{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T16:45:59Z","timestamp":1760978759009,"version":"3.40.4"},"reference-count":2,"publisher":"S. Karger AG","issue":"1","license":[{"start":{"date-parts":[[1998,1,1]],"date-time":"1998-01-01T00:00:00Z","timestamp":883612800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[1998,1,1]],"date-time":"1998-01-01T00:00:00Z","timestamp":883612800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron"],"published-print":{"date-parts":[[1998]]},"abstract":"In primary minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS), increased lymphocyte reactivity to renal antigens has been defined. Soluble HLA class I antigen (sHLA-I) is actively secreted by T and B lymphocytes when they are stimulated by mitogens, antigens and lymphokines. To determine if serum and urine sHLA-I levels could predict steroid response in patients with MCD and differentiate those from FSGS, we have investigated 45 healthy controls, biopsy-proven 17 patients with MCD (edema and 24-hour urine protein >3.5\u00a0g\/day), 8 patients with FSGS (24-hour urine protein >1\u00a0g\/day) and 10 patients with membranous nephropathy (MGN) (24-hour urine protein >1\u00a0g\/day). Before and after prednisone therapy (1\u00a0mg\/kg\/day or 2\u00a0mg\/kg\/EOD for 8 weeks), the levels of serum and urinary sHLA-I were measured by ELISA (sHLA-STAT; Sangstat Co., Calif., USA). After 8 weeks of treatment, 10 patients with MCD were responders (MCD-CR) while the other 7 patients with MCD were nonresponders (MCD-NR). Three of 7 patients with MCD-NR were re-biopsied and finally diagnosed as FSGS. They were included in the data of patients with FSGS. In healthy controls, serum sHLA-I was detected (415 \u00b1 256\u00a0ng\/ml), but urinary sHLA-I was not. At entry, there were no differences in age, sex, serum Cr and 24-hour urine protein among the patients with MCD-CR, MCD-NR and FSGS, but serum albumin was significantly elevated in patients with FSGS and MGN (p < 0.05). Serum sHLA-I levels were notably elevated in MCD-CR (1,040 \u00b1 1,066\u00a0ng\/ml), in MCD-NR (668 \u00b1 315\u00a0ng\/ml) and in FSGS (713 \u00b1 790\u00a0ng\/ml), but not in patients with MGN (444 \u00b1 86\u00a0ng\/ml) when compared with controls (p < 0.05). On the other hand, urinary sHLA-I levels in MCD-NR (541 \u00b1 239\u00a0ng\/mg Cr) and in FSGS (457 \u00b1 239\u00a0ng\/mg Cr) were significantly higher than those in MGN (125 \u00b1 28\u00a0ng\/mg Cr) and in MCD-CR (100 \u00b1 42\u00a0ng\/mg Cr, p < 0.05) and these substantial differences were maintained for 8 weeks. In all patients, serum and urinary sHLA-I levels were not reduced during 8 weeks of steroid therapy. We conclude that elevated serum and urinary sHLA-I levels reflect increased cellular immune response and disease activity in patients with MCD and FSGS. In patients with MCD, urinary sHLA-I may be an easily measurable indicator of predicting steroid response, while MCD-NR with high urinary sHLA-I levels might be re-evaluated for the possibility of FSGS.<\/jats:p>","DOI":"10.1159\/000044990","type":"journal-article","created":{"date-parts":[[2003,4,15]],"date-time":"2003-04-15T15:42:49Z","timestamp":1050421369000},"page":"44-49","source":"Crossref","is-referenced-by-count":1,"title":["Urinary Soluble HLA Class I Antigen in Patients with Minimal Change Disease: A Predictor of Steroid Response"],"prefix":"10.1159","volume":"79","author":[{"given":"Cheol Whee","family":"Park","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ho Chul","family":"Song","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Young Sin","family":"Shin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suk Joo","family":"Ahn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yong Soo","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suk Young","family":"Kim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eui Jin","family":"Choi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoon Sik","family":"Chang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Byung Kee","family":"Bang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[1998,4,29]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.42.1.25"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.med.39.1.517"}],"container-title":["Nephron"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/44990","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/44990","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:38:17Z","timestamp":1745469497000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000044990"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1998]]},"references-count":2,"journal-issue":{"issue":"1","published-online":{"date-parts":[[1998,5,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000044990","archive":["Portico"],"relation":{},"ISSN":["1660-8151","2235-3186"],"issn-type":[{"type":"print","value":"1660-8151"},{"type":"electronic","value":"2235-3186"}],"subject":[],"published":{"date-parts":[[1998]]}}}