ArticleAmerican journal of physiology. Renal physiology2011
Glomerular sclerosis is prevented during urinary tract obstruction due to podocyte protection.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 21 citations in OpenAlex.
- Evaluating renal function with intravoxel incoherent motion in a unilateral ureteral obstruction model.Current urology · 2026Article
- Stabilization of hypoxia-inducible factor ameliorates glomerular injury sensitization after tubulointerstitial injury.Kidney international · 2021Article
- Plasminogenuria is associated with podocyte injury, edema, and kidney dysfunction in incident glomerular disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Podocyte injury: the role of proteinuria, urinary plasminogen, and oxidative stress.American journal of physiology. Renal physiology · 2016Article
- Prevention of apoptosis averts glomerular tubular disconnection and podocyte loss in proteinuric kidney disease.Kidney international · 2016Article
- Unilateral ureteral obstruction attenuates intrarenal angiotensin II generation induced by podocyte injury.American journal of physiology. Renal physiology · 2015Article
- Causes and pathogenesis of focal segmental glomerulosclerosis.Nature reviews. Nephrology · 2015Review
- A potential role for mechanical forces in the detachment of podocytes and the progression of CKD.Journal of the American Society of Nephrology : JASN · 2015Review
- ELISA analysis of urinary nephrin and podocalyxin standardized by aquaporin-2 in adult patients with nephrotic syndrome.Journal of nephrology · 2014Article
- Podocyte injury enhances filtration of liver-derived angiotensinogen and renal angiotensin II generation.Kidney international · 2014Article
- Structural analysis of how podocytes detach from the glomerular basement membrane under hypertrophic stress.Frontiers in endocrinology · 2014Article
- ARB protects podocytes from HIV-1 nephropathy independently of podocyte AT1.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2012Article
- Liver angiotensinogen is the primary source of renal angiotensin II.Journal of the American Society of Nephrology : JASN · 2012Article
- Podocyte injury damages other podocytes.Journal of the American Society of Nephrology : JASN · 2011Article
- The targeted podocyte.The Journal of clinical investigation · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Urine outflow obstruction activates a variety of profibrotic factors, including the intrarenal renin-angiotensin system. However, the obstruction also nullifies the transmural hydraulic pressure difference across the glomerular capillary wall, an established inducer of glomerulosclerosis. In the present study, we investigated whether, and by what mechanism, urine outflow obstruction affects the process of progressive glomerulosclerosis. For this purpose, we tested the effect of unilateral ureteral obstruction (UUO) of 7 days duration in two distinct mouse models of glomerulosclerosis. In the human immunodeficiency virus (HIV) nephropathy model, where HIV-1 genes are selectively expressed in podocytes and develop progressive podocyte damage and glomerulosclerosis, UUO protected against sclerosis with preservation of podocytes morphologically and immunohistochemically. In contrast, the nonobstructed contralateral kidneys of these mice, as well as sham-operated HIV-1 mouse kidneys, developed severe podocyte injury and glomerulosclerosis. The protection against glomerulosclerosis imparted by ureteral obstruction was also documented in the NEP25 model of podocyte injury, in which a single injection of immunotoxin, LMB2, triggers selective podocyte injury followed by glomerulosclerosis, both of which were protected by UUO. Notably, intervention with an angiotensin II type 1 receptor antagonist provided only a partial protective effect in each of the models. These results demonstrate that urine outflow obstruction protects the glomerulus from progressive sclerosis. The results further reveal that this protection occurs at a very early stage of the pathologic process, namely, damage of podocytes.
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.