Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been known that morphological changes are predominant at the site of intercalated cells (IC-cells) of the rat outer medullary collecting duct (OMCD) under K depletion. The changes are characterized by an increase in microplica and the stud of the apical plasma membrane in association with a decrease in the tubulovesicular membrane compartment of the apical region of the cells. It has also been shown that significant K reabsorption and acceleration of H secretion are taking place in these cells of OMCD under the K depletion. In order to clarify whether the changes are directly related to K reabsorption or H secretion, the animal experiment was carried out under any condition. In the control group, G-I, rat was fed with standard diet of normal K content (serum K; 4.5 +/- 0.2 mEq/l), whereas K content was decreased in the K depletion group, G-II, (serum K; 2.7 +/- 0.6 mEq/l). In the acid loaded group, G-III, 4 mEq/100 g BW of 2N ammonium chloride was given every day (serum K; 4.0 +/- 0.2 mEq/l). Animals were sacrificed after 14 days and kidneys were removed for morphological and biochemical examinations. As a result, a significant cell proliferation and interstitial PAS positive granules are observed in K-depleted rats under the light microscopic study. Under the electron microscope, the changes of the intracellular ultrastructure are predominant in the IC-cells of OMCD, such as 'membrane recycling'. On the contrary, no particular changes are seen in acid loaded rats under the light microscope.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Morphological and functional alterations in the intercalated cells of outer medullary collecting duct in K-depleted rats--with special reference to ultrastructural change on electron microscopy]. 227 93

With established urinary markers of kidney integrity the early renal effects of lead have previously been considered to be mainly tubular or tubulointerstitial. In a cross-sectional study on 81 male lead-exposed workers and 45 age-matched controls (median blood lead concentrations 2.03 and 0.34 mumol/l respectively) not only well-established but also new urinary markers of renal integrity preferentially or exclusively located along the different nephron segments were analysed. Markers related to the glomerulus were 6-keto-prostaglandin 1 alpha, thromboxane B2, mainly produced in the glomerulus, and the extracellular matrix protein fibronectin. Markers of the proximal tubule were the brush-border antigens BBA, BB50, and HF5 and the intestinal alkaline phosphatase. Prostaglandin E2 and F2 alpha, preferentially synthesized in the collecting duct and medullary interstitial cells, served as markers of these more distal nephron segments. In contrast to previous studies on the early phase of lead nephrotoxicity, not only tubular but also glomerular involvement could be shown in the study presented here by increases in the median values of 6-keto-prostaglandin 1 alpha and decreases in fibronectin. The proximal tubular markers intestinal alkaline phosphatase and BBA confirmed that this particular segment of the nephron is affected by lead. Effects on the collecting tubule or medullary interstitial cells could also be observed. It is concluded that lead affects both the glomerulus and the tubular apparatus and that combinations of new and established markers could be valuable for a better definition and early detection of lead nephropathy.
Nephrol Dial Transplant 1994
PMID:Nephron target sites in chronic exposure to lead. 770 57

This study was carried out to investigate the role of aquaporin (AQP) in the peritoneum undergoing continuous ambulatory peritoneal dialysis (CAPD). Furthermore, we examined the effects of treatment with prednisolone (PSL) in a rat model of peritoneal sclerosis. We modelled peritoneal sclerosis by using dialysis solution with the addition of 0.1% chlorhexidine gluconate (CHG) for 10 days. Twenty male Wistar Kyoto (WKY) rats were divided into four groups and dialyzed with various solutions: (1) saline (NS group, n = 5); (2) 10% glucose (TZ group, n = 5); (3) 0.1% CHG (CHG group, n = 5); and (4) 0.1% CHG plus PSL (CHG + PSL group, n = 5). Expression of mRNA of AQPs (AQP-1-AQP-4) was studied by semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR). Expression of AQP-4 was also measured by Western blot analysis. Ultrafiltration volume and peritoneal function were measured by the peritoneal equilibration test. In the TZ group, expression of AQP-1 and AQP-4 were significantly enhanced, in parallel with an increment in ultrafiltration volume. On the other hand, in the CHG group, expression of AQP-1 and AQP-4 were significantly suppressed, and ultrafiltration volume was lost. The use of PSL with CHG completely restored the expression of AQP-1 and AQP-4, and peritoneal function improved. No expression of AQP-2 and AQP-3 was seen in the peritoneum. Our results suggest that AQP-1 and AQP-4 may be important factors in water transport in patients undergoing CAPD. PSL might be an effective treatment to prevent the progress of peritoneal sclerosis in patients undergoing CAPD.
Adv Perit Dial 2000
PMID:Glucocorticoid restores the deterioration of water transport in the peritoneum through increment in aquaporin. 1104 15

As metanephric mesenchyme converts into nephrons, the first step is aggregation into a 'condensate'. Precursors inside this structure are proliferative and have a low rate of apoptosis, accompanied by expression of PAX-2 and BCL-2 survival molecules; conversely, cells at the borders of the structure have a high rate of apoptosis, probably a normal mechanism to regulate the number of cells in each nephron. Ureteric bud/collecting duct survival and mitosis may be determined partly by renal mesenchymal secreted molecules such as hepatocyte growth factor (HGF) and glial cell line-derived neurotrophic factor. Human kidney malformations often occur with lower urinary tract obstruction, e.g. cystic dysplastic kidneys caused by urethral valves. Deregulation of cell turnover occurs in these organs, with enhanced proliferation in cystic epithelium, accompanied by PAX-2, BCL-2 and HGF receptor expression, and apoptosis in surrounding mesenchyme, which transdifferentiates under the influence of transforming growth factor-beta1 into smooth muscle instead of forming nephrons. Similar abnormalities of cell turnover and gene expression can be generated by experimental fetal urinary flow impairment. Finally, renal mesenchymal apoptosis, associated with renal hypoplasia, can be induced experimentally by maternal low protein diet.
Nephrol Dial Transplant 2002
PMID:Cell turnover in normal and abnormal kidney development. 1238 72

L1, a member of the immunoglobulin superfamily, is a cell adhesion and signal transducing molecule. In the kidney, L1 is expressed in the mesonephric duct and the metanephros throughout collecting duct development. We show that mice with a targeted deletion of the L1 gene display diverse renal malformations including (i) a duplex kidney with two ureters partially or totally separated, accompanied by hydronephrosis; and (ii) an enlarged elongated kidney with a malformed or incorrectly positioned inner medulla. The type, penetrance and severity of these phenotypes are influenced by the genetic background. The development of a duplex kidney is initiated by double ureteral budding from the Wolffian duct or by an accessory budding from the main ureter, whereas medullary malformation is due to an improper growth and branching pattern of ureteral branches. Multiple developmental defects in formation of the collecting system promote subsequent renal damage and progression to renal insufficiency. Various features of mouse ureteral duplication resemble the human congenital anomalies of the kidney and urinary tract (CAKUT) although disturbances of medulla development have not yet been reported in men.
Nephrol Dial Transplant 2002
PMID:Abnormal renal phenotype in L1 knockout mice: a novel cause of CAKUT. 1238 85

One of the most remarkable transformations of cells during organogenesis is the epithelial transformation of nephrogenic mesenchyme to secretory nephrons. During recent years, gene targeting and organ culture approaches have been used efficiently to resolve key molecules involved in this multistage process. Nephrons are induced by the tips of the branching ureteric bud that later forms the collecting duct network. The first signal in nephron induction is obviously maintaining the mesenchyme; the second enhances cell proliferation and brings together the set of cells that contribute to one single nephron. This stage is characterized by two types of condensations (first the cap stage and then pre-tubular condensation). The final step, epithelial transformation, is a cell-autonomous process. Although the molecular cascade in nephron induction is being resolved in the rat, the same signals seem to work less efficiently in the mouse. In the rat, fibroblast growth factor-2 maintains the nephrogenic mesenchyme; leukaemia inhibitory factor together with transforming growth factor beta-2 induce its condensation; and autocrine secretion of Wnt-4 converts it to epithelium.
Nephrol Dial Transplant 2002
PMID:Nephron induction. 1238 1

Though several suggestions have been put forward, the underlying mechanism of contrast medium-induced nephropathy (CIN) is not clear. Most probably, however, the culprit is a combination of various mechanisms working together to cause the development of CIN. The generally accepted main factors in the pathophysiology of CIN are the reduction in renal perfusion by contrast media (CM) combined with the toxic effects on the tubular cells. With regard to the literature, misconceptions are widespread when explaining the development of CIN, e.g. that osmolar challenge induces renal vasoconstriction due to the tubuloglomerular feedback mechanism (TGF). Although popular, this assumption is most probably false, since osmotic pressure is not the signal for the TGF. Much attention has been paid to reducing the osmolarity of CM further. In an effort to obtain iso-osmolar CM, dimers were formed. These CM have osmolarities in the near physiological range, but at the cost of increased viscosity. This seems to have adverse effects with regard to kidney haemodynamics. In contrast to the multifarious interpretations of CIN, it is generally accepted that hydration is effective in preventing CIN from occuring. There is no universally accepted explanation for the effect of hydration, but it may rely on enhancing renal medullary blood flow and reducing the viscosity of the fluid in the collecting duct.
Nephrol Dial Transplant 2005 Feb
PMID:Renal haemodynamic alterations in contrast medium-induced nephropathy and the benefit of hydration. 1570 45

In the present study, the effect of potassium depletion on the expression of acid-base transporters in the collecting duct was examined. Toward this end rats were fed a potassium-free diet for 3 weeks. Thereafter, the expression of the basolateral chloride/bicarbonate exchangers AE1 and SLC26A7 and the apical H(+)-ATPase was examined by northern hybridization, immunoblot analysis and immunofluorescence labelling. The mRNA expression of AE1 increased by a robust approximately 500% in the cortex and approximately 70% in the outer medulla, which translated into a huge increase in AE1 protein abundance in the cortex and a moderate increase in the outer medulla in K-depletion. The mRNA expression of SLC26A7 did not change significantly but its protein abundance showed a robust increase in the outer medulla. The expression of SLC26A7 remained undetected in the cortex in K-depleted rats. The post translational increase in SLC26A7 membrane abundance in potassium depletion was recapitulated in vitro using epitope-tagged SLC26A7. H(+)-ATPase displayed enhanced apical plasma membrane immunoreactivity in the OMCD in K-depletion. We suggest that the up-regulation of SLC26A7 and AE1 on the basolateral membrane of A-intercalated cells in the OMCD and CCD, respectively, along with H(+)-ATPase on the apical membrane, contributes to enhanced bicarbonate absorption in the collecting duct in K-depletion.
Nephrol Dial Transplant 2007 Dec
PMID:Regulation of the basolateral chloride/base exchangers AE1 and SLC26A7 in the kidney collecting duct in potassium depletion. 1780 57

The [Formula: see text] exchanger pendrin (SLC26A4, PDS) is located on the apical membrane of B-intercalated cells in the kidney cortical collecting duct and the connecting tubules and mediates the secretion of bicarbonate and the reabsorption of chloride. Given its dual function of bicarbonate secretion and chloride reabsorption in the distal tubules, it was thought that pendrin plays important roles in systemic acid-base balance and electrolyte and vascular volume homeostasis under basal conditions. Mice with the genetic deletion of pendrin or humans with inactivating mutations in PDS gene, however, do not display excessive salt and fluid wasting or altered blood pressure under baseline conditions. Very recent reports have unmasked the basis of incongruity between the mild phenotype in mutant mice and the role of pendrin as an important player in salt reabsorption in the distal tubule. These studies demonstrate that pendrin and the Na-Cl cotransporter (NCC; SLC12A3) cross compensate for the loss of each other, therefore masking the role that each transporter plays in salt reabsorption under baseline conditions. In addition, pendrin regulates calcium reabsorption in the distal tubules. Furthermore, combined deletion of pendrin and NCC not only causes severe volume depletion but also results in profound calcium wasting and luminal calcification in medullary collecting ducts. Based on studies in pathophysiological states and the examination of genetically engineered mouse models, the evolving picture points to important roles for pendrin (SLC26A4) in kidney physiology and in disease states. This review summarizes recent advances in the characterization of pendrin and the multiple roles it plays in the kidney, with emphasis on its essential roles in several diverse physiological processes, including chloride homeostasis, vascular volume and blood pressure regulation, calcium excretion and kidney stone formation.
Nephrol Dial Transplant 2015 Aug
PMID:The multiple roles of pendrin in the kidney. 2528 99

Classically, urate nephropathy has been postulated to cause kidney disease by depositing intraluminal crystal in the collecting duct. Recently, molecular mechanisms of inflammasome have been investigated. Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome. Against the lysosomal rupture and mitochondrial ROS production, autophagy acts to protect proximal tubular cells by isolating them from expanding the inflammation. In addition, increased cellular urate, directly or indirectly via xanthine oxidase-induced oxidative stress, may be associated with inflammasome. In addition to the traditional therapy against hyperuricemia, management of urate-induced inflammasome or augmentation of autophagy may offer the new effective therapies.
Nephrol Dial Transplant 2016 06
PMID:Hyperuricemia-induced inflammasome and kidney diseases. 2582 26


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