients with PA who did not receive KCl, there were no apparent changes in plasma potassium, NCC abundance, and phosphorylation status, but increases were observed in plasma aldosterone (from 178 to 418 pmol\/L;\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.006) and renin (from 2.0 to 3.0 mU\/L;\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.009). Plasma potassium correlated inversely with uEV levels of NCC (\n                      <jats:italic toggle=\"yes\">R<\/jats:italic>\n                      <jats:sup>2<\/jats:sup>\n                      =0.11;\n                      <jats:italic toggle=\"yes\">P=<\/jats:italic>\n                      0.01), pT60-NCC (\n                      <jats:italic toggle=\"yes\">R<\/jats:italic>\n                      <jats:sup>2<\/jats:sup>\n                      =0.11;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.01), and pT55\/60-NCC (\n                      <jats:italic toggle=\"yes\">R<\/jats:italic>\n                      <jats:sup>2<\/jats:sup>\n                      =0.11;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.01).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Acute oral KCl loading replenished plasma potassium in patients with PA and suppressed NCC abundance and phosphorylation, despite a significant rise in plasma aldosterone. This supports the view that potassium supplementation in humans with PA overrides the aldosterone stimulatory effect on NCC. The increased plasma aldosterone in patients with PA without KCl supplementation may be due to aldosterone response to posture challenge.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0003632022","type":"journal-article","created":{"date-parts":[[2022,8,26]],"date-time":"2022-08-26T15:45:13Z","timestamp":1661528713000},"page":"1909-1923","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":9,"title":["In Primary Aldosteronism Acute Potassium Chloride Supplementation Suppresses Abundance and Phosphorylation of the Sodium-Chloride Cotransporter"],"prefix":"10.34067","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9610-0943","authenticated-orcid":false,"given":"Aihua","family":"Wu","sequence":"first","affiliation":[{"name":"Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin J.","family":"Wolley","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia"},{"name":"Department of Nephrology, Royal Brisbane and Women\u2019s Hospital, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexandra","family":"Matthews","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane","family":"Cowley","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Welling","sequence":"additional","affiliation":[{"name":"Department of Medicine and Physiology, Johns Hopkins University, Baltimore, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1623-199X","authenticated-orcid":false,"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Aarhus University, Aarhus, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Stowasser","sequence":"additional","affiliation":[{"name":"Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2022,11,24]]},"reference":[{"key":"B1-20250825","doi-asserted-by":"crossref","first-page":"200","DOI":"10.1001\/jama.1965.03090030022005","article-title":"Normokalemic primary aldosteronism. 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