Dissertations / Theses: 'Proteinurie'

1

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

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2

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

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3

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

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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Zierhut, Ulf [Verfasser], Lorenz [Gutachter] Sellin, and Ralf [Gutachter] Kubitz. "Molekulare Signalkaskade der AngiotensinII-vermittelten Proteinurie, Nephrin, betaArrestin2 Interaktion / Ulf Zierhut ; Gutachter: Lorenz Sellin, Ralf Kubitz." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2019. http://d-nb.info/120154761X/34.

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12

GODFRIN, YANN. "Etude et mise en evidence de facteur(s) plasmatique(s) dans le syndrome nephrotique idiopathique." Nantes, 1998. http://www.theses.fr/1998NANT03VS.

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13

Schulz, Angela. "Genetische Charakterisierung der MWF-Ratte ein Rattenmodell zur Identifizierung genetischer Faktoren, die zu arterieller Hypertonie und Proteinurie führen /." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/169/index.html.

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14

Sohn, Andreas [Verfasser]. "Einfluss des mütterlichen Angiotensin-Converting-Enzym (ACE) Insertion / Deletion Polymorphismus auf Blutdruck und Proteinurie während der Schwangerschaft / Andreas Sohn." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1029845921/34.

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15

Schrader, Svenja [Verfasser], and Ulrich [Akademischer Betreuer] Seybold. "Bedeutung mittelgradiger Proteinurie bei Patienten mit HIV-Infektion für die Entwicklung eines chronischen Nierenversagens / Svenja Schrader ; Betreuer: Ulrich Seybold." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1192663381/34.

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16

LOUTFI, HAMID. "L'antiprotease acido-stable de l'urine humaine : etude structurale et determination chez le sujet sain et en cas de proteinurie." Lille 2, 1990. http://www.theses.fr/1990LIL2P253.

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17

Levrier, Frédéric. "Amylose primitive AL de révélation cutanée bulleuse secondaire à une protéinurie de Bence Jones idiopathique : revue de la littérature à propos d'une observation." Bordeaux 2, 1995. http://www.theses.fr/1995BOR2M109.

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18

Cedrone, Fabio [Verfasser]. "Pilotstudie zur Evaluation des Einflusses von Beschleunigungskräften auf das Auftreten einer Mikrohämaturie oder Proteinurie als Ausdruck einer möglichen Schädigung der Niere und der ableitenden Harnwege mittels Messung auf der Humanzentrifuge / Fabio Cedrone." Ulm : Universität Ulm, 2017. http://d-nb.info/1147484538/34.

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19

Vogel, Anna Dorothea [Verfasser], Marcel Ph [Akademischer Betreuer] Roos, Marcel Ph [Gutachter] Roos, and Uwe [Gutachter] Heemann. "Frühe postoperative C-terminal Agrin-Fragment (CAF)-Serum-Spiegel als prädiktiver Marker für Organversagen und Proteinurie bei nierentransplantierten Patienten / Anna Dorothea Vogel ; Gutachter: Marcel Ph. Roos, Uwe Heemann ; Betreuer: Marcel Ph. Roos." München : Universitätsbibliothek der TU München, 2018. http://d-nb.info/1153545667/34.

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20

Jepson, Rosanne Ellen. "Proteinuria and the feline kidney." Thesis, Royal Veterinary College (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497854.

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In human medicine proteinuria and systemic hypertension have been implicated in the development and progression of chronic kidney disease (CKD). Whilst the presence of increased concentrations of albumin within the urine may predominantly be associated with vascular changes at the level of the glomerulus, the presence of low molecular weight (LMW) proteins may be more indicative of damage at the level of the proximal tubules. In cats with CKD, proteinuria is an independent variable significantly associated with survival. To evaluate the role of clinical parameters, proteinuria and lifestyle factors in the development of feline CKD we have established a prospective stud/recruiting healthy geriatric cats and monitoring them until the development of azotaemia.

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21

Ihmoda, I. A. "The podocyte in proteinuric renal diseases." Thesis, University of Edinburgh, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.652796.

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Materials and Methods: 1. Total RNA was extracted from urine samples (20 ml each) of 70 protinuric renal patients at the renal outpatient department of Edinburgh Royal Infirmary. This was followed by RT-PCR for nephrin, podocalyxin (podocyte specific mRNAs) and β-actin (positive control) cDNAs. Induction of specific podocyte injury with diphtheria toxin (DT) in a transgenic mice expressing human diphtheria toxin receptor (hDTR) on podocytes. Mice DTR is normally resistant to the effects of DT. These transgenic mice were generated by male pronuclear microinjection of murine fertilized ova with the plasmid (pIN); a construct contains murine nephrin promoter (podocyte promoter) and hDTR gene which is human Heparin Binding-Epidermal Growth Factor cDNA (hHB-EGF cDNA). Results: 1. All of the 70 urine samples were negative for podocyte protein mRNAs by RT-PCR, although many samples gave positive β-actin results, and control human kidney cDNA gave consistently positive results. Of 100 urine samples examined by immunofluorescence, only one (1%) gave a positive result. The technique was tested with human cultured podocytes and found to detect 10-20% of the actual number of podocytes in urine, and a similar proportion of control cells. 2. Two trials of male pronuclear microinjection of fertilized murine ova with podocyte construct were undertaken. The first microinjection trial was unsuccessful but four hDTR transgenic founders (tg21.1, tg47.1, tg57.1, tg65.1) were established with the second round of microinjections. They gave identical results in two genotyping PCRs. These founders have shown the capability of passing the transgene to their phase 1 offspring. Conclusion: 1. Looking for urinary podocytes is not a clinically useful technique in patients with proteinuria. 2. Podocyte construct (pIN) has proved its validity by generating four transgenic founders by male pronuclear microinjection and furthermore, all of them have passed the transgene to their offspring.

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22

Vaškevičiūtė, Rasa. "Fizinio aktyvumo poveikis preeklampsijos pasireiškimui 20-35 nėštumo savaitėmis." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2006. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2006~D_20060510_210250-23785.

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Physical activity has versatile impact on female body and strengthens it in addition to improved physiological powers, more active performance of all systems and guaranteed normal course of pregnancy period. As a result, the cardiovascular condition is improved; placental circulation is more active, oxygen transopration and metabolism of the foetus is improved. The death-rate in pregnant women resulting from hypertension is the second after embolism. Preeclampsia is one of the hypertension-related failures, which affects 3 to 5 % of the pregnant women. The present research was targeted to women suffering from preeclampsia. The aim of the research was to investigate the impact of physical activity on manifestation of preeclampsia in pregnant women within 20-35 week of pregnancy. Tasks: 1. to assess arterial blood pressure (ABP) fluctuation of both groups of women (physically passive and physically active within 20-35 weeks of pregnancy; 2. to assess body weight index fluctuation of both groups of women (physically passive and physically active within 20-35 weeks of pregnancy; 3. to assess fluctuation of protein content in urine of both groups of women (physically passive and physically active within 20-35 weeks of pregnancy; 4. to assess life quality (sleep, headache, sight, right underrib pains, physical and physiological fatigue) of both groups of women (physically passive and physically active within 20-35 weeks of pregnancy. Hypothesis. Physical activity in pregnant women... [to full text]

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23

Hall, Matthew. "The predictive power of proteinuria in pregnancy." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/10811.

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Background- This thesis examines the power of urinary protein excretion – both quantitative and qualitative – during pregnancy in predicting maternal and fetal outcomes. The independent effect of proteinuria in predicting adverse outcomes for women with chronic kidney disease (CKD) has not been well characterised. Secondly, pre‐eclampsia is a leading cause of maternal and fetal morbidity and mortality worldwide. There are no tests to predict pre‐eclampsia in clinical use. Methods- Analysis of prospective data collected from pregnant women with CKD from multiple centres in the United Kingdom. A longitudinal prospective clinical study of urine proteomics in early pregnancy in women at high risk of pre‐eclampsia to identify putative predictive biomarkers. Results- Data was analysed from 313 pregnancies in 256 women with CKD from 2005 to 2010. Urine ACR or PCR is accurate in quantifying proteinuria in women with CKD during pregnancy. Women in whom pregnancy‐associated increases in proteinuria failed to return to baseline have increased progression of renal dysfunction compared to other women. Proteinuria at conception is not independently associated with pregnancy-associated accelerated loss of renal function but does predict preterm delivery. Nephrotic syndrome in pregnancy is not independently associated with adverse fetal outcomes. 145 participants were enrolled in a study of urine proteomics of whom 11 developed pre‐eclampsia. A panel of 5 peptides was identified in urine collected prior to 20 weeks gestation that predicted the subsequent development of pre‐eclampsia with 92% accuracy. A further peak was indentified in specimens collected from 20 to 25 weeks gestation with similar predictive performance. Summary- Maternal proteinuria at conception is associated with preterm delivery in women with CKD. Increased proteinuria that fails to resolve postpartum is associated with a more rapid decline. Accurate prediction of the development of pre‐eclampsia in women at high risk was achieved from urine proteomic analysis prior to 20 weeks gestation.

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24

Bull, Katherine Rose. "The genetics of autoimmune and proteinuric disease." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:5e93c208-c9df-44eb-87db-9c20622ca207.

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The genetics of complex common diseases are not fully understood, but rare variants with large phenotypic effects contribute to heritability. The objective of this thesis is to identify rare variants of relevance to autoimmune and renal disease, by developing ways of analysing whole genome sequencing (WGS) data and exploring the variants identified. Forward genetic experimental approaches are used, both in mutagenised mice, and in humans with extreme trait forms of the steroid resistant nephrotic syndrome (SRNS) and systemic lupus erythematosus (SLE). This work demonstrates that NâethylâNânitrosourea (ENU) mutations can be distinguished within WGS data, including a hypomorphic mutation in Lamb2 in a strain with the nephrotic syndrome, a murine model for the milder spectrum of human Pierson syndrome. In a Bâcell deficient ENU strain the causative mutation in Lyn was isolated by sequencing multiple affected mice and applying an implementation of the LanderâGreen algorithm to search for identity by descent. This method for the first time overcomes a rate-limiting step in ENU programmes and offers the potential to accelerate gene discovery, eliminating the need for outâcrossing and conventional linkage analysis. Knowledge of the ENU genomic intervals allowed calculation of a mutation frequency, 1.5 mutations per mega base, and modelling of an efficient ENU strategy. Shortâlists of candidate variants from 14 unrelated patients with steroid resistant nephrotic syndrome or systemic lupus erythematosus provide a substrate for future experiments, for example a candidate in the WiskottâAldrich syndrome gene was excluded using DNA from family members. In conclusion, WGS coupled with identity by descent analysis offers a powerful tool to improve the efficiency of ENU programmes. Rare variant discovery in humans without obvious Mendelian inheritance is more challenging and will require strategies to prioritise variants that combine bioinformatic filters and experimental verification in a high throughput way.

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25

Ferguson, Joanne Kathryn. "Glomerular and systemic permeability in proteinuric renal impairment." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535481.

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26

Wu, Haojia, and 吳浩佳. "Role of mesenchymal stem cells in proteinuric nephropathy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206678.

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Proteinuria has been recognized as a common feature in many forms of chronic kidney disease (CKD). As traditional medications for proteinuric nephropathy, such as blockade of the renin-angiotensin system (RAS), has only achieved limited clinical success, more effective renoprotective strategies need to be explored. Bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) have recently shown promise as a therapeutic tool in acute kidney injury (AKI) models. The therapeutic potential of bone marrow-derived mesenchymal stem cells (BM-MSCs) in proteinuric nephropathy models is unknown. Using a co-culture model of human proximal tubular epithelial cells (PTECs) and BM-MSCs, I first examined the potential effect of BM-MSCs in albumin-induced pro-inflammatory response and epithelial-to-mesenchymal transition (EMT) in PTECs. The unstimulated BM-MSCs exerted moderate suppressive effect on tubular inflammation as only albumin-induced CCL-2 and CCL-5 expression was attenuated in PTECs. When concomitantly stimulated by albumin excess, however, BM-MSCs remarkably suppressed albumin-induced tubular IL-6, IL-8, TNF-α, CCL-2, and CCL-5 expression, suggesting albumin overloaded milieu to be a prerequisite for them to fully exhibit their anti-inflammatory effects. This effect was mediated via deactivation of tubular NF-κB signaling as BM-MSCs prevented the overexpression of p-IκB and nuclear translocation of NF-κB. In addition, albumin-induced tubular EMT, as shown by the loss of E-cadherin and induction of α-SMA, FN-1 and collagen IV in PTECs, was also prevented by BM-MSC co-culture. To dissect the mechanism of action, I next explored the paracrine factors secreted by BM-MSCs under an albumin-overloaded condition and studied their contribution to the protective effect on tubular inflammation and EMT. Albumin-overloaded BM-MSCs per se overexpressed 34 paracrine factors, of which hepatocyte growth factor (HGF) and TNFα-stimulating gene (TSG)-6 were regulated by P38 and NF-κB signaling. These paracrine factors suppressed both the proinflammatory and profibrotic phenotypes in albumin-induced PTECs. Neutralizing HGF and TSG-6 abolished the anti-inflammatory and anti-EMT effects of BM-MSC co-culture in albumin-induced PTECs, respectively. Finally, in albumin-overloaded mice, a well established murine model reminiscent of human CKD, treatment with mouse BM-MSCs markedly reduced BUN, tubular CCL-2 and CCL-5 expression, interstitial macrophage, α-SMA and collagen IV accumulation independent of changes in proteinuria, together with upregulated renal cortical expression of HGF. Exogenous BM-MSCs were detected in their kidneys by PKH-26 staining. Collectively, these in vitro and in vivo data suggest a modulatory effect of BM-MSCs on albumin-induced tubular inflammation and fibrosis and underscore a therapeutic potential of BM-MSCs for CKD in the future.
published_or_final_version
Medicine
Doctoral
Doctor of Philosophy

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27

Gebrin, Adriana Celeste. "Proteinuria glomerular : correlação entre seletividade e disfunção tubular." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308689.

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Orientador: Celia Regina Garlip
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-07T12:25:34Z (GMT). No. of bitstreams: 1 Gebrin_AdrianaCeleste_M.pdf: 1300719 bytes, checksum: c4f0ce8c9284378c8180cddf34631ef6 (MD5) Previous issue date: 2006
Resumo: Proteinuria glomerular está freqüentemente associada à disfunção túbulo-intersticial. O índice de seletividade (IS) da proteinuria é usado para descrever mudanças na permeabilidade glomerular a macromoléculas. O presente estudo tem por objetivo analisar a correlação entre o grau de disfunção tubular (caracterizada pela excreção urinária de alfa 1 microglobulina), os níveis de excreção urinária de IgG e o índice de seletividade glomerular Foram estudadas 84 amostras de urina e soro de 47 pacientes com proteinuria glomerular de diversas etiologias. Albumina urinária, transferrina sérica e urinária, IgG sérica e urinária (IGU) e alfa 1 microglobulina urinária (AIM) foram dosadas por nefelometria. Proteinuria e creatinina urinária foram dosados através de método automatizado (vermelho de pirogalol e Jaffé modificado, respectivamente), sendo a creatinina utilizada para corrigir a excreção urinária de cada uma das proteínas específicas. O índice de seletividade (IS) foi calculado dividindo-se o depuração da transferrina pelo depuração do IgG. Teste de regressão, ANOVA e teste t não pareado foram utilizados para a análise estatística.Baseando-se no (IS), as proteinurias foram classificados em 3 grupos IS<0,10 = seletiva; IS entre 0,10 e 0,20 = seletividade intermediária e IS > 0,20 = não seletiva. Apesar da grande sobreposição de valores, verificamos que os níveis de AIM eram significativamente menores entre aqueles pacientes com proteinuria seletiva e que aumentavam à medida em que a proteinuria se tornava menos seletiva. A análise de regressão mostrou uma correlação significativa entre a excreção urinaria de IgG e AIM (r = 0,74 ; p < 0,05). Nossos dados sugerem que a excreção urinária de alfa 1-microglobulina é um marcador útil da disfunção tubular associada com proteinuria glomerular e que a alfa 1-microglobulina, a IgG e o índice de seletividade podem ter um valor preditivo significativo para a remissão e progressão da proteinuria em pacientes com doenças glomerulares
Abstract: Glomerular proteinuria is often associated with progressive tubulointerstitial dysfunction, which influences the degree of progression of renal failure. Alpha-1-microglobulin (AIM) is considered an indicator of tubular dysfunction. Proteinuria selectivity index (SI) is used to describe changes of the glomerular permeability for macromolecules. The aim of this study was to establish the relationship between SI, alpha-l-microglobulin and IgG urinary excretions. We compare the urinary excretion of AIM, IgG and SI among forty-seven patients with glomerular diseases. Serum and random urine samples were analyzed. Total protein, creatinine, alpha-1-microglobulin, transferrin, and IgG concentrations were determined and the SI was calculated. Based on SI, proteinuria were classified as Group 1: SI<0.10 = highly selective; Group 2: 0.200.20 = nonselective. Alpha-l-microglobulin levels were significantly lower among patients with highly selective proteinuria compared to patients with moderately and nonselective proteinuria. There was a significant relationship between AIM and urinary excretion of IgG (r = 0.74; p<0.05). These data suggest that urinary excretion of AIM is a useful marker of tubular dysfunction associated with glomerular proteinuria. AIM, IgG and SI may have a significant predictive value for both remission and progression of the proteinuria in patients with glomerular diseases
Mestrado
Patologia Clinica
Mestre em Ciências Médicas

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28

Iliescu, Eduard Andrei. "Prevalence of proteinuria in the obstructive sleep apnea syndrome." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0018/MQ54460.pdf.

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29

Vogt, Liffert. "Strategies to optimize renoprotective therapy in proteinuric renal patients." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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30

Hill, R. P. "A study of glycated proteins and proteinuria in diabetes." Thesis, Nottingham Trent University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283032.

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31

Ruotsalainen, V. (Vesa). "Nephrin:role in the renal ultrafilter and involvement in proteinuria." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514273494.

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Abstract Congenital nephrotic syndrome of the Finnish type (NPHS1, CNF) is an autosomal recessive disease that affects 1:8000 newborns in Finland. NPHS1 is characterised by heavy proteinuria already in utero and typical signs of nephrotic syndrome (NS) are present at or soon after birth. Due to the evident absence of extrarenal symptoms, NPHS1 has been considered a model disease for NS. In this study, the NPHS1 locus on chromosome 19q13.1 was sequenced and analysed with computer programs to identify new genes in the region. Genes were further characterised and sequenced from NPHS1 patient samples, as well as from controls. Analysis of the data resulted in the identification of the affected gene with two mutations that were found to explain 94% of the Finnish NPHS1 cases. The NPHS1 gene was found to encode a novel single-pass transmembrane protein, termed nephrin, which belongs to the immunoglobulin superfamily of cell adhesion molecules. The NPHS1 gene was cloned and recombinant nephrin fragments were produced in prokaryotic and eukaryotic expression systems. These fragments were used to raise antibodies that were utilized to characterise the spatial and temporal expression of nephrin in kidney glomeruli. Nephrin was localised by electron microscopy (EM) in ladder-like structures of the early junctional complexes of developing columnar podocytes at the capillary stage. In mature glomeruli, nephrin was localised to the slit diaphragm (SD) between adjacent glomerular podocyte foot processes. In order to investigate the more general involvement of nephrin in proteinuric disease, its expression was studied in primary acquired NS by immunofluorescence microscopy. The level of nephrin expression was found to be significantly reduced in membranous glomerulonephritis, minimal change disease and in focal segmental glomerulosclerosis. The known effects of nephrin mutations, together with the structure predicted from its sequence and localisation of the protein to the SD, emphasizes its indispensable role in maintaining the integrity of the glomerular filtration barrier. The glomerular basement membrane has long been considered to possess the size-selective filtration property of the filtration barrier. However, the identification of nephrin in the SD, as well as its alterations in proteinuria, has led us to reconsider SD as the final decisive size-selective filter.

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Gordana, Stražmešter Majstorović. "Biomarker lipokalin 2 u dijagnostici primarnih glomerulonefritisa." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2016. http://www.cris.uns.ac.rs/record.jsf?recordId=100906&source=NDLTD&language=en.

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Primarni glomerulonefritisi predstavljaju inflamatorna oboljenja bubrega, kod kojih su primarno zahvaćeni glomerulusi, ali promene na tubulointersticijumu imaju veliki značaj za tok i prognozu bolesti. Pored kliničko-laboratorijskih ispitivanja, perkutana biopsija bubrega zauzima značajno mesto u dijagnostici posebnih oblika glomerulonefritisa. Lipokalin vezan za neutrofilnu gelatinazu (NGAL) zauzima značajno mesto medju novijim biomarkerima u nefrologiji. Osnovna funkcija mu je transport gvoždja, ali ima ulogu i u regulaciji metabolizma gvoždja, regulaciji inflamacije, dok u masnom tkivu utiče na razvoj insulinske rezistencije i dijabetesa. Cilj ispitivanja je utvrditi nivo lipokalina 2 u serumu i urinu bolesnika sa primarnim glomerulonefritisom, te utvrditi postojanje korelacije izmedju nivoa lipokalina 2 i patohistološkog oblika glomerulonefritisa, stepenom bubrežne insuficijencije i brzinom progresije bubrežne insuficijencije. Takodje, cilj ispitivanja je bio analizirati povezanost lipokalina 2 sa odogovorom na primenjenu terapiju glomerulonefritisa. Ispitivanje je sprovedeno na 60 bolesnika sa dijagnozom primarnih glomerulonefritisa. Nivo lipokalina 2 je odredjivan pri postavljanju dijagnoze i nakon minimalno šest meseci lečenja. Rezultati studije ukazuju da bolesnici sa primarnim glomerulonefritisom imaju značajno veće nivoe lipokalina 2 u odnosu na zdrave osobe. Bolesnici sa proliferativnim oblicima primarnih glomerulonefritisa imaju veće nivoe NGAL-a u serumu i odnosa uNGAL/kreatinin, ali razlika nije statistički značajna. Nije utvrdjeno postojanje značajne razlike u prosečnim nivoima NGAL-a u serumu, niti urinu, pri postavljanju dijagnoze, izmedju bolesnika sa pozitivnim i negativnim efektom lečenja primarnog glomerulonefritisa. Utvrdjeno je postojanje korelacije izmedju nivoa NGAL-a u serumu i vrednosti kreatinina, ureje, mokraćne kiseline, klirensa kreatinina i broja leukocita, dok je sa nivoom NGAL-a u urinu utvrdjena korelacija sa klirensom kreatinina, dnevnom proteinurijom i serumskim albuminima. Utvrdjeno je postojanje statistički značajne razlike u prosečnim nivoima NGAL-a u serumu u zavisnosti od stadijuma bubrežne insufijencije. Nije utvrdjeno postojanje značajne razlike u prosečnim nivoima NGAL-a u serumu pri postavljanju dijagnoze, izmedju bolesnika sa povoljnim i nepovoljnim efektom lečenja na bubrežnu funkciju.
The primary glomerulonephritis are inflammatory kidney diseases. Glomerulus are primarily affected, but tubulointerstitial changes are very important for course and prognosis of the disease. In addition to clinical and laboratory testing, percutaneous renal biopsy has an important place in the diagnosis of specific forms of glomerulonephritis. Neutrophil gelatinaseassociated lipocalin (NGAL) occupies an important place among the newer biomarkers in nephrology. The main function of NGAL is transport of iron, whether it has a role in the regulation of iron metabolism, regulation of inflammation, while in adipose tissue affects the development of insulin resistance and diabetes. The aim of this study was to determine the level of lipocalin 2 in serum and urine of patients with primary glomerulonephritis and determine the existence of a correlation between the level of lipocalin 2 and histological forms of glomerulonephritis, the degree of renal insufficiency and speed of progression of renal insufficiency. Also, the aim of this study was to analyze the association of lipocalin 2 with the effect of therapy for glomerulonephritis. The study was conducted on 60 patients diagnosed with primary glomerulonephritis. The levels of lipocalin 2 were determined at diagnosis and after a minimum of six months of treatment. The study results show that patients with primary glomerulonephritis have significantly higher levels of lipocalin 2 compared to healthy people. Patients with proliferative forms of primary glomerulonephritis have higher levels of NGAL in serum and ratio uNGAL/creatinine, but the difference was not statistically significant. There was no significant differences in average levels of NGAL in serum or urine at the beginning, between patients with positive and negative effects of the treatment of primary glomerulonephritis. Correlation was found between the level of NGAL in serum and creatinine, urea, uric acid, creatinine clearance and the number of leukocytes, while the level of NGAL in urine correlated with creatinine clearance, the daily proteinuria and serum albumin. Statistically significant differences in mean levels of NGAL in serum depending on the severity of renal insufficiency were found. No evidence of significant differences in average levels of NGAL in serum at the beginning, among patients with favorable and unfavorable effects of treatment on renal function were found.

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33

Issler, N. "Clinical, genetic and molecular studies into hereditary renal tubular proteinuria." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1458544/.

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BACKGROUND We identified patients from consanguineous families from within a genetic isolate who presented with an unknown combination of renal tubular proteinuria and sensorineural hearing loss. METHODS Patients were carefully characterised concerning kidney function including 99m-Tc-DMSA scan and renal biopsy. We applied multipoint parametric whole-genome linkage analysis and haplotype reconstruction in four families with six affected children. We performed exome capture and next generation sequencing in five affected children. Newly identified mutations in a gene with presumed intracellular trafficking functions were evaluated with the use of different cell models. Protein expression within the kidney and intracellular trafficking were further investigated by immunocytochemical analysis. RESULTS All patients investigated had normal glomerular filtration rate, a pathological 99m-Tc-DMSA renal scan with no tracer uptake and abnormal electron microscopy finding within the microvilli of the proximal tubule. Linkage studies identified a single significant genome-wide locus with a LOD score of 7.2 on chromosome 11. This region of 1.5 million bases, contained a total of 48 annotated genes. Analysing the sequencing results of those genes within this linked region revealed a homozygous missense mutation in the EHD-1 gene in all affected individuals. The mutation segregated in an autosomal recessive fashion within the families and was absent from 196 healthy ethnically matched control alleles. This mutation, when expressed in HeLa and renal proximal tubular LLC-PK1 cells caused significant and specific changes in the endosomal recycling compartment, an intracellular compartment related to processing and recycling of cellular substrates. CONCLUSION We identified a founder mutation in a gene causing a previously unrecognised and undiagnosed rare autosomal recessive Mendelian disorder, showing clinically signs and symptoms of renal tubular low molecular weight proteinuria and hearing deficit. Our findings indicate that this gene plays a major role in renal tubular low molecular protein handling and inner ear function.

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Paisley, K. E. "Vascular function in human subjects with nephrotic syndrome and asymptomatic proteinuria." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427636.

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35

Isaya, Rosaria <1979&gt. "Proteinuria e sindrome nefrosica nel cane: studio reptrospettivo di 338 casi." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4830/.

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La sindrome nefrosica (SN) è definita come la presenza concomitante di una proteinuria maggiore di 3.5g/24 h, ipoalbuminemia, ipercolesterolemia e presenza di edemi. I pazienti con SN sono più a rischio di quelli che presentano una nefropatia glomerulare non nefrosica (NNGD) per lo sviluppo di ipertensione, ipernatremia, complicazioni tromboemboliche e comparsa di insufficienza renale. In Medicina Veterinaria, la Letteratura riguardante l’argomento è molto limitata e non è ben nota la correlazione tra SN e gravità della proteinuria, ipoalbuminemia e sviluppo di tromboembolismo. L’obiettivo del presente studio retrospettivo è stato quello di descrivere e caratterizzare le alterazioni cliniche e clinicopatologiche che si verificano nei pazienti con rapporto proteine urinarie:creatinina urinaria (UPC) >2 con lo scopo di inquadrare con maggiore precisione lo stato clinico di questi pazienti e individuare le maggiori complicazioni a cui possono andare incontro. In un periodo di nove anni sono stati selezionati 338 cani e suddivisi in base ad un valore cut-off di UPC≥3.5. Valori mediani di creatinina, urea, fosforo, albumina urinaria, proteina C reattiva (CRP) e fibrinogeno sono risultati al di sopra del limite superiore dell’intervallo di riferimento, valori mediani di albumina sierica, ematocrito, antitrombina al disotto del limite inferiore di riferimento. Pazienti con UPC≥3.5 hanno mostrato concentrazioni di albumine, ematocrito, calcio, Total Iron Binding Capacity (TIBC), significativamente minori rispetto a quelli con UPC<3.5, concentrazioni di CRP, di urea e di fosforo significativamente maggiori. Nessuna differenza tra i gruppi nelle concentrazioni di creatinina colesterolo, trigliceridi, sodio, potassio, cloro, ferro totale e pressione sistolica. I pazienti con UPC≥3.5 si trovano verosimilmente in uno “stato infiammatorio” maggiore rispetto a quelli con UPC<3.5, questa ipotesi avvalorata dalle concentrazioni minori di albumina, di transferrina e da una concentrazione di CRP maggiore. I pazienti con UPC≥3.5 non presentano concentrazioni di creatinina più elevate ma sono maggiormente a rischio di anemia.
Nephrotic syndrome (NS) is defined as the concurrent presence of proteinuria greater than 3.5g/24 h, hypoalbuminemia, hypercholesterolemia, and extravascular fluid accumulation. Patients with NS are at higher risk than those who have a non-nephrotic glomerular nephropathy (NNGD) for the development of hypertension, hypernatremia, thromboembolic complications and the onset of renal failure. In Veterinary Medicine, there are few studies and correlation between NS and proteinuria, hypoalbuminemia, hypertension, underlying glomerular disease and development of thromboembolism are unknow. The objective of this retrospective study is to describe and characterize the clinical and clinicopathological abnormalities in patients with a urine protein:creatinine ratio (UPC) greater than 2, with the aim to characterize with greater precision the clinical status of these patients and identify the major complications that can suffer. In a period of nine years, 338 dogs were selected and divided according to a cutoff value of UPC≥3.5. Median values of creatinine, BUN, phosphorus, urinary albumin, C-reactive protein (CRP) and fibrinogen were above the upper limit of the reference range, median values of serum albumin, hematocrit, antithrombin were below the lower limit of reference range. . Patients with ≥ 3.5 UPC showed concentrations of albumin, hematocrit, calcium, Total Iron Binding Capacity (TIBC), significantly lower than those with UPC <3.5, concentrations of CRP, BUN and phosphate significantly higher. No differences between groups in the concentrations of creatinine, cholesterol, triglycerides, sodium, potassium, chloride, total iron and systolic blood pressure. Patients with a UPC ≥ 3.5 are likely to find in an "inflammatory condition" greater than those with UPC <3.5, this hypothesis is strengthened by lower concentrations of albumin, TIBC and a greater concentration of CRP. Patients with a UPC ≥ 3.5 do not have higher concentrations of creatinine, but are at increased risk of anemia.

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Crawford, S. M. "Low molecular weight proteinuria and the natural history of multiple myeloma." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382055.

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Luimula, Pauliina. "Regulation of the key molecules of glomerular ultrafiltration in proteinuric models." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/luimula/.

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Conti, Luisa <1981&gt. "Metodi di misurazione e implicazioni dell'albuminuria e della proteinuria nel cane." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/6061/.

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La proteinuria è un marker di danno renale nel cane. L’obiettivo dello studio è di valutare la capacità del dipstick urinario e dell’UPC di diagnosticare precocemente l’albuminuria nel cane. Sono stati raccolti 868 campioni di urina, con sedimento spento e assenza di ematuria, nell’Ospedale Didattico Veterinario della Facoltà di Medicina Veterinaria di Bologna. Per 550 campioni è stata effettuata l’analisi delle urine, la misurazione dell’UPC e dell’UAC, mentre UPC e UAC sono stati misurati in tutti gli 868 campioni. I campioni di urina sono stati analizzati con il metodo dipstick mediante lettura automatizzata. Utilizzando come valore di riferimento l’UAC è stata valutata l’accuratezza diagnostica del dipstick urinario e dell’UPC. L’intervallo di riferimento dell’UAC (0-0,024) è stato determinato utilizzando 60 cani sani. I dati raccolti sono stati classificati utilizzando differenti cut-off per il peso specifico urinario (1012 o 1030), per la proteinuria al dipstick (30 o 100 mg/dl), per l’UPC (0,2) e per l’UAC (0,024). Sono stati valutati l’agreement diagnostico e la correlazione di Spearman tra dipstick, UPC e UAC. E’ stata stimata l’accuratezza diagnostica misurando l’area al di sotto della curva di ROC nell’analisi dell’UAC. Il livello di significatività è stato definito per p < 0,05. Indipendentemente dal peso specifico urinario, l’agreement diagnostico tra dipstick, UPC e UAC è risultato forte (k=0,62 e k=0,61, rispettivamente; p<0,001) con valori di dipstick ≥30 mg/dl, debole (k=0,27 e k=0,26, rispettivamente; p<0,001) con valori di dipstick ≥100 mg/dl. L’accuratezza diagnostica del dipstick messa a confronto con UPC e con UAC è molto buona (AUC 0,84 e 0,84, rispettivamente; p<0,001) e i risultati negativi al dipstick presentano il 100% di sensitività. UPC e UAC sono fortemente correlate (r=0,90; p<0,001). Mettendo a confronto UPC e UAC, l’accuratezza diagnostica è risultata eccellente (AUC 0,94; p<0,001), con massima sensitività e specificità per UPC≥0.3.
Proteinuria is considered a marker of kidney damage in dogs. The aim of the study was to evaluate the ability of a urine dipstick test and UPC to early recognize albuminuric dogs. 868 canine urine samples without active sediment and macroscopic hematuria were collected in our Teaching Hospital. Urinalysis, UPC and UAC were available for 550 samples, while UPC and UAC were performed in 868 specimens. Urine samples were dipstick tested, using an automated reader. Considering UAC as the reference method, the diagnostic accuracy of dipstick test and UPC was evaluated. UAC reference interval (0-0.024) was determined from 60 healthy dogs. Data collected were categorized using different cut-offs for urine specific gravity (1012 or 1030), dipstick proteinuria (30 or 100 mg/dl), UPC (0.2) and UAC (0.024). Diagnostic agreement and Spearman's correlation between dipstick, UPC and UAC were evaluated. The diagnostic accuracy was estimated with the area under the ROC curve (AUC) analysis. Significance level was set at p < 0.05. Independently of urine concentration, diagnostic agreement between dipstick and UPC or UAC was substantial (k=0.62 and k=0.61, respectively; p<0,001) with positive dipstick results ≥30 mg/dl, and was fair (k=0.27 and k=0.26, respectively; p<0,001) with positive dipstick results ≥100 mg/dl. Diagnostic accuracy of dipstick compared to UPC and UAC was very good (AUC 0.84 and 0.84, respectively; p<0,001) and negative dipstick results presented 100% sensitivity. UPC and UAC were highly correlated (r=0,90;p<0,001). Comparing UPC with UAC, diagnostic accuracy was excellent (AUC 0.94; p<0,001), with maximum sensitivity and specificity for UPC ≥0.3.

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Erdely, Aaron. "Progression of chronic renal disease in several animal models possible role of decreased renal nitric oxide production as a primary causative factor /." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2740.

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40

Tulloch, Inga Anne. "The anti-proteinuric effects of unsaturated fatty acid diets in healthy rats." Thesis, University of Glasgow, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295329.

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41

Marrón, Huamán Alexander. "PREVALENCIA DE PREECLAMPSIA EN GESTANTES ATENDIDAS EN EL SERVICIO DE EMERGENCIA. HOSPITAL DE VENTANILLA - 2014." Bachelor's thesis, Universidad Ricardo Palma, 2016. http://cybertesis.urp.edu.pe/handle/urp/551.

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OBJETIVOS: Determinar la prevalencia de Preeclampsia en gestantes atendidas en el servicio de emergencia del Hospital de Ventanilla en el 2014. MÉTODOS: Estudio Transversal Retrospectivo. LUGAR: Hospital de Ventanilla, entre enero y diciembre 2014. MATERIAL MÉTODOS: Se identificó 102 gestantes a través del registro de las historias clínicas, caracterizadas por edad, estado civil grado de instrucción y trimestre de desarrollo de la Preeclampsia. Se realizó análisis descriptivo mediante tablas de frecuencia y se estudiaron las variables mediante prueba chi cuadrado en SPSS versión 23 y Microsoft Excel. RESULTADOS: Las edad media de 28.46 ± 7,8 (IC 95% 20,66-36,26); 71.6% (73/102) estudios secundarios y 13.7% (14/102) primarios; el estado civil más frecuente fue “conviviente” en un 56.9% (58/102). La Preeclampsia se presentó con mayor frecuencia en el tercer trimestre con un 86.3% (88/102), 71.6% tuvo Preeclampsia leve y 28.4% Preeclampsia severa. La edad (p = 0.052), el estado civil (p = 0.032) no mostraron asociación significativa con el cuadro Leve o Severa clínica de Preeclamsia, contrario a ello el grado de instrucción nivel secundario (p = 0.000) se encuentra asociada al cuadro clínico de Preeclampsia Leve y Severa. CONCLUSIONES: La Preeclampsia está relacionada a una heterogeneidad de factores de riesgo. La prevalencia hospitalaria de Preeclampsia fue de 0.5%. Las gestantes deben ser cuidadosamente controladas durante su embarazo, para reducir la incidencia y complicaciones de este trastorno hipertensivo.

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42

Komuraiah, Myakala. "Proliferation Signal Inhibitor associated proteinuria in a renal transplant recipient: Dysfunction of proximal tubular epithelial cells is a result of decreased cubilinand/or megalin expression? : Proliferation Signal Inhibitor associated Proteinuria." Thesis, University of Skövde, School of Life Sciences, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-3885.

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Background The proliferation signal inhibitors (PSIs) sirolimus (SRL) and everolimus (ERL) are the potent immunosuppressive drugs using in organ transplantation and has been used successfully in renal transplant recipients (RTX) as well. PSIs are the key factors to overcome the allograft rejections after successful organ transplantation since the immune system starts to react against the graft. SRL and ERL prevents the action of immune system b inhibits the proliferation of T- and B-cells by inhibiting the intracellular signaling of interleukin-2. The presence of excess amount of serum proteins including albumin in the urine is considered as proteinuria, which reflects the loss of kidney function. The occurrence of proteinuria can be the result of abnormal glomerular filtration and/or impaired tubular endocytic function of renal proximal tubular epithelial cells (PTECs). Megalin and cubulin are two scavenger receptors present on epical surface of PTECs and involved in reabsorption of proteins after glomerular ultrafiltration process in the kidney. Proteinuria appears too high in renal transplanted patients during ongoing treatment with PSIs.

Aim Our study aimed to investigate and correlate the expression level of megalin and cubilin and albumin uptake in PTEC of renal transplanted patients before and after conversion to PSI.

Methods To retrieve the maximal expression of our interest molecules in renal PTECs, we optimized antigen retrieval (AR) method and primary antibody dilution for each molecule separately. An optimization experiment was performed on 3 different normal patients renal biopsies were used. Later, human renal biopsy specimens originated from 4 different renal transplanted patients were used in this study. From all the 4 patients biopsy specimens were taken before and ongoing administration of PSIs (SRL, ERL). The expression of megalin, cubilin and albumin uptake in PTEC of renal transplant patients was determined by immunohistochemical staining.

Results Based on the optimization experiments, we selected the AR method and primary antibody dilution for the expression of megalin, cubilin and albumin uptake. In 4 renal transplanted patients following administration of PSIs results in patients 1, 2, 3 expression of megalin, cubilin and albumin uptake during ongoing PSI treatment was not comparable or even more intense than before PSIs introduction. The expression of megalin, cubilin and albumin uptake was reduced in patient 4 during ongoing PSI treatment.

Conclusion Our findings suggest that the renal transplant patient 4 developed proteinuria during PSI medication. The expression of megalin, cubilin and albumin uptake was markedly decreased during ongoing PSI treatment in patient 4. We concluded that there is a direct link between PSI medication and tubular dysfunction, which might cause proteinuria

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43

Haltia, Anni. "Pathogenetic features of proteinuria studies on congenital nephrotic syndrome of the Finnish type." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/haltia/.

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44

Sancho, Calabuig Mª Asunción. "Incidencia, factores de riesgo y significado pronóstico de la proteinuria en el trasplante renal. Valor predictivo de la proteinuria precoz sobre la función renal y las supervivencias del injerto y del paciente." Doctoral thesis, Universitat de València, 2010. http://hdl.handle.net/10803/52156.

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La proteinuria es el principal marcador independiente de progresión de enfermedad renal en riñones nativos. En el trasplante renal es indicativa de lesión renal a nivel glomerular y tubulointersticial, y se ha relacionado con una peor supervivencia del injerto y del paciente. No obstante, existen pocas evidencias acerca del papel pronóstico y predictivo de la proteinuria en el trasplante renal, sobre todo en lo que respecta a la proteinuria precoz y de bajo grado. En este trabajo de investigación se ha intentado profundizar en el conocimiento de la proteinuria en nuestra población trasplantada renal que incluye una elevada prevalencia de trasplantes con órganos de donantes con criterios expandidos. Nuestra hipótesis de trabajo fue que la proteinuria es un evento frecuente y precoz en la evolución del trasplante renal, que posee valor pronóstico sobre la función renal, la supervivencia del injerto y del paciente, y cuya disminución durante el primer año se asocia a una mejoría en la supervivencia del injerto y del paciente a largo plazo. Se realizó un estudio retrospectivo de cohortes que incluyó 401 trasplantados renales en nuestro centro en los primeros 9 años del programa de trasplante renal. La presencia de proteinuria se definió como aquella con valores mayores o iguales a 0,1 g/24h, valor cercano al límite inferior de detección de la técnica empleada en nuestro centro. Se analizó la relación entre la magnitud de la proteinuria durante el primer año y el pronóstico del injerto y del paciente. Posteriormente se analizaron los factores de riesgo y el significado pronóstico de dicha proteinuria, categorizada según diferentes criterios: proteinuria al tercer mes como expresión de proteinuria precoz postrasplante, proteinuria al duodécimo mes como presentación tardía de la misma, disminución o no disminución durante el primer año de trasplante y proteinuria de muy bajo rango mantenida durante el primer año. Finalmente analizamos la capacidad predictiva de la proteinuria sobre la función renal subóptima, el fracaso del injerto y la muerte del paciente con injerto funcionante mediante estudios de sensibilidad, especificidad, valores predictivos, cocientes de probabilidades o cálculo del área bajo la curva ROC. La realización de este trabajo de investigación ha demostrado la elevada prevalencia de proteinuria en estadios precoces del trasplante, correspondiendo la mayor proporción de pacientes con proteinuria a aquellos con cifras inferiores a 0,5g/24h. La proteinuria en el primer año de trasplante se asoció a factores de riesgo, relacionados con el donante, riesgo inmunológico del receptor, evolución en el postrasplante inmediato, inmunosupresión, función renal y control tensional. La presencia de proteinuria durante el primer año resultó un factor de riesgo independiente del fracaso del injerto y muerte del paciente trasplantado, incluso aquellas proteinurias mantenidas de muy bajo grado inferiores a 0,5 g/24h. La presencia de proteinuria predijo mejor la función subóptima del injerto, que el fracaso del injerto o la muerte del paciente, siendo la capacidad predictiva de la proteinuria al tercer mes muy similar a la de la proteinuria al año del trasplante. La ausencia de proteinuria resultó ser signo de buen pronóstico. La disminución de la proteinuria a lo largo del primer año del trasplante se acompañó de un riesgo de fracaso del injerto y de muerte del paciente similar al de los pacientes sin proteinuria. Todo ello incide en la necesidad de establecer una vigilancia exquisita ante la aparición de cualquier grado medible de proteinuria desde el postrasplante inmediato, sobre todo si se mantiene a partir del tercer mes, independientemente de su cuantía, con el fin de adoptar precozmente medidas diagnósticas, para filiar su causa, y de nefroprotección dirigidas a la reducción de la proteinuria y la progresión de la insuficiencia renal.
Proteinuria is the best independet predictor of developement of end stage renal disease in general population. Its presence in renal transplantation is a marker of glomerular pathology and tubulointerstitial lesions. It has been related to graft failure and a worse patient survival. In this cohort retrospective study of 401 kidney transplant performed in our unit we analyzed the presence of proteinuria ≥ 0,1 g/24h and its prognostic significance as well as its predictive value by means of a sensitivity, specificity, positive and negative predictive values and the value of the area under the curve ROC. The presence of proteinuria at third month after transplantation, at first year, reduction of proteinuria and very low range proteinuria in the first year after transplantation were analyzed. Proteinuria resulted highly prevalent in the first year after transplantation. Its presence was associated with donor age and cause of death, recipient age, number of HLA missmatches, immunosuppression, delayed graft function, worse renal function and blood pressure control. Proteinuria, including that of less than 0,5g/24h at first year after transplantation was related to graft failure and a worse patient survival. Absence of proteinuria was a sign of good prognosis, and predictive value of early proteinuria on suboptimal renal function, graft failure and patient death was similar to that of proteinuria at first year after transplantation. It must be necessary to extreme diagnostic measures to detect early proteinuria and to establish nephroprotective measures to avoid the progression of renal disease and to improve graft and patient survival.

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Yasuda, Nobuo. "Effects of Long-term Strenuous Exercise on Oxidative DNA Damage and Proteinuria in Humans." The University of Montana, 2007. http://etd.lib.umt.edu/theses/available/etd-12282007-160926/.

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The purpose of this study consisting of three projects was to determine the effects of long-term strenuous exercise on oxidative DNA damage and proteinuria in trained individuals. In the first project, four successive triathlons accompanied by long-term training in a triathlete was chosen as the experimental design and procedure. In the second project, repeated 5-h bouts of cycling exercise at 52 %VO2peak and a 40 km time trial with carbohydrate and potential antioxidant supplementation (fenugreek seed extract) were carried out with trained individuals. In the third project, a wildland firefighting three-day work shift was conducted with active duty military personnel. Assessment of oxidative DNA damage was based on urinary and muscle 8-hydroxy-2'-deoxyguanosine. Post-exercise proteinuria was determined with several biomarkers including urinary total protein, albumin, beta2-microglobulin, N-acetyl-beta-D-glucosaminidase, and creatinine. The overall results showed that there were significant whole-body DNA oxidation and post-exercise proteinuria after the half- and full-Ironman triathlon races, but these levels gradually returned to baseline. In contrast, no significant alterations were observed in either oxidative DNA damage at the muscle and tissue level or proteinuria after the 5 h of cycling exercise at 52 %VO2peak and the 40 km time trial. Arduous work during wildland fire suppression induced proteinuria, which tended to be accumulated as the work shift progressed. These findings indicate that moderate exercise may not reach the threshold to cause oxidative DNA damage and proteinuria, whereas long-lasting strenuous exercise appears to induce oxidative DNA modification and exceed normal range of urinary protein excretion.

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Tatjana, Stojšić Vuksanović. "Uticaj holekalciferola na proteinuriju kod bolesnika sa tipom 2 dijabetesa mellitus." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2020. https://www.cris.uns.ac.rs/record.jsf?recordId=114771&source=NDLTD&language=en.

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Zastupljenost deficita vitamina D3 je mnogo veći kod bolesnika sa dijabetesnom bolesti tipa 2 nego u populaciji zdravih osoba. Bolesnici sa DM tipa 2 i deficitom vitamina D3 imaju veći rizik za razvoj dijabetesne nefropatije. Eksperimenti na životinjama i neka klinička istraživanja ukazuju da bi primena nižih doza vitamina D3 mogla imati renoproktektivno delovanje. Cilj istraživanja je bio da se utvrdi zastupljenost deficita vitamina D3 u populaciji bolesnika sa dijabetesnom nefropatijom koja je definisana proteinurijom ˃0,150 g/du. Drugi cilj je bio da se utvrdi da li primena holekaciferola u dozi koja predstavlja razliku između utvrđenog i optimalnog nivoa vitamina D3 dovodi do statistički značajnog smanjenja proteinurije. Bolesnici sa dijabetesom tipa 2 i proteinurijom ˃0,150 g/du su uključivani u skrining na nivo vitamina D3 (25(OH)D) nakon čega su svrstavani u grupe sa deficitom i normalnim nivoom vitamina D3. Granična vrednost za utvrđivanje deficita vitamina D3 je odreĎivana na osnovu tabele koja definiše ove vrednosti za svaki mesec tokom godine, posebno za muškarce i žene. Bolesnici sa deficitom vitamina D3 su podeljeni u 2 grupe od po 45 ispitanika. Studijska grupa je primala holekaciferol u dozi koja je izračunata na osnovu razlike između izmerene vrednosti i određenog optimalnog nivoa vitamina D3 od 90-100 nmol/L. Kontrolna grupa bolesnika je uzimala svoju uobičajenu terapiju. Istraživanje je trajalo 24 nedelje tokom koje su na drugi mesec praćeni parametri bubrežne funkcije, parametri inflamacije i koštanog metabolizma. Na početku i kraju istraživanja su odreĎeni nivo vitamina D3 u studijskoj grupi, dok su u obe grupe određivani vrednost HbA1c i lipidni profil. Analizom dobijenih podataka je utvrđeno da je zastupljenost deficita vitamina D3 kod bolesnika sa dijabetesnom nefropatijom, uzimajući u obzir sezonske varijacije u nivou ovog vitamina, bila veća od vrednosti od 30-50% koje su postavljene u radnoj hipotezi. Učestalost bolesnika sa nedostakom vitamina D3 je u ispitivanom uzorku je bila 82,56% , dok je normalne vrednosti vitamina D3 imalo 17,43% ispitanika, od toga je bilo 10 (52,63%) muškaraca i 9 (47,36%) žena. Sniženje vrednosti vitamina D3 u odnosu na donje granične vrednosti je bilo izraženije u letnjem periodu i bilo je statistički značajno kod svih ispitanika zajedno, potom u studijskoj grupi, dok je utvrđeno i u kontrolnoj grupi ali je u njoj bilo bez statisičke značajnosti. Utvrđen je porast HbA1c koji je bio veći u kontrolnoj grupi ispitanika. Suplementacija vitaminom D3 je imala povoljan efekat na lipidni profil. Registrovan je porast vrednosti ukupnog holesterola koji je bio izraženiji u kontrolnoj grupi, pad vrednosti triglicerida u grupi bolesnika koji su uzimali vitamin D3 i njihov porast u kontrolnoj grupi ispitanika. U studijskoj grupi je registrovan porast vrednosti HDL-holesterola koji je bio na granici statističke značajnosti dok je istovremeno nađeno njegovo smanjenje u kontrolnoj grupi. Vrednost LDL-holesterola je ostala bez promene pod delovanjem vitamina D3, dok je u kontrolnoj grupi došlo do njegovog porasta. Utvrđeno je snižavanje vrednosti sedimentije, CRP-a i fibrinogena koje je bilo bez statističke značajnosti. Bezbednosni profil vrednosti kalcijuma u serumu i urinu tokom dugotrajnije primene je dobar. Primenom vitamina D3 je došlo do signifikatnog smanjenja proteinurije u grupi bolesnika koji su primali holekaciferol čime je ujedno i potvrđena radna hipoteza.
The prevalence of vitamin D3 deficiency is much higher in patients with type 2 diabetes than in the healthy population. Patients with type 2 DM and vitamin D3 deficiency are at increased risk for developing diabetic nephropathy. Animal experiments and some clinical studies suggest that administration of lower doses of vitamin D3 could have renoprotective effect. The aim of the study was to determine the prevalence of vitamin D3 deficiency in the population of patients with diabetic nephropathy defined by proteinuria ˃0.150 g / du. The second goal was to determine whether the use of cholecaciferol in a dose that represents the difference between the established and optimal levels of vitamin D3 leads to a statistically significant reduction in proteinuria. Patients with type 2 diabetes and proteinuria ˃0.150 g / du were screened for vitamin D3 (25 (OH) D) levels and then classified as deficient and normal vitamin D3. The limit value for determining vitamin D3 deficiency was set on the basis of a table defining these values for each month during the year, separately for men and women. Patients with vitamin D3 deficiency were divided into 2 groups of 45 subjects each. The study group received cholecaciferol at a dose calculated on the basis of the difference between the measured value and the set optimal vitamin D 3 level of 90-100 nmol/L. The control group of patients was taking their usual therapy. The study lasted 24 weeks during which the parameters of renal function, parameters of inflammation and bone metabolism were monitored every second month. At the beginning and end of the study, the levels of vitamin D3 in the study group were determined, while in both groups HbA1c and lipid profile were determined. The analysis of the obtained data showed that the prevalence of vitamin D3 deficiency in patients with diabetic nephropathy, taking into account seasonal variations in the level of this vitamin, was higher than the values of 30-50%, which were set in the working hypothesis. The frequency of patients with vitamin D3 deficiency in the study sample was 82.56%, while the normal values of vitamin D3 were in 17.43% of the subjects, of which 10 (52.63%) were men and 9 (47.36%) woman. The decrease in vitamin D3 compared to the lower limit values was more pronounced in the summer and was statistically significant in all subjects together, as well in the study group, while it was also found in the control group but was not statistically significant. An increase in HbA1c was found to be higher in the control group. Vitamin D3 supplementation had a beneficial effect on the lipid profile. An increase in the total cholesterol level that was more pronounced in the control group, a decrease in triglyceride values in the group of patients taking vitamin D3 and its increase in the control group of subjects were registered. An increase in HDL-cholesterol was reported in the study group, which was at the limit of statistical significance, while at the same time a decrease was found in the control group. LDL-cholesterol levels remained unchanged under the influence of vitamin D3, while in the control group it increased. The decrease in sedimentation, CRP and fibrinogen values was found to be of no statistical significance. The safety profile of serum and urine calcium during long-term administration is good. The use of vitamin D3 resulted in a significant decrease in proteinuria in the group of patients receiving cholecaciferol, which also confirmed the working hypothesis.

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47

Menahem, Solomon. "Apoptosis in the progression of IGA nephropathy." Monash University, Faculty of Medicine, Nursing and Health Sciences, 2003. http://arrow.monash.edu.au/hdl/1959.1/9449.

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Kramer, Andrea Brechtsje. "Proteinuria-associated renal injury and the effects of intervention in the renin-angiotensin-aldosterone system." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/293118337.

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49

Surman, Sean T. "The Relationships Between Systemic Hypertension, Proteinuria, and Renal Histopathology in Clinically Healthy Retired Racing Greyhounds." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1276873953.

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50

Russo, Samanta <1984&gt. "Valutazione della proteinuria e del follow-up clinico e clinicopatologico in cani affetti da Leishmaniosi canina." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/6053/.

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Introduzione: la leishmaniosi canina (CanL) è una malattia infettiva, trasmessa da vettore e sostenuta da un protozoo, la Leishmania infantum. La CanL ha assunto sempre più importanza sia in medicina veterinaria che in medicina umana. La leishmaniosi è fortemente associata allo sviluppo di una nefropatia cronica. Disegno dello studio: studio di coorte retrospettivo. Obiettivo: individuare le alterazioni clinico-patologiche prevalenti al momento dell’ammissione e durante il follow-up del paziente, per identificare quelle con un valore prognostico maggiore. Materiali e metodi: 167 cani, per un totale di 187 casi trattati, con diagnosi sierologica e/o citologica di Leishmaniosi e dati ematobiochimici completi, elettroforesi sierica, analisi delle urine e biochimica urinaria comprensiva di proteinuria (UPC) ed albuminuria (UAC), profilo coagulativo (ATIII, d-Dimeri, Fibrinogeno) e marker d’infiammazione (CRP). Dei pazienti inclusi è stato seguito il follow-up clinico e clinicopatologico per un periodo di tempo di due anni e sono stati considerati. Risultati: Le alterazione clinicopatologiche principali sono state anemia (41%), iperprotidemia (42%), iperglobulinemia (75%), ipoalbuminemia (66%), aumento della CRP (57%), incremento dell’UAC (78%), aumento dell’UPC (70%), peso specifico inadeguato (54%) e riduzione dell’ATIII (52%). Il 37% dei pazienti non era proteinurico e di questi il 27% aveva già un’albuminuria patologica. Il 38% dei pazienti aveva una proteinuria nefrosica (UPC>2,5) e il 22% era iperazotemico. I parametri clinicopatologici hanno mostrato una tendenza a rientrare nella normalità dopo il 90° giorno di follow-up. La creatinina sierica, tramite un analisi multivariata, è risultata essere il parametro correlato maggiormente con l’outcome del paziente. Conclusione: i risultati ottenuti in funzione dell’outcome dei pazienti hanno mostrato che i soggetti deceduti durante il follow-up, al momento dell’ammissione avevano valori di creatinina, UPC e UAC più elevati e ingravescenti. Inoltre l’UAC può venire considerato un marker precoce di nefropatia e la presenza di iperazotemia all’ammissione, in questi pazienti, ha un valore prognostico negativo.
Introduction: Canine Leishmaniasis (CanL) is an infectious disease transmitted by the carrier and supported by a protozoan, Leishmania infantum. The CanL has become increasingly important in both veterinary medicine than in human medicine. Leishmaniasis is strongly associated with the development of a chronic nephropathy. Study design: retrospective cohort study. Objective: To identify the clinicopathologic changes prevailing at the time of admission and during follow-up of the patient, to identify those with a greater prognostic value. Materials and methods: 167 dogs, for a total of 187 cases treated with serological diagnosis and / or cytological diagnosis of leishmaniasis and complete data biochemistry, serum electrophoresis, urinalysis and urinary biochemistry including proteinuria (UPC) and albuminuria (UAC), coagulation profile (ATIII, d-dimers, fibrinogen) and markers of inflammation (CRP). Of patients included was followed the clinical follow-up and clinicopathologic for a time period of two years and were considered. Results: The main alteration clinicopathological were anemia (41%), iperprotidemia (42%), hyperglobulinaemia (75%), hypoalbuminemia (66%), increased CRP (57%), increased UAC (78%), increased UPC (70%), inadequate urine specific gravity (54%) and reduction of ATIII (52%). 37% of patients were not proteinuric and of these 27% had pathologic albuminuria. 38% of patients had a nephrotic proteinuria (UPC> 2.5) and 22% was azotemic. The clinicopathological parameters showed a tendency to return to normal after the 90th day of follow-up. Serum creatinine, using a multivariate analysis, was found to be the parameter most correlated with patient outcome. Conclusion: results obtained on the basis of the outcome of the patients showed that the patients who died during follow-up, at the time of admission had higher and worsening serum Creatinine, UAC and UPC. In addition, the UAC can be considered an early marker of kidney disease and the presence of azotemia on admission, in these patients, it has a negative prognostic value.

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