Total serum magnesium in cats with chronic kidney disease with nephrolithiasis.

OBJECTIVES: Magnesium has been 'the forgotten ion' for many years. Over the past decade, however, the role of magnesium in essential physiological functions and several illness conditions have been elucidated. Nevertheless, the investigation of magnesium in cats with chronic kidney disease (CKD) and nephrolithiasis is yet to be determined. The purpose of this study was to investigate whether CKD cats with nephrolithiasis have changes in total serum magnesium concentrations, and whether magnesium disorders may be associated with other electrolyte disturbances, as well as with prognosis. We also aimed to evaluate whether total serum magnesium concentration differs between CKD cats with and without nephrolithiasis. METHODS: Total serum magnesium concentrations were assessed in 42 cats with CKD with stage 1-4 nephrolithiasis. The correlation between magnesium and other electrolytes, as well as Kaplan-Meier survival analysis, were performed. We also selected 14 control cats with CKD without nephrolithiasis age-matched with 14 cats with CKD with nephrolithiasis. RESULTS: Hypermagnesemia was observed in 16/42 (38.1%) and hypomagnesemia in 6/42 (14.3%) cats. Serum magnesium abnormalities were observed in cats of all stages, and marked hypermagnesemia was noted in cats with stage 4 CKD with nephrolithiasis (P <0.001). There was a negative correlation between total serum magnesium and ionized calcium (r = -0.64; P <0.01), and a positive correlation between total serum magnesium and serum phosphorus (r = 0.58, P = 0.01). Cats with CKD with nephrolithiasis and hypomagnesemia or hypermagnesemia had higher mortality than those with normal total serum magnesium concentration (P <0.01), regardless of CKD stage. There was no difference in total serum magnesium concentration between CKD cats with and without nephrolithiasis. CONCLUSIONS AND RELEVANCE: Cats with CKD with nephrolithiasis have magnesium abnormalities. Hypomagnesemia and hypermagnesemia were associated with an increase in mortality, and thus total serum magnesium abnormalities may be used as prognostic factors in these cases.

Blood lactate concentration in diabetic dogs.

Human diabetic patients may have increased lactate levels compared to non-diabetics. Despite the use of lactate levels in critical care assessment, information is lacking for diabetic dogs. Therefore, this prospective cross-sectional clinical study aimed to determine lactate concentrations in 75 diabetic dogs [25 newly diagnosed non-ketotic diabetics, 25 under insulin treatment, and 25 in diabetic ketoacidosis (DKA)], compared to 25 non-diabetic dogs. Lactate levels (mmol/L) were not different among groups (P = 0.20); median and 25th to 75th percentile were 2.23 and P25-75 = 1.46 to 2.83 for controls, 1.69 and P25-75 = 1.09 to 2.40 for newly diagnosed non-ketotic diabetics, 2.27 and P25-75 = 1.44 to 2.90 for dogs under insulin treatment for at least 30 days, and 2.40 and P25-75 = 1.58 to 3.01 for dogs in DKA. Longitudinal studies assessing both isomers (L- and D-lactate) are needed to better elucidate the role of lactate in the pathophysiology of diabetes acid-base status in dogs.

La concentration de lactate de sang chez les chiens diabétiques. Des patients humains avec diabète peuvent présenter augmentation des niveaux de lactate, quand comparés aux non diabetiques. Bien que est utilisé d'évaluer les patients dans un état critique, cette information manque pour les chiens diabétiques. Par conséquent, cette étude clinique s'agit d'une prospective transversale en vue de detérminer les concentrations du lactate en 75 chiens diabétiques [25 au moment du diagnostic, 25 sous traitement à l'insuline et 25 dans l'acido-cétose diabétique (ACD)], par rapport aux 25 chiens non diabétiques. Les niveaux de L-lactate ne différaient pas entre les groupes (P = 0,20). Les valeurs médianes et les centiles 25 % et 75 % étaient de 2,23 mmol/L (P25­75 = 1,46 à 2,83) pour les contrôles, 1,69 mmol/L (P25­75 = 1,09 à 2,40) au diagnostic, 2,27 mmol/L (P25­75 = 1,44 à 2,90) sous traitement à l'insuline pendant au moins 30 jours, et 2,40 mmol/L (P25­75 = 1,58 à 3,01) dans ACD. Des études longitudinales évaluant les deux isomères (L et D-lactate) sont nécessaires pour élucider son rôle dans la physiopathologie et le déséquilibre acide-base chez les chiens diabétiques.(Traduit par Ana Carolina Possas Viana).

Urine protein electrophoresis study in dogs with pituitary dependent hyperadrenocorticism during therapy with trilostane / Avaliação da proteína urinária por eletroforese em cães com hiperadrenocorticismo hipófise dependente durante a terapia com trilostano

Hyperadrenocorticism is one of the most common endocrine disorders in dogs. Regarding to the kidneys, chronic hypercortisolemia can cause damage to the glomerulus, and evolve into chronic kidney disease. This study evaluated nine normotensive dogs with pituitary dependent hyperadrenocorticism, before and after therapy with trilostane, during the follow-up period of six months, in order to investigate the development of pathological proteinuria by quantitative (urinary protein-to-creatinine ratio) and qualitative (urinary protein electrophoresis) methods, and also to monitor its intensity over the course of the disease and therapy. The main renal lesion detected in dogs with hyperadrenocorticism was in the tubular segment, evidenced by the prevalence of urinary protein bands of lower molecular weight, indicating the lack absorption of these proteins in the proximal segment of the nephron. Low molecular weight proteins persisted throughout the follow-up. Regarding the future of routine veterinary medical clinic in the care of patients with hyperadrenocorticism, the assessments of proteinuria determinations by the urinary protein-to-creatinin ratio and urinary protein electrophoresis, according to the results obtained in this study, can add more information about the renal damage in these animals, and contribute to the prognosis.(AU)

Hiperadrenocorticismo (HAC) é uma das doenças endócrinas mais comuns em cães. A hipercortisolemia crônica pode causar danos glomerulares, pelo aumento da taxa de filtração glomerular, podendo levar ao desenvolvimento de doença renal crônica. Este estudo avaliou nove cães normotensos com hiperadrenocorticismo hipófise-dependente, antes e após a terapia com trilostano, durante o período de acompanhamento de seis meses, a fim de investigar o desenvolvimento de proteinúria patológica por métodos quantitativo (relação proteína e creatinina urinária) e qualitativos (eletroforese de proteínas urinárias) e também para monitorar a sua intensidade ao longo do curso da doença e terapia. A principal lesão renal detectada em cães com HAC foi no segmento tubular, evidenciada pela prevalência de bandas de proteínas urinárias de peso molecular mais baixo, indicando a falta de absorção destas proteínas no segmento proximal do néfron. A proteinúria de baixo peso molecular persistiu durante todo o acompanhamento. Em relação ao futuro da rotina clínica médica veterinária no tratamento de cães com hiperadrenocorticismo, as avaliações de proteinúria pela relação proteína e creatinina urinária e eletroforese de proteínas urinárias, de acordo com os resultados obtidos neste estudo, podem adicionar mais informações sobre a lesão renal nestes animais e contribuir para o prognóstico.(AU)