The kidneys have vital functions to the organism, such as catabolites excretion, maintenance of salt and water concentrations, hormone production, and acid-basic regulation. Retention of nitrogen products of the protein catabolism occurs, with the severe loss of the renal function, a condition called azotemia. Uremia is understood as a condition resulting from prolonged azotemia and is considered an important cause of death in dogs. Aiming to determine the epidemiology, prevalence, and morphological characteristics (including the anatomic localization) of the extrarenal uremic lesions, as well as to determine the main lesions of the urinary system associated to the occurrence of uremia, the protocols of necropsies performed in dogs between January 1996 and December 2012 (17 years) at the Laboratório de Patologia Veterinária of the Universidade Federal de Santa Maria were analyzed. A total of 4,201 dogs were necropsied and 161 (3,8%) had extrarenal uremic lesions. Clinical signs associated to uremia were reported in 134 dogs (83,2%). The extrarenal lesions more often observed, in descending order of prevalence, were: ulcerative and hemorrhagic gastritis (56,5%), soft-tissue mineralization (55,9%), pulmonary edema (47,2%), ulcerative stomatitis and/or glossitis (30,4%), endocarditis/atrial and aortic thrombosis (28,6%), parathyroid hyperplasia (9,3%), fibrous osteodytrophy (8,1%), anemia (6,2%), ulcerative laryngitis (5%), ulcerative and hemorrhagic enteritis (3,7%), fibrinonecrotic esophagitis (1,9%), and fibrinous pericarditis (1,9%). In most of the cases, the extrarenal lesions of uremia were due to prolonged azotemia secondary to severe renal lesions, such as interstitial nephritis and glomerulonephritis (the most prevalent ones). / Os rins exercem funções vitais para o organismo como a excreção de resíduos, manutenção das concentrações de sal e água, produção de hormônios e regulação do equilíbrio ácido-básico. Com a redução severa da função renal, ocorre a retenção de produtos nitrogenados do catabolismo das proteínas, condição denominada de azotemia. A uremia pode ser entendida como uma condição resultante de azotemia prolongada e é uma importante causa de morte em cães. Com o objetivo de determinar a epidemiologia, a prevalência e as características morfológicas, incluindo a localização anatômica, das lesões extrarrenais de uremia, bem como determinar as principais lesões do sistema urinário associadas à ocorrência de uremia, foram revisados os protocolos de necropsias de cães realizadas no Laboratório de Patologia Veterinária da Universidade Federal de Santa Maria entre janeiro de 1996 e dezembro de 2012 (17 anos). Nesse período foram necropsiados um total de 4.201 cães, sendo que 161 (3,8% ) apresentaram lesões extrarrenais de uremia. Em 134 cães (83,2%) foram descritos sinais clínicos associados à uremia. As lesões extrarrenais mais frequentes, em ordem decrescente foram: a gastrite ulcerativa e hemorrágica (56,5%), mineralização de tecidos moles (55,9%), edema pulmonar (47,2%), estomatite e/ou glossite ulcerativa (30,4%), endocardite/trombose atrial e aórtica (28,6%), hiperplasia da paratireoide (9,3%), osteodistrofia fibrosa (8,1%), anemia (6,2%), laringite ulcerativa (5%), enterite ulcerativa/hemorrágica (3,7%), esofagite fibrinonecrótica (1,9%) e pericardite fibrinosa (1.9%). Na maioria dos casos, as lesões extrarrenais de uremia foram decorrentes de azotemia prolongada por lesões renais graves, sendo as mais prevalentes a nefrite intersticial e a glomerulonefrite.

Made available in DSpace on 2014-06-11T19:25:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-06-22Bitstream added on 2014-06-13T20:14:20Z : No. of bitstreams: 1 barbosa_ts_me_araca.pdf: 548631 bytes, checksum: f32592933503d19bda6a960ab1bf825c (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Embora a insuficiência renal ocorra com bastante freqüência na espécie canina, não se sabe se essa condição, a semelhança do que ocorre em humano, compromete o funcionamento dos poliformonucleares (PMN). O superóxido produzido pelo metabolismo oxidativo dos PMN exerce importante papel na resposta imune inata, destruído os patógenos fagocitados, entretanto, quando em excesso age de modo deletério promovendo a aceleração da apoptose. Testou-se a hipótese de que, a semelhança do que ocorrer em humanos, as toxinas presentes no soro de cães urêmicos alteram o metabolismo oxidativo e acelera a morte celular programada dos neutrófilos de cães normais. Para tal o sangue total e polimorfonucleares isolados de dez cães sadios foram incubados com soro urêmico. A produção de superóxido foi quantificada pelo teste de redução do tetrazólio nitroazul (NBT) e o índice apoptótico calculado pelo método morfométrico. A produção de superóxido gerada dos neutrófilos de sangue total tratados com soro urêmico apresentou significante redução (p < 0,05). Quando isolados e incubados com soro urêmico, apenas na metade das amostras os PMN apresentaram concomitantemente diminuição da produção de superóxido e aumento do índice apoptótico. Foi possível concluir que os componentes presentes no soro urêmico alteram ex vivo o metabolismo oxidativo e a apoptose dos PMN, fortalecendo a hipótese de que cães com de insuficiência renal têm sua imunidade inata comprometida. / Although kidney failure occurs frequently on canine species, it is unknown if this condition, being similar to what occurs in human beings, jeopardized the functioning of the polymorphonuclear (PMN). The superoxide produced by the oxidative metabolism of the PMN plays an important role in the immune inherent answer, having destroyed the pathogenic phagocytized. However, when in excess it acts in a deleterious way promoting the acceleration of apoptosis. It was tested by the hypothesis that, similar to what occurs in humans, the toxins present in the serum of uremic dogs alter the oxidative metabolism and accelerates the programmed cellular death of the neutrophis of normal dogs. For that, the total blood and polymorphonuclears isolated from ten healthy dogs were incubated with uremic serum. The production of superoxide was quantified by nitroblue tetrazolium reduction test (NBT) and the index apoptic was calculated by the morphometric method. The production of superoxide generated from the neutrophil of total blood treated with uremic serum presented significant reduction (P<0.05). When isolated and incubated with uremic serum, only on half of the sample the PMN presented concomitantly a reduction of production of superoxide and increase of apoptotic index. It was possible deduct that the components present in the uremic serum alter ex vivo the oxidative metabolism and the apoptosis of the PMN, consolidating the hypothesis that dogs having kidney failure have their inherent immunity jeopardized.

A uremia é uma desordem sistêmica que pode estar associada à disfunção plaquetária adquirida, levando a alterações na hemostasia primária. Vários modelos de interferência entre a uremia e a falha na hemostasia já foram propostos, porém o mecanismo exato é desconhecido, e a tendência ao sangramento parece ser de origem multifatorial. O teste do tempo de sangramento da mucosa oral (TSMO) pode ser utilizado na avaliação da hemostasia primária em animais. O fator de von Willebrand (FvW:Ag) normal ou aumentado, observado na maioria dos cães urêmicos, contribui para o diagnóstico de uma alteração plaquetária adquirida. A contagem de plaquetas e os testes de coagulação normais associados a um aumento no TSMO dão suporte à suspeita de um defeito qualitativo. O objetivo deste trabalho foi investigar possíveis anormalidades na hemostasia, buscando estabelecer uma relação entre os resultados de exames laboratoriais e alterações no tempo de sangramento. A hemostasia foi avaliada em quarenta cães azotêmicos, urêmicos ou não. O aumento no TSMO foi observado em 35% dos cães azotêmicos. O teste de Spearman demonstrou haver correlação entre o TSMO e os valores de creatinina, uréia e hematócrito, porém, o ajuste pela Regressão Linear Múltipla evidenciou o hematócrito como única variável associada com o TSMO. Valores de hematócrito abaixo do intervalo de referência para a espécie foram observados em 92,86% dos pacientes que apresentaram aumento no TSMO. Esses valores reduzidos parecem contribuir para a tendência ao sangramento, embora não possam ser considerados como fator determinante preditivo, uma vez que sua ocorrência nem sempre se associou com interferências no TSMO. / Uremia is a systemic disorder that may be associated with acquired platelet dysfunction, leading to changes in primary hemostasis. Several interference models between uremia and hemostasis failure have been proposed, but the exact mechanism is unknown, and bleeding tendencies seem to have a multifactorial origin. The buccal mucosal bleeding time (BMBT) test can be used in the assessment of primary hemostasis in animals. Normal or increased von Willebrand factor (vWF:Ag), observed in most uremic dogs, contributes to the diagnosis of an acquired platelet alteration. Normal platelet counts and coagulation tests associated with BMBT raises support the suspicion of a qualitative defect. The aim of this study was to investigate possible hemostasis abnormalities, trying to establish a relation between the results of laboratory tests and changes in bleeding times. Hemostasis was evaluated in forty azotemic dogs, uremic or not. Increase in BMBTs was observed in 35% of the azotemic dogs. Spearman’s test showed a correlation between BMBT and the values of creatinine, urea and hematocrit; however, adjusting for Multiple Linear Regression showed hematocrit as the only variable associated with BMBT. Hematocrit values below reference range for the species was observed in 92,86% of the patients showed an increase in BMBT. These low values appear to contribute to the tendency to bleed, although they cannot be considered as a preditive determining factor, since their occurrence is not always associated with interference in BMBT.

Made available in DSpace on 2014-06-11T19:23:46Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-02-25Bitstream added on 2014-06-13T19:30:23Z : No. of bitstreams: 1 galvao_alb_me_jabo.pdf: 779106 bytes, checksum: 2a6c1389b9e11842f7a627985c3a1d30 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / O objetivo do presente trabalho foi avaliar os efeitos da n-acetilcisteína (NAC) na função renal, na pressão arterial, no perfil hematológico, hepático e eletrolítico em cães saudáveis e com doença renal crônica. Quatro grupos de cães foram avaliados, grupo normal controle (N-C), grupo normal tratado (N-T), grupo doente renal crônico controle (DRC-C) e grupo doente renal crônico tratado (DRCT). Os grupos N-T e DRC-T foram submetidos ao tratamento com NAC (VO) na dose de 10mg/kg b.i.d, durante 60 dias. Nos grupos N-C e DRC-C não foi realizado qualquer tipo de tratamento. Hemograma, perfil renal, hepático, eletrolítico e pressão arterial sistólica (PAS) foram avaliados previamente, 15, 30, 45 e 60 dias após o tratamento com NAC. A NAC não exerceu qualquer efeito sobre a PAS e o perfil hepático, em nenhum dos grupos estudados (p>0,05). A concentração sérica de uréia e de creatinina do grupo DRC-C (93,42±17,28; 2,52±0,23mg/dL), foi significativamente maior, em relação ao N-C (20,44±3,43; 0,87±0,14mg/dL) e N-T (30,97±1,05; 1,09±0,05mg/dL) (p<0,05). O clereance creatinina do grupo DRC-C (1,13±0,07mL/min/kg) foi significativamente menor, relativamente ao N-C (2,29±0,13mL/min/kg) (p<0.05). O grupo DRC-T apresentou valor de excreção fracionada de sódio (1,19±0,29%) significativamente maior, comparativamente aos grupos N-C (0,25±0,03%) e N-T (0,30±0,08%) (p<0,05). A contagem de hemácias no grupo N-T (7,05±0,48x106/μL) foi significativamente superior, em relação ao grupo DRC-C (5,50±0,11x106/μL) (p<0,05). O grupo N-T apresentou hematócrito (49,44±3,13%) superior ao grupo DRC-C (38,73±1,02%) e DRC-T (43,46±1,42%) (p<0,05). A concentração sérica de sódio no grupo N-T (149±4,99mg/dL) foi superior, em relação ao N-C (141±1,32mg/dL) (p<0,05). / The present study aimed to evaluate the effects of n-acetylcysteine in dogs with chronic kidney disease. To this end, the animals were devided in four groups: healthy control group (H-C), healthy treated group (H-T), control chronic kidney disease (C-CKD), and treated chronic kidney disease (T-CKD). H-T and TCKD groups received 10mg/kg of NAC, PO, q 12h, during 60 days. H-C and TCKD did not receive any treatment. Cell blood count, kidney, hepatic, and electrolytic profile, and systolic blood pressure (SBP) were evaluated previously, 15, 30, 45, and 60 days after treatment with NAC. NAC did not exert any effect on SBP and hepatic profile, in any studied group (P > 0.05). Serum Urea and creatinine values in the group C-CKD (93.42±17.28; 2.52±0.23mg/dL) was significantly higher, in comparison to H-C (20,44±3,43; 0,87±0,14mg/dL) and H-T (30,97±1,05; 1,09±0,05mg/dL) (P < 0.05). Average creatinine clearance of C-CKD group (1.13±0.07 mL/min./kg) was significantly lower than H-C group (2.29±0.13mL/min./kg) (P < 0.05). Excretion fraction of sodium was significantly higher in group T-CKD (1.19±0.29%), than in H-C (0.25±0.03%) and H-T (0.30±0.08%) groups (P < 0.05). Erythrocytes count in the H-T (7.05±0.48x106/μL) increased significantly in comparison to C-CKD (5.50±0.11x106/μL) (P < 0.05). Average hematocrit values changed significantly in the H-T group (49.44±3.13%), when compared to C-CKD (38.73±1.02%) and T-CKD (43.46±1.42%) groups (P < 0.05). Serum sodium concentration in the group H-T (149±4.99mg/dL) increased significantly, when compared to H-C (141±1.32mg/dL) (P < 0.05).

Orientadora: Marileda Bonafim Carvalho / Banca: Luciane Helena Gargaglioni Batalhão / Banca: Angela Akamatsu / Resumo: O objetivo do presente trabalho foi avaliar os efeitos da n-acetilcisteína (NAC) na função renal, na pressão arterial, no perfil hematológico, hepático e eletrolítico em cães saudáveis e com doença renal crônica. Quatro grupos de cães foram avaliados, grupo normal controle (N-C), grupo normal tratado (N-T), grupo doente renal crônico controle (DRC-C) e grupo doente renal crônico tratado (DRCT). Os grupos N-T e DRC-T foram submetidos ao tratamento com NAC (VO) na dose de 10mg/kg b.i.d, durante 60 dias. Nos grupos N-C e DRC-C não foi realizado qualquer tipo de tratamento. Hemograma, perfil renal, hepático, eletrolítico e pressão arterial sistólica (PAS) foram avaliados previamente, 15, 30, 45 e 60 dias após o tratamento com NAC. A NAC não exerceu qualquer efeito sobre a PAS e o perfil hepático, em nenhum dos grupos estudados (p>0,05). A concentração sérica de uréia e de creatinina do grupo DRC-C (93,42±17,28; 2,52±0,23mg/dL), foi significativamente maior, em relação ao N-C (20,44±3,43; 0,87±0,14mg/dL) e N-T (30,97±1,05; 1,09±0,05mg/dL) (p<0,05). O clereance creatinina do grupo DRC-C (1,13±0,07mL/min/kg) foi significativamente menor, relativamente ao N-C (2,29±0,13mL/min/kg) (p<0.05). O grupo DRC-T apresentou valor de excreção fracionada de sódio (1,19±0,29%) significativamente maior, comparativamente aos grupos N-C (0,25±0,03%) e N-T (0,30±0,08%) (p<0,05). A contagem de hemácias no grupo N-T (7,05±0,48x106/μL) foi significativamente superior, em relação ao grupo DRC-C (5,50±0,11x106/μL) (p<0,05). O grupo N-T apresentou hematócrito (49,44±3,13%) superior ao grupo DRC-C (38,73±1,02%) e DRC-T (43,46±1,42%) (p<0,05). A concentração sérica de sódio no grupo N-T (149±4,99mg/dL) foi superior, em relação ao N-C (141±1,32mg/dL) (p<0,05). / Abstract: The present study aimed to evaluate the effects of n-acetylcysteine in dogs with chronic kidney disease. To this end, the animals were devided in four groups: healthy control group (H-C), healthy treated group (H-T), control chronic kidney disease (C-CKD), and treated chronic kidney disease (T-CKD). H-T and TCKD groups received 10mg/kg of NAC, PO, q 12h, during 60 days. H-C and TCKD did not receive any treatment. Cell blood count, kidney, hepatic, and electrolytic profile, and systolic blood pressure (SBP) were evaluated previously, 15, 30, 45, and 60 days after treatment with NAC. NAC did not exert any effect on SBP and hepatic profile, in any studied group (P > 0.05). Serum Urea and creatinine values in the group C-CKD (93.42±17.28; 2.52±0.23mg/dL) was significantly higher, in comparison to H-C (20,44±3,43; 0,87±0,14mg/dL) and H-T (30,97±1,05; 1,09±0,05mg/dL) (P < 0.05). Average creatinine clearance of C-CKD group (1.13±0.07 mL/min./kg) was significantly lower than H-C group (2.29±0.13mL/min./kg) (P < 0.05). Excretion fraction of sodium was significantly higher in group T-CKD (1.19±0.29%), than in H-C (0.25±0.03%) and H-T (0.30±0.08%) groups (P < 0.05). Erythrocytes count in the H-T (7.05±0.48x106/μL) increased significantly in comparison to C-CKD (5.50±0.11x106/μL) (P < 0.05). Average hematocrit values changed significantly in the H-T group (49.44±3.13%), when compared to C-CKD (38.73±1.02%) and T-CKD (43.46±1.42%) groups (P < 0.05). Serum sodium concentration in the group H-T (149±4.99mg/dL) increased significantly, when compared to H-C (141±1.32mg/dL) (P < 0.05). / Mestre

A uremia é uma desordem sistêmica que pode estar associada à disfunção plaquetária adquirida, levando a alterações na hemostasia primária. Vários modelos de interferência entre a uremia e a falha na hemostasia já foram propostos, porém o mecanismo exato é desconhecido, e a tendência ao sangramento parece ser de origem multifatorial. O teste do tempo de sangramento da mucosa oral (TSMO) pode ser utilizado na avaliação da hemostasia primária em animais. O fator de von Willebrand (FvW:Ag) normal ou aumentado, observado na maioria dos cães urêmicos, contribui para o diagnóstico de uma alteração plaquetária adquirida. A contagem de plaquetas e os testes de coagulação normais associados a um aumento no TSMO dão suporte à suspeita de um defeito qualitativo. O objetivo deste trabalho foi investigar possíveis anormalidades na hemostasia, buscando estabelecer uma relação entre os resultados de exames laboratoriais e alterações no tempo de sangramento. A hemostasia foi avaliada em quarenta cães azotêmicos, urêmicos ou não. O aumento no TSMO foi observado em 35% dos cães azotêmicos. O teste de Spearman demonstrou haver correlação entre o TSMO e os valores de creatinina, uréia e hematócrito, porém, o ajuste pela Regressão Linear Múltipla evidenciou o hematócrito como única variável associada com o TSMO. Valores de hematócrito abaixo do intervalo de referência para a espécie foram observados em 92,86% dos pacientes que apresentaram aumento no TSMO. Esses valores reduzidos parecem contribuir para a tendência ao sangramento, embora não possam ser considerados como fator determinante preditivo, uma vez que sua ocorrência nem sempre se associou com interferências no TSMO. / Uremia is a systemic disorder that may be associated with acquired platelet dysfunction, leading to changes in primary hemostasis. Several interference models between uremia and hemostasis failure have been proposed, but the exact mechanism is unknown, and bleeding tendencies seem to have a multifactorial origin. The buccal mucosal bleeding time (BMBT) test can be used in the assessment of primary hemostasis in animals. Normal or increased von Willebrand factor (vWF:Ag), observed in most uremic dogs, contributes to the diagnosis of an acquired platelet alteration. Normal platelet counts and coagulation tests associated with BMBT raises support the suspicion of a qualitative defect. The aim of this study was to investigate possible hemostasis abnormalities, trying to establish a relation between the results of laboratory tests and changes in bleeding times. Hemostasis was evaluated in forty azotemic dogs, uremic or not. Increase in BMBTs was observed in 35% of the azotemic dogs. Spearman’s test showed a correlation between BMBT and the values of creatinine, urea and hematocrit; however, adjusting for Multiple Linear Regression showed hematocrit as the only variable associated with BMBT. Hematocrit values below reference range for the species was observed in 92,86% of the patients showed an increase in BMBT. These low values appear to contribute to the tendency to bleed, although they cannot be considered as a preditive determining factor, since their occurrence is not always associated with interference in BMBT.

Call number: LD2668 .T4 1955 C68 / Master of Science

by Wing-cheung Pang. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1988. / Bibliography: leaves 45-56.

No description available.

Mortality from cardiovascular disease in patients on chronic hemodialysis (HD) is 10 to 20 times greater than in the general population. One major risk factor is renal dyslipidemia, characterised by an impaired catabolism of triglyceride (TG)-rich lipoproteins with accumulation of atherogenic remnant particles. A contributing factor may be derangement of the lipoprotein lipase (LPL) system, the major lipase in the catabolism of TG-rich lipoproteins. The functional pool of LPL is located at vascular surfaces, and is released by heparin into the circulating blood and extracted and degraded by the liver. Unfractionated heparin (UFH) is commonly used during dialysis to avoid clotting in the extracorporeal devices, but is increasingly replaced by various low molecular weight heparin (LMWH) preparations. Plasma LPL activity is usually lower after injection of LMWH which is therefore said to release less LPL and cause less disturbance of lipoprotein metabolism than UFH. However, animal studies have revealed that LMWH is as efficient as UFH in releasing LPL but is less efficient in retarding hepatic uptake. The aim of this study was to explore the effects of UFH and a LMWH (dalteparin) on LPL activity and TG concentrations in HD-patients compared with healthy controls, matched for age and gender. A disturbed LPL system might contribute to an impaired lipoprotein metabolism, and hence, an aggravated cardiovascular condition. An 8-hour primed infusion of UFH to controls gave rise to an initial peak of LPL activity within 30 minutes. The activity then dropped by almost 80% over the next two hours and levelled off to a plateau that corresponded to 15% of the peak level. When UFH was infused to HD-patients the curve for LPL activity resembled that for controls, but was reduced by 50% during the peak, while the plateau activities were comparable. The interpretation was that the functional pool, represented by the initial peak, was impaired in HD-patients, while the production of lipase molecules, reflected by the plateau, was only marginally reduced. During the peak of LPL activity TG decreased in both groups, but less in HD-patients, as was expected from the lower circulating lipase activity. During the plateau phase with low lipase activity, TG increased towards and beyond baseline values. When dalteparin was infused, the same pattern of plasma LPL activity was observed, although remarkably reduced. In controls the peak was only 30% and the subsequent plateau 40% compared with the activities during the UFH infusion. A bolus of UFH given when the LPL activity had levelled off to a plateau brought out about the same amount of activity, regardless of whether dalteparin or UFH had been infused. The conclusion was that both heparin preparations had reduced endothelial LPL to a similar extent, but that dalteparin less efficiently retarded the hepatic uptake of the enzyme. As a consequence to this, TG tended to reach higher levels after the dalteparin infusion. The LPL activities were further reduced in HD-patients during infusion with dalteparin, the peak was only 27% and the plateau 35% compared with the activities when UFH was infused. There was no decrease in TG, but rather a continuous increase, suggesting a profound depletion of functional LPL. In another study in HD-patients, two anticoagulation regimes based on present clinical practice were compared, and the doses were adjusted to the respective manufacturers recommendation. UFH was administered as a primed infusion, whereas dalteparin was given only as a single bolus pre-dialysis, not followed by an infusion. The results were in line with those in the experimental studies and indicate that also in the clinical setting LMWH interferes with the LPL system as least as much as an infusion of UFH does, and temporarily impairs lipolysis of TG. This interference might, in consequence, contribute to an aggravated cardiovascular condition in HD-patients.