Durante a evolução da doença renal crônica (DRC) em cães, um dos mecanismos importantes envolvidos na autoperpetuação e progressão da lesão renal envolvem, teoricamente, o comprometimento inicial do glomérulo pelo mecanismo de hiperfiltração glomerular, e este processo pode acarretar no desenvolvimento de microalbuminúria ou de proteinúria pela presença de proteínas de alto peso molecular (albumina). Com o progredir da doença, as altas concentrações de proteína no filtrado glomerular pode também desencadear lesões tubulares e intersticiais, ocasionando a perda urinária também de proteínas de baixo peso molecular (PM) pelo comprometimento da reabsorção dessas proteínas pelos túbulos renais. Outras teorias de progressão da lesão renal também são suscitadas tais como o comprometimento inicial da porção túbulo-intersticial. Assim, espera- -se que durante a evolução da DRC, a avaliação das proteínas urinárias quanto à qualidade (determinação de albumina e os pesos moleculares) e a quantidade possam trazer informações relevantes sobre a velocidade de progressão e o local da lesão renal. O objetivo deste estudo foi de avaliar, sequencialmente, a albuminúria e a proteinúria (pelos métodos quantitativos e qualitativos - eletroforese de proteínas) dos cães com DRC nos estágios 1, 2 ou 3 ao longo do período de pelo menos 5 meses, e verificar a existência de alterações na intensidade ou no aparecimento de proteinúria e/ou albuminuria. Dezesseis cães (Grupo 1= 5 cães do estágio 1; Grupo 2= 5 cães do estágio 2 e Grupo 3= 6 cães do estágio 3), 9 fêmeas e 7 machos de raças variadas e idades entre 24 a 168 meses, foram acompanhados por 5 a 18 meses e os exames clínico e laboratorial realizados a cada 30 dias. Os cães dos Grupos 1 e 2 apresentaram bom controle clínico, entretanto o Grupo 3 apresentou evolução mais rápida da doença (3 cães vieram a óbito). No Grupo 1, o aumento da razão proteína:creatinina urinária (RPC; variação de 0,154 a 1,14) foi observada somente em um dos cães (no 1) e esta não era decorrente de albuminúria, mas sim da presença de proteínas de baixo peso molecular (lesão tubular) e também foi constatada diminuição progressiva da taxa de filtração glomerular pelo o aumento das concentrações de cistatina C sérica; os demais cães deste grupo apresentaram RPC e razão albumina:creatinina urinária (RAC) normais, entretanto com predomínio de proteínas de baixo peso molecular em 2 cães. No Grupo 2 fato semelhante também foi constatado, nos cães no 6 (inicialmente hipertenso) e 8 em que a RPC variou de 4,89 a 12,77 e 0,5 a 1,0, respectivamente; no cão no6 foi não foi detectada macroalbuminuria, mas somente microalbuminúria e com o predomínio de proteínas de baixo PM (lesão tubular), como também no cão no 8 (ausência de micro ou macroalbuminuria) em que houve o predomínio de 78 a 100% de proteínas de baixo PM e com 3 a 6 bandas. No Grupo 3, proteinúria foi constatada nos cães de no 11, 13 e 15 e a microalbuminúria somente no cão no11; o predomínio de proteínas de baixo PM foi observada nos cães no 11 e 13 e proteinúria mista no cão no 15. Assim, a avaliação sequencial ou seriada da proteinúria, pelo conjunto de informações obtido pela RPC, RAC e eletroforese de proteínas urinárias nos com cães com doença renal crônica, ao longo de um período, trouxe informações mais precisas acerca da qualidade das proteínas, identificando os segmentos do néfron que provavelmente foram comprometidos ao longo da evolução da doença. / During the course of chronic kidney disease (CKD) in dogs, one of the mechanisms involved in the autoperpetuation and progression of renal disease, in theory, is glomerular hyperfiltration, and this process may result in the development of microalbuminuria or proteinuria due to the presence of high molecular weight proteins (albumin). As the disease progresses, the presence of high concentrations of proteins in the glomerular filtrate may also cause the development of interstitial and tubular injuries, and in consequence the presence of low molecular weight proteins in urine as the impairment of tubular reabsorption mechanism of proteins is affected. Other theories of progression of renal injury are also raised such as the initial involvement of the tubulointerstitial segment. Thus, it is expected that during the course of CKD, the evaluation of the quality (determination of albumin and molecular weights) and quantity of urinary proteins may indicate relevant information about the location and rate of progression of renal injury. The objective of this study was to evaluate, longitudinally, albuminuria and proteinuria (by quantitative and qualitative methods - protein electrophoresis) of dogs with CKD in stages 1, 2 and 3 over the period of at least 5 months, and observe the changes in intensity or the appearance of proteinuria and / or albuminuria. Sixteen dogs (Group 1 = 5 dogs in stage 1, Group 2 = 5 dogs in stage 2 and Group 3 = 6 dogs in stage 3), 9 females and 7 males of various breeds and ages ranging from 24 to 168 months, were followed-up for 5-18 months and medical and laboratory monitoring data were recorded every 30 days. Dogs of Groups 1 and 2 showed good clinical control, however the Group 3 had a progressive deterioration of the disease (3 dogs died). In Group 1, the increase in urinary protein-to-creatinine ratio (UPC; ranging from 0.154 to 1.14) was observed in only one dog (no. 1) and albuminuria was not involved, however low molecular weights proteins (LMWP) were detected (tubular injury) and also the progressive decrease in glomerular filtration rate was noticed by the increase of serum concentrations of cystatin C; the remaining dogs in this group demonstrated normal UPC and UAC (urinary albumin-to-creatinine ratio), however the predominance of LMWP in 2 dogs was observed. In Group 2, similar findings were also noticed in CKD dogs no. 6 (initially hypertensive) and 8 , UPC ranged from 4.89 to 12.77 and 0.5 to 1.0, respectively; dog no. 6 demonstrated no macroalbuminuria but only microalbuminuria, and the predominance of LMWP (tubular injury) was observed as well as the dog no. 8 that had 78 to 100% of LMWP with 3 to 6 bands and no micro or macroalbuminuria was detected. Group 3 presented proteinuria in dogs no. 11, 13 and 15 and microalbuminuria was only observed in dog no. 11; the predominance of LMWP was noticed in dogs no.11 and 13, and mixed proteinuria in dog no. 15. Thus, the sequential or longitudinal study of proteinuria by means of several information obtained of UPC, UAC and urine protein electrophoresis in dogs with chronic kidney disease, followed-up over a period, could give more accurate information about the quality of proteins, allowing the possible identification of the segments of the nephron involved that could probably be affected throughout the course of the disease.

Submitted by Rosina Valeria Lanzellotti Mattiussi Teixeira (rosina.teixeira@unisantos.br) on 2016-08-11T18:51:28Z No. of bitstreams: 1 Polianne Brito.pdf: 1107426 bytes, checksum: 5c3c4fadb4db605f31557ca7bf8c3609 (MD5) / Made available in DSpace on 2016-08-11T18:51:29Z (GMT). No. of bitstreams: 1 Polianne Brito.pdf: 1107426 bytes, checksum: 5c3c4fadb4db605f31557ca7bf8c3609 (MD5) Previous issue date: 2016-04-14 / Introduction: Chronic renal disease is considered nowadays, as one of the main public health problems in the world, being an important cause of morbidity and mortality. The diagnosis leads to the need for continuous treatment, submitting the patient to a constant coming and going to the hospital, and this impacting and wearing routine, many times moves the individual partially or totally away from work activities, bringing consequences with the family income, limiting their lives in many aspects, submitting the individual to the dependence of the family or health service. Objective: To analyze from the perspective of the patient with chronic renal disease, the repercussions of the disease and strategies to confront the treatment in a hemodialysis unit in the municipality of Patos-PB. Methodology: This was a qualitative study with chronic renal patients who were in hemodialysis treatment in a private clinic in the municipality of Patos-PB, where SUS (which is a Unified Health System) is the financial transfer so that the carriers are not charged for the treatment. The data was collected by means of a semi-structured interview, in the pre-dialysis period. Preliminary information regarding the study was provided, the signature of the informed consent form was requested and then the interview was recorded with the consent of the participants and fictitious names were used. After the collection, the interviews were transcribed and categories and sub-categories were established for Bardin¿s qualitative content analysis. Results: 06 chronic renal disease patients were interviewed; where, 03 were men and 03 were women in hemodialysis treatment, ageing between 20 to 55 years. The majority of the participants were single and catholic, with educational levels varying from illiterate to complete secondary level, none of them were working at the time of the interviews and 05 of them received a health care benefit of a minimum salary. All the interviewed were referred from a public hospital service, with immediate access to the hemodialysis treatment. Changes occurred in the social and daily life, work, feeding and leisure of all the participants. Alterations in general health due to the treatment were also reported by the majority of the clients. The main confrontation strategies found to deal with the disease and the treatment were the support of the family, partners, and religion. The main difficulties to start and maintain the hemodialysis treatment were the lack of knowledge about the disease and the treatment and the lack of transportation, in order to dislocate the patients to the hemodialysis service .The friendly reception of the multi-professional team, faith and the support of the family and other clinically well patients, were pointed out as being facilitator factors to start and maintain the treatment. Conclusion: the study revealed that the chronic renal disease causes great repercussions in the life of the hemodialysis patients, altering their lifestyle and daily routine; the support of the family, religion and the multi-professional team represented the main confronting strategies for the adhesion to and maintenance of the treatment of the interviewed patients. / Introdução: A doença renal crônica é considerada hoje, um dos principais problemas de saúde pública no mundo, sendo importante causa de morbidade e mortalidade. O diagnóstico conduz à necessidade de um tratamento continuado, submetendo o paciente a idas e vindas ao hospital e essa rotina impactante e desgastante muitas vezes afasta o indivíduo parcial ou totalmente das atividades laborais, com consequências na renda familiar, limitando sua vida em vários aspectos, submetendo-o à dependência da família e de um serviço de saúde. Objetivo: Analisar a partir da perspectiva do portador de doença renal crônica as repercussões da doença e estratégias de enfrentamento para seu tratamento em uma unidade de hemodiálise no município de Patos-PB. Metodologia: tratou-se de um estudo qualitativo com doentes renais crônicos e em tratamento de hemodiálise em uma clínica privada do município de Patos-PB, onde o SUS faz o repasse financeiro para que os portadores realizem sem custo próprio. Os dados foram coletados por meio de entrevista semiestruturada, no período pré-dialítico, foram fornecidas informações prévias sobre o estudo e solicitada a assinatura do termo de consentimento livre e esclarecido e a entrevista foi gravada com consentimento dos participantes e uso de nomes fictícios. Após a coleta, as entrevistas foram transcritas e estabelecidas categorias e subcategorias para análise qualitativa de conteúdo de Bardin. Resultados: foram entrevistados 06 portadores de doença renal crônica, sendo 03 homens e 03 mulheres em tratamento de hemodiálise, com idade entre 20 e 55 anos. A maioria dos participantes era solteira e católica, com escolaridade variando de não alfabetizado a ensino médio completo, nenhum trabalhava na ocasião das entrevistas e 05 recebiam auxílio-doença de um salário mínimo. Todos os entrevistados foram encaminhados de serviço público hospitalar, com acesso imediato ao tratamento de hemodiálise. Ocorreram mudanças na vida social, no cotidiano, trabalho, alimentação e lazer de todos os participantes. Alterações na saúde geral em virtude do tratamento também foi relatada pela maioria dos clientes. As principais estratégias de enfrentamento encontradas para lidar com a doença e tratamento foram apoio familiar, do companheiro e religioso. As principais dificuldades para iniciar e manter o tratamento de hemodiálise foram a falta de conhecimento sobre a patologia e o tratamento e a falta de transporte para se deslocarem até o serviço de hemodiálise. O acolhimento da equipe multiprofissional, a fé, o apoio familiar e a convivência com outros pacientes clinicamente bem, foram apontados como facilitadores para iniciar e manter o tratamento. Conclusão: o estudo revelou que a doença renal crônica causa grandes repercussões na vida dos doentes em hemodiálise, alterando seu estilo de vida e rotina diária. O apoio familiar, a religião e a equipe multiprofissional representaram as principais estratégias de enfrentamento para a adesão e manutenção do tratamento dos entrevistados

Addenda held in pocket pasted onto back end paper. / Bibliography: leaves 137-165. / xvi, 165 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / This thesis involves the retrospective investigation of the insulin-like growth factors and their binding proteins in the serum of children with chronic renal failure (CRF) and transplantation, before and after treatment with recombinant human growth hormone (rhGH). IGF-IGFBP complexes in pooled serum from prepubertal and pubertal children of both sexes with CRF and renal transplantation, before and after treatment with rhGH, are analysed by fast protein liquid chromatography under neutral conditions. / Thesis (M.D.)--University of Adelaide, Dept. of Paediatrics, 1997?

<p>Cardiovascular disease (CVD) is the major cause of death in patients with chronic renal failure (CRF). Endothelial function and oxidative stress (OS) have previously been shown to be important in the pathogenesis of CVD. In this thesis, the endothelium-dependent vasodilatation (EDV) and OS were investigated in the patients with CRF. Also the influence of L-arginine, erythropoietin and diclofenac on EDV were evaluated in patients with CRF. </p><p>Patients with CRF were found to be characterized by a defect EDV even after correction for traditional cardiovascular risk factors. This impairment was related to the degree of renal failure. </p><p>Measurement of OS markers in CRF patients demonstrated that these patients were in a state of OS compared to healthy controls. The most informative indices to evaluate the degree of OS in CRF were: oxidized glutathione (GSSG) level, ratio between oxidized and reduced glutathione (GSSG/GSH ratio), lag phase of lipoprotein fraction (LPF) and baseline diene conjugation level of LPF. </p><p>Simultaneously investigated OS markers and EDV demonstrated a relationship between OS and EDV in patients with CRF. EDV was positively correlated with total antioxidative activity, reduced glutathione (GSH) and lag phase of LDL. </p><p>Local infusion of L-arginine as a substrate for nitric oxide synthesis and diclofenac as an inhibitor of cyclooxygenase-derived vasoconstrictive agents augmented EDV in patients CRF. In contrast, the erythopoietin treatment (both acute and long-term) impaired EDV in CRF patients. </p><p>In conclusion, patients with CRF have increased levels of OS markers and impaired endothelial vasodilatory function. These factors may be important with respect to the high morbidity and mortality of CVD found in patients with CRF. One possible mechanism to reduce CVD in patients with CRF is to improve endothelial function and eliminate OS. Locally administrated L-arginine and diclofenae improved EDV but erythropoietin administration impaired EDV in patients with CRF. </p>

Cardiovascular disease (CVD) is the major cause of death in patients with chronic renal failure (CRF). Endothelial function and oxidative stress (OS) have previously been shown to be important in the pathogenesis of CVD. In this thesis, the endothelium-dependent vasodilatation (EDV) and OS were investigated in the patients with CRF. Also the influence of L-arginine, erythropoietin and diclofenac on EDV were evaluated in patients with CRF. Patients with CRF were found to be characterized by a defect EDV even after correction for traditional cardiovascular risk factors. This impairment was related to the degree of renal failure. Measurement of OS markers in CRF patients demonstrated that these patients were in a state of OS compared to healthy controls. The most informative indices to evaluate the degree of OS in CRF were: oxidized glutathione (GSSG) level, ratio between oxidized and reduced glutathione (GSSG/GSH ratio), lag phase of lipoprotein fraction (LPF) and baseline diene conjugation level of LPF. Simultaneously investigated OS markers and EDV demonstrated a relationship between OS and EDV in patients with CRF. EDV was positively correlated with total antioxidative activity, reduced glutathione (GSH) and lag phase of LDL. Local infusion of L-arginine as a substrate for nitric oxide synthesis and diclofenac as an inhibitor of cyclooxygenase-derived vasoconstrictive agents augmented EDV in patients CRF. In contrast, the erythopoietin treatment (both acute and long-term) impaired EDV in CRF patients. In conclusion, patients with CRF have increased levels of OS markers and impaired endothelial vasodilatory function. These factors may be important with respect to the high morbidity and mortality of CVD found in patients with CRF. One possible mechanism to reduce CVD in patients with CRF is to improve endothelial function and eliminate OS. Locally administrated L-arginine and diclofenae improved EDV but erythropoietin administration impaired EDV in patients with CRF.

Activated coagulation Factor XII (FXIIa) elevates blood pressure (BP) acutely by stimulating adrenomedullary catecholamine (CA) release in Brown Norway (BN) bioassay rats. These effects are absent in kininogen-deficient BN Katholiek (BNK) bioassay rats, indicating that these FXIIa-induced responses require an intact kallikrein-kinin system (KKS). In three hypertensive anephric pediatric patients, ΔFXIIa concentrations tracked peri-dialytic ΔBP. We hypothesized that FXIIa exerts a vasoconstrictor pro-hypertensive action, via the KKS, particularly evident in chronic renal failure (CRF). In CRF patients (n=11) receiving conventional hemodialysis, mean plasma FXIIa concentrations were 3-fold (p<0.05) greater than in healthy controls. Although conversion from conventional to nocturnal hemodialysis did not change mean FXIIa concentrations there was intra-session variation within individuals, such that ΔFXIIa concentrations correlated with changes in mean arterial pressure (MAP, r=0.66, p=0.026) and total peripheral resistance (TPR, r=0.75, p=0.007). In normotensive BN rats, FXIIa infusion (85 ng/min/kg for 60 mins) increased MAP (10±1 mmHg), TPR (0.5±0.1 Units), and CA, whilst left-ventricular end-diastolic volume (LVEDV) and heart rate decreased (all p<0.05). After adrenalectomy, FXIIa infusion decreased MAP (5±1 mmHg), did not raise CA or induce sustained vasoconstriction, and caused a greater fall in LVEDV (all p<0.05). In the 5/6 nephrectomized (NX) rodent CRF model, MAP and TPR were significantly greater in BN NX (n=16) than in BNK NX (n=15) (147±4 vs. 133±2 mmHg, 2.8±0.2 vs. 2.3±0.2 Units; all p<0.05). Plasma FXIIa measured using our semi-quantitive ELISA was 3-fold higher in both BN NX and BNK NX than in controls (p<0.01), but only correlated with MAP (r=0.48, p=0.01) in the BN NX. Plasma CA were elevated in the BN NX (p<0.05) but not in BNK NX. Infusion of a specific FXIIa inhibitor into BN NX decreased MAP (-12 mmHg) and TPR (-0.5 Units) proportionally to baseline FXIIa (ΔMAP: r=-0.72, p=0.002; ΔTPR: r=-0.57, p=0.021), and plasma CA fell by 40-67% (all p<0.05). No such changes occurred in the BNK NX. In summary, a significant component of the hypertension of CRF can be attributed to FXIIa-induced vasoconstriction mediated via the KKS and stimulated CA release. In normal rats, FXIIa appears also to directly or indirectly decrease preload and heart rate.

Activated coagulation Factor XII (FXIIa) elevates blood pressure (BP) acutely by stimulating adrenomedullary catecholamine (CA) release in Brown Norway (BN) bioassay rats. These effects are absent in kininogen-deficient BN Katholiek (BNK) bioassay rats, indicating that these FXIIa-induced responses require an intact kallikrein-kinin system (KKS). In three hypertensive anephric pediatric patients, ΔFXIIa concentrations tracked peri-dialytic ΔBP. We hypothesized that FXIIa exerts a vasoconstrictor pro-hypertensive action, via the KKS, particularly evident in chronic renal failure (CRF). In CRF patients (n=11) receiving conventional hemodialysis, mean plasma FXIIa concentrations were 3-fold (p<0.05) greater than in healthy controls. Although conversion from conventional to nocturnal hemodialysis did not change mean FXIIa concentrations there was intra-session variation within individuals, such that ΔFXIIa concentrations correlated with changes in mean arterial pressure (MAP, r=0.66, p=0.026) and total peripheral resistance (TPR, r=0.75, p=0.007). In normotensive BN rats, FXIIa infusion (85 ng/min/kg for 60 mins) increased MAP (10±1 mmHg), TPR (0.5±0.1 Units), and CA, whilst left-ventricular end-diastolic volume (LVEDV) and heart rate decreased (all p<0.05). After adrenalectomy, FXIIa infusion decreased MAP (5±1 mmHg), did not raise CA or induce sustained vasoconstriction, and caused a greater fall in LVEDV (all p<0.05). In the 5/6 nephrectomized (NX) rodent CRF model, MAP and TPR were significantly greater in BN NX (n=16) than in BNK NX (n=15) (147±4 vs. 133±2 mmHg, 2.8±0.2 vs. 2.3±0.2 Units; all p<0.05). Plasma FXIIa measured using our semi-quantitive ELISA was 3-fold higher in both BN NX and BNK NX than in controls (p<0.01), but only correlated with MAP (r=0.48, p=0.01) in the BN NX. Plasma CA were elevated in the BN NX (p<0.05) but not in BNK NX. Infusion of a specific FXIIa inhibitor into BN NX decreased MAP (-12 mmHg) and TPR (-0.5 Units) proportionally to baseline FXIIa (ΔMAP: r=-0.72, p=0.002; ΔTPR: r=-0.57, p=0.021), and plasma CA fell by 40-67% (all p<0.05). No such changes occurred in the BNK NX. In summary, a significant component of the hypertension of CRF can be attributed to FXIIa-induced vasoconstriction mediated via the KKS and stimulated CA release. In normal rats, FXIIa appears also to directly or indirectly decrease preload and heart rate.

The Severity of Renal Disease Scale (SORDS) was developed to provide a single score reflecting disease severity of renal patients independent of confounding psychosocial influences. This study examined SORDS' reliability and validity and its relevance as a research tool assessing the psychological effect of illness severity. Data was collected from 127 renal patients (predialysis, HD, CAPD). SORDS was compared with the Endstage Renal Disease Severity Index (ESRD-SI), the SF-36, the Beck Depression Inventory - 2nd Edition and a subset of BDI-II items reflecting cognitive features only at differing stages of renal disease and time on dialysis. SORDS and ESRD-SI data from twenty-two CAPD patients was included in reliability analyses. SORDS reliability estimates were low suggesting that the use of SORDS with medical chart data at this time is problematic. SORDS should be used only by medical practitioners who are aware of patients' standing on SORDS variables. There was however strong support for SORDS' validity. Validity was demonstrated by correlations between SORDS and the ESRD-SI. Compared to the ESRD-SI, SORDS was better able to discriminate between dialysis and pre-dialysis patients. SORDS and ESRD-SI scores were related to self-perceptions of decreased health status on the SF-36 independent of dialysis duration and age. SORDS utility in psychosocial research with renal patients was demonstrated by a finding that disease severity differentially impacts levels of depression for HD versus CAPD patients independent of age or dialysis duration. At the lowest level of illness severity as assessed by SORDS, CAPD patients scored in the moderate range of depression and were significantly more depressed than HD patients. Using the same analyses but with the ESRD-SI, no differences in level of depression were detected. These results imply a relationship between adjustment to treatment and illness severity. It is concluded that SORDS is a valid index of renal disease severity and that illness severity as assessed by SORDS may have an important role as a moderator variable in psychosocial research with renal patients. These results may have important implications for treatment assignment and psychosocial assessment and intervention of renal patients and their families.

Thesis (M.S.W.)--University of Hong Kong, 1982.

published_or_final_version / Nursing Studies / Master / Master of Nursing in Advanced Practice