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Intraperitoneal protein injection in the axolotl: the amphibian kidney as a novel model to study tubulointerstitial activation.

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TLDR
The axolotl kidney provides a novel in vivo model to study tubulointerstitial activation and induction of interstitial fibrosis by protein loading, independent of alterations of glomerular function that may have potential confounding effects on peritubular hemodynamics, pO2, cell traffic, etc.
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This article is published in Kidney International.The article was published on 2002-07-01 and is currently open access. It has received 42 citations till now. The article focuses on the topics: Peritoneal cavity & Kidney.

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How Does Proteinuria Cause Progressive Renal Damage

TL;DR: Evidence indicating that proteinuria may accelerate kidney disease progression to end-stage renal failure is reviewed, and proximal tubular cell receptors for uptake of plasma proteins that are under investigation may provide activation signals on excess tubular protein handling.
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Cell Biology and Pathology of Podocytes

TL;DR: A membrane biologist's view of the podocyte is taken, examining the many membrane receptors, channels, and other signaling molecules that have been implicated in podocyte biology and emphasizing that this approach may be fruitful in understanding the podocytes and its unique properties.
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Combination therapy with ACE inhibitors and angiotensin II receptor blockers to halt progression of chronic renal disease: pathophysiology and indications.

TL;DR: Japanese authors avoided this confounder and demonstrated that combination therapy reduced hard end-points (end stage renal failure or doubling of serum creatinine concentration) by 50% compared to the respective monotherapies.
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Proteinuria: an enzymatic disease of the podocyte?

TL;DR: In this article, the authors review recent insights into the pathogenesis and treatment of proteinuria, with a special emphasis on the emerging concept that proteinuria can result from enzymatic cleavage of essential regulators of podocyte actin dynamics by cytosolic cathepsin L (CatL), resulting in a motile podocyte phenotype.
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Why is proteinuria an ominous biomarker of progressive kidney disease

TL;DR: It is believed that the strongly predictive inverse relationship between level of proteinuria and long-term renal survival currently justifies aggressive antiproteinuric treatment strategies, with a goal of reducing protein excretion rate to the lowest level possible without the induction of symptoms or undue risk.
References
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Understanding the nature of renal disease progression

TL;DR: This article reviewed the abundant evidence in the literature that the process of reabsorption of filtered proteins activates the proximal tubular epithelium and gave rise to an inflammatory reaction that in most forms of glomerulonephritis consistently precede renal scarring.
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Relationship between renal function and histological changes found in renal-biopsy specimens from patients with persistent glomerular nephritis.

TL;DR: It is concluded that in persistent glomerular nephritis the glomersular filtration-rate is more affected by changes in the tubules than by changesinine clearance, and that in some patients with extensiveglomerular changes but little or no tubular damage, the creatinine clearances were normal.
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Structural-functional correlations in renal disease

TL;DR: The most interesting and perhaps unexpected finding was that regardless of the basic disease in the kidney, impaired renal function was most closely related to changes in the tubules and in the interstitium.
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Impaired Angiogenesis in the Remnant Kidney Model: II. Vascular Endothelial Growth Factor Administration Reduces Renal Fibrosis and Stabilizes Renal Function

TL;DR: In conclusion, VEGF treatment reduces fibrosis and stabilizes renal function in the RK model of progressive renal failure and may represent a new approach to the treatment of kidney disease.
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