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Relevant bibliographies by topics / Proteinurie

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Academic literature on the topic 'Proteinurie'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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Journal articles on the topic "Proteinurie"

1

Elke, Ludin, and Fehr. "Proteinurie." Praxis 97, no. 15 (July 1, 2008): 811–18. http://dx.doi.org/10.1024/1661-8157.97.15.811.

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Ritz, E. "Proteinurie." DMW - Deutsche Medizinische Wochenschrift 118, no. 50 (July 17, 2009): 1853–54. http://dx.doi.org/10.1055/s-0029-1235274.

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Naujoks, H., and C. Wanner. "Proteinurie." Der Urologe B 39, no. 4 (August 1999): 358–70. http://dx.doi.org/10.1007/s001310050321.

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Menne, J., C. Chatzikyrkou, and H. Haller. "Proteinurie." Der Nephrologe 7, no. 1 (January 2012): 28–34. http://dx.doi.org/10.1007/s11560-011-0583-x.

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Haller, H., and G. Mayer. "Proteinurie." Der Nephrologe 8, no. 2 (February 24, 2013): 117–18. http://dx.doi.org/10.1007/s11560-012-0667-2.

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Naujoks, H., and C. Wanner. "Proteinurie." Der Internist 39, no. 9 (September 1998): 955–68. http://dx.doi.org/10.1007/s001080050265.

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Meyer, Tobias N. "Proteinurie." Uro-News 21, no. 10 (September 29, 2017): 38–41. http://dx.doi.org/10.1007/s00092-017-1625-0.

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Bohnert, Bernhard N. "Proteinurie." Dialyse aktuell 25, no. 02 (March 2021): 68–75. http://dx.doi.org/10.1055/a-1269-6168.

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ZUSAMMENFASSUNGDie Proteinurie ist ein empfindlicher Marker für eine Nierenschädigung und ein guter Prädiktor für das Fortschreiten einer chronischen Nierenschädigung hin zu einer terminalen Nierenerkrankung. Ob die Proteinurie dabei allerdings nur einen Risikomarker darstellt, der lediglich die Nierenschädigung widerspiegelt, oder ob sie durch toxische Effekte auf Podozyten und Nierentubuli selbst einen Risikofaktor darstellt, ist bisher nicht klar. Während der Fokus aktueller Leitlinien im Wesentlichen auf der Quantität der Proteinurie liegt, zeigen immer mehr experimentelle Daten, dass auch der Qualität der Proteinurie eine wesentliche Rolle hinsichtlich ihres Schädigungspotenzials und ihres Risikos zukommt.

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Dendorfer, U., H. J. Anders, and D. Schlöndorff. "Urindiagnostik: Proteinurie." DMW - Deutsche Medizinische Wochenschrift 126, no. 46 (November 15, 2001): 1310–13. http://dx.doi.org/10.1055/s-2001-18467.

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Galle, J. "Zufallsbefund Proteinurie." Der Internist 55, no. 10 (September 3, 2014): 1165–70. http://dx.doi.org/10.1007/s00108-014-3487-9.

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Dissertations / Theses on the topic "Proteinurie"

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Gozlan, Patricia. "Proteinurie orthostatique : etude qualitative de la proteinurie." Limoges, 1989. http://www.theses.fr/1989LIMOO117.

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Laaser, Mark Kore. "Pathologische Proteinurie nach einseitiger Nephrektomie /." Köln, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000252833.

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Bachmann, Friederike. "Chronisches Transplantatversagen Einfluß einer arteriellen Hypertonie auf die Langzeitfunktionsrate nach Nierentransplantation /." [S.l. : s.n.], 2007.

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VUILLEMIN, THIERRY. "Comparaison des effets de l'enalapril et de la nitrendipine sur la proteinurie d'effort." Nantes, 1991. http://www.theses.fr/1991NANT099M.

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Unland, Johannes [Verfasser]. "Einfluss von Testosteron auf Proteinurie und Nephropathie in Rattenmodellen chronischer Nierenerkrankungen / Johannes Unland." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1179777689/34.

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Grigoleit, Felix Heinrich [Verfasser]. "Entwicklung der Proteinurie und der Nierenfunktion beim Nephrotischen Syndrom unter Pentoxifyllin / Felix Heinrich Grigoleit." Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1084767686/34.

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CLEDAT, WENDEL CATHERINE. "Le depistage systematique de l'hematurie et de la proteinurie en milieu scolaire : rapport d'une enquete toulousaine sur 11459 enfants." Toulouse 3, 1989. http://www.theses.fr/1989TOU31040.

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Diekmann, Fritz [Verfasser]. "Chronische Allograftdysfunktion nach Nierentransplantation - Rolle der mTOR-Inhibition und prädiktiver Wert der Proteinurie / Fritz Diekmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023783487/34.

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Hügle, Sophia [Verfasser]. "Auswirkungen des eNOS-G894T-Polymorphismus auf den Blutdruck und die Proteinurie bei Schwangeren / Sophia Hügle." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1202044646/34.

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Zeder, Andreas [Verfasser], and Johannes [Akademischer Betreuer] Bogner. "Prävalenz, Risikofaktoren und Bedeutung mittelgradiger Proteinurie bei HIV-positiven Patienten / Andreas Zeder ; Betreuer: Johannes Bogner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1117474267/34.

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Books on the topic "Proteinurie"

1

Avram, M. M., ed. Proteinuria. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2477-5.

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1946-, Smith Michael C., ed. Proteinuria and the nephrotic syndrome. Chicago: Year Book Medical Publishers, 1986.

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Parker, James N., and Philip M. Parker. The official patient's sourcebook on proteinuria. Edited by Icon Group International Inc and NetLibrary Inc. San Diego, Calif: Icon Health Publications, 2002.

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Blaine, Judith, ed. Proteinuria: Basic Mechanisms, Pathophysiology and Clinical Relevance. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43359-2.

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H, Brouhard Ben, and Kalia Alok, eds. An approach to the child with hematuria and proteinuria. Norwalk, Conn: Appleton-Century-Crofts, 1985.

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6

D, Bianchi Claudio M., ed. Kidney and proteins in health and disease: Fifth International Symposium of Nephrology at Montecatini, Montecatini Terme, July 21-23, 1987. Basel: Karger, 1988.

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D, Bianchi Claudio M., ed. Kidney, proteins, and drugs: 6th International Symposium of Nephrology at Montecatini, Montecatini Terme, June 1-3, 1989. Basel: Karger, 1990.

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D, Bianchi Claudio M., ed. Kidney, proteins, and drugs: An update : 7th International Symposium of Nephrology at Montecatini, Montecatini Terme, October 14-16, 1991. Basel: Karger, 1993.

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9

Wheeler, Linda A. Maternal assessment: Blood pressure. Edited by Raff Beverly S, Albers Lolita, and March of Dimes Birth Defects Foundation. 2nd ed. White Plains, N.Y: March of Dimes Birth Defects Foundation, 1988.

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Wheeler, Linda A. Maternal assessment: Urine evaluation. Edited by Raff Beverly S, Albers Lolita, and March of Dimes Birth Defects Foundation. 2nd ed. White Plains, N.Y: March of Dimes Birth Defects Foundation, 1987.

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Book chapters on the topic "Proteinurie"

1

Weber, L. T. "Proteinurie." In Pädiatrische Differenzialdiagnostik, 157–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-29798-4_39.

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Naujoks, H., and C. Wanner. "Proteinurie." In Kompendium der praktischen Medizin, 1319–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59754-1_112.

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Ehrich, J. H. H., and U. Wurster. "Proteinurie." In Nephrologie — Urologie, 1–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70602-8_1.

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Schärer, K. "Isolierte Proteinurie." In Pädiatrische Nephrologie, 203–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56378-2_25.

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Boesken, W. H. "Aussagefähigkeit der Proteinurie." In Verhandlungen der Deutschen Gesellschaft für Innere Medizin, 473–78. Munich: J.F. Bergmann-Verlag, 1987. http://dx.doi.org/10.1007/978-3-642-85460-6_118.

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Frei, U. "Proteinurie nach Nierentransplantation." In Verhandlungen der Deutschen Gesellschaft für Innere Medizin, 480–81. Munich: J.F. Bergmann-Verlag, 1987. http://dx.doi.org/10.1007/978-3-642-85460-6_121.

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Scherberich, J. E. "Proteinurie bei Systemerkrankungen." In Verhandlungen der Deutschen Gesellschaft für Innere Medizin, 481–93. Munich: J.F. Bergmann-Verlag, 1987. http://dx.doi.org/10.1007/978-3-642-85460-6_122.

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Roth, Stephan, Axel Semjonow, and Peter Rathert. "Proteinurie — Was tun?" In Klinische Urologie, 15–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-97417-5_2.

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Habbig, Sandra, Max C. Liebau, and Lutz T. Weber. "Hämaturie und Proteinurie." In Repetitorium Kinder- und Jugendmedizin, 633–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-56790-6_37.

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Roth, Stephan, Burkhard Ubrig, Axel Semjonow, and Peter Rathert. "Proteinurie - Was tun?" In Klinische Urologie, 13–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-59541-7_2.

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Conference papers on the topic "Proteinurie"

1

Strong, KJ, CM Kahler, and SA Webb. "Hypoalbuminemia Is Associated with Proteinuria in Experimental Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1160.

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Stemeier, K., J. Mertin, J. Pill, and F. Hartig. "EFFECTS OF THROMBOXANE RECEPTOR BLOCKER BM 13.505 ON THE DEVELOPMENT OF PROTEINURIA IN AUTOIMMUNE NZB/W MICE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643757.

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Female F1 hybrid of New Zealand black and white mice(NZB/W) spontaneouslydevelop an autoimmune disease characterize by afatal immune complex glomerulonephritis.Theyare considered to be a relevant model of human systemic lupus erythematosus. We observeda doubling of the concentration of TXB2 in urine at the same time when onset of proteinuria was noticed. This suggests that TXA2 synthetized by mesangial and epithelial cells of the glomeruli as well as by some inflammatory cells and platelets might be an important mediator in the pathogenesis of thi auto immune-mediated glomerular disease. Weused BM 13.505 as an long-acting TX receptor blocker for evaluating the importance of TXA2 on the development of proteinuria and compared its effects with that of the immunsuppressive agent cyclophosphamide.NZB/W mice were distributed to vehicle-treated (V-)group 20 mg/kg BM 13.505 (BM-) group and 20 mg/kgcyclophosphamide (C-) group( = 13 -14).Daily dosing by gavage was startedat the age of12 weeks. Every fourth week theurinary concentrations of proteins were measured by th biuret method and TXB2by a RIA. An increasein TXB2 was seen in the V- and BM-group, while in the C-group TXB2 was lowered. At 36 weeks of age 8of 14 animals of the V-group were proteinuria positive (>100 mg/100 ml). The study was finished at 44 weeks because more than 2/3 of the animals of the V-group haddeveloped a proteinuria. Previously four animals died and in most of other the disease was faradvanced. In the BM-group no animal had diedor showed signs of illness. However seven ofthe animals had slightly elevated protein concentrations in urine and two moderate elevated values. In the C-group no proteinuria was detected. Histological examinations of thekidneys showed a correlation in individualanimals of the V-group between the duration and extent of proteinuria and changes in the morphology of the glomeruli. In the BM-treated animals slight to moderate protein deposits were detectable, while in cyclophosphamide-treated animals glomeruli were of normal structure. This study presents someevidence that TXA2 may be an important mediator in the pathogenesis of this immune-mediated renal disease. Manifestation of this disease is delayed by the administration of thespecific TX receptor blocker BM 13.505.

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Moenardi, VN, BS Suryajaya, I. I. Hidayat, and L. Hamijoyo. "163 Association between hypertension and proteinuria in systemic lupus erythematosus." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.163.

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Algergawy, S. "PS7:138 New strategy therapy for lupus nephritis with persistent proteinuria." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.181.

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Delani, F., M. Tagliaferri, D. Macconi, C. Lupini, N. Perico, and G. Rumuzzi. "PLATELET ACTIVATING FACTOR (PAF) AS A MEDIATOR OF PROTEINURIA IN ISOLATED PERFUSED KIDNEY (IPK)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643485.

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PAF amplifies tissue damage in glomerulonephritis and can promote proteinuria stimulating platelet and neutrophil cationic protein release. We used IPK to establish whether PAF directly causes proteinuria. Kidneys were isolated from male Sprague-Dawley rats and perfused at constant pressure (100 mmHg) in a closed circuit with a Krebs-Henseleit buffer containing glucose urea creatinine, BSA (1%), Ficoll 70 (3.5%) and amino acids. After 25 min stabilization period, a basal 10 min clearance period was followed by PAF (1.8 nM f.c. n = 6) or vehicle (n = 5) injection into the renal artery. As seen in the figure PAF but not vehicle significantly (p<0.01) increased urine protein excretion. No significant changes in GFR (as creatinine clearance) were observed after PAF or vehicle injection (Basal: 0.786 ± 0.075 PAF: 0.658 ± 0.070. Basal 0.653 ± 0.081, vehicle 0.639 ± 0.074 ml/min/g kidney). The data indicate that PAF may directly increase glomerular permeability to proteins.

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Gadelha-Parente, T., M. Gouault-Heilmann, G. Rostoker, M. Levent, S. Rafowicz, L. Intrator, and G. Lagrue. "TOTAL AND FREE PROTEIN S IN NEPHROTIC SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644296.

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25 consecutive patients (15M, 10F ; mean age 30 years) with nephrotic syndrome (NS) of different grade were studied. Control group consisted in 18 healthy adult volunteers. Total protein S antigen (TPS:Ag) and free protein S antigen (FPS:Ag) after precipitation of C4-BP-bound protein S by PEG 3-5 % final concentration were measured by Laurell's technique. PS:Ag was also searched in concentrated urine of 9 patients by ELISA method, more sensitive than the Laurell's technique. In the same plasma samples we measured C4-BP, Protein C Ag and AT III biological activity (all reagents from D.Stago). Serum albumin level, proteinuria, proteinuria selectivity index, triglycerides, cholesterol levels were recorded. TPS:Ag was found elevated in NS (1.30±0.3 U/ml) in comparison with control group (1.09±0.32 U/ml) and the difference was statistically significant (p<0.05). The mean values of FPS:Ag observed in patients and controls were not statistically different, but if we consider 95 % confidence limits (0.99-1-35 U/ml), 16 pts had normal or elevated FPS:Ag level, whereas 9 had decreased FPS:Ag level. A positive correlation was found between TPS:Ag and FPS:Ag in control group (r=0.66 ; p< 0.001) and in patients with NS (r=0.4l, p<0.05). C4-BP was significantly (p<0.01) increased in nephrotic patients ( 1.37 ± 0.36 U/ml) in comparison with control group (1.04±0.27 U/ml). A negative correlation was found between FPS:Ag and C4-BP levels in control group (r = −0.57, P< 0.01) but not in nephrotic patients. A positive correlation was found between FPS:Ag and albumin level and between FPS:Ag and cholesterol level. No correlation was found between TPS:Ag or FPS:Ag and proteinuria, proteinuria selectivity index, AT III and protein C levels. Traces of PS were found in urine (0. to 2.5 U/day) in 9 patients tested. 2/25 pts suffered thromboembolic events : one had a very low level of FPS:Ag in addition to a decreased level of AT III. The other one had normal FPS:Ag and AT III level but a borderline Protein C level. In conclusion. An acquired FPS:Ag deficiency was observed in 9/25 pts with NS despite an increased level of TPS:Ag. In this small series of patients the acquired FPS deficiency does not seem to be related either to an urinary loss of FPS or to an increased binding to C4-BP, as suggested by some authors.

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Takahashi, H., Y. Nasa, E. Takamasu, S. Sugii, and N. Yokogawa. "AB0514 The effect of hydroxychloroquine on reducing proteinuria in stable sle patients." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2249.

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Mayer, AL, K. Amann, T. Klein, and C. Daniel. "Linagliptin reduced proteinuria and renal injury in a rat model of crescentic nephritis." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688338.

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Lee, Seung Min, Minseon Park, and Hyung-Jin Yoon. "Association of Body Mass Index with Estimated Glomerular Filtration Rate and Incident Proteinuria." In 11th International Conference on Health Informatics. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0006716905870590.

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Blockmans, D., M. J. Heynen, J. Vermylen, and R. Verwilghen. "CONGENITAL MACROTHROMBOCYTOPENIA, LEUCOCYTE INCLUSIONS, DEAFNESS AND PROTEINURIA: FUNCTIONAL AND ELECTR0NMICROSCOPIC OBSERVATIONS ON PLATELETS AND MEGAKARYOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643928.

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We report here a female patient of 33 years with a variant of Alport's syndrome (macrothrombocytopenia, leucocyte inclusions, deafness and proteinuria). The bleeding problems consisted of ecchymoses and menorrhagia, the deafness was of the ^ensorineural type. The platelet count in whole blood was 14.109/I, the mean platelet volume 22.8 μm3 . The template bleeding time exceeded 30 minutes. Ultrastructural studies of the peripheral blood revealed giant spheroid platelets with a high density of organelles, an abundance of vacuoles and an apparently disorganized microtubular system. In addition, unusual granule free areas were observed in the neutrophils of the patient and her mother. Granulocyte function was normal, except for a low myeloperoxidase content.Functional studies of the platelets in platelet rich plasma showed normal aggregation curves related to the low platelet number, although no shape change could be elicited. Platelet aggregation studies in whole blood (impedance method) gave supernormal aggregation curves; this suggests the limited usefulness of this technique in patients with such large platelets.The bone marrow contained numerous dysplastic megakaryocytes. In the mature granular megakaryocytes vacuoles and cysternae were organized in a radiating pattern demarkating elongated platelet territories. The platelet producing megakaryocytes showed fragmentation of the central zone and discharge of platelets through openings of the peripheral zone. These megakaryocytes had an immunological phenotype resembling that of very young cells (TR 14%, GP IIa 17% and GP IIIa 7%). The conversion of the elongated platelet territories into giant spheroid platelets probably results from remodelling within the circulation. The internalisation of plasma membranes would give rise to the extended invaginated canalicular system. Further studies are needed to explain the exact pathogenesis of this syndrome.

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Reports on the topic "Proteinurie"

1

Filipov, Jean, Tania Metodieva, Nikolay Hubanov, Emil Dimitiro, and Dobrin Svinarov. Cholecalciferol Supplementation and Its Effect on Proteinuria in Bulgarian Kidney Transplant Recipients. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2021. http://dx.doi.org/10.7546/crabs.2021.06.15.

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