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Journal articles on the topic 'Renal systems'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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1

Yuan, Zhi-xiang, Zhenghui Shang, Jian Gu, and Lili He. "Renal targeting delivery systems." Future Medicinal Chemistry 11, no. 17 (September 2019): 2237–40. http://dx.doi.org/10.4155/fmc-2019-0152.

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2

Zeikus, Eric, Giri Sura, Nicole Hindman, and Julia R. Fielding. "Tumors of Renal Collecting Systems, Renal Pelvis, and Ureters." Magnetic Resonance Imaging Clinics of North America 27, no. 1 (February 2019): 15–32. http://dx.doi.org/10.1016/j.mric.2018.09.002.

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3

Stokes, M. Barry. "Classification Systems in Renal Pathology." Surgical Pathology Clinics 7, no. 3 (September 2014): 427–41. http://dx.doi.org/10.1016/j.path.2014.04.007.

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4

Hennefer, Dawn, and Elizabeth Lawson. "Pharmacology - a systems approach: renal system." British Journal of Healthcare Assistants 4, no. 1 (January 2010): 38–41. http://dx.doi.org/10.12968/bjha.2010.4.1.46073.

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5

Novara, Giacomo, Guido Martignoni, Walter Artibani, and Vincenzo Ficarra. "Grading Systems in Renal Cell Carcinoma." Journal of Urology 177, no. 2 (February 2007): 430–36. http://dx.doi.org/10.1016/j.juro.2006.09.034.

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6

Schafer, James A. "RENAL WATER AND ION TRANSPORT SYSTEMS." Advances in Physiology Education 275, no. 6 (December 15, 1998): S119—S131. http://dx.doi.org/10.1152/advances.1998.275.6.s119.

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7

Rhee, Eugene P. "A Systems-Level View of Renal Metabolomics." Seminars in Nephrology 38, no. 2 (March 2018): 142–50. http://dx.doi.org/10.1016/j.semnephrol.2018.01.005.

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8

Nishimura, M., A. Milsted, C. H. Block, K. B. Brosnihan, and C. M. Ferrario. "Tissue renin-angiotensin systems in renal hypertension." Hypertension 20, no. 2 (August 1992): 158–67. http://dx.doi.org/10.1161/01.hyp.20.2.158.

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9

Brown, Anthony, Mitchell Smith, Paul Rochon, and Charles Ray. "Percutaneous Access of Nondilated Renal Collecting Systems." Seminars in Interventional Radiology 31, no. 01 (February 20, 2014): 098–100. http://dx.doi.org/10.1055/s-0033-1363849.

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10

Pilz, Stefan, Andreas Meinitzer, Martin Gaksch, Martin Grübler, Nicolas Verheyen, Christiane Drechsler, Bríain ó. Hartaigh, et al. "Homoarginine in the renal and cardiovascular systems." Amino Acids 47, no. 9 (May 1, 2015): 1703–13. http://dx.doi.org/10.1007/s00726-015-1993-2.

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11

Jindal, Nikita, Jimmy Singla, Balwinder Kaur, Harsh Sadawarti, Deepak Prashar, Sudan Jha, Gyanendra Prasad Joshi, and Changho Seo. "Fuzzy Logic Systems for Diagnosis of Renal Cancer." Applied Sciences 10, no. 10 (May 17, 2020): 3464. http://dx.doi.org/10.3390/app10103464.

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Renal cancer is a serious and common type of cancer affecting old ages. The growth of such type of cancer can be stopped by detecting it before it reaches advanced or end-stage. Hence, renal cancer must be identified and diagnosed in the initial stages. In this research paper, an intelligent medical diagnostic system to diagnose renal cancer is developed by using fuzzy and neuro-fuzzy techniques. Essentially, for a fuzzy inference system, two layers are used. The first layer gives the output about whether the patient is having renal cancer or not. Similarly, the second layer detects the current stage of suffering patients. While in the development of a medical diagnostic system by using a neuro-fuzzy technique, the Gaussian membership functions are used for all the input variables considered for the diagnosis. In this paper, the comparison between the performance of developed systems has been done by taking some suitable parameters. The results obtained from this comparison study show that the intelligent medical system developed by using a neuro-fuzzy model gives the more precise and accurate results than existing systems.
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12

Volpe, Alessandro, and Carlo Terrone. "Anatomic Classification Systems of Renal Tumors: New, Useful Tools in Renal Surgical Oncology." European Urology 60, no. 4 (October 2011): 731–33. http://dx.doi.org/10.1016/j.eururo.2011.07.038.

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13

Tsyrlin, V. A., N. V. Kuzmenko, M. G. Pliss, and N. S. Rubanova. "BAROREFLEX AND ADAPTATION OF VISCERAL SYSTEMS IN RENOVASCULAR HYPERTENSION." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 1 (February 28, 2013): 32–37. http://dx.doi.org/10.18705/1607-419x-2013-19-1-32-37.

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Objective. To test the hypothesis, that the arterial baroreceptor refl ex plays the key role for the phenomenon of visceral systems adaptation for long-term afferent drive. Design and methods. In Wistar rats the model of the «two kidneys, one clip» vasorenal hypertension was carried out. The sino-aortic denervation was performed in one group — before the left renal artery clipping, in the other group — 8 weeks after the left renal artery clipping. Results. The renal artery clipping led to the increase of blood pressure only in 17 % of animals with intact sino-carotid-aortic mechanoreceptor zones. The absence of hypertension in these animals might be due to the cardiovascular adaptation phenomenon to prolonged afferent action from ischemic kidney. Denervation of mechanoreceptor zones before the clipping of the renal artery contributes to the development of hypertension in 100 %. However, the denervation of sino-carotid and aortic zones performed 8 weeks after the renal artery clipping in rats without hypertension, does not affect blood pressure level.Conclusion. We suggest, that the absence of hypertension after renal artery clipping is due to the adaptation of the circulatory system to a long-term afferentation from the kidney, and the denervation of large vessels mechanoreceptor zones does not alter this process. At the same time, the damage of the arterial baroreceptor refl ex before renal artery clipping interferes in the visceral systems adaptation to afferent action and contributes to the arterial hypertension development.
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14

Pinto, Vanda, Maria João Pinho, and Patrício Soares‐da‐Silva. "Renal amino acid transport systems and essential hypertension." FASEB Journal 27, no. 8 (April 24, 2013): 2927–38. http://dx.doi.org/10.1096/fj.12-224998.

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15

Kapoor, Anil. "Renal tumour scoring systems: How useful are they?" Canadian Urological Association Journal 9, no. 1-2 (February 5, 2015): 46. http://dx.doi.org/10.5489/cuaj.2740.

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16

Gohar, Eman Y., Malgorzata Kasztan, and David M. Pollock. "Interplay between renal endothelin and purinergic signaling systems." American Journal of Physiology-Renal Physiology 313, no. 3 (September 1, 2017): F666—F668. http://dx.doi.org/10.1152/ajprenal.00639.2016.

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Alterations in extracellular fluid volume regulation and sodium balance may result in the development and maintenance of salt-dependent hypertension, a major risk factor for cardiovascular disease. Numerous pathways contribute to the regulation of sodium excretion and blood pressure, including endothelin and purinergic signaling. Increasing evidence suggests a link between purinergic receptor activation and endothelin production within the renal collecting duct as a means of promoting natriuresis. A better understanding of the relationship between these two systems, especially in regard to sodium homeostasis, will fill a significant knowledge gap and may provide novel antihypertensive treatment options. Therefore, this review focuses on the cross talk between endothelin and purinergic signaling as it relates to the renal regulation of sodium and blood pressure homeostasis.
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17

Weale, Andy R. "THE SAFER CLINICAL SYSTEMS PROJECT IN RENAL CARE." Journal of Renal Care 39, S2 (August 13, 2013): 19–22. http://dx.doi.org/10.1111/j.1755-6686.2013.12031.x.

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18

Lory, Peter. "A mathematical modeling technique for renal counterflow systems." Applied Mathematics Letters 6, no. 2 (March 1993): 83–87. http://dx.doi.org/10.1016/0893-9659(93)90018-i.

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19

Nastase, Madalina V., Jinyang Zeng-Brouwers, Malgorzata Wygrecka, and Liliana Schaefer. "Targeting renal fibrosis: Mechanisms and drug delivery systems." Advanced Drug Delivery Reviews 129 (April 2018): 295–307. http://dx.doi.org/10.1016/j.addr.2017.12.019.

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20

Berthier, Celine C., Matthias Kretzler, and Anne Davidson. "A systems approach to renal inflammation in SLE." Clinical Immunology 185 (December 2017): 109–18. http://dx.doi.org/10.1016/j.clim.2016.08.015.

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21

Scully, Christopher G., Nicholas Mitrou, Branko Braam, William A. Cupples, and Ki H. Chon. "Detecting physiological systems with laser speckle perfusion imaging of the renal cortex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 11 (June 1, 2013): R929—R939. http://dx.doi.org/10.1152/ajpregu.00002.2013.

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Laser speckle perfusion imaging (LSPI) has become an increasingly popular technique for monitoring vascular perfusion over a tissue surface. However, few studies have utilized the full range of spatial and temporal information generated by LSPI to monitor spatial properties of physiologically relevant dynamics. In this study, we extend the use of LSPI to analyze renal perfusion dynamics over a spatial surface of ∼5 × 7 mm of renal cortex. We identify frequencies related to five physiological systems that induce temporal changes in renal vascular perfusion (cardiac flow pulse, respiratory-induced oscillations, baroreflex components, the myogenic response, and tubuloglomerular feedback) across the imaged surface and compare the results with those obtained from renal blood flow measurements. We find that dynamics supplied from global sources (cardiac, respiration, and baroreflex) present with the same frequency at all locations across the imaged surface, but the local renal autoregulation dynamics can be heterogeneous in their distribution across the surface. Moreover, transfer function analysis with forced blood pressure as the input yields the same information with laser speckle imaging or renal blood flow as the output during control, intrarenal infusion of Nω-nitro-l-arginine methyl ester to enhance renal autoregulation, and intrarenal infusion of the rho-kinase inhibitor Y-27632 to inhibit vasomotion. We conclude that LSPI measurements can be used to analyze local as well as global renal perfusion dynamics and to study the properties of physiological systems across the renal cortex.
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22

Reilly, Sharon L., Charles F. Sing, Michael A. Savageau, and Stephen T. Turner. "Analysis of systems influencing renal hemodynamics and sodium excretion. I. Biochemical systems theory." Integrative Physiological and Behavioral Science 29, no. 1 (January 1994): 55–73. http://dx.doi.org/10.1007/bf02691281.

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23

Zhu, Zixuan, Cai Yue, Ying Sun, Xuemei Li, and Mingxi Li. "Light-chain amyloidosis with renal involvement: renal outcomes and validation of two renal staging systems in the Chinese population." Amyloid 26, no. 4 (July 24, 2019): 186–91. http://dx.doi.org/10.1080/13506129.2019.1639149.

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24

Puppala, Naresh, and Gantala Alekhya Reddy. "Review on Effects of NSAID`S on Different Systems." Asian Journal of Pharmaceutical Research and Development 8, no. 1 (February 14, 2020): 100–109. http://dx.doi.org/10.22270/ajprd.v8i1.621.

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Non steroidal anti-inflammatory drugs (NSAIDs) are amongst the most commonly prescribed medication. Some are available over the counter and likely to be abused. The gastrointestinal (GI), renal and cardiovascular (CV) side effects limit NSAIDs use. These side effects occurred at a rate as low as 1%–5% for NSAID users. The gastrointestinal (GI), renal and cardiovascular (CV) side effects limit NSAIDs use. Some studies have shown that an extra 2to8 per 1000 people per year may have a major vascular event from using an NSAID. Several studies demonstrated that conventional NSAIDs were associated with a higher risk of AKI and GN and decreased kidney hemodynamic functions, including sodium excretion. NSAIDs have a range of adverse effects mainly affecting the GI, renal and CV systems.
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25

Koepsell, Hermann, Andreas Busch, Valentin Gorboulev, and Petra Arndt. "Structure and Function of Renal Organic Cation Transporters." Physiology 13, no. 1 (February 1998): 11–16. http://dx.doi.org/10.1152/physiologyonline.1998.13.1.11.

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Polyspecific transport systems in the kidney mediate the excretion and reabsorption of organic cations. Electrogenic import systems and electroneutral export systems in the basolateral and luminal plasma membranes of proximal renal tubules are involved. Two subtypes of electrogenic import systems have been cloned from rats and humans and functionally characterized.
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26

Vanni, Alex J., Jim Hotaling, Christian Hamlat, Gregory J. Jurkovich, and Bryan B. Voelzke. "Do inclusive trauma systems improve outcomes after renal trauma?" Journal of Trauma and Acute Care Surgery 72, no. 2 (February 2012): 385–89. http://dx.doi.org/10.1097/ta.0b013e3182411c67.

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27

Dirkes, Susan. "How To Use The New CWH Renal Replacement Systems." AJN, American Journal of Nursing 94, no. 5 (May 1994): 67–73. http://dx.doi.org/10.1097/00000446-199405000-00028.

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28

LANIGAN, D., R. CONROY, C. BARRY-WALSH, B. LOFTUS, D. ROYSTON, and M. LEADER. "A comparative analysis of grading systems in renal adenocarcinoma." Histopathology 24, no. 5 (May 1994): 473–76. http://dx.doi.org/10.1111/j.1365-2559.1994.tb00557.x.

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29

Zhang, R., and E. Reisin. "Obesity-hypertension: the effects on cardiovascular and renal systems." American Journal of Hypertension 13, no. 12 (December 1, 2000): 1308–14. http://dx.doi.org/10.1016/s0895-7061(00)01254-1.

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30

Yee, Jerry, and Eric G. Neilson. "Immune modulation of biologic systems in renal somatic cells." Kidney International 43, no. 1 (January 1993): 128–34. http://dx.doi.org/10.1038/ki.1993.21.

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31

WRIGHT, MALCOLM. "Physiology for General Practitioners. 2: Cardiovascular and Renal Systems." Family Practice 5, no. 2 (1988): 145–53. http://dx.doi.org/10.1093/fampra/5.2.145.

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32

Ficarra, Vincenzo, Antonio Galfano, Gregory Verhoest, Stefano Cavalleri, Guido Martignoni, Walter Artibani, and Jean-Jacques Patard. "Prognostic Factors and Staging Systems for Renal Cell Carcinoma." European Urology Supplements 6, no. 10 (May 2007): 623–29. http://dx.doi.org/10.1016/j.eursup.2007.03.008.

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33

Zobel, Gerfried, Ekkehard Ring, and Veronika Zobel. "Continuous arteriovenous renal replacement systems for critically ill children." Pediatric Nephrology 3, no. 2 (1989): 140–43. http://dx.doi.org/10.1007/bf00852895.

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34

James, Charles A. "Morphology and function in MRI. Cardiovascular and renal systems." Pediatric Nephrology 7, no. 3 (June 1993): 329. http://dx.doi.org/10.1007/bf00853241.

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35

Kumar, Ravi M., Luke T. Lavallée, Darren Desantis, Sonya Cnossen, Ranjeeta Mallick, Ilias Cagiannos, Chris Morash, and Rodney H. Breau. "Are renal tumour scoring systems better than clinical judgement at predicting partial nephrectomy complexity?" Canadian Urological Association Journal 11, no. 6 (June 13, 2017): 199. http://dx.doi.org/10.5489/cuaj.4228.

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Introduction: We aimed to determine how renal tumour scoring systems, such as RENAL, PADUA, and Centrality (C)-index, compare to clinical judgement at predicting time required for tumour removal and kidney reconstruction during partial nephrectomy.Methods: A consecutive cohort of partial nephrectomy patients treated at The Ottawa Hospital, a tertiary care uro-oncological centre, was retrospectively reviewed. Preoperative axial images were reviewed by four experienced urological oncologists who independently rated the complexity of a partial nephrectomy from 1‒10 to generate a clinical judgement score. Two independent reviewers determined the RENAL, PADUA, and C-index scores. The time to complete tumour resection and renal reconstruction during partial nephrectomy was prospectively recorded.Results: During the study period, 104 partial nephrectomies were performed. The mean partial nephrectomy complexity score based on clinical judgement was 3.4 (standard deviation [SD] 2.1) out of 10. There was good agreement between surgeons in assessing tumour complexity (intraclass correlation coefficient 0.72; 95% confidence interval [CI] 0.65, 0.78). The mean RENAL score was 6.7 (SD 1.6) out of a maximum of 12, the mean PADUA score was 8.5 (SD 1.5) out of a maximum of 14, and the mean C-index score was 3.8 (SD 2). Mean resection and reconstruction time was 24 minutes (SD 10 minutes). The correlation between clinical judgement score and time was 0.27 (p=0.005). The correlation between renal tumour scoring systems and time was 0.20 (p=0.04) for RENAL, 0.21 (p=0.03) for C-index, and 0.26 (p=0.007) for PADUA. RENAL and PADUA scores were significantly associated with surgical and total complications.Conclusions: The majority of variance in ischemia time is not explained by clinical judgement or renal tumour scoring systems. Renal tumour scoring systems were not better than the clinical judgement of urological oncologists at predicting ischemia time during partial nephrectomy.
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36

Motte, Sophie, Ronald van Beneden, José Mottet, Benoit Rondelet, Myrielle Mathieu, Xavier Havaux, Pascale Lause, et al. "Early activation of cardiac and renal endothelin systems in experimental heart failure." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 6 (December 2003): H2482—H2491. http://dx.doi.org/10.1152/ajpheart.00419.2003.

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We investigated the time course of the expression of cardiac and renal endothelin systems in tachycardia-induced heart failure in dogs. Eleven beagles underwent rapid pacing at a progressively increased rate over a period of 5 wk, with a weekly clinical examination, echocardiography, measurement of circulating and urinary endothelin-1 (ET-1), and myocardial and renal tissue biopsies. Real-time quantitative PCR was used for determinations of tissue prepro-ET-1 (ppET-1), ET-1-converting enzyme (ECE-1), and ETA and ETB receptor mRNA. Cardiac and renal tissue ET-1 contents were evaluated by immunostaining and measured by radioimmunoassay at autopsy. Rapid pacing caused a progressive increase in end-systolic and end-diastolic ventricular volumes ( P < 0.05) from week 2 together with a decrease in ejection fraction and in mean velocity of circumferential shortening ( P < 0.05) from week 1. These changes were tightly correlated to myocardial ppET-1 and renal ETA receptor mRNA and less so to myocardial ECE-1 mRNA, and they occurred before any increase in plasma and urinary ET-1 ( P < 0.05 from week 4) and clinical signs of heart failure. Renal ppET-1 did not change. Both cardiac and renal ET-1 peptide contents were increased at autopsy. We conclude that tachycardia-induced heart failure in dogs is characterized by an early activation of the cardiac and renal tissue endothelin systems, which occurs before any changes in circulating and urinary ET-1 and is closely related to altered ventricular function.
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37

Nair, Nikhil, Ronith Chakraborty, Zubin Mahajan, Aditya Sharma, Sidarth Sethi, and Rupesh Raina. "Renal Manifestations of Tuberous Sclerosis Complex." Journal of Kidney Cancer and VHL 7, no. 3 (August 27, 2020): 5–19. http://dx.doi.org/10.15586/jkcvhl.v7i3.131.

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Tuberous sclerosis complex (TSC) is a genetic condition caused by a mutation in either the TSC1 or TSC2 gene. Disruption of either of these genes leads to impaired production of hamartin or tuberin proteins, leading to the manifestation of skin lesions, tumors and seizures. TSC can manifests in multiple organ systems with the cutaneous and renal systems being the most commonly affected. These manifestations can secondarily lead to the development of hypertension, chronic kidney disease, and neurocognitive declines. The renal pathologies most commonly seen in TSC are angiomyolipoma, renal cysts and less commonly, oncocytomas. In this review, we highlight the current understanding on the renal manifestations of TSC along with current diagnosis and treatment guidelines.
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38

Eveloff, J., and D. G. Warnock. "K-Cl transport systems in rabbit renal basolateral membrane vesicles." American Journal of Physiology-Renal Physiology 252, no. 5 (May 1, 1987): F883—F889. http://dx.doi.org/10.1152/ajprenal.1987.252.5.f883.

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The transport pathways for chloride in basolateral membrane vesicles from the rabbit renal cortex were investigated. 36Cl uptake was stimulated by the presence of potassium in the uptake media compared with sodium or N-methyl-D-glucamine. In addition, potassium (86Rb) uptake was stimulated more by chloride than by nitrate or gluconate. Neither of these processes was further stimulated by potassium gradients plus valinomycin, suggesting the presence of an electrically neutral K-Cl cotransport system. A magnesium-induced chloride conductance was also found in the basolateral membrane vesicles. In the absence of magnesium, the chloride conductance was low; valinomycin and an inwardly directed potassium gradient did not stimulate 36Cl uptake, anthracene-9-carboxylic acid did not inhibit 36Cl uptake, and valinomycin did not stimulate chloride-dependent 86Rb uptake. However, in the presence of 1 mM magnesium, opposite results were obtained; valinomycin and an inwardly directed potassium gradient stimulated 36Cl uptake, anthracene-9-carboxylic acid inhibited 36Cl uptake, and valinomycin stimulated chloride-dependent 86Rb uptake. Therefore, an electrically neutral K-Cl cotransport and magnesium-induced chloride conductance were found in renal cortical basolateral membrane vesicles prepared from the rabbit renal cortex.
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39

Shatylko, T. V., V. M. Popkov, A. Yu Korolev, and D. A. Chausovsky. "COMPARISON OF NEPHROMETRIC SYSTEMS IN PARTIAL NEPHRECTOMY FOR RENAL CELL CARCINOMA." I.P.Pavlov Russian Medical Biological Herald 25, no. 1 (March 31, 2017): 110–17. http://dx.doi.org/10.23888/pavlovj20171110-117.

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Evaluation of efficacy of using nephrometry scores was performed on our own cohort of patients. Correlation between them and clinical variables was studied. All nephrometry scores - RENAL, PADUA and C-index - correlate significantly with ischemia time during partial nephrectomy, but not with total operative time. Kidney resection for intermediate and high complexity tumors caused chronic kidney disease (CKD) de novo or CKD upstaging more often than resection for low complexity tumors. Low complexity tumors on RENAL and PADUA were characterized by significantly lower renal parenchyma ischemia time required for resection. Complications of partial nephrectomy were observed only in groups with intermediate and high tumor complexity, while differences between intermediate and high complexity seemed practically insignificant. Nephrometry systems are useful in clinical practice, but require further improvement.
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40

O’Brien, Brendan M., Steven P. Meyers, and Benjamin T. Crane. "Brachio-Oto-Renal Syndrome." Otology & Neurotology 36, no. 6 (July 2015): e110-e111. http://dx.doi.org/10.1097/mao.0000000000000409.

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41

Lynch, JO, A. Cox, B. Rawal, S. Shelmerdine, N. Vasdev, and A. Patel. "Bilateral obstruction of bilaterally duplicated collecting systems requiring upper and lower moiety drainage." Annals of The Royal College of Surgeons of England 98, no. 04 (April 1, 2016): e55-e58. http://dx.doi.org/10.1308/rcsann.2016.0077.

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A 60-year-old woman with a history of breast cancer presented with bilateral obstruction of bilaterally duplicated renal collecting systems secondary to extrinsic compression from metastatic pelvic lymphadenopathy. Bilateral JJ ureteric stents were inserted, resulting in some improvement of renal function but a failure to normalise completely. Repeat computed tomography demonstrated bilateral duplex collecting systems with persisting obstruction of the undrained moieties. Selective puncture was performed to decompress the obstructed renal moieties for bilateral nephrostomy catheter insertion. This allowed renal function to improve sufficiently for the patient to be discharged and commence chemotherapy. This is the first reported case of bilaterally obstructed partially duplicated collecting systems and it illustrates the importance of recognising anatomical variants to tailor treatment appropriately. It also highlights the important relationship between urology and interventional radiology in the management of such complex patients.
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42

Jönsson, Sofia, Mediha Becirovic Agic, Fredrik Narfström, Jacqueline M. Melville, and Michael Hultström. "Renal neurohormonal regulation in heart failure decompensation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 5 (September 1, 2014): R493—R497. http://dx.doi.org/10.1152/ajpregu.00178.2014.

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Decompensation in heart failure occurs when the heart fails to balance venous return with cardiac output, leading to fluid congestion and contributing to mortality. Decompensated heart failure can cause acute kidney injury (AKI), which further increases mortality. Heart failure activates signaling systems that are deleterious to kidneys such as renal sympathetic nerve activity (RSNA), renin-angiotensin-aldosterone system, and vasopressin secretion. All three reduce renal blood flow (RBF) and increase tubular sodium reabsorption, which may increase renal oxygen consumption causing AKI through renal tissue hypoxia. Vasopressin contributes to venous congestion through aquaporin-mediated water retention. Additional water retention may be mediated through vasopressin-induced medullary urea transport and hyaluronan but needs further study. In addition, there are several systems that could protect the kidneys and reduce fluid retention such as natriuretic peptides, prostaglandins, and nitric oxide. However, the effect of natriuretic peptides and nitric oxide are blunted in decompensation, partly due to oxidative stress. This review considers how neurohormonal signaling in heart failure drives fluid retention by the kidneys and thus exacerbates decompensation. It further identifies areas where there is limited data, such as signaling systems 20-HETE, purines, endothelin, the role of renal water retention mechanisms for congestion, and renal hypoxia in AKI during heart failure.
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43

Couchoud, Cecile, and Mohamed Benghanem Gharbi. "Advocacy for renal replacement therapy: the role of renal registries." Clinical Kidney Journal 13, no. 5 (July 29, 2020): 742–44. http://dx.doi.org/10.1093/ckj/sfaa067.

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Abstract The paper by Jardine et al. reporting results from the South African Renal Registry describes a 2-fold success. First, even in a limited-resource environment, survival of patients on renal replacement therapy (RRT) is favourable. Secondly, this information is available because a few years ago, South African nephrologists started a renal registry. These successes cannot conceal, however, that numerous patients are not offered RRT. Robust health information systems make it possible to define chronic kidney disease and end-stage kidney disease (ESKD) burdens, guide resource allocation, inform service planning and enable policy. Registries can highlight inequitable RRT access and help support advocacy in favour of additional resources for ESKD care.
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44

Shimamoto, Kazuaki, Nobuyuki Ura, Toshiya Ishiguro, Motoya Nakagawa, and Osamu Iimura. "The Role of Renal Natriuretic Depressor Systems on Hypertensive Mechanisms in Reduced Renal Mass Hypertensive Rats." Hypertension Research 18, SupplementI (1995): S53—S57. http://dx.doi.org/10.1291/hypres.18.supplementi_s53.

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45

Navar, L. G., E. W. Inscho, S. A. Majid, J. D. Imig, L. M. Harrison-Bernard, and K. D. Mitchell. "Paracrine regulation of the renal microcirculation." Physiological Reviews 76, no. 2 (April 1, 1996): 425–536. http://dx.doi.org/10.1152/physrev.1996.76.2.425.

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There has been an explosive growth of interest in the multiple interacting paracrine systems that influence renal microvascular function. This review first discusses the membrane activation mechanisms for renal vascular control. Evidence is provided that there are differential activating mechanisms regulating pre- and postglomerular arteriolar vascular smooth muscle cells. The next section deals with the critical role of the endothelium in the control of renal vascular function and covers the recent findings related to the role of nitric oxide and other endothelial-derived factors. This section is followed by an analysis of the roles of vasoactive paracrine systems that have their origin from adjoining tubular structures. The interplay of signals between the epithelial cells and the vascular network to provide feedback regulation of renal hemodynamics is developed. Because of their well-recognized contributions to the regulation of renal microvascular function, three major paracrine systems are discussed in separate sections. Recent findings related to the role of intrarenally formed angiotensin II and the prominence of the AT1 receptors are described. The possible contribution of purinergic compounds is then discussed. Recognition of the emerging role of extracellular ATP operating via P2 receptors as well as the more recognized functions of the P1 receptors provides fertile ground for further studies. In the next section, the family of vasoactive arachidonic acid metabolites is described. Possibilities for a myriad of interacting functions operating both directly on vascular smooth muscle cells and indirectly via influences on endothelial and epithelial cells are discussed. Particular attention is given to the more recent developments related to hemodynamic actions of the cytochrome P-450 metabolites. The final section discusses unique mechanisms that may be responsible for differential regulation of medullary blood flow by locally formed paracrine agents. Several sections provide perspectives on the complex interactions among the multiple mechanisms responsible for paracrine regulation of the renal microcirculation. This plurality of regulatory interactions highlights the need for experimental strategies that include integrative approaches that allow manifestation of indirect as well as direct influences of these paracrine systems on renal microvascular function.
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46

Zhang, Ming-Zhi, Bing Yao, James A. McKanna, and Raymond C. Harris. "Cross talk between the intrarenal dopaminergic and cyclooxygenase-2 systems." American Journal of Physiology-Renal Physiology 288, no. 4 (April 2005): F840—F845. http://dx.doi.org/10.1152/ajprenal.00240.2004.

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In mammalian kidney, dopamine produced in the proximal tubule (PT) acts as an autocrine/paracrine natriuretic hormone that inhibits salt and fluid reabsorption in the PT. In high-salt-treated animals, PT dopamine activity increases and inhibits reabsorption, leading to increased salt and fluid delivery to the macula densa (MD) and subsequent natriuresis and diuresis. Regulated cyclooxygenase-2 (COX-2) in the MD represents another intrinsic system mediating renal salt and water homeostasis. Renal cortical COX-2 is inversely related to salt intake, and decreased extracellular NaCl stimulates COX-2 expression in cultured MD/cortical thick ascending limb cells. The current study investigated interactions between renal dopamine and cortical COX-2 systems. In rats fed a control diet, the dopamine precursor l-dihydroxyphenylalanine (l-DOPA) or the DA1 receptor agonist SKF-81297 suppressed cortical COX-2 expression. High salt suppressed cortical COX-2 expression, which was attenuated by inhibition of dopamine production with benserazide or the DA1 receptor antagonist, SCH-23390. In contrast, l-DOPA or the dopamine-metabolizing enzyme inhibitor entacapone suppressed low-salt-induced cortical COX-2 expression. Inhibition of PT reabsorption with the carbonic anhydrase inhibitor acetazolamide suppressed cortical COX-2 expression. In contrast, treatment with distally acting diuretics led to elevation of cortical COX-2. These results indicate that dopamine modulates renal cortical COX-2 expression by modifying PT reabsorption.
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47

Gawlik, Alexander, and Susan E. Quaggin. "Deciphering the Renal Code: Advances in Conditional Gene Targeting." Physiology 19, no. 5 (October 2004): 245–52. http://dx.doi.org/10.1152/physiol.00009.2004.

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Several powerful new techniques can examine gene function in mammals. Recombinase systems and kidney-specific promoters enable gene knockout and overexpression. Genetic systems induced on administration or removal of antibiotics or hormones permit control of gene expression. Gene silencing using short interfering RNA expression systems should accelerate loss-of-function studies. Thorough characterization of animals that have undergone conditional gene targeting has already provided insights into renal development and diseases. Here we discuss the advantages and pitfalls of currently available gene-targeting systems.
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48

Huber, Korinna, Uta Roesler, Alexandra Muscher, Kathrin Hansen, Irkham Widiyono, Ernst Pfeffer, and Gerhard Breves. "Ontogenesis of epithelial phosphate transport systems in goats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 2 (February 1, 2003): R413—R421. http://dx.doi.org/10.1152/ajpregu.00357.2002.

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The rapid development of precocial goats in the first weeks after birth requires an adequate adaptation of phosphate transport systems to maintain the P homeostasis at each developmental stage. Here we examined the age-related development of Na+-Pitransport systems in small intestines, kidneys, and parotid glands of goats. Kinetic parameters were determined by brush-border membrane vesicle uptake studies, and relative expression of NaPi type II mRNA and protein was recorded by molecular biological methods. High intestinal Pi transport capacity was already present on the first day of life. Within the first 3 wk of life there seemed to be a change in the type of Na+-dependent Pitransporter, and NaPi IIb was expressed increasingly up to the fifth month of life. Renal Na+-Pi transport capacity was also high at birth, and this was associated with high expression levels of NaPi IIa mRNA, indicating the important role of this transporter for renal Pi reabsorption. At weaning an increase in both intestinal and renal Na+-Pitransport balanced the increasing requirements for Pi to establish the endogenous Pi cycle. Salivary Piconcentration and parotid NaPi II mRNA rose markedly to guarantee an adequate Pi supply for rumen microbes. We concluded that the high demand for Pi in young goats was assured by high basal Na+-Pi transport capacity of small intestines and kidney expressed continuously during ontogenesis.
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Dirkes, Susan. "ClinicalSavvy: How to Use the New CVVH Renal Replacement Systems." American Journal of Nursing 94, no. 5 (May 1994): 67. http://dx.doi.org/10.2307/3464642.

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50

Ahmad, Ashfaq, Sara Dempsey, Zdravka Daneva, Maleeha Azam, Ningjun Li, Pin-Lan Li, and Joseph Ritter. "Role of Nitric Oxide in the Cardiovascular and Renal Systems." International Journal of Molecular Sciences 19, no. 9 (September 3, 2018): 2605. http://dx.doi.org/10.3390/ijms19092605.

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The gasotransmitters are a family of gaseous signaling molecules which are produced endogenously and act at specific receptors to play imperative roles in physiologic and pathophysiologic processes. As a well-known gasotransmitter along with hydrogen sulfide and carbon monoxide, nitric oxide (NO) has earned repute as a potent vasodilator also known as endothelium-derived vasorelaxant factor (EDRF). NO has been studied in greater detail, from its synthesis and mechanism of action to its physiologic, pathologic, and pharmacologic roles in different disease states. Different animal models have been applied to investigate the beneficial effects of NO as an antihypertensive, renoprotective, and antihypertrophic agent. NO and its interaction with different systems like the renin–angiotensin system, sympathetic nervous system, and other gaseous transmitters like hydrogen sulfide are also well studied. However, links that appear to exist between the endocannabinoid (EC) and NO systems remain to be fully explored. Experimental approaches using modulators of its synthesis including substrate, donors, and inhibitors of the synthesis of NO will be useful for establishing the relationship between the NO and EC systems in the cardiovascular and renal systems. Being a potent vasodilator, NO may be unique among therapeutic options for management of hypertension and resulting renal disease and left ventricular hypertrophy. Inclusion of NO modulators in clinical practice may be useful not only as curatives for particular diseases but also for arresting disease prognoses through its interactions with other systems.
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