{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T17:08:16Z","timestamp":1771002496948,"version":"3.50.1"},"reference-count":51,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2006,2,27]],"date-time":"2006-02-27T00:00:00Z","timestamp":1140998400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Proteomics"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hypokalemic nephropathy caused by prolonged K<jats:sup>+<\/jats:sup> deficiency is associated with metabolic alkalosis, polydipsia, polyuria, growth retardation, hypertension, and progressive tubulointerstitial injury. Its pathophysiology, however, remains unclear. We performed gel\u2010based, differential proteomics analysis of kidneys from BALB\/c mice fed with high\u2010normal\u2010K<jats:sup>+<\/jats:sup> (HNK), low\u2010normal\u2010K<jats:sup>+<\/jats:sup> (LNK), or K<jats:sup>+<\/jats:sup>\u2010depleted diet for 8\u2009wk (<jats:italic>n<\/jats:italic>\u2005=\u20056 in each group). Plasma K<jats:sup>+<\/jats:sup> levels were 4.62\u2005\u00b1\u20050.35, 4.46\u2005\u00b1\u20050.23, and 1.51\u2005\u00b1\u20050.21\u2009mmol\/L for HNK, LNK, and KD mice, respectively (<jats:italic>p<\/jats:italic>\u2005&lt;\u20050.0001; KD <jats:italic>vs.<\/jats:italic> others). With comparable amounts of food intake, the KD mice drank significantly more water than the other two groups and had polyuria. Additionally, the KD mice had growth retardation, metabolic alkalosis, markedly enlarged kidneys, renal tubular dilation, intratubular deposition of amorphous and laminated hyaline materials, and tubular atrophy. A total of 33 renal proteins were differentially expressed between the KD mice and others, whereas only eight proteins were differentially expressed between the HNK and LNK groups, as determined by quantitative intensity analysis and ANOVA with Tukey's post hoc multiple comparisons. Using MALDI\u2010MS and\/or quadrupole\u2010TOF MS\/MS, 30 altered proteins induced by K<jats:sup>+<\/jats:sup>\u2010depletion were identified as metabolic enzymes (<jats:italic>e.g.<\/jats:italic>, carbonic anhydrase II, aldose reductase, glutathione <jats:italic>S<\/jats:italic>\u2010transferase GT41A, <jats:italic>etc.<\/jats:italic>), signaling proteins (14\u20133\u20103 \u03b5, 14\u20133\u20103 \u03b6, and cofilin 1), and cytoskeletal proteins (\u03b3\u2010actin and tropomyosin). Some of these altered proteins, particularly metabolic enzymes and signaling proteins, have been demonstrated to be involved in metabolic alkalosis, polyuria, and renal tubular injury. Our findings may lead to a new road map for research on hypokalemic nephropathy and to better understanding of the pathophysiology of this medical disease when the functional and physiological significances of these altered proteins are defined.<\/jats:p>","DOI":"10.1002\/pmic.200500530","type":"journal-article","created":{"date-parts":[[2006,2,27]],"date-time":"2006-02-27T05:18:12Z","timestamp":1141017492000},"page":"2273-2285","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Proteomic identification of alterations in metabolic enzymes and signaling proteins in hypokalemic nephropathy"],"prefix":"10.1002","volume":"6","author":[{"given":"Visith","family":"Thongboonkerd","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Somchai","family":"Chutipongtanate","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rattiyaporn","family":"Kanlaya","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Napat","family":"Songtawee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Supachok","family":"Sinchaikul","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paisal","family":"Parichatikanond","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shui\u2010Tein","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Prida","family":"Malasit","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,3,22]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.160.16.2429"},{"key":"e_1_2_1_3_2","first-page":"997","volume-title":"Brenner & Rector's The Kidney","author":"Mount D. 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