Academic literature on the topic 'Proximal renal tubules'
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Journal articles on the topic "Proximal renal tubules"
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Dominguez, J. H., M. Juhaszova, S. B. Kleiboeker, C. C. Hale, and H. A. Feister. "Na(+)-Ca2+ exchanger of rat proximal tubule: gene expression and subcellular localization." American Journal of Physiology-Renal Physiology 263, no. 5 (November 1, 1992): F945—F950. http://dx.doi.org/10.1152/ajprenal.1992.263.5.f945.
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The activity of the Na(+)-Ca2+ exchanger, a membrane transporter that mediates Ca2+ efflux, has been described in amphibian and mammalian renal proximal tubules. However, demonstration of cell-specific expression of the Na(+)-Ca2+ exchanger in proximal renal tubules has been restricted to functional assays. In this work, Na(+)-Ca2+ exchanger gene expression in rat proximal tubules was characterized by three additional criteria: functional assay of transport activity in membrane vesicles derived from proximal tubules, expression of specific Na(+)-Ca2+ exchanger protein detected on Western blots, and determination of specific mRNA encoding Na(+)-Ca2+ exchanger protein on Northern blots. A new transport activity assay showed that proximal tubule membranes contained the highest Na(+)-Ca2+ exchanger transport activity reported in renal tissues. In dog renal proximal tubules and sarcolemma, a specific protein of approximately 70 kDa was detected, whereas in rat proximal tubules and sarcolemma, the specific protein approximated 65 kDa and was localized to the basolateral membrane. On Northern blots, a single 7-kb transcript isolated from rat proximal tubules, whole kidney, and heart hybridized under high-stringency conditions with rat heart cDNA. These data indicate that Na(+)-Ca2+ exchanger protein expressed in rat proximal tubule is similar, if not identical, to the cardiac protein. We suggest that the tubular Na(+)-Ca2+ exchanger characterized herein represents the Na(+)-Ca2+ exchanger described in functional assays of renal proximal tubules.
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Ramachandran, C., and M. G. Brunette. "The renal Na+/Ca2+ exchange system is located exclusively in the distal tubule." Biochemical Journal 257, no. 1 (January 1, 1989): 259–64. http://dx.doi.org/10.1042/bj2570259.
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The movement of Ca2+ across the basolateral plasma membrane was determined in purified preparations of this membrane isolated from rabbit proximal and distal convoluted tubules. The ATP-dependent Ca2+ uptake was present in basolateral membranes from both these tubular segments, but the activity was higher in the distal tubules. A very active Na+/Ca2+ exchange system was also demonstrated in the distal-tubular membranes, but in proximal-tubular membranes this exchange system was not demonstrable. The presence of Na+ outside the vesicles gradually inhibited the ATP-dependent Ca2+ uptake in the distal-tubular-membrane preparations, but remained without effect in those from the proximal tubules. The activity of the Na+/Ca2+ exchange system in the distal-tubular membranes was a function of the imposed Na+ gradient. These results suggest that the major differences in the characteristics of Ca2+ transport in the proximal and in the distal tubules are due to the high activity of a Na+/Ca2+ exchange system in the distal tubule and its virtual absence in the proximal tubule.
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Beyenbach, Klaus W. "Kidneys sans glomeruli." American Journal of Physiology-Renal Physiology 286, no. 5 (May 2004): F811—F827. http://dx.doi.org/10.1152/ajprenal.00351.2003.
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The evolution of the vertebrate kidney records three occasions, each separated by about 50 million years, when fish have abandoned glomeruli to produce urine by tubular mechanisms. The recurring dismissal of glomeruli suggests a mechanism of aglomerular urine formation intrinsic to renal tubules. Indeed, the transepithelial secretion of organic solutes and of inorganic solutes such as sulfate, phosphate, and magnesium can all drive secretory water flow in renal proximal tubules of fish. However, the secretion of NaCl via secondary active transport of Cl is the primary mover of secretory water flow in, surprisingly, proximal tubules of both glomerular and aglomerular fish. In filtering kidneys, the tubular secretion of solute and water is overshadowed by reabsorptive transport activities, but secretion progressively comes to light as glomerular filtration decreases. Thus the difference between glomerular and aglomerular urine formation is more a difference of degree than of kind. At low rates of glomerular filtration in seawater fish, NaCl-coupled water secretion serves to increase the renal excretory capacity by increasing the luminal volume into which waste, excess, and toxic solutes can be secreted. The reabsorption of NaCl and water in the distal nephron and urinary bladder concentrates unwanted solutes for excretion while minimizing renal water loss. In aglomerular fish, NaCl-coupled water secretion across proximal tubules replaces glomerular filtration to increase renal excretory capacity. A review of the literature suggests that tubular secretion of NaCl and water is an early function of the vertebrate proximal tubule that has been retained throughout evolution. Active transepithelial Cl secretion takes place in gall bladders studied as models of the mammalian proximal tubule and in proximal tubules of amphibians and apparently also of mammals. The tubular secretion of Cl is also observed in mammalian distal tubules. The evidence consistent with and for Cl secretion in, respectively, proximal and distal tubules of the mammalian kidney calls for a reexamination of basic assumptions in renal physiology that may lead to new opportunities for managing some forms of renal disease.
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Miller, D. S. "Daunomycin secretion by killfish renal proximal tubules." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 2 (August 1, 1995): R370—R379. http://dx.doi.org/10.1152/ajpregu.1995.269.2.r370.
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Epifluorescence microscopy and video-image analysis were used to measure the uptake of the fluorescent anthracycline daunomycin by intact killifish renal proximal tubules. When tubules were incubated in medium containing 2-5 microM daunomycin, the drug accumulated in the cells and the tubular lumen. At steady state, luminal fluorescence was two to three times greater than cellular fluorescence. Luminal accumulation of daunomycin was reduced when tubules were exposed to the multidrug-resistance (MDR) transporter modifiers verapamil and cyclosporin A (CSA), but not tetraethylammonium (TEA), a model substrate for the renal organic cation transport system. NaCN and vanadate reduced luminal drug accumulation. In contrast, cellular daunomycin accumulation was not affected by verapamil, CSA, TEA, or vanadate and was only slightly reduced by NaCN. When the pH of the buffer solution was decreased from 8.25 to 7.25, luminal, but not cellular, accumulation of daunomycin was again reduced by CSA; however, TEA now reduced cellular and luminal accumulation. These findings are consistent with daunomycin being actively secreted in killifish proximal tubule by two mechanisms. At pH 8.25, daunomycin crossed the basolateral membrane by simple diffusion and was secreted into the tubular lumen by the MDR transporter. At pH 7.25, daunomycin was transported across the basolateral membrane by simple diffusion and carrier-mediated uptake on the organic cation transporter and was secreted into the lumen by the MDR transporter and the organic cation/H+ exchanger.
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Maurel, Agnès, Odile Spreux-Varoquaux, Francesco Amenta, Seyed Khosrow Tayebati, Daniele Tomassoni, Marie-Hélène Seguelas, Angelo Parini, and Nathalie Pizzinat. "Vesicular monoamine transporter 1 mediates dopamine secretion in rat proximal tubular cells." American Journal of Physiology-Renal Physiology 292, no. 5 (May 2007): F1592—F1598. http://dx.doi.org/10.1152/ajprenal.00514.2006.
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Renal dopamine, synthesized by proximal tubules, plays an important role in the regulation of renal sodium excretion. Although the renal dopaminergic system has been extensively investigated in both physiological and pathological situations, the mechanisms whereby dopamine is stored and secreted by proximal tubule cells remain obscure. In the present study we investigated whether vesicular monoamine transporters (VMAT)-1 and -2, which participate in amine storing and secretion, are expressed in rat renal proximal tubules, and we defined their involvement in dopamine secretion. By combining RT-PCR, Western blot, and immunocytochemistry we showed that VMAT-1 is the predominant isoform expressed in isolated proximal tubule cells. These results were confirmed by immunohistochemistry analysis of rat renal cortex showing that VMAT-1 was found in proximal tubules but not in glomeruli. Functional studies showed that, as previously reported for VMAT-dependent amine transporters, dopamine release by cultured proximal tubule cells was partially inhibited by disruption of intracellular H+ gradient. In addition, dopamine secretion was prevented by the VMAT-1/VMAT-2 inhibitor reserpine but not by the VMAT-2 inhibitor tetrabenazine. Finally, we demonstrated that tubular VMAT-1 mRNA and protein expression were significantly upregulated during a high-sodium diet. In conclusion, our results show for the first time the expression of a VMAT in the renal proximal tubule and its involvement in regulation of dopamine secretion. These data represent the first step toward the comprehension of the role of this transporter in renal dopamine handling and its involvement in pathological situations.
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Miller, D. S., and J. B. Pritchard. "Nocodazole inhibition of organic anion secretion in teleost renal proximal tubules." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 3 (September 1, 1994): R695—R704. http://dx.doi.org/10.1152/ajpregu.1994.267.3.r695.
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The impact of the microtubule-disrupting drug nocodazole on renal tubular secretion of organic anions was examined in vitro using proximal tubular masses from teleost fish. Nocodazole reversibly inhibited 20-30% of the tubular accumulation of two model organic anions, p-aminohippurate and fluorescein (FL), by winter flounder tubular masses. However, the drug had no effect on the initial rate of organic anion uptake. Thus it did not reduce transport into the cells at the basolateral membrane, either directly by affecting basolateral organic anion transport proteins or indirectly by altering metabolism or ion gradients. Instead, epifluorescence video microscopy and digital image analysis of killifish tubules showed that nocodazole greatly reduced luminal accumulation of FL and had a smaller effect on cellular dye accumulation. Luminal FL accumulation returned to control levels when tubules were incubated in drug-free medium. Confocal fluorescence microscopy confirmed the marked reduction in luminal FL concentration and demonstrated that intracellular punctate FL accumulation was also markedly reduced. Finally, immunohistochemistry with an anti-tubulin antibody showed that the concentrations of nocodazole used in the above experiments reversibly disrupted microtubules within renal epithelial cells. These data indicate that a component of organic anion secretion in teleost proximal tubule is dependent on an intact microtubular network.
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Gewin, Leslie S. "Sugar or Fat? Renal Tubular Metabolism Reviewed in Health and Disease." Nutrients 13, no. 5 (May 9, 2021): 1580. http://dx.doi.org/10.3390/nu13051580.
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The kidney is a highly metabolically active organ that relies on specialized epithelial cells comprising the renal tubules to reabsorb most of the filtered water and solutes. Most of this reabsorption is mediated by the proximal tubules, and high amounts of energy are needed to facilitate solute movement. Thus, proximal tubules use fatty acid oxidation, which generates more adenosine triphosphate (ATP) than glucose metabolism, as its preferred metabolic pathway. After kidney injury, metabolism is altered, leading to decreased fatty acid oxidation and increased lactic acid generation. This review discusses how metabolism differs between the proximal and more distal tubular segments of the healthy nephron. In addition, metabolic changes in acute kidney injury and chronic kidney disease are discussed, as well as how these changes in metabolism may impact tubule repair and chronic kidney disease progression.
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GOBÉ, GLENDA, XIAO-JU ZHANG, DESLEY A. WILLGOSS, ESTELLE SCHOCH, NICOLE A. HOGG, and ZOLTÁN H. ENDRE. "Relationship between Expression of Bcl-2 Genes and Growth Factors in Ischemic Acute Renal Failure in the Rat." Journal of the American Society of Nephrology 11, no. 3 (March 2000): 454–67. http://dx.doi.org/10.1681/asn.v113454.
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Abstract. The promotion of cell survival and regeneration in acute renal failure (ARF) is important for restitution of renal function. This study analyzes the temporal and spatial relationship between expression of pro- and anti-apoptotic members of the Bcl-2 gene family (Bcl-2, Bcl-XL, Bax) and epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), and transforming growth factor-β (TGF-β), growth factors that are thought to be reparative in ARF. A rat model of ischemic ARF involving 30 min of bilateral renal artery occlusion followed by reperfusion for 0 to 14 d was used. Apoptosis and mitosis were quantified and qualitative assessment was made of other cellular damage including necrosis and loss of cellular adhesion. Locality and level of expression of the Bcl-2 and growth factor proteins were determined using immunohistochemistry. Apoptosis peaked between 4 and 14 d postischemia in both proximal and distal tubules. Mitosis peaked at 2 d in proximal tubules and 4 to 14 in the distal tubules. A spatio-temporal relationship was observed between anti-apoptotic Bcl-2 gene family members and growth factors after ischemia-reperfusion. In control kidneys, expression of Bcl-2, Bcl-XL was low in epithelium of distal tubules, Bax had low-to-moderate expression in the proximal tubule and had low expression in the distal tubule, EGF and IGF-1 had low-to-moderate expression in the distal tubule, and TGF-β had low expression in the proximal tubule. In contrast, within 24 h of reperfusion, distal tubules showed a marked increase in expression of Bcl-2 and a moderate increase in Bcl-XL and Bax. Proximal tubules showed a marked increase in Bax expression and a moderate increase in Bcl-XL. Twenty-four hours after expression of the Bcl-2 proteins was increased, IGF-1 and EGF protein levels were increased in the distal tubule, similar to the Bcl-2 anti-apoptotic proteins, and were also detected in the adjacent proximal tubules, suggestive of paracrine action in these tubules. TGF-β expression was moderately increased in regenerating proximal tubules, but no relationship was seen with the pattern of expression of the Bcl-2 genes. An explanation of these results is that the distal tubule is adaptively resistant to ischemic injury via promotion of survival by anti-apoptotic Bcl-2 genes, and its survival allows expression of growth factors critical not only to the maintenance and regeneration of its own cell population (autocrine action), but also to the adjacent ischemia-sensitive proximal tubular cells (paracrine action).
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Shah, Mehul, Raymond Quigley, and Michel Baum. "Maturation of rabbit proximal straight tubule chloride/base exchange." American Journal of Physiology-Renal Physiology 274, no. 5 (May 1, 1998): F883—F888. http://dx.doi.org/10.1152/ajprenal.1998.274.5.f883.
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The present in vitro microperfusion study compared the mechanism and rates of NaCl transport in neonatal and adult rabbit proximal straight tubules. In proximal straight tubules perfused with a late proximal tubular fluid and bathed in a serumlike albumin solution, the rate of volume absorption ( J V) was 0.54 ± 0.10 and 0.12 ± 0.05 nl ⋅ mm−1 ⋅ min−1in adults and neonates, respectively ( P < 0.05). With the addition of 10−5 M bath ouabain, J Vdecreased to 0.27 ± 0.07 and −0.03 ± 0.04 nl ⋅ mm−1 ⋅ min−1in adult and neonatal tubules, respectively ( P < 0.05), consistent with lower rates of active and passive NaCl transport in the neonatal proximal straight tubule. The effect of luminal sodium and chloride removal on intracellular pH was used to assess the relative rates of Na+/H+and Cl−/base exchange. The rates of Na+/H+and Cl−/base exchange were approximately fivefold less in neonatal proximal straight tubules than adult tubules. In both neonatal and adult proximal straight tubules, the rate of Cl−/base exchange was not affected by formate, bicarbonate, or cyanide and acetazolamide, consistent with Cl−/OH−exchange. These data demonstrate an increase in proximal straight tubule NaCl transport during postnatal renal development.
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Tripathi, S., E. L. Boulpaep, and A. B. Maunsbach. "Isolated perfused Ambystoma proximal tubule: hydrodynamics modulates ultrastructure." American Journal of Physiology-Renal Physiology 252, no. 6 (June 1, 1987): F1129—F1147. http://dx.doi.org/10.1152/ajprenal.1987.252.6.f1129.
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A method using a pressure-sensing servo-pipette is described for measuring downstream transepithelial pressure within isolated renal tubules perfused at flow rates designed to keep luminal solution composition constant. The hydrodynamics of in vitro microperfusion of isolated proximal tubules of Ambystoma tigrinum was varied and different states of transepithelial hydrostatic pressure difference, axial tubule flow, and transepithelial transport were correlated with epithelial ultrastructure. Tubules analyzed by ultrastructural morphometry were as follows: unperfused with and without ouabain, perfused single-end cannulated with and without ouabain, and perfused double-end cannulated tubules incubated in substrate Ringer. The results indicate that proximal tubule fine structure is well preserved for more than 3 h in unperfused and perfused tubules. Small transepithelial hydrostatic pressure gradients (less than 162 Pa) increase tubule diameters and decrease cell height without changing volumes of the cells, lateral intercellular spaces (LIS), or the basal extracellular labyrinth (BEL). Pressure gradients of 271 Pa have no further effect on tubule diameters or cell height, but significantly reduce volumes of LIS and BEL. Transport inhibition and axial flow changes have minor structural effects. This study demonstrates a close dependence of tubule ultrastructure on hydrodynamic conditions and provides guidelines for optimizing the latter during perfusion of isolated renal tubules.
Dissertations / Theses on the topic "Proximal renal tubules"
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SILBER, PAUL MICHAEL. "EARLY INDICATION AND PATHOGENESIS OF RENAL PROXIMAL TUBULE INJURY (ENZYMURIA)." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184097.
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It is well known that a variety of toxicants can cause damage to the renal proximal tubule. However, the early pathogenesis of these deleterious interactions between a toxicant and this region of the nephron remain poorly understood. Thus, the purpose of this research was to attempt to answer three interrelated questions. First, what are the earliest changes in kidney function and structure after administration of tubule toxicants in vivo? Secondly, how do these structural/functional alterations change over time? Finally, are certain indicators of renal "dysfunction" more sensitive then others to the early stages of proximal tubule injury? The basic experimental approach consisted of injecting laboratory animals with a selective proximal tubule toxicant, and then collecting blood and/or urine at several timepoints after dosing; a variety of renal function indicators were evaluated at each of these timepoints. These included blood urea nitrogen (BUN), the glomerular filtration rate (GFR), and the excretion of glucose, protein, salts, glutathione, enzymes, and other endogenous molecules into the urine. At the termination of the exposure period the kidneys were evaluated histopathologically, and were also assayed for levels of specific enzymes and glutathione. Enzyme histochemistry was used to visualize changes in renal enzyme distribution, and protein electrophoretic methods permitted quantification of urinary proteins. These studies showed that specific markers of renal dysfunction were more sensitive to acute proximal tubule injury than other indicators. Specifically, the urinary excretion of proteins and the brush border membrane marker γ-glutamyl transpeptidase (GGT) were the best indicators of proximal tubule injury. Glucosuria, lysozymuria, and glutathionuria were all less sensitive markers, and changes in BUN or GFR were the poorest indicators of acute proximal tubule injury. These results indicated that the brush border membrane is one of the most susceptible regions of the proximal tubule to acute renal injury. Analysis of urinary protein electrophoresis patterns and kidney histopathology confirmed this hypothesis. This research also demonstrated the progression of the toxicant-tubule interaction over time, and showed that both tubule structure and function may be altered within minutes of administering a nephro-toxicant.
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Shuprisha, Apichai. "Real-time assessment of organic anion secretion in isolated, perfused rabbit renal proximal tubules." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/289029.
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A newly developed epifluorescense microscopy system has been employed to measure net transepithelial secretion of fluorescein (FL) in real time in isolated perfused S2 segments of rabbit renal proximal tubules. Net FL secretion (K(t), ∼4 μM, and J(max), ∼280 fmol·min⁻¹·mm⁻¹) shares the same transport system with that of para -aminohippurate (PAH). The basolateral Na-DC cotransporter supports ∼25% of the "basal" FL secretion in the absence of exogenous αKG via recycling of αKG that has been exchanged for FL. Physiological αKG concentrations in the bath (∼10 μM) or in the perfusate (∼50 μM) stimulated net secretion of FL by ∼30 or ∼20%, respectively. These data indicate that the basolateral Na-DC cotransporter supports ∼42% of the net FL secretion. The luminal and basolateral effects of physiological concentrations of αKG were additive. Together, the basolateral and luminal Na-DC cotransporters can directly support ∼50% of the net FL secretion, apparently, by their establishing and maintaining the outwardly directed αKG gradient responsible for driving basolateral FL/αKG exchange. The remaining ∼50% would be maintained by metabolic production of αKG in the cells. Adding of 100 nM phorbol 12-myristate 13-acetate (PMA), a known PKC activator, to the bath decreased steady-state secretion of FL by ∼30% after 25 min incubation. This inhibition was irreversible and increased to ∼60% 25 min following removal of PMA. The inhibition produced by PMA was blocked when 100 nM of either staurosporine (ST) or bisindolylmaleimide I (BIM), both known PKC inhibitors, was added to the bath. ST or BIM alone had no significant effect on FL secretion, suggesting that the basal FL secretion was not under the influence of PKC. Adding of 1 μM of either the peptide hormone bradykinin (BK) or the α₁-receptor agonist phenylephrine (PE), to the bath both of which stimulate PKC via a ligand-receptor-PKC coupling reaction, inhibited FL secretion by ∼22% and ∼27%, respectively. The inhibition was completely reversible after removal of BK or PE. In conclusion, PKC negatively regulates the net secretion of FL in rabbit renal proximal tubules. The data indicate that BK or catecholamines can play a physiological role in regulating organic anion secretion via PKC activation.
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RUEGG, CHARLES EDWARD. "MECHANISMS UNDERLYING REGIOSELECTIVE ACUTE TUBULAR NECROSIS OF RENAL PROXIMAL TUBULAR SEGMENTS." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184162.
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The convoluted (CPT) and straight (SPT) portions of the renal proximal tubule are susceptible to injury by a wide variety of chemical agents. These agents often affect the CPT or SPT selectively by proposed mechanisms usually attributed to tubular concentration, blood flow delivery patterns and tubuloglomerular feedback responses within the intact kidney. The innate cellular responses to chemical exposures remain virtually unexplored. Hence, the basic goal of this research was to develop an in vitro system that was conducive to examining the innate cellular differences in susceptibility between the CPT and SPT following in vitro exposure to mercuric chloride (HgCl₂), potassium dichromate (K₂Cr₂O₇)$ or hypoxic conditions. A renal cortical slicing technique was developed for these studies to position the CPT and SPT within discrete regions of slices made perpendicular to the cortical-papillary axis. An incubation vessel that could maintain the morophological and biochemical viability of slices for at least 12 hr was also developed. The selective necrosis of CPT induced by K₂Cr₂O₇ or hypoxic exposure, and SPT induced by HgCl₂, observed in vivo was reproduced in renal cortical slices exposed in vitro. Innate cellular uptake mechanisms were then investigated since the tissue distribution of each metal was found to be most concentrated within their respective injured cell type. The transport of PAH, TEA, phosphate, sulfate, glutathione and cysteine were examined as potential mechanisms for selective accumulation of these metals. K₂Cr₂O₇ caused a dose-dependent reduction in the uptake rate of sulfate by cortical slices, while phosphate, PAH, and TEA uptake were unaffected. Although HgCl₂ has a high affinity for sulfhydryl groups its uptake as a complex to glutathione or cysteine was not enhanced. HgCl₂ also had no affect on the uptake rate of PAH or TEA even though both HgCl₂ and K₂Cr₂O₇ were able to reduce the steady state accumulation of these organic substrates.
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Tang, Chi-wai Sydney. "The many facets of the renal proximal tubular epithelial cell in human." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31992468.
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Tang, Chi-wai Sydney, and 鄧智偉. "The many facets of the renal proximal tubular epithelial cell inhuman." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31992468.
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Reece, Mark T. "Functional characterization of OCTRL2 : an organic cation transporter expressed in the renal proximal tubules." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=20973.
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Chromosome 11p15.5 harbors a gene or genes involved in Beckwith Wiedemann Syndrome (BWS) and that confer(s) susceptibility to Wilms' tumor, rhabdomyosarcoma, and hepatoblastoma. PowerBLAST of P1 artificial chromosome clones from this region identified two novel transcripts with open reading frames encoding putative proteins of 253 and 424 amino acids. The larger of the transcripts was shown by Northern blot to be predominantly expressed in the fetal and adult liver and kidney. This transcript shares homology with integral membrane organic cation transporters, such as the tetracycline resistance proteins and bacterial multidrug resistance proteins; and was therefore designated ORCTL2 (organic cation transporter-like 2). An expressed sequence polymorphism provided evidence that the ORCTL2 gene exhibits "leaky" imprinting in both human fetal kidney and human fetal liver. Given the expression pattern of ORCTL2, it is possible that this gene may have a role in the development of phenotypes associated with BWS, including Wilms' tumor (WT). SSCP analysis on 51 sporatic WT samples did not identify any mutations in ORCTL2 which would implicate it in disease. Investigation of the transport properties of ORCTL2 show that this protein can confer resistance to chloroquine and quinidine when overexpressed in bacteria. Immunohistochemistry performed with anti-ORCTL2 polyclonal antibodies on human renal sections indicate that ORCTL2 is localized on the apical membrane surface of the proximal tubules. These results suggest that ORCTL2 may play a role in the transport of chloroquine and quinidine related compounds within the kidney.
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Branco, Regiane Cardoso Castelo. "Efeito da angiotensina-(1-7) no fluxo reabsortivo de bicarbonato (JHCO3-) e na concentração citosólica de cálcio ([Ca2+]i): estudo por microperfusão tubular proximal, in vivo." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-25072012-135726/.
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O estudo avaliou os efeitos agudos da Ang-(1-7) na reabsorção de bicarbonato (JHCO3-) no túbulo proximal cortical de rato, in vivo, medindo o pH intratubular pelo microeletródio sensível a H+. O JHCO3- controle é 2,84 ± 0,08 nmol. cm-2. s-1 (49), a Ang-(1-7; 10-12 ou 10-9 M) o reduz (35 ou 61 %) e a Ang-(1-7; 10-6 M) o eleva (56 %). A inibição do receptor Mas (por A779) eleva o JHCO3- (30 %), abole o efeito inibidor da Ang-(1-7), mas não afeta seu efeito estimulador. A inibição do NHE3 (por S3226) diminui o JHCO3- (45 %), não altera o efeito inibidor da Ang-(1-7), mas transforma seu efeito estimulador em inibidor. A concentração de cálcio citosólico ([Ca2+]i), medida pelo FURA-2-AM, controle é 100 ± 2,47 nM (35) e a Ang-(1-7; 10-12, 10-9 ou 10-6 M) a aumenta (152, 103 ou 53 %) transientemente (3 min). A inibição do receptor Mas aumenta a [Ca2+]i (26 %), mais inibe o efeito estimulador de todas as doses de Ang-(1-7). Os resultados indicam que o efeito bifásico dose-dependente da Ang-(1-7) sobre o JHCO3- no túbulo proximal é via receptor Mas e isoforma NHE3 e sugerem estimulação desse trocador por moderado aumento da [Ca2+]i na presença de Ang-(1-7; 10-6 M) e sua inibição por pronunciado aumento da [Ca2+]i na vigência de Ang-(1-7; 10-12 ou 10-9 M).The action of Ang-(1-7) on bicarbonate reabsorption (JHCO3-) was evaluated in vivo middle proximal tubule of rat kidney, using H ion-sensitive microelectrodes. The control JHCO3- is 2,84 ± 0.08 nmol. cm-2. s-1 (49), Ang-(1-7; 10-12 or 10-9 M) decreases it (35 and 61 %) but Ang-(1-7; 10-6 M) increased it (56 %). A779 (an Ang-(1-7) receptor Mas antagonist) increases the JHCO3- (30 %), prevents the inhibitory effect of Ang-(1-7) and does not affect the stimulatory effect of Ang-(1-7). S3226 (10-6 M; an inhibitor of NHE3) decreases the JHCO3- (45 %), does not affect the inhibitory effect of Ang-(1-7) and changes its stimulatory effect on an inhibitory effect. The control cytosolic free calcium ([Ca2+]i), monitored by FURA-2-AM, is 100 ± 2,47 nM (35) and Ang-(1-7; 10-12, 10-9 or 10-6 M) causes a transient (3 min) increase of it (152, 103 or 53 %). A779 increases the [Ca2+]i (26 %) but impaired the stimulatory effect of Ang-(1-7). Our results indicate the biphasic dose-dependent effect of Ang-(1-7) on JHCO3- in proximal tubule is mediated via Mas receptor and NHE3 and are compatible with stimulation of this exchanger by a moderate increase in [Ca2+]i in the presence of Ang-(1-7, 10-6 M), and its inhibition by large increase in [Ca2+]i with Ang-(1-7, 10-12 or 10-9 M).
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Pergher, Patrícia e. Silva. "Efeitos não-genômicos dos hormônios esteróides - aldosterona e corticosterona - sobre a acidificação do túbulo proximal (S2) de ratos: estudos de microperfusão tubular e capilar, in vivo." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-10122010-144456/.
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O objetivo foi determinar se aldosterona e corticosterona agem sobre a acidificação do túbulo proximal e se esses efeitos são genômicos e/ou não-genômicos. A reabsorção de HCO3- foi avaliada por microperfusão estacionária. Aldosterona e corticosterona perfundidas na luz tubular causaram aumento significante do JHCO3-. Na presença de etanol, actinomicina D, cicloheximida ou espironolactona, o JHCO3- foi estatisticamente igual ao valor controle (2,84 ± 0,079 nmol.cm-2.s-1). RU486 sozinho inibiu o efeito estimulador da aldosterona e corticosterona. Losartan não alterou o JHCO3-. Concanomicina ou S3226 diminuiram o efeito estimulador da corticosterona. A aldosterona perfundida nos capilares peritubulares aumentou o JHCO3-. Assim, a aldosterona e corticosterona tem um efeito rápido, não-genômico, estimulante do JHCO3-, provavelmente com a participação do GR e pela ativação do NH3 e da H+-ATPase luminais. Além disto, a aldosterona e corticosterona endógenas estimulam o JHCO3- no túbulo proximal.The purpose was to determine if aldosterone and corticosterone act on the acidification of proximal tubule and if these hormonal effects are genomic and/or nongenomic. Bicarbonate reabsorption was evaluated by microperfusion. Aldosterone and corticosterone caused a significant increase in JHCO3-. In the presence of ethanol, actinomycin D, cycloheximide or espironolactone, the JHCO3- was not different from the control value (2.84 ± 0.079 nmol.cm-2.s-1). However, in the presence of RU486 a decrease on JHCO3- was observed. Losartan inhibited the JHCO3-. Concanamicyn or S3226 decreased the stimulatory effect of corticosterone. Aldosterone perfused into peritubular capillaries also increased JHCO3-. Our results indicate that: aldosterone and corticosterone has a rapid, nongenomic, stimulatory effect on JHCO3-; probably, GR participates in this process and; this effect, probably, occurs by activation of luminal NH3 and H+-ATPase. Besides, endogenous aldosterone and corticosterone stimulate JHCO3-.
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Farah, Livia Xavier Soares. "Efeito do peptídeo-1 semelhante ao glucagon endógeno sobre a atividade do NHE3 em túbulo proximal renal." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5166/tde-05102015-114814/.
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O peptídeo-1 semelhante ao glucagon (GLP-1) é um hormônio incretina secretado pelas células L do trato gastrointestinal e liberado imediatamente após a ingestão de alimento. O GLP-1 estimula a secreção de insulina pós-prandial moderando a elevação precoce da glicose no sangue. Embora primariamente envolvido na homeostase da glicose, o GLP-1 é capaz de induzir a diurese e natriurese, quando administrado em doses farmacológicas em humanos e em roedores. Estudos prévios do nosso laboratório demonstraram que o mecanismo de ação renal do GLP-1, bem como de agonistas sintéticos do receptor GLP-1R, envolve o aumento do fluxo plasmático renal (FPR) e do ritmo de filtração glomerular (RFG) bem como a diminuição da reabsorção de sódio dependente da isoforma 3 do trocador Na?/H? (NHE3) em túbulo proximal renal. Entretanto, até o momento, nenhum estudo investigou se o GLP-1 endógeno exerce efeitos sobre o manuseio renal de sal e água, nem o seu papel fisiológico sobre a regulação da atividade do NHE3. Portanto, o objetivo deste estudo foi testar a hipótese que o GLP-1 endógeno modula a função renal de ratos, ao menos em parte, via inibição da atividade do NHE3 em túbulo renal. Para este fim, ratos Wistar (2-3 meses de idade) foram devidamente anestesiados, submetidos à traqueostomia e tiveram a veia jugular e a bexiga canuladas para infusão de uma solução contendo 100 ug/kg/min do antagonista do receptor GLP-1R exendin-9 (Ex-9, 40 uL/min) por um período de 30 minutos e para a coleta de urina, respectivamente. A infusão sistêmica de Ex-9 diminuiu a concentração de AMPc urinário e atividade da PKA cortical renal consistente com o bloqueio da sinalização deflagrada pela interação GLP-1/GLP-1R no rim. Além disso, a administração sistêmica de Ex-9 reduziu a diurese, natriurese, RFG, FPR, clearance de lítio e pH urinário. Em experimentos de microperfusão estacionária in vivo, não foram observadas diferenças no fluxo de bicarbonato dependente de NHE3 entre os túbulos proximais perfundidos com exendin-9 (2 uM) e os túbulos perfundidos com solução controle. No entanto, a perfusão tubular proximal com Ex-9 foi capaz de bloquear completamente as ações inibitórias do GLP-1 (20 nM) sobre a atividade do NHE3. Por outro lado, a infusão sistêmica do Ex-9 reduziu os níveis de fosforilação da serina 552, sítio consenso para a fosforilação por PKA localizado na região C-terminal do NHE3, e que está associado à inibição da atividade de troca Na+/H+ mediada por este transportador. Baseando-se nos achados que a infusão sistêmica do Ex-9 aumenta a reabsorção de sódio e secreção de H?, reduz o clearance do lítio e os diminui os níveis de fosforilação do NHE3 na serina 552 são consistentes com um aumento na atividade deste transportador na ausência/redução da sinalização mediada pela interação do GLP-1 endógeno com seu receptor no rim. Por sua vez, o fato do Ex-9 não afetar a atividade do NHE3 sob as condições experimentais da microperfusão estacionária in vivo é condizente com o fato do GLP-1 não ser sintetizado no néfron e sugere fortemente que é o GLP-1 filtrado que se liga ao seu receptor no túbulo proximal renal resultando na diminuição da reabsorção de bicarbonato de sódio mediada pelo NHE3. Em conjunto, estes resultados sugerem que o GLP-1 endógeno exerce efeito tônico sobre o manuseio renal de sódio e água, mediando portanto, uma relação funcional entre a homeostase glicêmica e volêmicaThe glucagon like peptide-1 (GLP-1) is an incretin hormone secreted by the L-cells of the gastrointestinal tract and released immediately after ingestion of food. GLP-1 stimulates postprandial insulin secretion moderating early increase in blood glucose. Although primarily involved in glucose homeostasis, GLP-1 is capable of inducing diuresis and natriuresis when administered in pharmacologic doses in humans and rodents. Previous studies from our laboratory have shown that the renal mechanism of action of GLP-1 and synthetic agonists of GLP-1R receptor, involves an increase of renal plasma flow (RPF) and glomerular filtration rate (GFR) as well a decrease in reabsorption of sodium mediated by the Na? / H? exchanger (NHE3) isoform 3 in the renal proximal tubule. However, to date, no study has investigated whether endogenous GLP-1 exerts effects on the renal handling of salt and water, or its physiological role in the regulation of the activity of NHE3. Therefore, the aim of this study was to test the hypothesis that endogenous GLP-1 modulates renal function in rats, at least in part, via inhibition of the NHE3 in renal tubule. To this end, male Wistar rats (2-3 months old) were properly anesthetized, tracheostomized and the jugular vein and the bladder were cannulated to the infusion of a solution containing 100 ug / kg / min GLP-1R antagonist receiver exendin-9 (Ex-9, 40 uL/min) for a period of 30 minutes and to collect urine, respectively. Systemic infusion of Ex-9 reduced the urinary concentration of cAMP and the renal cortical PKA activity, consistent with the blockage of the signal triggered by the interaction of GLP-1 / GLP-1R in the kidney. Furthermore, systemic administration of ex-9 reduced diuresis, natriuresis, GFR, RPF, lithium clearance and urinary pH. In experiments of in vivo stationary microperfusion, no differences were observed in the NHE3-mediated net bicarbonate flow between proximal tubules perfused with exendin-9 (2 mM) and perfused tubules with control solution. However, the tubular proximal perfusion with Ex-9 was able to completely block the inhibitory actions of GLP-1 (20 nM) on the activity of NHE3. On the other hand, systemic infusion of Ex-9 reduced phosphorylation levels of serine 552, a consensus site for phosphorylation by PKA located in the C-terminal region of NHE3, which is associated with inhibition of exchange activity of Na+/H+ mediated by this transporter. Collectively, the findings that systemic infusion of Ex-9 increases sodium reabsorption and secretion of H+, reduces the lithium clearance and decreases the NHE3 phosphorylation at serine 552 levels are consistent with the idea that NHE3 activity is upregulated in the absence/reduction of the signaling cascade mediated by the interaction of the endogenous GLP-1 with its receptor in the kidney. In turn, the fact Ex-9 does not affect the activity of NHE3 under the experimental conditions of stationary microperfusion in vivo is consistent with the fact that GLP-1 is not synthesized in the nephron. Besides, it strongly suggests that is the filtrated GLP-1 that binds to its receptor in renal proximal tubule, resulting in a decrease in NHE3-mediated sodium bicarbonate reabsorption. Taken together, these results suggest that endogenous GLP-1 exerts a tonic effect on renal sodium and water handling, mediating therefore a functional relationship between volume and glucose homeostasis
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Lee, Sarah Angeline. "Curcumin Protects against Renal Ischemia by Activating the Unfolded Protein Response and Inducing HSP70." Yale University, 2009. http://ymtdl.med.yale.edu/theses/available/etd-04062009-215154/.
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The purpose of this study was to establish whether curcumin protects renal proximal tubule cells against ischemic injury, determine whether this postulated cytoprotective effect is mediated through the upregulation of HSP70, and investigate whether the mechanism by which curcumin induces HSP70 expression and confers its protective effect is through activation of the Unfolded Protein Response. LLC-PK1 cells were cultured on collagen-coated filters to mimic conditions of in vivo renal proximal tubule cells and induce cell polarization. Injury with and without curcumin treatment was studied by using chemically-induced ATP-depletion which mimics renal ischemic injury. Cell injury was assessed using a TUNEL assay in order to evaluate DNA cleavage associated with ischemia-induced apoptosis and actin staining used to assess cytoskeletal disruption. Renal ischemic damage was further investigated by determining detachment of the Na-K ATPase from the basolateral membrane, which represents loss of cell polarity. Cells were incubated with curcumin in a dose- and time-response fashion and subsequent levels of HSP70 expression were assessed. Cells were then incubated with AEBSF, an inhibitor of the Unfolded Protein Response (UPR) and HSP70 and BiP/GRP78 (an ER resident chaperone that is upregulated by the UPR) expression levels were evaluated. Results demonstrated that treatment with curcumin during two hours of injury results in significantly less injury-related apoptosis and cytoskeletal disruption compared to control injured cells. It was demonstrated that curcumin induces HSP70 in both a dose- and time-response fashion. Moreover, curcumin treatment resulted in profound stabilization of Na-K ATPase on the basolateral membranes as there was significantly less Na-K ATPase detachment in cells treated with curcumin during two hours of injury compared to control injured cells. Finally, treatment with AEBSF inhibited HSP70 upregulation in curcumin-treated cells as well as inhibiting the GRP78 over-expression otherwise demonstrated in curcumin-treated cells. Protection of proximal tubule cells against renal ischemic injury by curcumin was therefore indicated to be mediated by the activation of the UPR through which HSP70 is upregulated. Curcumins activation of the UPR and induction of HSP70 explains the stabilization of Na-K ATPase on the cytoskeleton and also provides a potential mechanism explaining many of curcumins therapeutic and protective qualities.
Books on the topic "Proximal renal tubules"
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Najjar, Samer. Effects of ischemia and reperfusion on mitochondrial phosphate uptake in rat renal proximal tubules. [New Haven, Conn: s.n.], 1993.
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Wong, P. S. K. The use of NMR spectroscopy to follow intracellular sodium content in rat rental proximal tubules. Birmingham: University of Birmingham, 1994.
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Jones, Caroline Elizabeth Mary. The development, evaluation and use of freshly isolated renal proxinal tubule systems in the fischer rat. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1990.
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Speeckaert, Marijn, and Joris Delanghe. Tubular function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0008.
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Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is characterized by hypophosphataemia, and a variety of other abnormalities characteristics of the renal Fanconi syndrome. Distinguishing the location of the lesion in Renal Tubular Acidosis is considered in Chapter 35.
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Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.
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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanced conditions, absorption of dietary Pi along the small intestine equals the output of Pi via kidney and faeces. Renal excretion of Pi represents the key determinant for the adjustment of normal Pi plasma concentrations. Renal reabsorption of Pi occurs along the proximal tubules by sodium-dependent Pi cotransporters that are strictly localized at the apical brush border membrane. Parathyroid hormone (PTH) and FGF23 are key regulators amongst a myriad of factors controlling excretion of Pi in urine, mostly by changes of the apical abundance of Na/Pi cotransporters. Hypophosphataemia may result in osteomalacia, rickets, muscle weakness, and haemolysis. Hyperphosphataemia can lead to hyperparathyroidism and severe calcifications in different tissues.
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Bockenhauer, Detlef, and Robert Kleta. Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0041_update_001.
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Up to 80% of filtered salt and water is returned back into the circulation in the proximal tubule. Several solutes, such as phosphate, glucose, low-molecular weight proteins, and amino acids are exclusively reabsorbed in this segment, so their appearance in urine is a sign of proximal tubular dysfunction. An entire orchestra of specialized apical and basolateral transporters, as well as paracellular molecules, mediate this reabsorption. Defects in proximal tubular function can be isolated (e.g. isolated renal glycosuria, aminoacidurias, or hypophosphataemic rickets) or generalized. In the latter case it is called the Fanconi–Debre–de Toni syndrome, based on the initial clinical descriptions. However, in clinical practice it is usually referred to as just the ‘renal Fanconi syndrome’. Severity of proximal tubular dysfunction can vary, and may coexist with some degree of loss of glomerular filtration capacity. Causes include a wide range of insults to proximal tubular cells, including a number of genetic conditions, drugs and poisons.
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Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.
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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
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Schreuder, Michiel F. Renal tubular dysgenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0350.
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Renal tubular dysgenesis involves the absence or incomplete differentiation of proximal tubular nephron segments. Due to the lack of a patent nephron, it is characterized by (fetal) anuria and subsequent oligohydramnios, pulmonary hypoplasia, premature birth with severe and refractory arterial hypotension, and fetal or neonatal death. The main cause for renal tubular dysgenesis is a genetic mutation in the renin–angiotensin system, which has shown an autosomal recessive trait. Maternal use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers during pregnancy can have similar blocking effects on the fetal renin–angiotensin system, which may lead to renal tubular dysgenesis. Even though there is no actual renal function, ultrasound usually shows kidneys of normal size and architecture with an intact corticomedullary differentiation. Most patients with renal tubular dysgenesis do not survive beyond the neonatal period. A few patients have been described to survive with respiratory support, vasopressor treatment, and dialysis.
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Walsh, Stephen B. Approach to the patient with renal tubular acidosis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0036.
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The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α-intercalated cells in the distal nephron. Proximal (Type 2) renal tubular acidosis is a syndrome of metabolic acidosis that is almost always accompanied by the Fanconi syndrome of glycosuria, phosphaturia, uricosuria, aminoaciduria, and low-molecular-weight proteinuria. It is caused by a failure of bicarbonate reabsorption by the proximal tubular cells. Type 3 or mixed renal tubular acidosis, as originally described, has vanished (or was originally incompletely described). It is sometimes used to describe a mutation of carbonic anhydrase II, which causes both proximal and distal renal tubular acidosis, as well as cerebral calcification and osteopetrosis. Type 4 or hypoaldosteronism is a syndrome of hyperkalaemia and mild metabolic acidosis. It is due to a lack of aldosterone or resistance to its action.
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
Book chapters on the topic "Proximal renal tubules"
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Pavelka, Margit, and Jürgen Roth. "Parathyroid Hormone Response of Renal Proximal Tubules." In Functional Ultrastructure, 230–31. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_119.
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Green, Carol E., Jack E. Dabbs, Katherine L. Allen, Charles A. Tyson, and Elmer J. Rauckman. "Characterization of Isolated Renal Proximal Tubules for Nephrotoxicity Studies." In Nephrotoxicity, 719–23. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_111.
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Mandel, Lazaro J., William R. Jacobs, Rick Schnellmann, Maria Sgambati, Ann LeFurgey, and Peter Ingram. "Mechanisms of Anoxic Injury to Transport and Metabolism of Proximal Renal Tubules." In Cell Calcium Metabolism, 471–77. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5598-4_49.
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Kaimori, Jun-ya, Masaru Takenaka, and Kousaku Okubo. "16 Quantification of Gene Expression in Mouse and Human Renal Proximal Tubules." In Laser Capture Microdissection, 209–20. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-853-6:209.
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Christensen, Erik Ilsø, and Søren Nielsen. "Protein Handling from Apical and Basolateral Surfaces in Rat and Rabbit Renal Proximal Tubules." In Endocytosis, 325–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_40.
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Chobanian, M. C., L. A. Fahien, and P. C. Brazy. "Metabolic Requirement for Inorganic Phosphate by Renal Proximal Tubules: Influence upon L-Glutamine Metabolism." In Contributions to Nephrology, 85–92. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000059849.
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Yanagawa, Norimoto, and Ok D. Jo. "Possible Role of Calcium in Parathyroid Hormone Action on Phosphate Transport in Rabbit Renal Proximal Tubules." In Phosphate and Mineral Homeostasis, 125–32. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_13.
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Lote, Christopher J. "The Proximal Tubule." In Principles of Renal Physiology, 51–66. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3785-7_5.
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Lote, Christopher J. "The proximal tubule." In Principles of Renal Physiology, 51–67. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-6470-2_5.
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Lote, Chris. "The proximal tubule." In Principles of Renal Physiology, 53–69. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4086-7_5.
Full textConference papers on the topic "Proximal renal tubules"
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Westwood, Brian M., Hossam A. Shaltout, and Mark C. Chappell. "Modeling of Angiotensin Peptide Metabolism in Renal Proximal Tubules." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-190990.
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The recent discovery of angiotensin converting enzyme 2 (ACE2) as a functional peptidase within the renin-angiotensin system (RAS) has added a new layer of complexity to the enzymatic cascade of this hormonal system. ACE2 is highly expressed in the proximal tubules of the kidney, an important tissue site involved in blood pressure regulation. Therefore, we derived a model for the processing of Ang I which is the immediate precursor to the biologically active peptides Ang II and Ang-(1-7) based on metabolism data in isolated proximal tubules of the sheep kidney (1). Given the individual experimental velocities for several peptidases expressed in the proximal tubules including ACE, ACE2 and neprilysin, rate constants were calculated to describe the conservation equations for the processing of Ang I, Ang II and Ang-(1-7) We modeled the system with Ang I as the initial substrate and peptide concentrations for the downstream products were calculated using Euler’s method.
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Safithri, Fathiyah, Desy Andari, and Fifa Yuniarmi. "Improvement of Renal Proximal Tubules after Black Cumin (Nigella Sativa) Extract Administration in Rat with CCl4-induced Chronic Renal Damage." In The Health Science International Conference. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0009120000210026.
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Hansson, Jennifer, Kjell Hultenby, Catharina Cramnert, David Lindgren, Håkan Axelson, and Martin E. Johansson. "Abstract 5010: Characterization of a novel cell type in human renal proximal tubules with connection to renal cell carcinoma development." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5010.
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Brandão, Joana Bader Sadala, Isabela Abud De Andrade, Maria Eduarda Alencar Santos, Paula Cristina Rios Rodriguez, and Rafael Xavier Cunha. "INFECÇÃO POR SARS-COV-2 E RELAÇÃO FISIOPATOLÓGICA COM INJÚRIA RENAL." In I Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/1000.
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INTRODUÇÃO: A Covid-19 é caracterizada por sua alta transmissibilidade e, em casos graves, pela sua acentuada resposta imune e sua tempestade de citocinas, que pode resultar em perda da tolerância periférica dos órgãos, ocasionando uma inflamação exacerbada e destruição tecidual. É sabido que o vírus Sars-CoV-2 pode gerar injúrias em órgãos e sistemas além do pulmonar e imune, como o sistema renal. Um importante ponto de análise foi a ação da enzima conversora de angiotensina 2 (ACE2), altamente presente nas células tubulares proximais e podócitos, levando a um quadro de hematúria e proteinúria. OBJETIVO: Validar a importância de observar-se a evolução do quadro renal em pacientes enfermos de Covid-19. MÉTODO: Trata-se de uma Revisão Integrativa de Literatura do tipo qualitativo-descritivo. A busca automática utilizou-se das bases SCIELO e PUBMED, adotando como critérios de inclusão artigos, publicados no período de 2017 a 2021, dentro da abordagem temática proposta e no idioma Inglês, e nos de exclusão, enquadrou-se aqueles divergentes das diretrizes estipuladas. RESULTADOS: Dentre os 10 artigos selecionados, foi factível analisar as características imunológicas da Insuficiência Renal Aguda (IRA) em pacientes com Covid-19. Evidenciou-se a presença de proteína do nucleocapsídeo, macrófagos CD68+ e C5b-9 na região tubular proximal, demonstrando que o novo coronavírus é capaz de lesionar direta e indiretamente, mediante células do complemento e ação dos macrófagos. Análises imuno-histoquímicas observaram a presença de neutrófilos nos glomérulos e tubulointersticial, agregados de eritrócitos bloqueando capilares peritubulares e trombos de fibrina segmentar na região glomerular. Ademais, o Sars-CoV-2 apresenta tropismo com células que expressam ACE2, de modo que envolve uma resposta adaptativa inadequada do sistema imunológico, acarretando em tempestade de citocinas e lesão renal. CONCLUSÃO: Em conformidade com os dados apresentados, conclui-se que as lesões renais se devem à superexpressão de ACE2 nas células tubulares proximais. A proteinúria, consequência desse mecanismo lesivo, é um fator importante para o desenvolvimento de IRA. A incidência desta é aumentada em grau conformativo com a gravidade do paciente com Covid-19, o que foi indicado pelos valores prognósticos. Devendo, portanto, haver uma maior preocupação com a função renal no cuidado desses pacientes.
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Taub, Mary L., and Sunil Sudarshan. "Abstract 4364: Oncometabolite L-2-hydroxyglutarate blocks differentiation of renal proximal tubule cells in matrigel." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4364.
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Taub, Mary L., and Sunil Sudarshan. "Abstract 4364: Oncometabolite L-2-hydroxyglutarate blocks differentiation of renal proximal tubule cells in matrigel." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4364.
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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, Giovanna A. Giannico, Roy Zent, Raymond Clement Harris, Peter Clark, Punita Dhawan, and Amar B. Singh. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1767.
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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, Giovanna A. Giannico, Roy Zent, Raymond Clement Harris, Peter Clark, Punita Dhawan, and Amar B. Singh. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1767.
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