ArticleHypertension (Dallas, Tex. : 1979)2026
Urokinase Promotes Redundantly Intratubular C3a-Formation But Not ENaC-Driven Hypertension in DOCA/Salt Kidney Injury.
Article in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgrounduPA (urokinase-type plasminogen activator) inhibitors mitigate salt retention, plasmin, and complement activation in acute proteinuric kidney diseases. We hypothesized that in chronic kidney injury with albuminuria, uPA contributes to hypertension and complement-dependent tissue inflammation and injury.
methodsWild-type and uPA KO (knockout) mice underwent either sham surgery or unilateral nephrectomy, followed by insertion of deoxycorticosterone acetate (DOCA)- or sham pellets and a high (4%) or control (0.5%) sodium chloride diet for 21 days. Glomerular filtration rate was estimated by transcutaneous fluorescein-isothiocyanate-sinistrin, and arterial blood pressure was recorded continuously by indwelling femoral catheters. Urine was analyzed for albumin, plasmin(ogen), electrolytes, kidney injury markers (neutrophil gelatinase-associated lipocalin), and complement proteins (C3, C3a). Kidney tissue was examined for neutrophil gelatinase-associated lipocalin, epithelial sodium channel, C3, C3a, C5a, cytokines, inflammation, and macrophage polarization markers (CD16
resultsDOCA-salt increased diuresis, Na
conclusionsWhile not essential for filtration barrier injury, glomerular filtration rate decline, and hypertension in DOCA-salt-induced kidney injury, uPA, through plasmin, generates anaphylatoxins with effects on specific cytokines.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.