ArticleBMC nephrology2026
Voclosporin ameliorates proteinuria in a model of non-inflammatory glomerular disease.
Article in BMC nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundIdiopathic nephrotic syndrome (INS) is among the most common glomerular diseases in children with standard first line treatment of glucocorticoids. However, there has been no definitive treatment that can completely cure disease with few side effects for steroid resistant INS patients. Voclosporin (VCS) is a second generation calcineurin inhibitor (CNI) approved in multiple countries for the treatment of adults with active lupus nephritis. VCS does not require therapeutic drug monitoring due to an improved pharmacokinetic profile compared to other CNIs. Based on this, we assessed the ability of VCS to ameliorate proteinuria and hypoalbuminemia in a non-inflammatory glomerular disease using an animal model of NS.
methodsRats received 50 mg/kg puromycin aminonucleoside (PAN) IV to induce NS. Rats were gavaged BID with vehicle or VCS (4 mg/kg/dose), a clinically relevant dose. Outcome measures included proteinuria, hypoalbuminemia, serum lipid profiles, glomerular podocyte injury, renal tubular injury, and hypercoagulopathy. Human podocytes were also treated with PAN +/- VCS and assessed for cell viability and stress using XTT and LDH release assays.
resultsVCS treatment significantly ameliorated PAN-induced proteinuria (61% median reduction; P < 0.05) and tubular injury (P < 0.05) in rats. VCS also numerically but insignificantly improved hypoalbuminemia (P = 0.16), hypercoagulopathy (P = 0.099), and glomerular podocyte injury (P = 0.11). VCS did not exacerbate serum lipid profiles of rats with PAN-induced disease. In vitro, VCS significantly protected podocyte viability from PAN-induced toxicity and reduced PAN-induced stress, though not significantly.
conclusionsVCS significantly ameliorated proteinuria in a non-inflammatory model of glomerular disease, and compared favorably regarding improvements in hypoalbuminemia, hypercoagulopathy, dyslipidemia, and podocyte injury. These findings suggest that VCS could be clinically efficacious in patients with primary or secondary NS, without need for drug level testing and with decreased risk of exacerbation of known CNI-related dyslipidemia. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
What Socratic 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 Socratic graph.