<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>478(1)</volume><submitter>Essigke D</submitter><pubmed_abstract>The complement component C3, factor B (FB) and factor D (FD) belong to the alternative complement pathway and have been identified in urine samples from nephrotic mice. However, it is not yet known whether these factors are involved in mediating sodium retention in nephrotic syndrome (NS). Here we used a genetic mouse model of NS based on an inducible podocin deletion (Nphs2&lt;sup>Δipod&lt;/sup>). These mice were intercrossed with mice deficient for FB, FD or C3, yielding Nphs2&lt;sup>Δipod&lt;/sup>*Cfb&lt;sup>-/-&lt;/sup>, Nphs2&lt;sup>Δipod&lt;/sup>*Cfd&lt;sup>-/-&lt;/sup> or Nphs2&lt;sup>Δipod&lt;/sup>*C3&lt;sup>-/-&lt;/sup> mice, respectively. NS was induced after oral doxycycline treatment for 14 days. C3, FB and FD were detected in the nephrotic urine of Nphs2&lt;sup>Δipod&lt;/sup> mice as well as fragments of C3 and FB, indicati</pubmed_abstract><journal>Pflugers Archiv : European journal of physiology</journal><pagination>16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12764515</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.</pubmed_title><pmcid>PMC12764515</pmcid><pubmed_authors>Bohnert BN</pubmed_authors><pubmed_authors>Essigke D</pubmed_authors><pubmed_authors>Kong L</pubmed_authors><pubmed_authors>Artunc F</pubmed_authors><pubmed_authors>Worn M</pubmed_authors><pubmed_authors>Atkinson JP</pubmed_authors><pubmed_authors>Kalo MZ</pubmed_authors><pubmed_authors>Saad MK</pubmed_authors><pubmed_authors>Omage K</pubmed_authors><pubmed_authors>Birkenfeld AL</pubmed_authors><pubmed_authors>Wu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.</name><description>The complement component C3, factor B (FB) and factor D (FD) belong to the alternative complement pathway and have been identified in urine samples from nephrotic mice. However, it is not yet known whether these factors are involved in mediating sodium retention in nephrotic syndrome (NS). Here we used a genetic mouse model of NS based on an inducible podocin deletion (Nphs2&lt;sup>Δipod&lt;/sup>). These mice were intercrossed with mice deficient for FB, FD or C3, yielding Nphs2&lt;sup>Δipod&lt;/sup>*Cfb&lt;sup>-/-&lt;/sup>, Nphs2&lt;sup>Δipod&lt;/sup>*Cfd&lt;sup>-/-&lt;/sup> or Nphs2&lt;sup>Δipod&lt;/sup>*C3&lt;sup>-/-&lt;/sup> mice, respectively. NS was induced after oral doxycycline treatment for 14 days. C3, FB and FD were detected in the nephrotic urine of Nphs2&lt;sup>Δipod&lt;/sup> mice as well as fragments of C3 and FB, indicati</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Jan</publication><modification>2026-07-16T09:39:36.549Z</modification><creation>2026-07-09T10:46:57.722Z</creation></dates><accession>S-EPMC12764515</accession><cross_references><pubmed>41483032</pubmed><doi>10.1007/s00424-025-03136-x</doi></cross_references></HashMap>