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style="display:none">Search</button></div></aside><main id="maincontent"><section class="o-columnbox1"><header><h2 class="o-columnbox1__heading" aria-live="polite">Scholarly Works (2 results)</h2></header><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/0vc567rk"><div class="c-clientmarkup">A randomized trial of albumin infusion to prevent intradialytic hypotension in hospitalized hypoalbuminemic patients</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3AMacedo%2C%20Etienne">Macedo, Etienne</a>; </li><li><a href="/search/?q=author%3AKarl%2C%20Bethany">Karl, Bethany</a>; </li><li><a href="/search/?q=author%3ALee%2C%20Euyhyun">Lee, Euyhyun</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3AMehta%2C%20Ravindra%20L">Mehta, Ravindra L</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (2021)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup"><h3>Background</h3>Intradialytic hypotension (IDH) is a frequent complication of intermittent hemodialysis (IHD), occurring from 15 to 50% of ambulatory sessions, and is more frequent among hospitalized patients with hypoalbuminemia. IDH limits adequate fluid removal and increases the risk for vascular access thrombosis, early hemodialysis (HD) termination, and mortality. Albumin infusion before and during therapy has been used for treating IDH with the varying results. We evaluated the efficacy of albumin infusion in preventing IDH during IHD in hypoalbuminemic inpatients.<h3>Methods</h3>A randomized, crossover trial was performed in 65 AKI or ESKD patients with hypoalbuminemia (albumin < 3 g/dl) who required HD during hospitalization. Patients were randomized to receive 100 ml of either 0.9%sodium chloride or 25% albumin intravenously at the initiation of each dialysis. These two solutions were alternated for up to six sessions. Patients' vital signs and ultrafiltration removal rate were recorded every 15 to 30 min during dialysis. IDH was assessed by different definitions reported in the literature. All symptoms associated with a noted hypotensive event as well as interventions during the dialysis were recorded.<h3>Results</h3>Sixty-five patients were submitted to 249 sessions; the mean age was 58 ([Formula: see text] 12), and 46 (70%) were male with a mean weight of 76 ([Formula: see text] 18) kg. The presence of IDH was lower during albumin sessions based on all definitions. The hypotension risk was significantly decreased based on the Kidney Disease Outcomes Quality Initiative definition; (15% with NS vs. 7% with albumin, p = 0.002). The lowest intradialytic SBP was significantly worse in patients who received 0.9% sodium chloride than albumin (NS 83 vs. albumin 90 mmHg, p = 0.035). Overall ultrafiltration rate was significantly higher in the albumin therapies [NS - 8.25 ml/kg/h (- 11.18 5.80) vs. 8.27 ml/kg/h (- 12.22 to 5.53) with albumin, p = 0.011].<h3>Conclusion</h3>In hypoalbuminemic patients who need HD, albumin administration before the dialysis results in fewer episodes of hypotension and improves fluid removal. Albumin infusion may be of benefit to improve the safety of HD and achievement of fluid balance in these high-risk patients. ClinicalTrials.gov Identifier: NCT04522635.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div><div class="c-scholworks__ancillary"><a class="c-scholworks__thumbnail" href="/uc/item/0vc567rk"><img src="/cms-assets/8f8e843a00f210dfb3db4364f0e69fb5ba6eb8545834386c87a5c78a83ea33a7" alt="Cover page: A randomized trial of albumin infusion to prevent intradialytic hypotension in hospitalized hypoalbuminemic patients"/></a><a href="https://creativecommons.org/licenses/by/4.0/" class="c-scholworks__license"><img class="c-lazyimage" data-src="/images/cc-by-small.svg" alt="Creative Commons 'BY' version 4.0 license"/></a></div></section><section class="c-scholworks"><div class="c-scholworks__main-column"><ul class="c-scholworks__tag-list"><li class="c-scholworks__tag-article">Article</li><li class="c-scholworks__tag-peer">Peer Reviewed</li></ul><div><h3 class="c-scholworks__heading"><a href="/uc/item/79s7m1nn"><div class="c-clientmarkup">Metabolomics Reveals Signature of Mitochondrial Dysfunction in Diabetic Kidney Disease</div></a></h3></div><div class="c-authorlist"><ul class="c-authorlist__list"><li class="c-authorlist__begin"><a href="/search/?q=author%3ASharma%2C%20Kumar">Sharma, Kumar</a>; </li><li><a href="/search/?q=author%3AKarl%2C%20Bethany">Karl, Bethany</a>; </li><li><a href="/search/?q=author%3AMathew%2C%20Anna%20V">Mathew, Anna V</a>; </li><li><a href="/search/?q=author%3AGangoiti%2C%20Jon%20A">Gangoiti, Jon A</a>; </li><li><a href="/search/?q=author%3AWassel%2C%20Christina%20L">Wassel, Christina L</a>; </li><li><a href="/search/?q=author%3ASaito%2C%20Rintaro">Saito, Rintaro</a>; </li><li><a href="/search/?q=author%3APu%2C%20Minya">Pu, Minya</a>; </li><li><a href="/search/?q=author%3ASharma%2C%20Shoba">Sharma, Shoba</a>; </li><li><a href="/search/?q=author%3AYou%2C%20Young-Hyun">You, Young-Hyun</a>; </li><li><a href="/search/?q=author%3AWang%2C%20Lin">Wang, Lin</a>; </li><li><a href="/search/?q=author%3ADiamond-Stanic%2C%20Maggie">Diamond-Stanic, Maggie</a>; </li><li><a href="/search/?q=author%3ALindenmeyer%2C%20Maja%20T">Lindenmeyer, Maja T</a>; </li><li><a href="/search/?q=author%3AForsblom%2C%20Carol">Forsblom, Carol</a>; </li><li><a href="/search/?q=author%3AWu%2C%20Wei">Wu, Wei</a>; </li><li><a href="/search/?q=author%3AIx%2C%20Joachim%20H">Ix, Joachim H</a>; </li><li><a href="/search/?q=author%3AIdeker%2C%20Trey">Ideker, Trey</a>; </li><li><a href="/search/?q=author%3AKopp%2C%20Jeffrey%20B">Kopp, Jeffrey B</a>; </li><li><a href="/search/?q=author%3ANigam%2C%20Sanjay%20K">Nigam, Sanjay K</a>; </li><li><a href="/search/?q=author%3ACohen%2C%20Clemens%20D">Cohen, Clemens D</a>; </li><li><a href="/search/?q=author%3AGroop%2C%20Per-Henrik">Groop, Per-Henrik</a>; </li><li><a href="/search/?q=author%3ABarshop%2C%20Bruce%20A">Barshop, Bruce A</a>; </li><li><a href="/search/?q=author%3ANatarajan%2C%20Loki">Natarajan, Loki</a>; </li><li><a href="/search/?q=author%3ANyhan%2C%20William%20L">Nyhan, William L</a>; </li><li class="c-authorlist__end"><a href="/search/?q=author%3ANaviaux%2C%20Robert%20K">Naviaux, Robert K</a> </li></ul></div><div class="c-scholworks__publication"><a href="/uc/ucsd_postprints">UC San Diego Previously Published Works</a> (2013)</div><div class="c-scholworks__abstract"><div class="c-clientmarkup">Diabetic kidney disease is the leading cause of ESRD, but few biomarkers of diabetic kidney disease are available. This study used gas chromatography-mass spectrometry to quantify 94 urine metabolites in screening and validation cohorts of patients with diabetes mellitus (DM) and CKD(DM+CKD), in patients with DM without CKD (DM-CKD), and in healthy controls. Compared with levels in healthy controls, 13 metabolites were significantly reduced in the DM+CKD cohorts (P≤0.001), and 12 of the 13 remained significant when compared with the DM-CKD cohort. Many of the differentially expressed metabolites were water-soluble organic anions. Notably, organic anion transporter-1 (OAT1) knockout mice expressed a similar pattern of reduced levels of urinary organic acids, and human kidney tissue from patients with diabetic nephropathy demonstrated lower gene expression of OAT1 and OAT3. Analysis of bioinformatics data indicated that 12 of the 13 differentially expressed metabolites are linked to mitochondrial metabolism and suggested global suppression of mitochondrial activity in diabetic kidney disease. Supporting this analysis, human diabetic kidney sections expressed less mitochondrial protein, urine exosomes from patients with diabetes and CKD had less mitochondrial DNA, and kidney tissues from patients with diabetic kidney disease had lower gene expression of PGC1α (a master regulator of mitochondrial biogenesis). We conclude that urine metabolomics is a reliable source for biomarkers of diabetic complications, and our data suggest that renal organic ion transport and mitochondrial function are dysregulated in diabetic kidney disease.</div></div><div class="c-scholworks__media"><ul class="c-medialist"></ul></div></div></section></section></main></form></div><div><div class="c-toplink"><a href="javascript:window.scrollTo(0, 0)">Top</a></div><footer class="c-footer"><nav class="c-footer__nav"><ul><li><a href="/">Home</a></li><li><a href="/aboutEschol">About eScholarship</a></li><li><a href="/campuses">Campus Sites</a></li><li><a href="/ucoapolicies">UC Open Access Policy</a></li><li><a href="/publishing">eScholarship Publishing</a></li><li><a href="https://www.cdlib.org/about/accessibility.html">Accessibility</a></li><li><a href="/privacypolicy">Privacy Statement</a></li><li><a href="/policies">Site Policies</a></li><li><a href="/terms">Terms of Use</a></li><li><a href="/login"><strong>Admin Login</strong></a></li><li><a href="https://help.escholarship.org"><strong>Help</strong></a></li></ul></nav><div class="c-footer__logo"><a href="/"><img class="c-lazyimage" data-src="/images/logo_footer-eschol.svg" alt="eScholarship, University of California"/></a></div><div class="c-footer__copyright">Powered by the<br/><a href="http://www.cdlib.org">California Digital Library</a><br/>Copyright © 2017<br/>The Regents of the University of California</div></footer></div></div></div></div> <script src="/js/vendors~app-bundle-7424603c338d723fd773.js"></script> <script src="/js/app-bundle-63f992b6abba5f8338a3.js"></script> </body> </html>