PS 04-30 THE EFFECT OF EPLERENONE ON CELL PROLIFERATION IN CONTRALATERAL KIDNEY OF RATS WITH UNILATERAL URETERAL OBSTRUCTION

2016 ◽  
Vol 34 (Supplement 1) ◽  
pp. e141 ◽  
Author(s):  
Conghui Wang ◽  
Zheng Wang ◽  
Lijuan Lang ◽  
Qingyou Xu ◽  
Tatsuo Shimosawa
Keyword(s):  
Cell Proliferation ◽  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Contralateral Kidney

Renal hydrogen ion secretion after release of unilateral ureteral obstruction

1976 ◽  
Vol 231 (4) ◽  
pp. 1233-1239 ◽  
Author(s):  
K Thirakomen ◽  
N Kozlov ◽  
JA Arruda ◽  
NA Kurtzman
Keyword(s):  
Ureteral Obstruction ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Unilateral Ureteral Obstruction ◽  
Outer Cortex ◽  
Urinary Ph ◽  
Contralateral Kidney ◽  
Saline Loading ◽  
K Secretion ◽  
Inner Cortex

The effect of 24 h of unilateral ureteral obstruction on HCO3 reabsroption and urinary acidification was studied in dogs. The postobstructed kidney (EK) had a significantly lower glomerular filtration rate and renal plasma flow than the contralateral kidney (CK). Urinary pH prior to HCO3 loading was significantly higher in the EK as was maximal HCO3 reabsorption. Saline loading depressed HCO3 reabsorption to the same degree in both kidneys. Urinary PCO2, during HCO3 loading, and during phosphate infusion, was significantly lower in the EK than the CK. Fractional Na excretion was significantly higher in the EK than the CK after deoxycorticosterone acetate administration. Na2SO4 administration enhanced acid excretion only in the CK. K excretion was significantly lower in the EK than the CK both during HCO3 loading and Na2SO4 administration. There was redistribution of cortical blood flow from the outer cortex toward the inner cortex in the EK as compared to the CK. There was no difference in plasma renin activity from both renal veins. These data demonstrate enhanced proximal H+ secretion (which is abolished by volume expansion) and impaired distal H+ secretion by the postobstructed kidney. The distal defect is likely an effect of a generalized disorder of distal transport in that both K secretion and steroid-responsive Na reabsorption were impaired in the postobstructed kidney.

scholarly journals INK4a knockout mice exhibit increased fibrosis under normal conditions and in response to unilateral ureteral obstruction

2010 ◽  
Vol 299 (6) ◽  
pp. F1486-F1495 ◽  
Author(s):  
Jesse M. Wolstein ◽  
David H. Lee ◽  
Jennine Michaud ◽  
Venessa Buot ◽  
Beth Stefanchik ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Knockout Mice ◽  
Ureteral Obstruction ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Collecting Duct ◽  
Mesenchymal Cell ◽  
Transforming Growth Factor Β ◽  
Unilateral Ureteral Obstruction ◽  
Matrix Deposition

The INK4a proteins p16INK4a and p19ARF regulate cell cycle arrest and senescence. However, the role of these proteins in controlling these processes in the normal kidney and following injury is unknown. We performed unilateral ureteral obstruction (UUO) to induce fibrosis in 2- to 3-mo-old wild-type (WT) C57/B6 and INK4a knockout mice. By quantitative RT-PCR, p16INK4a levels were increased sixfold in WT mice 7 days after UUO and p19ARF remained undetectable. Kidney sections were examined to determine levels and localization of p16INK4a, apoptosis, fibrosis, and senescent cells. INK4a knockout mice displayed mesangial cell proliferation, increased matrix deposition, and myofibroblast differentiation under normal conditions. Following UUO, INK4a knockout mice displayed 10-fold increased tubular and interstitial cell proliferation, 75% decreased collecting duct apoptosis, 2-fold greater collagen and fibronectin deposition, and no cell senescence by senescence-associated β-galactosidase staining compared with WT mice. Both INK4a knockout mesangial cells and kidney lysates from knockout mice following injury showed elevated levels of IL-6 by ELISA compared with WT samples. INK4a knockout epithelial cell cultures displayed increased mesenchymal cell markers when exposed to transforming growth factor-β. These results confirm that p16INK4a controls cell proliferation and matrix production and mitigates fibrosis following injury and suggest that the mechanism involves a role in limiting inflammation and cell proliferation.

scholarly journals Kidney-Draining Lymph Node Fibrosis Following Unilateral Ureteral Obstruction

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaofei Li ◽  
Jing Zhao ◽  
Said Movahedi Naini ◽  
Gianmarco Sabiu ◽  
Stefan G. Tullius ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
Lymph Node ◽  
Ureteral Obstruction ◽  
Immune Cell ◽  
Ischemia Reperfusion ◽  
Unilateral Ureteral Obstruction ◽  
Immunofluorescence Staining ◽  
Contralateral Kidney ◽  
Draining Lymph Node

Although the primary organ has been the subject of intense investigation in the field of organ fibrosis over the past several decades, the presence of lymph node fibrosis due to persistent activation of the immune response in its partner organ remains largely unknown. Previously, we demonstrated that activation of the immune response following ischemia-reperfusion injury (IRI) and crescentic glomerulonephritis (CGN) in the kidney was associated with extracellular matrix (ECM) production by fibroblastic reticular cells (FRCs) of the kidney-draining lymph node (KLN). Here, we sought to determine whether FRCs in the KLN become similarly fibrogenic following unilateral ureteral obstruction (UUO) of the kidney. We subjected 6–8-week-old C57BL/6J mice to UUO for 2, 7, and 14 days. We examined the microarchitecture of the kidney and KLN by immunofluorescence staining at each timepoint, and we quantified immune cell populations in the KLN by flow cytometry. The contralateral kidney unaffected by UUO and its partner KLN were used as controls. We found through immunofluorescence staining that FRCs increased production of ECM fibers and remodeled the microarchitecture of the UUO KLN, contributing to fibrosis that mirrored the changes in the kidney. We also observed by flow cytometry that the populations of CD11b+ antigen-presenting cells, CD11c+ dendritic cells, and activated CD4+ and CD8+ T cells were significantly higher in the UUO KLN than the KLN draining the unaffected contralateral kidney. Expression of the TGFβ/TGFβR signaling pathway was upregulated and colocalized with FRCs in the UUO KLNs, suggesting a possible mechanism behind the fibrosis. Both release of ureteral ligation at 2 days following UUO and depletion of FRCs at the time of injury onset halted the progression of fibrosis in both the kidney and the KLN. These findings for the first time highlight the association between fibrosis both in the kidney and the KLN during UUO, and they lay the groundwork for future studies that will investigate more deeply the mechanisms behind the connection between FRCs and KLN fibrosis.

A fetal sheep model for studying compensatory mechanisms in the healthy contralateral kidney after unilateral ureteral obstruction

2015 ◽  
Vol 11 (6) ◽  
pp. 352.e1-352.e7 ◽  
Author(s):  
Alexander Springer ◽  
Klaus Kratochwill ◽  
Helga Bergmeister ◽  
Dagmar Csaicsich ◽  
Johann Huber ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Compensatory Mechanisms ◽  
Sheep Model ◽  
Fetal Sheep ◽  
Contralateral Kidney

scholarly journals The changes of the tubular epithelium phenotype in the contralateral kidney nephrons while developing unilateral ureteral obstruction: an experimental study

2021 ◽  
Vol 9 (3) ◽  
pp. 5-11
Author(s):  
M. A. Akimenko ◽  
O. V. Voronova ◽  
T. S. Kolmakova
Keyword(s):  
Ureteral Obstruction ◽  
Urinary Tract Obstruction ◽  
Smooth Muscle Actin ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Unilateral Ureteral Obstruction ◽  
Renal Diseases ◽  
Tissue Samples ◽  
Contralateral Kidney ◽  
Compensatory Reserve

Introduction. The high prevalence of renal diseases caused by urinary tract obstruction led to the need for experimental research of compensatory and pathological processes with kidney injury. It is also of relevance to study key mechanisms providing a compensatory function of the contralateral kidney for early diagnosis, treatment, and prognosis of obstructive renal diseases.Purpose of the study. To examine epithelial nephron cells phenotype dynamics changes in contralateral kidney using unilateral ureteral obstruction experimental model.Materials and methods. Model of unilateral ureteral obstruction was established using adult rabbits. The studies were carried out on days 7, 14 and 21 of complete obstruction of the left ureter. Immunophenotyping was performed on contralateral kidney tissue samples using epithelial (cytokeratin 7, E-cadherin) and mesenchymal (vimentin, α-smooth muscle actin) markers.Results. The contralateral kidney under additional load can maintain the morphological and functional characteristics of the nephron for a long time. The first transmogrify signs in the nephron epithelium phenotype were detected by day 21 as the diffuse appearance of mesenchymal marker vimentin with unaltered visualization of epithelial phenotype markers.Conclusion. The results obtained allow us to assume that the compensatory reserve of the contralateral kidney is gradually decreasing when the duration of the obstruction increases. Thus, the likelihood of developing negative disorders increases.

Ureteral occlusion decreases phospholipid and cholesterol of renal tubular membranes

1986 ◽  
Vol 250 (1) ◽  
pp. F136-F143
Author(s):  
J. Morrissey ◽  
D. Windus ◽  
S. Schwab ◽  
J. Tannenbaum ◽  
S. Klahr
Keyword(s):  
Ureteral Obstruction ◽  
Unilateral Ureteral Obstruction ◽  
Phospholipid Content ◽  
Contralateral Kidney ◽  
Basolateral Membranes ◽  
Renal Tubular Cells ◽  
Altered Response ◽  
Renal Tubular ◽  
Tubular Membranes ◽  
Ureteral Occlusion

Unilateral ureteral obstruction of 24 h duration in the dog results in a 20% decrease in the amount of total phospholipids present in basolateral membranes of renal tubular cells obtained from the experimental kidney as compared with the amount of phospholipid in basolateral membranes prepared from the contralateral kidney of the same dogs or from the kidneys of normal sham-operated dogs. There was also a decrease in the content of cholesterol and cholesterol esters of the basolateral membranes from the experimental kidney. By contrast, no significant change in lipid content was observed in brush border membranes obtained from the experimental kidney of dogs with unilateral ureteral obstruction. The decrease in phospholipid content of basolateral membranes was accompanied by a 40% fall in the content of phosphatidylcholine and a 12% fall in sphingomyelin. There was a small (12%) but significant increase in the content of phosphatidylethanolamine in basolateral membranes. The mechanisms responsible for the selective decrease in phospholipid content of basolateral membranes remain to be established. It is postulated that changes in solute transport and altered response to hormones observed in the postobstructed kidney of animals with unilateral ureteral obstruction may be explained, at least in part, by changes in the lipid composition of basolateral membranes.

scholarly journals Chronic unilateral ureteral obstruction in the neonatal mouse delays maturation of both kidneys and leads to late formation of atubular glomeruli

2013 ◽  
Vol 305 (12) ◽  
pp. F1736-F1746 ◽  
Author(s):  
Michael S. Forbes ◽  
Barbara A. Thornhill ◽  
Carolina I. Galarreta ◽  
Jordan J. Minor ◽  
Katherine A. Gordon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ureteral Obstruction ◽  
Smooth Muscle Actin ◽  
Unilateral Ureteral Obstruction ◽  
Obstructive Nephropathy ◽  
Contralateral Kidney ◽  
Mitochondrial Superoxide ◽  
Atubular Glomeruli ◽  
Proximal Tubular ◽  
Papillary Growth

Unilateral ureteral obstruction (UUO) in the adult mouse is the most widely used model of progressive renal disease: the proximal tubule is the nephron segment most severely affected and atubular glomeruli are formed after only 7 days of UUO. To determine the proximal nephron response to UUO in the maturing kidney, neonatal mice were examined 7 to 28 days following complete UUO under general anesthesia. Proximal tubular mass and maturation were determined by staining with Lotus tetragolonobus lectin. Superoxide was localized by nitroblue tetrazolium and collagen by Sirius red. Cell proliferation, cell death, PAX-2, megalin, α-smooth muscle actin (α-SMA), renin, and fibronectin were identified by immunohistochemistry. During the first 14 days of ipsilateral UUO, despite oxidative stress (4-hydroxynonenal staining), glomerulotubular continuity was maintained and mitochondrial superoxide production persisted. However, from 14 to 28 days, papillary growth was impaired and proximal tubules collapsed with increased apoptosis, autophagy, mitochondrial loss, and formation of atubular glomeruli. Fibronectin, α-SMA, and collagen increased in the obstructed kidney. Oxidative stress was present also in the contralateral kidney: renin was decreased, glomerulotubular maturation and papillary growth were delayed, followed by increased cortical and medullary growth. We conclude that neonatal UUO initially delays renal maturation and results in oxidative stress in both kidneys. In contrast to the adult, proximal tubular injury in the neonatal obstructed kidney is delayed at 14 days, followed only later by the formation of atubular glomeruli. Antioxidant therapies directed at proximal tubular mitochondria during early renal maturation may slow progression of congenital obstructive nephropathy.

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