Visão geral sobre a doença renal crônica em gatos e cães / Overview of chronic kidney disease in cats and dogs

A Doença Renal Crônica (DRC) é uma condição que afeta a capacidade dos rins de filtrar o sangue e eliminar substâncias tóxicas do organismo. É uma doença degenerativa e que progride para estágios avançados sem que os animais apresentem sinais claros ou visíveis inicialmente. A doença renal crônica pode afetar gatos e cães de todas as idades, porém sua prevalência aumenta com o avançar da idade.(AU)

Nasal mucosal mineralization, ulceration and epistaxis in a dog with uremia caused by chronic renal failure / Mineralização, ulceração e epistaxe em um cão com uremia causada por insuficiência renal crônica

Soft tissue mineralization and epithelial ulceration are common findings in dogs with uremia, being commonly reported in the gastrointestinal tract, lungs and pleura. This report described a case of nasal mucosal mineralization and ulceration contributing to recurrent epistaxis in a dog with chronic renal failure and uremia. A dog with recurrent epistaxis accompanied by elevated urea and creatinine was hospitalized. Platelet count and coagulation tests were within normal limits. Chronic renal failure was diagnosed, and the dog was euthanized. On necropsy, the kidneys were small, with an irregular capsular surface. The nasal conchae were slightly reddish. Histopathology revealed chronic glomerulonephritis, with gastric mineralization and bilateral parathyroid hyperplasia. Vascular and basal lamina mineralization, epithelial ulceration and hemorrhage were seen in the nasal conchae. The observed findings indicated that nasal mineralization and ulceration were caused by uremia. The severity of histopathological findings suggested that nasal mineralization/ulceration may have caused or at least contributed to epistaxis in this dog. We hope to stimulate further investigations into possible association between uremia, nasal mucosa mineralization/ulceration and epistaxis in dogs.

Mineralização dos tecidos moles e ulceração epitelial são achados comuns em cães com uremia, sendo geralmente observados no trato gastrointestinal, pulmões e pleura. O objetivo desse relato é reportar um caso de mineralização e ulceração da mucosa nasal contribuindo para epistaxe recorrente em um cão com insuficiência renal crônica e uremia. Um cão com epistaxe recorrente e aumento da ureia e creatinina foi hospitalizado. A contagem plaquetária e os testes de coagulação não tinham alterações. Foi diagnosticado insuficiência renal crônica, e o cão foi submetido a eutanásia. Na necropsia, o cão tinha os rins diminuídos, com superfície irregular. As conchas nasais estavam levemente avermelhadas. Histologicamente, foi diagnosticada uma glomerulonefrite crônica com mineralização gástrica e hiperplasia das paratireoides. As conchas nasais tinham mineralização da parede de vasos e membrana basal, úlceras e hemorragia. Os achados histopatológicos indicam que a mineralização e ulceração nasal foram causadas pela uremia. A severidade das lesões histológicas sugere que a mineralização/ulceração nasal pode ter causado, ou pelo menos contribuído, para a epistaxe deste cão. Espera-se, com esse relato, estimular futuros estudos que investiguem uma possível associação entre uremia, mineralização/ulceração nasal e epistaxe em cães.

Doença policística felina tratada com homeopatia: relato de caso / Feline polycystic disease treated withhomeopathy: case report

Foi avaliado o tratamento homeopático de um felino com doença renal policística, moléstia hereditária muito comum na espécie felina. Por ser progressiva, o prognóstico depende do estágio de evolução da doença renal crônica, da resposta do felino ao tratamento inicial e do desejo do tutor em dar continuidade ao tratamento. A observação teve duração de 9 (nove) meses e a avaliação dos resultados foi realizada com o emprego de exame clínico e de exames complementares como imagens ultrassonográficas e exames laboratoriais. A terapia foi composta por medicamento homeopático constitucional Phosphorus 30CH e episódico Kresolum 6CH associado à introdução de dieta renal (ração seca adjuvante). O medicamento homeopático não provocou eventos adversos no animal. Os resultados sugerem que um animal com doença policística felina pode ser tratado pela homeopatia.(AU)

The homeopathic treatment of a feline with polycystic kidney disease was evaluated, a common hereditary disease in the feline species. Because it is progressive, the prognosis depends on the stage of evolution of the chronic kidney disease, the feline response to the initial treatment and the guardian's desire to continue the treatment. The observation lasted 9 (nine) months and the evaluation of the results was performed through clinical examination and complementary tests such as ultrasound images and laboratory tests. The therapy was composed of constitutional Phosphorus 30CH and episodic Kresolum 6CH homeopathic medication associated with the introduction of diet kidney diet (adjunct dry feed). The homeopathic medicine did not cause adverse events in the animal. The results suggest that an animal with feline polycystic disease can be treated by homeopathy.(AU)

B-mode and Doppler ultrasound of bitches' kidneys with mammary neoplasia submitted to adjuvant chemotherapy / Ultrassonografia modo-B e Doppler dos rins de cadelas com neoplasias mamárias submetidas à quimioterapia adjuvante

Mammary neoplasia represents the most frequently diagnosed type of neoplasia in bitches. Although surgical removal is the procedure of choice for therapeutic management, chemotherapy protocols appear as important allies and adjuvants. Despite the great advances that have occurred in the field of cancer therapy, the systemic repercussions of these drugs still impose important limitations on their use. In this sense, the development of increasingly targeted therapeutic protocols and preventive monitoring of patients represent important strategies to avoid possible complications - among them, Acute Kidney Injury (AKI). Routinely, ultrasound evaluation is used to identify morphological or metastatic variations in abdominal cavity organs. Acting complementary to the B-mode evaluation, Doppler mapping proves to be efficient in recognizing alterations in vascular hemodynamics. Therefore, the objective of the present study was to evaluate the use of B-mode and Doppler ultrasound to identify renal morphological and hemodynamic alterations in bitches with mammary neoplasia submitted to adjuvant chemotherapy protocols that associate gemcitabine with carboplatin. Thirteen bitches were included, without distinction of breed and between seven and 13 years of age. The animals were evaluated ultrasonographically at two different times during three consecutive chemotherapy cycles: before (T0) and one and a half hours after each cycle (T1), for 42 days. No morphological changes were observed in B-mode throughout the chemotherapy protocol. However, the Doppler velocimetry indices demonstrated statistical differences before (T0) and after (T1) the administration of the drugs. It was concluded that Doppler ultrasound could be used as a complementary method for monitoring the renal response of patients exposed to nephrotoxic drugs and potentially causing renal injury.

As neoplasias mamárias representam o tipo de neoplasma mais frequentemente diagnosticado em fêmeas da espécie canina. Embora a remoção cirúrgica seja o procedimento de eleição para a conduta terapêutica, os protocolos quimioterápicos aparecem como importantes aliados e adjuvantes. Apesar dos grandes avanços ocorridos na área da terapia oncológica, as repercussões sistêmicas destes fármacos ainda impõem importantes limitações ao seu uso. Neste sentido, o desenvolvimento de protocolos terapêuticos cada vez mais direcionados e o monitoramento preventivo dos pacientes representam estratégias importantes para evitar possíveis complicações - dentre elas, a injúria renal aguda (IRA). Rotineiramente, a avaliação ultrassonográfica é utilizada para identificação de variações morfológicas ou metastáticas em órgãos da cavidade abdominal. Atuando de forma complementar à avaliação em modo-B, o mapeamento Doppler mostra-se eficiente no reconhecimento de alterações na hemodinâmica vascular. Portanto, o objetivo do presente estudo foi avaliar a utilização da ultrassonografia modo-B e Doppler como método para identificação de alterações morfológicas e hemodinâmicas renais em cadelas com neoplasias mamárias submetidas a protocolos quimioterápicos adjuvantes que associam a gencitabina à carboplatina. Foram incluídas 13 fêmeas caninas, sem distinção quanto a raça e com idades entre sete e 13 anos. Os animais foram avaliados ultrassonograficamente em dois momentos distintos durante três ciclos quimioterápicos consecutivos: antes (T0) e uma hora e meia após a realização de cada ciclo (T1), totalizando 42 dias. Não foram observadas alterações morfológicas em modo-B ao longo do protocolo quimioterápico. Entretanto, os índices dopplervelocimétricos demonstraram diferenças estatísticas antes (T0) e após (T1) a administração dos fármacos. Concluiu-se que a ultrassonografia Doppler pode ser utilizada como método complementar para o monitoramento da resposta renal de pacientes expostos a fármacos nefrotóxicos e potencialmente causadores de injúrias renais.

Puerarin alleviated oxidative stress and ferroptosis during renal fibrosis induced by ischemia/reperfusion injury via TLR4/Nox4 pathway in rats

Purpose: To investigate the role of puerarin on renal fibrosis and the underlying mechanism in renal ischemia and reperfusion (I/R) model. Methods: Rats were intraperitoneally injected with puerarin (50 or 100 mg/kg) per day for one week before renal I/R. The level of renal collagen deposition and interstitial fibrosis were observed by hematoxylin and eosin and Sirius Red staining, and the expression of α-smooth muscle actin (α-SMA) was examined by immunohistochemical staining. The ferroptosis related factors and TLR4/Nox4-pathway-associated proteins were detected by Western blotting. Results: Puerarin was observed to alleviate renal collagen deposition, interstitial fibrosis and the α-SMA expression induced by I/R. Superoxide dismutase (SOD) activities and glutathione (GSH) level were decreased in I/R and hypoxia/reoxygenation (H/R), whereas malondialdehyde (MDA) and Fe2+ level increased. However, puerarin reversed SOD, MDA, GSH and Fe2+ level changes induced by I/R and H/R. Besides, Western blot indicated that puerarin inhibited the expression of ferroptosis related factors in a dose-dependent manner, which further demonstrated that puerarin had the effect to attenuate ferroptosis. Moreover, the increased expression of TLR/Nox4-pathway-associated proteins were observed in I/R and H/R group, but puerarin alleviated the elevated TLR/Nox4 expression. Conclusions: Our results suggested that puerarin inhibited oxidative stress and ferroptosis induced by I/R and, thus, delayed the progression of renal fibrosis, providing a new target for the treatment of renal fibrosis.

Doxorubicin nephrotoxicity in cats (Felis catus) with malignant mammary neoplasms / Nefrotoxicidade da doxorrubicina em gatas (Felis catus) com neoplasias mamárias malignas

The aim of the study was to investigate the nephrotoxicity of doxorubicin in cats with malignant neoplasms of the mammary gland. All selected cats did not present comorbidities such as nephropathies and/or cardiomyopathies, confirmed by physical and laboratory tests, underwent radical mastectomy associated with regional lymph node excision and were treated with a protocol based on doxorubicin. Renal markers of urea, creatinine, symmetrical dimethylarginine were evaluated during all the treatment, and two months after the end. Abdominal ultrasound, urinalysis and biochemical analysis of protein, urinary creatinine and urinary GGT were performed in the beginning and two months after the end of the treatment, to evaluate possible renal alterations. Six cats did not present renal alterations in any exams performed during the study. Two cats presented azotemia during this study, and one of them stopped the treatment early, because of the intense azotemia. Clinical imaging and laboratory monitoring of patients throughout the treatment is essential, including the measurement of analytes that detect kidney changes early. Thus, it is emphasized that doxorubicin is a safe drug for use in non-nephropathic cats.

O objetivo do estudo foi investigar a nefrotoxicidade da doxorrubicina em gatas com neoplasias malignas da glândula mamária. Todas as gatas selecionadas não apresentaram comorbidades como nefropatias e/ou cardiomiopatias, comprovadas por exames físicos e laboratoriais, foram submetidas à mastectomia radical associada à exérese de linfonodos regionais e tratadas com protocolo baseado em doxorrubicina. Os marcadores renais ureia, creatinina, dimetilarginina simétrica foram avaliados durante todo o tratamento e dois meses após o término. Ultrassonografia abdominal, urinálise e análise bioquímica de proteínas, creatinina urinária e GGT urinária foram realizadas no início e dois meses após o término do tratamento, para avaliar possíveis alterações renais. Seis gatas não apresentaram alterações renais em nenhum dos exames realizados durante o estudo. Duas gatas apresentaram azotemia durante este estudo, e uma delas interrompeu o tratamento precocemente, devido à intensa azotemia. A individualidade de cada paciente deve ser sempre considerada, pois são muitas as variáveis. O monitoramento clínico, com exames complementares, tais como bioquímicos séricos e de imagem dos pacientes durante todo o tratamento, é essencial, especialmente a mensuração de analitos que detectam alterações renais precocemente. Diante disso, ressalta-se que a doxorrubicina é um medicamento seguro para utilização em gatas não nefropatas.

Distúrbios hidroeletrolíticos no hipoadrenocorticismo primário agudo em cães: Uma revisão / Hydroelectrolytic disorders in acute primary hypoadrenocorticism in dogs: A review

O hipoadrenocorticismo canino é uma endocrinopatia caracterizada, na sua forma mais comum, pela deficiência de glicocorticoides e mineralocorticoides. Pacientes não tratados podem desenvolver a forma aguda da doença (crise addisoniana), apresentação grave com risco de óbito, caso não sejam realizadas as intervenções adequadas. Entre as alterações apresentadas estão: distúrbios eletrolíticos (como hiponatremia, hipercalemia, hiperfosfatemia e hipercalcemia), desequilíbrio hídrico (desidratação e choque hipovolêmico) e acidobásico. Fluidoterapia intravenosa adequada é a base do manejo inicial da crise addisoniana, que irá reestabelecer o volume intravascular e hidratação, reduzindo a concentração sérica de fósforo e potássio, a acidose lática, a azotemia pré-renal e a acidose metabólica. A reposição de glicocorticoides também contribui para a normalização dessas alterações. Entre as possíveis complicações do tratamento está a mielinólise pontina, decorrente de aumento rápido na concentração sérica de sódio. Diante disso, o conhecimento dos distúrbios associados à essa endocrinopatia auxilia na suspeição e manejo adequado da doença.(AU)

Canine hypoadrenocorticism is an endocrinopathy characterized, in its most common form, by glucocorticoid and mineralocorticoid deficiency, often resulting from immune-mediated destruction of the adrenal glands. Untreated patients may develop the acute form of the disease (Addisonian crisis), a severe presentation with a risk of death if appropriate interventions are not performed. Among the changes presented are: electrolyte disorders (such as hyponatremia, hyperkalemia, hyperphosphatemia and hypercalcemia), water imbalance (dehydration and hypovolemic shock) and acid-base disorder. Adequate intravenous fluid therapy is the basis for the initial management of Addisonian crisis, which will restore intravascular volume and hydration, reducing serum phosphorus and potassium concentrations, lactic acidosis, pre-renal azotemia and metabolic acidosis. Glucocorticoid replacement also contributes to the normalization of these changes. Among the possible complications of the treatment is pontine myelinolysis, resulting from a rapid increase in serum sodium concentration. In view of this, knowledge of the disorders associated with this endocrinopathy helps in the suspicion and adequate management of the disease.(AU)

Gota úrica visceral em pato-do-mato (Cairina moschata) / Visceral uric gout in muscovy duck (Cairina moschata)

Background: Gout, a metabolic disease affecting multiple species, is frequent in birds which are uricotelic animals. It is primarily caused by hyperuricemia originating from birds' renal disorders with subsequent deposition of urate crystals into tissue. The location of the crystals determines the type of disease. Joint disease occurs with deposition inside and around joints, joint capsules, and tandine hems, while visceral disease occurs when the serous surface of visceral organs (mainly pericardium, liver, kidneys, air sacs, peritoneum, and spleen) are affected. This report describes a case of visceral uric gout in a Muscovy duck, which is rare. Case: An adult, male, Muscovy duck (Cairina moschata), kept under human care in a zoo, was referred to a veterinary clinic. The animal presented suddenly with prostration, ataxia, and anorexia, and died the following day. The body was sent to the Pathology Sector of Ritter dos Reis University Center (UniRitter) for a necropsy. During the necropsy, it was observed that white membranes, presenting a "chalk dust" appearance, were deposited under the serous layer of organs including the liver, kidneys, and pericardium. Following the necropsy and macroscopic evaluations, fragments of multiple organs were fixed in 10% formalin and processed routinely with hematoxylin and eosin (HE) staining for histopathological evaluation in an analysis laboratory in Porto Alegre city. A deposition of amorphous eosinophilic material was identified in the intestine, liver (serous), kidneys, lungs, and heart (epicardium) with findings of serositis, nephritis, and fibrinous epicarditis. The liver parenchyma and lungs had areas of congestion. There was both moderate and intense hepatocellular degeneration as well as degeneration in the renal tubular cells. These macro and microscopic changes were compatible with urate crystal deposition which represents visceral uric gout. Discussion: As opposed to free-living birds, birds in captivity have easy access to food and are sedentary. These factors, together with inadequate food management, make nutritional disorders the main predisposing cause of uric gout in these animals. Since it was not possible to determine the causative factors of this individual animal's disease due to the absence of examinations while alive, a nutritional origin of this animal's demise was considered. According to prior reports, an important cause of avian disease can be attributed directly or indirectly to kidney dysfunction. In addition to a deposition of amorphous material in the renal cortex, this Muscovy duck had areas of tubular cell degeneration and proliferation of fibrous connective tissue. However, it was not possible to establish a cause and effect relationship between the renal damage and the uric gout. Despite being common in birds under human care, the disease still is challenging for veterinarians, since the diagnosis is often late and treatment is often ineffective. The absence of documentation of this disease in the Muscovy duck contributes to the difficulty in establishing predisposing factors and a distinct disease etiology. This highlights the importance of the present report and the need for new studies. To the best of our knowledge, this is the first report of visceral uric gout in a Muscovy duck (Cairina moschata). This highlights the importance of necroscopic examinations and the impact they can have in the clinical arena, especially in wild animals.

Thalassemia, a human blood disorder

Abstract A group of inherited blood defects is known as Thalassemia is among the worlds most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning and globin proteins, respectively. In some cases, one of these proteins may be completely absent. and globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, globin proteins partner with globin and are later replaced by globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Resumo Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina e formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas globina se associam à globina e, posteriormente, são substituídas pela proteína globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, já que os cientistas ainda não conseguiram encontrar uma cura permanente para essa doença mortal depois de mais de 87 anos desde que foi descrita pela primeira vez em 1925.

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, [...].

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.(AU)

Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, [...].(AU)

Hipertensão situacional em cães dóceis adultos / Situational hypertension in docile adult dogs

A hipertensão arterial sistêmica (HAS) é uma enfermidade silenciosa que pode afetar gatos e cães. Embora bastante descrita em felinos, a "Síndrome do Jaleco Branco", ou hipertensão situacional, é pouco relatada em cães. Assim, este trabalho tem como objetivo mostrar a importância do estresse na aferição da pressão arterial de cães adultos. O estudo foi realizado com 46 cães de ambos os sexos, dóceis, adultos, e aparentemente saudáveis. Após anamnese, exame físico, ambientação e manejo amigável dos animais, mensurou-se a pressão arterial sistólica (PAS) pelo método Doppler no membro torácico. Foram feitas várias aferições para obtenção de média aritmética. Animais com até 160mmHg de PAS, na primeira aferição, foram considerados normotensos (36 cães, correspondente a 78,26%). Para os que tiveram PAS maior ou igual a 160mmHg (dez cães, equivalente a 21,74%), realizou-se um segundo momento de aferição, após 15 a 30 minutos, com os animais em repouso. Assim, seis desses cães apresentaram PAS entre 154mmHg e 200mmHg, sendo, então, um considerado pré-hipertenso e cinco hipertensos, e outros quatro considerados normotensos. Para o animal com pré-hipertensão e para os hipertensos, realizaram-se exames complementares, pelos quais quatro cães foram diagnosticados com doença renal crônica e dois com dislipidemia familiar dos Schnauzers. Dessa forma, pode-se concluir que, dos 46 cães avaliados, 36 apresentaram-se normotensos (78,26%), um pré-hipertenso (2,17%), cinco hipertensos (10,87%) e quatro com hipertensão situacional (8,7%). Portanto, para cães em ambiente hospitalar, é importante realizar um manejo amigável e, quando necessário, mais de um momento de aferição de PAS para evitar diagnósticos errôneos de HAS.

Systemic arterial hypertension (SAH) is a silent disease that can affect cats and dogs. Although well described in felines, "white coat syndrome", or situational hypertension, is little reported in dogs. Thus, this paper aims to show the importance of stress in the measurement of blood pressure from adult dogs. The study was conducted with 46 dogs of both sexes, docile, adults, apparently healthy. After anamnesis, physical examination, ambiance, and friendly management of animals, systolic blood pressure (SBP) was measured by the doppler method in the thoracic limb. Several measurements were made to obtain an arithmetic average. Animals up to 160mmHg of SBP, in the first measurement, were considered normotensive (36 dogs, corresponding to 78.26%). For those with SBP higher than or equal to 160mmHg (10 dogs, equivalent to 21.74%), a second measurement was performed after 15 to 30 minutes, with the animals at rest. Therefore, six of these dogs presented SBP between 154mmHg and 200mmHg (one considered prehypertense and five hypertensives) and four normotensives. For the animal with prehypertension and the hypertensives, complementary examinations were performed, in which four dogs were diagnosed with chronic kidney disease and two with family dyslipidemia of the Schnauzers. Thus, it can be concluded that among the 46 dogs evaluated, there were 36 normotenses (78.26%), a one prehypertense (2.17%), five hypertensives (10.87%), and four with situational hypertension (8.7%). Therefore, regarding dogs in a hospital environment, it is important to perform friendly management and, when necessary, more than one moment of SBP measurement to avoid erroneous diagnoses of SAH.

Urethral obstruction due to seminal vesiculitis in a sheep: case report / Obstrução uretral por vesiculite seminal em ovino: relato de caso

We report a case of urethral obstruction due to seminal vesiculitis in a Dorper sheep, with symptoms of anuria, rectal prolapse, orchitis/epididymitis, and uroperitoneum and biochemical tests indicating severe azotemia. The animal died due to advanced azotemia, and necropsy revealed kidneys with cortical and medullary necrosis, pyelonephritis of renal calyces, hydronephrosis, ruptured and necrotic bladder, and vesicular, bulbourethral, and ampoule accessory sex glands. There was prostate hyperplasia that revealed a large amount of pus in the cross section, which was also observed bilaterally in the epididymis and right testis. Morphotintorial and biochemical analyses of bacteria obtained from microbiological culture revealed Corynebacterium sp. and Escherichia coli. Infection, hyperplasia, and abscessation of accessory sex glands caused urethral compression, resulting in an obstructive condition, similar to urolithiasis, in addition to bacteremia. Hyperplastic seminal vesiculitis, although rare, must be included among the differential diagnoses of obstructive processes in the urinary tract of sheep.

Relata-se um caso de obstrução uretral decorrente de vesiculite seminal em carneiro da raça Dorper, com quadro de anúria, prolapso retal, orquite/epididimite e uroperitôneo, com exames bioquímicos indicativos de severa azotemia. Devido ao quadro avançado de azotemia, o animal faleceu e, na necropsia, foi observado:: rins com necrose de cortical e medular, pielonefrite dos cálices renais e hidronefrose, bexiga rompida e necrosada, assim como glândulas sexuais acessórias vesiculares, bulbouretrais e ampola. Havia hiperplasia de próstata que, ao corte transversal, revelou grande quantidade de pus, que também foi observado bilateralmente no epidídimo e no testículo direito. As análises morfotintoriais e bioquímicas das bactérias obtidas a partir do cultivo microbiológico foram compatíveis com Corynebacterium sp. e Escherichia coli. A infecção, a hiperplasia e a abscedação das glândulas sexuais acessória, causaram compressão uretral, levando a um quadro obstrutivo, semelhante à urolitíase, somado à bacteremia. A vesiculite seminal hiperplásica, apesar de rara, deve ser incluída entre os diagnósticos diferenciais dos processos obstrutivos do trato urinário de carneiros.

Toxicological effects of thimerosal on rat kidney: a histological and biochemical study / Efeitos toxicológicos do timerosal no rim de rato: um estudo histológico e bioquímico

Thimerosal is an organomercurial compound, which is used in the preparation of intramuscular immunoglobulin, antivenoms, tattoo inks, skin test antigens, nasal products, ophthalmic drops, and vaccines as a preservative. In most of animal species and humans, the kidney is one of the main sites for mercurial compounds deposition and target organs for toxicity. So, the current research was intended to assess the thimerosal induced nephrotoxicity in male rats. Twenty-four adult male albino rats were categorized into four groups. The first group was a control group. Rats of Group-II, Group-III, and Group-IV were administered with 0.5µg/kg, 10µg/kg, and 50µg/kg of thimerosal once a day, respectively. Thimerosal administration significantly decreased the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione reductase (GR), glutathione (GSH), and protein content while increased the thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) levels dose-dependently. Blood urea nitrogen (BUN), creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, urinary albumin and creatinine clearance was reduced dose-dependently in thimerosal treated groups. The results demonstrated that thimerosal significantly increased the inflammation indicators including nuclear factor kappaB (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activities, DNA and histopathological damages dose-dependently. So, the present findings ascertained that thimerosal exerted nephrotoxicity in male albino rats.

O timerosal é um composto organomercurial, utilizado na preparação de imunoglobulina intramuscular, antivenenos, tintas de tatuagem, antígenos de teste cutâneo, produtos nasais, gotas oftálmicas e vacinas como conservante. Na maioria das espécies animais e nos humanos, o rim é um dos principais locais de deposição de compostos de mercúrio e órgãos-alvo de toxicidade. Assim, a presente pesquisa teve como objetivo avaliar a nefrotoxicidade induzida pelo timerosal em ratos machos. Vinte e quatro ratos albinos machos adultos foram categorizados em quatro grupos. O primeiro grupo era um grupo de controle. Ratos do Grupo II, Grupo III e Grupo IV receberam 0,5µg / kg, 10µg / kg e 50µg / kg de timerosal uma vez ao dia, respectivamente. A administração de timerosal diminuiu significativamente as atividades de catalase (CAT), superóxido dismutase (SOD), peroxidase (POD), glutationa redutase (GR), glutationa (GSH) e conteúdo de proteína, enquanto aumentou as substâncias reativas ao ácido tiobarbitúrico (TBARS) e peróxido de hidrogênio (H2O2) níveis dependentes da dose. Os níveis de nitrogênio ureico no sangue (BUN), creatinina, urobilinogênio, proteínas urinárias, molécula de lesão renal-1 (KIM-1) e lipocalina associada à gelatinase de neutrófilos (NGAL) aumentaram substancialmente. Em contraste, a albumina urinária e a depuração da creatinina foram reduzidas de forma dependente da dose nos grupos tratados com timerosal. Os resultados demonstraram que o timerosal aumentou significativamente os indicadores de inflamação, incluindo fator nuclear kappaB (NF-κB), fator de necrose tumoral-α (TNF-α), interleucina-1β (IL-1β), níveis de interleucina-6 (IL-6) e atividades da ciclooxigenase-2 (COX-2), DNA e danos histopatológicos dependentes da dose. Portanto, os presentes achados verificaram que o timerosal exerceu nefrotoxicidade em ratos albinos machos.

Toxicological effects of thimerosal on rat kidney: a histological and biochemical study / Efeitos toxicológicos do timerosal no rim de rato: um estudo histológico e bioquímico

Thimerosal is an organomercurial compound, which is used in the preparation of intramuscular immunoglobulin, antivenoms, tattoo inks, skin test antigens, nasal products, ophthalmic drops, and vaccines as a preservative. In most of animal species and humans, the kidney is one of the main sites for mercurial compounds deposition and target organs for toxicity. So, the current research was intended to assess the thimerosal induced nephrotoxicity in male rats. Twenty-four adult male albino rats were categorized into four groups. The first group was a control group. Rats of Group-II, Group-III, and Group-IV were administered with 0.5µg/kg, 10µg/kg, and 50µg/kg of thimerosal once a day, respectively. Thimerosal administration significantly decreased the activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), glutathione reductase (GR), glutathione (GSH), and protein content while increased the thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) levels dose-dependently. Blood urea nitrogen (BUN), creatinine, urobilinogen, urinary proteins, kidney injury molecule-1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels were substantially increased. In contrast, urinary albumin and creatinine clearance was reduced dose-dependently in thimerosal treated groups. The results demonstrated that thimerosal significantly increased the inflammation indicators including nuclear factor kappaB (NF-κB), tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6) levels and cyclooxygenase-2 (COX-2) activities, DNA and histopathological damages dose-dependently. So, the present findings ascertained that thimerosal exerted nephrotoxicity in male albino rats.(AU)

O timerosal é um composto organomercurial, utilizado na preparação de imunoglobulina intramuscular, antivenenos, tintas de tatuagem, antígenos de teste cutâneo, produtos nasais, gotas oftálmicas e vacinas como conservante. Na maioria das espécies animais e nos humanos, o rim é um dos principais locais de deposição de compostos de mercúrio e órgãos-alvo de toxicidade. Assim, a presente pesquisa teve como objetivo avaliar a nefrotoxicidade induzida pelo timerosal em ratos machos. Vinte e quatro ratos albinos machos adultos foram categorizados em quatro grupos. O primeiro grupo era um grupo de controle. Ratos do Grupo II, Grupo III e Grupo IV receberam 0,5µg / kg, 10µg / kg e 50µg / kg de timerosal uma vez ao dia, respectivamente. A administração de timerosal diminuiu significativamente as atividades de catalase (CAT), superóxido dismutase (SOD), peroxidase (POD), glutationa redutase (GR), glutationa (GSH) e conteúdo de proteína, enquanto aumentou as substâncias reativas ao ácido tiobarbitúrico (TBARS) e peróxido de hidrogênio (H2O2) níveis dependentes da dose. Os níveis de nitrogênio ureico no sangue (BUN), creatinina, urobilinogênio, proteínas urinárias, molécula de lesão renal-1 (KIM-1) e lipocalina associada à gelatinase de neutrófilos (NGAL) aumentaram substancialmente. Em contraste, a albumina urinária e a depuração da creatinina foram reduzidas de forma dependente da dose nos grupos tratados com timerosal. Os resultados demonstraram que o timerosal aumentou significativamente os indicadores de inflamação, incluindo fator nuclear kappaB (NF-κB), fator de necrose tumoral-α (TNF-α), interleucina-1β (IL-1β), níveis de interleucina-6 (IL-6) e atividades da ciclooxigenase-2 (COX-2), DNA e danos histopatológicos dependentes da dose. Portanto, os presentes achados verificaram que o timerosal exerceu nefrotoxicidade em ratos albinos machos.(AU)

Amelioration of exosome and mesenchymal stem cells in rats infected with diabetic nephropathy by attenuating early markers and aquaporin-1 expression / Melhoria das células-tronco exossomais e mesenquimais em ratos infectados com nefropatia diabética atenuando marcadores precoces e expressão de aquaporina-1

Diabetic nephropathy (DN) is a prevalent diabetic microvascular condition. It is the leading cause of kidney disease in the advanced stages. There is no currently effective treatment available. This research aimed to investigate the curative potentials of exosomes isolated from mesenchymal stem cells affecting DN. This study was performed on 70 male adult albino rats. Adult rats were randomized into seven groups: Group I: Negative control group, Group II: DN group, Group III: Balanites treated group, Group IV: MSCs treated group, Group V: Exosome treated group, Group VI: Balanites + MSCs treated group and Group VII: Balanites + exosome treated group. Following the trial period, blood and renal tissues were subjected to biochemical, gene expression analyses, and histopathological examinations. Results showed that MDA was substantially increased, whereas TAC was significantly decreased in the kidney in the DN group compared to normal health rats. Undesired elevated values of MDA levels and a decrease in TAC were substantially ameliorated in groups co-administered Balanites aegyptiacae with MSCs or exosomes compared to the DN group. A substantial elevation in TNF-α and substantially diminished concentration of IGF-1 were noticed in DN rats compared to normal health rats. Compared to the DN group, the co-administration of Balanites aegyptiacae with MSCs or exosomes substantially improved the undesirable elevated values of TNF-α and IGF-1. Furthermore, in the DN group, the mRNA expression of Vanin-1, Nephrin, and collagen IV was significantly higher than in normal healthy rats. Compared with DN rats, Vanin-1, Nephrin, and collagen IV Upregulation were substantially reduced in groups co-administered Balanites aegyptiacae with MSCs or exosomes. In DN rats, AQP1 expression was significantly lower than in normal healthy rats. Furthermore, the groups co-administered Balanites aegyptiacae with MSCs or exosomes demonstrated a substantial increase in AQP1 mRNA expression compared to DN rats.

A nefropatia diabética (ND) é uma condição microvascular diabética prevalente. É a principal causa de doença renal em estágios avançados. Atualmente, não há tratamento eficaz disponível. Esta pesquisa teve como objetivo investigar os potenciais curativos de exossomos isolados de células-tronco mesenquimais que afetam a ND. Este estudo foi realizado em 70 ratos albinos adultos machos. Ratos adultos foram randomizados em sete grupos: Grupo I: Grupo de controle negativo, Grupo II: Grupo DN, Grupo III: Grupo tratado com Balanites, Grupo IV: Grupo tratado com MSCs, Grupo V: Grupo tratado com exossomos, Grupo VI: Grupo tratado com Balanites + MSCs e Grupo VII: Balanites + grupo tratado com exossomas. Após o período experimental, o sangue e os tecidos renais foram submetidos a análises bioquímicas, de expressão gênica e exames histopatológicos. Os resultados mostraram que o MDA aumentou substancialmente, enquanto o TAC diminuiu significativamente no rim no grupo DN em comparação com ratos saudáveis normais. Valores elevados indesejados de níveis de MDA e uma diminuição no TAC foram substancialmente melhorados em grupos coadministrados Balanites aegyptiacae com MSCs ou exossomas em comparação com o grupo DN. Uma elevação substancial em TNF-α e uma concentração substancialmente diminuída de IGF-1 foram observadas em ratos DN em comparação com ratos saudáveis normais. Em comparação com o grupo DN, a coadministração de Balanites aegyptiacae com MSCs ou exossomas melhorou substancialmente os valores elevados indesejáveis de TNF-α e IGF-1. Além disso, no grupo DN a expressão de mRNA de vanina-1, nefrina e colágeno IV foi significativamente maior do que em ratos saudáveis normais. Comparado com ratos DN, Vanin-1, Nephrin e colágeno IV Upregulation foram substancialmente reduzidos em grupos co-administrados Balanites aegyptiacae com MSCs ou exossomos. Em ratos DN, a expressão de AQP1 foi significativamente menor do que em ratos saudáveis normais. Além disso, os grupos que coadministraram Balanites aegyptiacae com MSCs ou exossomos demonstraram um aumento substancial na expressão de mRNA de AQP1 em comparação com ratos DN.

Thalassemia, a human blood disorder / Talassemia, uma doença do sangue humano

Abstract A group of inherited blood defects is known as Thalassemia is among the world's most prevalent hemoglobinopathies. Thalassemias are of two types such as Alpha and Beta Thalassemia. The cause of these defects is gene mutations leading to low levels and/or malfunctioning α and β globin proteins, respectively. In some cases, one of these proteins may be completely absent. α and β globin chains form a globin fold or pocket for heme (Fe++) attachment to carry oxygen. Genes for alpha and beta-globin proteins are present in the form of a cluster on chromosome 16 and 11, respectively. Different globin genes are used at different stages in the life course. During embryonic and fetal developmental stages, γ globin proteins partner with α globin and are later replaced by β globin protein. Globin chain imbalances result in hemolysis and impede erythropoiesis. Individuals showing mild symptoms include carriers of alpha thalassemia or the people bearing alpha or beta-thalassemia trait. Alpha thalassemia causes conditions like hemolytic anemia or fatal hydrops fetalis depending upon the severity of the disease. Beta thalassemia major results in hemolytic anemia, growth retardation, and skeletal aberrations in early childhood. Children affected by this disorder need regular blood transfusions throughout their lives. Patients that depend on blood transfusion usually develop iron overload that causes other complications in the body systems like renal or hepatic impairment therefore, thalassemias are now categorized as a syndrome. The only cure for Thalassemias would be a bone marrow transplant, or gene therapy with currently no significant success rate. A thorough understanding of the molecular basis of this syndrome may provide novel insights and ideas for its treatment, as scientists have still been unable to find a permanent cure for this deadly disease after more than 87 years since it is first described in 1925.

Resumo Um grupo de defeitos sanguíneos hereditários é conhecido como talassemia e está entre as hemoglobinopatias mais prevalentes do mundo. As talassemias são de dois tipos, como talassemia alfa e beta. As causas desses defeitos são as mutações genéticas que levam a níveis baixos e/ou proteínas de globina com mau funcionamento, respectivamente. Em alguns casos, uma dessas proteínas pode estar completamente ausente. As cadeias de globina α e β formam uma dobra ou bolsa de globina para a fixação de heme (Fe ++) para transportar oxigênio. Os genes das proteínas alfa e beta globina estão presentes na forma de um cluster nos cromossomos 16 e 11, respectivamente. Diferentes genes de globina são usados ​​em diferentes estágios do curso de vida. Durante os estágios de desenvolvimento embrionário e fetal, as proteínas γ globina se associam à α globina e, posteriormente, são substituídas pela proteína β globina. Os desequilíbrios da cadeia de globina resultam em hemólise e impedem a eritropoiese. Indivíduos que apresentam sintomas leves incluem portadores de talassemia alfa ou as pessoas com traços de talassemia alfa ou beta. A talassemia alfa causa condições como anemia hemolítica ou hidropsia fetal fatal, dependendo da gravidade da doença. A beta talassemia principal resulta em anemia hemolítica, retardo de crescimento e aberrações esqueléticas na primeira infância. As crianças afetadas por esse distúrbio precisam de transfusões de sangue regulares ao longo da vida. Os pacientes que dependem de transfusão de sangue geralmente desenvolvem sobrecarga de ferro que causa outras complicações nos sistemas do corpo, como insuficiência renal ou hepática, portanto as talassemias agora são classificadas como uma síndrome. A única cura para as talassemias seria um transplante de medula óssea ou terapia genética sem atualmente uma taxa de sucesso significativa. Uma compreensão completa da base molecular dessa síndrome pode fornecer novos insights e ideias para seu tratamento, já que os cientistas ainda não conseguiram encontrar uma cura permanente para essa doença mortal depois de mais de 87 anos desde que foi descrita pela primeira vez em 1925.

Experimental model of nephropathy associated with diabetes mellitus in mice

Purpose: Nontransmissible chronic diseases, such as diabetes mellitus (DM) and nephropathy, affect a significant portion of the population, often treated due to injuries that require healing and regeneration. To create an experimental model of associated comorbidities, for healing and regeneration studies, protocols for induction of nephropathy by ischemia and reperfusion (I/R) and induction of DM by injection of streptozotocin (STZ) were associated. Methods: Sixty-four mice (Mus musculus), female, adult, Swiss strain, weighing approximately 20 g, were divided into four groups: G1: control (n = 24), G2: nephropathy group (N) (n = 7), G3, DM (n = 9), and G4: N+DM (n = 24). Arteriovenous stenosis (I/R) of the left kidney was performed as the first protocol. The animals received a hyperlipidemic diet for 7 days after the injection of STZ (150 mg/kg, via i.p.) and an aqueous glucose solution (10%) for 24 h. The animals in the G3 and G4 groups were observed for 14 days before receiving the diet and STZ. The evolution of nephropathy was observed using a urine test strip and the DM, through the analysis of blood glucose with a reagent strip on a digital monitor. Results: The ischemic induction protocols of nephropathy and DM with STZ, associated, were sustainable, low-cost, and without deaths. There were alterations compatible with initial renal alterations, in the first 14 days, such as increased urinary density, pH alteration, presence of glucose, proteins and leukocytes, when compared to the control group. DM was confirmed by the presence of hyperglycemia 7 days after induction and its evolution after 14 days. The animals in the G4 group showed constant weight loss when compared to the other groups. It was possible to observe morphological alterations in the kidneys submitted to I/R, regarding coloration, during surgery and after the end of the observation period, in the volume and size of the left kidney, when compared to the contralateral kidney. Conclusion: It was possible to induce nephropathy and DM associated in the same animal, in a simple way, confirmed with rapid tests, without losses, providing a basis for future studies.

Pyometra in queens - changes in haemato-biochemical parameters

Background: Pyometra is a bacterial and hormone-induced reproductive disease that occurs in the post-estrus luteal phase in intact queens. Pyometra is more common in the diestrus period due to the high progesterone concentration (in queens that mated, spontaneously ovulated, or were induced to ovulate). However, it can also be seen due to the use of exogenous hormones such as progesterone for the suppression of estrus. More research is needed in cases of pyometra in queens, as well as in bitches. Because, considering that the pathogenesis and characteristics of feline pyometra is similar to bitches, studies on pyometra-affected bitches are taken as reference in studies and applications on queens. From this point of view, the aims of this study were to reveal the changes in complete blood count, blood gas, and serum biochemistry parameters in feline pyometra cases and to determine the correlation between the mentioned parameters. Materials, Methods & Results: In the study, a total of 25 female cats of different breeds were used, between the ages of 6 months and 7 years, 15 were diagnosed with pyometra, and 10 healthy. Anamnesis, clinical findings, and ultrasonographic examinations were used in the diagnosis of pyometra. Abdominal ultrasonography was performed on queens brought to the clinic with complaints such as anorexia, polydipsia, polyuria, abdominal tension, and fever. The control group (n =10) consisted of queens that were introduced to the clinic and were reproductively healthy. Before any treatment in queens with pyometra and the control group, 1 mL blood samples were taken from v. cephalica to evaluate complete blood count, blood gases and serum biochemistry parameters. In complete WBC, Lym, Mon, Gra, RBC, Hb, HCT, MCV, MCH and PLT parameters and, blood gas parameters such as pH, pCO2 , pO2 , sO2 , Na, K, Cl, lactate, glucose, HCO3 , and BE were also evaluated in taken blood samples. Biochemical parameters BUN, creatinine, ALT, AST, ALP, amylase, T.BIL, D.BIL, P, CHOL, TG, LDH, TP, CPK, ALP, Ca, GGT were measured in serum samples. After examination and laboratory analysis, ovariohysterectomy was performed on queens as a treatment. Granulocyte, WBC, HCT and MCH levels of the pyometra group were higher (P < 0.05) and Lym levels were lower (P < 0.05) compared to the control group. According to these results, pH, HCO3 , and BE were lower (P < 0.05) in queens with pyometra than those in the control group, while Na and lactate parameters were higher (P < 0.05). According to the results of biochemical analysis, it was determined that BUN, creatinine levels, GGT, and LDH enzyme activities were found to be higher in the pyometra group compared to the control group, while the Ca level was found to be low (P < 0.05). A positive correlation was observed between BUN and creatinine and LDH, WBC, granulocyte, HCT, and lactate, and a negative correlation between lymphocytes, pH, and BE in the correlation analysis performed on queens with pyometra and control group. However, a positive correlation was observed between creatinine and LDH and HCT, and a negative correlation between lymphocyte, pH and BE. Discussion: There is not enough information about pyometra in queens. As a result, it was determined that there were significant changes in complete blood count, blood gases and serum biochemical parameters in queens with pyometra in this study. These changes were generally thought to be related to dehydration and sepsis or endotoxemia. In addition, it was evaluated that prerenal azotemia occurring in pyometra affected queens may cause renal dysfunction. For this reason, it is thought that the results obtained in the presented study may contribute to the diagnosis, treatment, and prognosis of pyometra cases in queens.

Protective effect and mechanism of Shenkang injection on adenine-induced chronic renal failure in rats

Purpose: To investigate the protective effects of Shenkang injection (SKI) on adenine-induced chronic renal failure (CRF) in rat. Methods: Sprague Dawley rats were randomly divided into five groups: control, model, and SKI groups (5, 10, 20 mL/kg). Rats in model and SKI groups were treated with adenine i.g. at a dose of 150 mg/kg every day for 12 weeks to induce CRF. Twelve weeks later, SKI was administered to the rat i.p. for four weeks. The effects of SKI on kidney injury and fibrosis were detected. Results: SKI inhibited the elevation of the urine level of N-acetyl-b-D-glucosaminidase, kidney injury molecule-1, beta-2-microglobulin, urea protein in CRF rats. The serum levels of uric acid and serum creatinine increased and albumin decreased in the model group, which was prevented by SKI. SKI inhibited the release of inflammatory cytokines and increasing the activities of antioxidant enzymes in serum. SKI inhibited the expression of transforming growth factor-β1, vascular cell adhesion molecule 1, intercellular adhesion molecule 1, collagen I, collagen III, endothelin-1, laminin in kidney of CRF rats. Conclusions: SKI protected against adenine-induced kidney injury and fibrosis and exerted anti-inflammatory, and antioxidant effects in CRF rats.