<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wewers TM</submitter><funding>Deutsche Forschungsgemeinschaft</funding><pagination>1853-1863</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8455271</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>32(8)</volume><pubmed_abstract>Soluble Fms-like tyrosine kinase (sFlt-1/sVEGFR1) is a naturally occurring antagonist of vascular endothelial growth factor (VEGF). Despite being a secreted, soluble protein lacking cytoplasmic and transmembrane domains, sFlt-1 can act locally and be protective against excessive microenvironmental VEGF concentration or exert autocrine functions independently of VEGF. Circulating sFlt-1 may indiscriminately affect endothelial function and the microvasculature of distant target organs. The clinical significance of excess sFlt-1 in kidney disease was first shown in preeclampsia, a major renal complication of pregnancy. However, circulating sFlt-1 levels appear to be increased in various diseases with varying degrees of renal impairment. Relevant clinical associations between circulating sFlt-1 and severe outcomes (&lt;i>e.g.,&lt;/i> endothelial dysfunction, renal impairment, cardiovascular disease, and all-cause mortality) have been observed in patients with CKD and after kidney transplantation. However, sFlt-1 appears to be protective against renal dysfunction-associated aggravation of atherosclerosis and diabetic nephropathy. Therefore, in this study, we provide an update on sFlt-1 in several kidney diseases other than preeclampsia, discuss clinical findings and experimental studies, and briefly consider its use in clinical practice.</pubmed_abstract><journal>Journal of the American Society of Nephrology : JASN</journal><pubmed_title>Circulating Soluble Fms-like Tyrosine Kinase in Renal Diseases Other than Preeclampsia.</pubmed_title><pmcid>PMC8455271</pmcid><funding_grant_id>SE2824/3-1</funding_grant_id><pubmed_authors>Pavenstadt H</pubmed_authors><pubmed_authors>Schulz A</pubmed_authors><pubmed_authors>Brand M</pubmed_authors><pubmed_authors>Nolte I</pubmed_authors><pubmed_authors>Wewers TM</pubmed_authors><pubmed_authors>Di Marco GS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Circulating Soluble Fms-like Tyrosine Kinase in Renal Diseases Other than Preeclampsia.</name><description>Soluble Fms-like tyrosine kinase (sFlt-1/sVEGFR1) is a naturally occurring antagonist of vascular endothelial growth factor (VEGF). Despite being a secreted, soluble protein lacking cytoplasmic and transmembrane domains, sFlt-1 can act locally and be protective against excessive microenvironmental VEGF concentration or exert autocrine functions independently of VEGF. Circulating sFlt-1 may indiscriminately affect endothelial function and the microvasculature of distant target organs. The clinical significance of excess sFlt-1 in kidney disease was first shown in preeclampsia, a major renal complication of pregnancy. However, circulating sFlt-1 levels appear to be increased in various diseases with varying degrees of renal impairment. Relevant clinical associations between circulating sFlt-1 and severe outcomes (&lt;i>e.g.,&lt;/i> endothelial dysfunction, renal impairment, cardiovascular disease, and all-cause mortality) have been observed in patients with CKD and after kidney transplantation. However, sFlt-1 appears to be protective against renal dysfunction-associated aggravation of atherosclerosis and diabetic nephropathy. Therefore, in this study, we provide an update on sFlt-1 in several kidney diseases other than preeclampsia, discuss clinical findings and experimental studies, and briefly consider its use in clinical practice.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-26T16:33:18.572Z</modification><creation>2025-04-06T15:12:53.316Z</creation></dates><accession>S-EPMC8455271</accession><cross_references><pubmed>34155060</pubmed><doi>10.1681/asn.2020111579</doi><doi>10.1681/ASN.2020111579</doi></cross_references></HashMap>