Doença de chagas em cães / Chagas disease in dogs

A doença de Chagas, também chamada de tripanossomíase americana, é uma antropozoonose causada por um protozoário flagelado denominado Trypanosoma cruzi. A transmissão ocorre de diversas maneiras, sendo as mais relatadas: a forma vetorial, que ocorre quando o paciente inocula as fezes do vetor infectadas pelo tripanossomo por meio do orifício que foi aberto no momento do repasto sanguíneo, ou por via oral, devido principalmente a ingestão de alimentos contaminados com o tripanossomo. Diferentes espécies de animais domésticos e silvestres podem ser acometidas pela doença; contudo, o objetivo deste trabalho é descrever a doença em cães os quais são capazes de desenvolver o curso crônico, assim como os humanos, e são importantes marcadores de saúde pública para a doença, tendo em vista que são animais considerados sentinelas para o seu aparecimento.

Chagas disease, also called American trypanosomiasis, is an anthropozoonosis caused by the flagellated protozoan Trypanosoma cruzi. The transmission occurs in several ways, and the most reported are: the vector form, which occurs when the patient inoculates the feces of the vector infected by the trypanosome, through the hole that was opened during the blood meal, or orally, mainly due to the ingestion of food contaminated with trypanosome. Different species of domestic and wild animals can be affected by the disease; however, this study aims to describe the disease in dogs, which are capable of developing the chronic course, just like humans, and are also important public health indicators for the disease, since they are animals considered sentinels to its appearance.

Evaluation of Serum and Urine Amino Acids in Dogs with Chronic Kidney Disease and Healthy Dogs Fed a Renal Diet.

This observational study aimed to evaluate serum and urinary amino acid (AA) concentrations in healthy dogs and dogs with chronic kidney disease (CKD) fed a commercial therapeutic renal diet with reduced protein and phosphorus levels. Ten dogs with CKD stages 3 or 4 composed the study group and received the renal diet for 180 days (RG T180). A control group (CG T30) composed of seven healthy dogs was fed a renal diet for 30 days. When comparing serum AA between RG T180 and CG T30, histidine, isoleucine, leucine, lysine, phenylalanine, tryptophan, cysteine, citrulline, ornithine, taurine, branched-chain amino acids (BCAA), and total essential amino acids (EAA) were higher in RG T180. Meanwhile, arginine, asparagine, aspartate, glutamine, serine, and tyrosine were higher in CG T30. Serum phenylalanine, tryptophan, and hydroxyproline were higher in RG T0 (dogs with CKD before consuming a renal diet) when compared to RG T180. In addition, the serum ratios of arginine/citrulline, tyrosine/phenylalanine, and serine/glycine were higher in CG T30 than in RG T180. Concerning urinary AA concentrations in CKD dogs, isoleucine, phenylalanine, tryptophan, aspartate, cysteine, and BCAA were higher in RG T180. In urine, the total EAA/total non-essential AA ratio in RG T180 was higher than in CG T30 as well as tyrosine/phenylalanine ratio higher in CG T30. In conclusion, the combination of renal diet and conservative treatment over 6 months in dogs with CKD stages 3 or 4 affected the AAs metabolism when compared to healthy adult dogs.

Healthy and Chronic Kidney Disease (CKD) Dogs Have Differences in Serum Metabolomics and Renal Diet May Have Slowed Disease Progression.

Chronic kidney disease (CKD) is highly prevalent in dogs, and metabolomics investigation has been recently introduced for a better understanding of the role of diet in CKD. This study aimed to compare the serum metabolomic profile of healthy dogs (CG) and dogs with CKD (CKD-T0 and CKD-T6) to evaluate whether the diet would affect metabolites. Six dogs (5 females; 1 male; 7.47 ± 2.31 years old) with CKD stage 3 or 4 (IRIS) were included. CG consisted of 10 healthy female dogs (5.89 ± 2.57 years old) fed a maintenance diet. Serum metabolites were analyzed by 1H nuclear magnetic resonance (1H NMR) spectra. Principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) were performed to assess differences in metabolomic profiles between groups and before (CKD-T0) and after renal diet (CKD-T6). Data analysis was performed on SIMCA-P software. Dogs with CKD showed an altered metabolic profile with increased urea, creatinine, creatine, citrate, and lipids. Lactate, branched-chain amino acids (BCAAs), and glutamine were decreased in the CKD group. However, after 6 months of diet, the metabolite profiles of CKD-T0 and CKD-T6 were similar. Metabolomics profile may be useful to evaluate and recognize metabolic dysfunction and progression of CKD, and the diet may have helped maintain and retard the progression of CKD.

Evaluation of Electrolyte Concentration and Pro-Inflammatory and Oxidative Status in Dogs with Advanced Chronic Kidney Disease under Dietary Treatment.

An integrated study on the effect of renal diet on mineral metabolism, fibroblast growth factor 23 (FGF-23), total antioxidant capacity, and inflammatory markers has not been performed previously. In this study, we evaluated the effects of renal diet on mineral metabolism, oxidative stress and inflammation in dogs with stage 3 or 4 of chronic kidney disease (CKD). Body condition score (BCS), muscle condition score (MCS), serum biochemical profile, ionized calcium (i-Ca), total calcium (t-Ca), phosphorus (P), urea, creatinine, parathyroid hormone (PTH), FGF-23, interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor alpha (TNF-α) and total antioxidant capacity (TAC) were measured at baseline (T0) and after 6 months of dietary treatment (T6). Serum urea, P, t-Ca, i-Ca, PTH, FGF-23, IL-6, IL-10, TNF-α and TAC measurements did not differ between T0 and T6. Serum creatinine (SCr) was increased at T6 and serum PTH concentrations were positively correlated with serum SCr and urea. i-Ca was negatively correlated with urea and serum phosphorus was positively correlated with FGF-23. Urea and creatinine were positively correlated. The combination of renal diet and support treatment over 6 months in dogs with CKD stage 3 or 4 was effective in controlling uremia, acid-base balance, blood pressure, total antioxidant capacity, and inflammatory cytokine levels and in maintaining BCS and MCS.

Nefropatia diabética em cães: revisão de literatura / Diabetic nephropathy in dogs: literature review

O diabetes mellitus que se desenvolve por deficiência de insulina e hiperglicemia crônica usualmente apresenta complicações que incluem catarata, retinopatia, infecções recorrentes e cetoacidose. A hiperglicemia crônica pode promover complicações a longo prazo como a nefropatia diabética. Nos humanos, a nefropatia diabética é caracterizada principalmente por lesão glomerular e geralmente está associada a hipertensão arterial sistêmica. Dentre os mecanismos propostos para a fisiopatologia da nefropatia diabética tem sido referida a lesão glomerular, assim como a lesão nos túbulos renais. Contudo, até o momento existem poucos estudos investigando a relação entre diabetes mellitus e lesão renal em cães. Esta revisão tem por objetivos esclarecer os possíveis mecanismos fisiopatológicos da nefropatia diabética e discutir o conhecimento disponível sobre sua ocorrência em cães.

Diabetes mellitus caused by insulin deficiency and chronic hyperglycemia usually presents complications including cataract, retinopathy, recurrent infections and ketoacidosis. Chronic hyperglycemia can cause long-term complications such as diabetic nephropathy. In humans, diabetic nephropathy is characterized mainly by glomerular injury and usually it is associated with systemic hypertension. The mechanisms proposed for the pathogenesis of diabetic nephropathy could be glomerular injury, as well as renal tubular damage. However, there are few studies analyzing the relationship between diabetes mellitus and kidney damage in dogs. The objective of this review is to clarify the pathophysiological mechanisms of diabetic nephropathy and to analyze the available information about its occurrence in dogs.

Nefropatia diabética em cães: revisão de literatura / Diabetic nephropathy in dogs: literature review

O diabetes mellitus que se desenvolve por deficiência de insulina e hiperglicemia crônica usualmente apresenta complicações que incluem catarata, retinopatia, infecções recorrentes e cetoacidose. A hiperglicemia crônica pode promover complicações a longo prazo como a nefropatia diabética. Nos humanos, a nefropatia diabética é caracterizada principalmente por lesão glomerular e geralmente está associada a hipertensão arterial sistêmica. Dentre os mecanismos propostos para a fisiopatologia da nefropatia diabética tem sido referida a lesão glomerular, assim como a lesão nos túbulos renais. Contudo, até o momento existem poucos estudos investigando a relação entre diabetes mellitus e lesão renal em cães. Esta revisão tem por objetivos esclarecer os possíveis mecanismos fisiopatológicos da nefropatia diabética e discutir o conhecimento disponível sobre sua ocorrência em cães.(AU)

Diabetes mellitus caused by insulin deficiency and chronic hyperglycemia usually presents complications including cataract, retinopathy, recurrent infections and ketoacidosis. Chronic hyperglycemia can cause long-term complications such as diabetic nephropathy. In humans, diabetic nephropathy is characterized mainly by glomerular injury and usually it is associated with systemic hypertension. The mechanisms proposed for the pathogenesis of diabetic nephropathy could be glomerular injury, as well as renal tubular damage. However, there are few studies analyzing the relationship between diabetes mellitus and kidney damage in dogs. The objective of this review is to clarify the pathophysiological mechanisms of diabetic nephropathy and to analyze the available information about its occurrence in dogs.(AU)

Urinary Fractional Excretion of Phosphorus in Dogs with Spontaneous Chronic Kidney Disease.

The increase of urinary fractional excretion of phosphorus (uFEP) may indicate phosphorus retention before the onset of hyperphosphatemia in the early stages of chronic kidney disease (CKD). The hypothesis of this study is whether uFEP may increase during the early stage of CKD as a compensatory mechanism to prevent hyperphosphatemia as well as whether hyperphosphatemia in the late stages is associated with increase or decrease in uFEP in dogs with naturally occurring CKD; therefore, the aim of this study was to determine the uFEP in CKD dogs with different stages. Forty-nine CKD dogs were included, and they were divided into stage 1 (serum creatinine < 1.4 mg/dL), stage 2 (serum creatinine 1.5 to 2.0 mg/dL), stage 3 (serum creatinine 2.1 to 5.0 mg/dL) and stage 4 (serum creatinine > 5.0 mg/dL), according to the IRIS staging criteria. The stage 3 was subdivided into stage 3-A (serum creatinine 2.1 to 3.5 mg/dL) and stage 3-B (serum creatinine 3.6 to 5.0 mg/dL). The control group comprised 10 dogs, and uFEP ≤ 40% was considered as normal. A progressive increase in uFEP along the progression of CKD was found. However, similar results of uFEP levels were observed in late CKD, since there were no differences between stages 3 (A, B) and 4. Interestingly, some CKD dogs with stage 4 showed normal or reduced uFEP, besides hyperphosphatemia; conversely, some dogs in early CKD had increased uFEP values and normophosphatemia. Our findings suggest that uFEP may act as a compensatory mechanism to avoid the onset of hyperphosphatemia in early CKD, but not in later stages. uFEP assessment may be considered as an additional tool for the diagnostic and monitoring of phosphate disorders in dogs with CKD, since it may help to identify disturbances of phosphorus balance. More studies are needed to elucidate the role of uFEP in phosphorus homeostasis in dogs with CKD.