{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:40:07Z","timestamp":1745469607033,"version":"3.40.4"},"reference-count":2,"publisher":"S. Karger AG","issue":"2","license":[{"start":{"date-parts":[[2004,1,1]],"date-time":"2004-01-01T00:00:00Z","timestamp":1072915200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2004,1,1]],"date-time":"2004-01-01T00:00:00Z","timestamp":1072915200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Kidney Blood Press Res"],"published-print":{"date-parts":[[2004]]},"abstract":"<jats:p>&lt;i&gt;Background:&lt;\/i&gt; Patients with chronic glomerulonephritis exhibit salt-sensitive (SS) hypertension. In the early stage, however, the exact characteristics are still unclear. A decrease in renal dopamine production under basal conditions or after a sodium load has been reported in a subset of patients with SS primary hypertension. &lt;i&gt;Aims:&lt;\/i&gt; The present study examined 17 untreated IgA-N patients with near-normal renal function, to determine whether salt sensitivity appears before hypertension and whether this sensitivity is related to renal dopamine production. &lt;i&gt;Methods:&lt;\/i&gt; Daily urinary excretion of dopamine, the amine precursor \u2013 L-DOPA, and metabolites was monitored in conditions of basal sodium ingestion, followed by three consecutive 5-day periods of 100, 20 and 350\u00a0mmol\/day sodium intake. The sodium sensitivity index (SSI) was evaluated in each patient. In addition, the patients were considered SS when showing an increase \u22675 mm Hg in 24-hour mean BP when they changed from a 20- to a 350-mmol\/day sodium diet. &lt;i&gt;Results:&lt;\/i&gt; Urinary dopamine output was lower in SS than in salt-resistant patients throughout the study (p &lt; 0.001). This was accompanied by lower creatinine clearance values and higher urinary protein excretion in SS IgA-N patients. A strong negative relationship was observed in these 17 IgA-N patients between the SSI and the daily urinary excretion of dopamine in conditions of both 20 mmol\/day sodium intake (r&lt;sup&gt;2&lt;\/sup&gt; = 0.592; p = 0.0003) and 350 mmol\/day sodium diet (r&lt;sup&gt;2&lt;\/sup&gt; = 0.352; p = 0.01). However, urinary dopamine output varied appropriately throughout the study in SS patients, in agreement with changes in sodium intake. &lt;i&gt;Conclusion:&lt;\/i&gt; We conclude that in IgA-N patients, a rightward shift in the \u2018pressure natriuresis\u2019 can appear before hypertension and is related with a reduced renal production of dopamine. It is suggested that decreased renal dopamine synthesis in SS IgA-N patients results from acquired tubulointerstitial injury. In contrast to what has been found in SS primary hypertension, renal dopamine may behave appropriately in SS IgA-N patients, as a compensatory hormone.<\/jats:p>","DOI":"10.1159\/000076022","type":"journal-article","created":{"date-parts":[[2004,1,9]],"date-time":"2004-01-09T11:23:35Z","timestamp":1073647415000},"page":"78-87","source":"Crossref","is-referenced-by-count":2,"title":["Renal Dopamine and Salt Sensitivity of Blood Pressure in IgA Nephropathy"],"prefix":"10.1159","volume":"27","author":[{"given":"Manuel","family":"Pestana","sequence":"first","affiliation":[]},{"given":"Joana","family":"Santos","sequence":"additional","affiliation":[]},{"given":"Alejandro","family":"Santos","sequence":"additional","affiliation":[]},{"given":"Andreia","family":"Coroas","sequence":"additional","affiliation":[]},{"given":"Flora","family":"Correia","sequence":"additional","affiliation":[]},{"given":"Paula","family":"Serr\u00e3o","sequence":"additional","affiliation":[]},{"given":"Carmen","family":"Valbuena","sequence":"additional","affiliation":[]},{"given":"Patr\u00edcio","family":"Soares-da-Silva","sequence":"additional","affiliation":[]}],"member":"127","published-online":{"date-parts":[[2004,5,3]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1159\/000025844"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra011078"}],"container-title":["Kidney and Blood Pressure Research"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/76022","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/76022","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:08:51Z","timestamp":1745467731000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000076022"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004]]},"references-count":2,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2004,7,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000076022","archive":["Portico"],"relation":{},"ISSN":["1420-4096","1423-0143"],"issn-type":[{"type":"print","value":"1420-4096"},{"type":"electronic","value":"1423-0143"}],"subject":[],"published":{"date-parts":[[2004]]}}}