ArticleThe American journal of pathology2014
Tubular obstruction leads to progressive proximal tubular injury and atubular glomeruli in polycystic kidney disease.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Trial
- Preterm birth increases susceptibility to hyperglycemia induced glomerular alterations in male mice.Scientific reports · 2025Article
- Stenosis of the glomerulotubular neck in progressive chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Permanent defects in renal medullary structure and function after reversal of urinary obstruction.JCI insight · 2025Article
- Epithelial tubule interconnection driven by HGF-Met signaling in the kidney.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Epithelial tubule interconnection driven by HGF-Met signaling in the kidney.bioRxiv : the preprint server for biology · 2024Article
- ALTERATIONS IN HISTIDINE METABOLISM IS A FEATURE OF EARLY AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE (ADPKD).Transactions of the American Clinical and Climatological Association · 2024Article
- Wall Tension and Tubular Resistance in Kidney Cystic Conditions.Biomedicines · 2023Review
- Overexpression of notch signaling in renin cells leads to a polycystic kidney phenotype.Clinical science (London, England : 1979) · 2023Article
- Functional differentiation and scalable production of renal proximal tubular epithelial cells from human pluripotent stem cells in a dynamic culture system.Cell proliferation · 2022Article
- The presence of simple renal cysts is associated with an increased risk of albuminuria in young adults.The Korean journal of internal medicine · 2022Article
- Tubular mitochondrial AKT1 is activated during ischemia reperfusion injury and has a critical role in predisposition to chronic kidney disease.Kidney international · 2021Article
- Magnetic resonance imaging accurately tracks kidney pathology and heterogeneity in the transition from acute kidney injury to chronic kidney disease.Kidney international · 2021Article
- Beyond the tubule: pathological variants ofAmerican journal of physiology. Renal physiology · 2020Article
- The effect of size, charge, and peptide ligand length on kidney targeting by small, organic nanoparticles.Bioengineering & translational medicine · 2020Article
- Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
- Evolution, kidney development, and chronic kidney disease.Seminars in cell & developmental biology · 2019Review
- ADPKD-what the radiologist should know.The British journal of radiology · 2019Review
- Long-term trajectory of kidney function in autosomal-dominant polycystic kidney disease.Kidney international · 2019Observational
- Polycystic kidney disease.Nature reviews. Disease primers · 2018Review
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6 authors at 2 institutions in 1 country.
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Abstract
In polycystic kidney disease (PKD), renal parenchyma is destroyed by cysts, hypothesized to obstruct nephrons. A signature of unilateral ureteral obstruction, proximal tubular atrophy leads to formation of atubular glomeruli. To determine whether this process occurs in PKD, kidneys from pcy mice (moderately progressive PKD), kidneys from cpk mice (rapidly progressive PKD), and human autosomal dominant PKD were examined in early and late stages. Integrity of the glomerulotubular junction and proximal tubular mass were determined in sections stained with Lotus tetragonolobus lectin. Development of proximal tubular atrophy and atubular glomeruli was determined in serial sections of individual glomeruli. In pcy mice, most glomerulotubular junctions were normal at 20 weeks, but by 30 weeks, 56% were atrophic and 25% of glomeruli were atubular; glomerulotubular junction integrity decreased with increasing cyst area (r = 0.83, P < 0.05). In cpk mice, all glomerulotubular junctions were normal at 10 days, but by 19 days, 26% had become abnormal. In early-stage autosomal dominant PKD kidneys, 50% of glomeruli were atubular or attached to atrophic tubules; in advanced disease, 100% were abnormal. Thus, proximal tubular injury in cystic kidneys closely parallels that observed with ureteral obstruction. These findings support the hypothesis that, in renal cystic disorders, cyst-dependent obstruction of medullary and cortical tubules initiates a process culminating in widespread destruction of proximal convoluted tubules at the glomerulotubular junction.
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