TY - JOUR A1 - Weingart, C. A1 - Raila, Jens A1 - Lübke-Becker, A. A1 - Kershaw, O. A1 - Brunnberg, M. A1 - Kohn, B. T1 - Calcitriol induced hypercalcemia in a hunting dog with a disseminated Paecilomyces variotii infection T1 - Calcitriol-bedingte Hyperkalzämie bei einem Jagdhund mit disseminierter Paecilomyces variotii-Infektion JF - Schweizer Archiv für Tierheilkunde N2 - A 5-year old hunting dog was presented with reduced appetite, weight loss and polyuria/polydipsia. Hematology and clinical chemistry revealed anemia, leukocytosis, increased liver enzymes, hypoalbuminemia and hypercalcemia. The cytological, pathohistological and microbiological examination identified a disseminated infection with the saprophytic mould fungus Paecilomyces variotii in the biopsies of the spleen and a lymph node. Determination of vitamin D metabolites confirmed a calcitriol induced hypercalcemia. N2 - Ein 5-jähriger Jagdhund wurde wegen verminderter Futteraufnahme, Gewichtsverlust und Polyurie/Polydipsie vorgestellt. In der hämatologischen und klinisch-chemischen Blutuntersuchung wurde neben einer Anämie und Leukozytose eine Erhöhung der Leberenzyme, Hypoalbuminämie und Hyperkalzämie festgestellt. Durch zytologische, pathohistologische und mikrobiologische Untersuchungen von Biopsien aus Milz und Lymphknoten konnte eine systemische Schimmelpilzinfektion mit Paecilomyces variotii nachgewiesen werden. Die Bestimmung der Vitamin-D-Metabolite bestätigte das Vorliegen einer Hyperkalzämie infolge einer Erhöhung der Calcitriolkonzentration. KW - mould fungus KW - calcium KW - polyuria/polydipsia KW - dog KW - Schimmelpilzinfektion KW - Kalzium KW - Polyurie/ Polydipsie KW - Hund Y1 - 2018 U6 - https://doi.org/10.17236/sat00161 SN - 0036-7281 SN - 1664-2848 IS - 5 SP - 313 EP - 319 PB - Gesellschaft Schweizer Tierärztinnen und Tierärzte CY - Bern ET - 160 ER - TY - JOUR A1 - Raila, Jens A1 - Schweigert, Florian J. A1 - Kohn, Barbara T1 - Relationship between urinary Tamm-Horsfall protein excretion and renal function in dogs with naturally occurring renal disease JF - Veterinary clinical pathology N2 - Background Tamm-Horsfall protein (THP) is physiologically excreted in urine, but little is known about the role of THP in the diagnosis of renal disease in dogs. Objective The aim of this study was to evaluate to which extent naturally occurring renal disease affects the urinary excretion of THP. Methods Dogs were divided into 5 groups according to plasma creatinine concentration, urinary protein-to-creatinine ratio (UP/UC), and exogenous plasma creatinine clearance (P-ClCr) rates: Group A (healthy control dogs; n=8), nonazotemic and nonproteinuric dogs, with P-ClCr rates > 90mL/min/m2; group B (n=25), nonazotemic and nonproteinuric dogs with reduced P-ClCr rates (51-89mL/min/m2); group C (n=7), nonazotemic but proteinuric dogs with P-ClCr rates 53-98mL/min/m2; group D (n=8), azotemic and borderline proteinuric dogs (P-ClCr rates: 22-45mL/min/m2); and group E (n=15), azotemic and proteinuric dogs (not tested for P-ClCr). THP was measured by quantitative Western blot analysis, and the ratio of THP-to-urinary creatinine (THP/UC) was calculated. Results The THP/UC concentrations were not different among dogs of groups A-D, but were reduced in dogs of group E (P<.001). THP/UC correlated negatively with serum creatinine (P<.01) and UP/UC (P<.01), but was not significantly associated with P-ClCr. Conclusions Decreased levels of THP/UC were present in moderately to severely azotemic and proteinuric dogs. This suggests tubular injury in these dogs and that THP might be useful as urinary marker to study the pathogenesis of renal disease. KW - Distal tubules KW - dog KW - kidney KW - lower nephron KW - proteinuria KW - urine Y1 - 2014 U6 - https://doi.org/10.1111/vcp.12143 SN - 0275-6382 SN - 1939-165X VL - 43 IS - 2 SP - 261 EP - 265 PB - Wiley-Blackwell CY - Hoboken ER - TY - JOUR A1 - Krupkova, Olga A1 - Smolders, Lucas A1 - Würtz-Kozak, Karin A1 - Cook, James A1 - Pozzi, Antonio T1 - The pathobiology of the meniscus BT - a comparison between the human and dog JF - Frontiers in veterinary science N2 - Serious knee pain and related disability have an annual prevalence of approximately 25% on those over the age of 55 years. As curative treatments for the common knee problems are not available to date, knee pathologies typically progress and often lead to osteoarthritis (OA). While the roles that the meniscus plays in knee biomechanics are well characterized, biological mechanisms underlying meniscus pathophysiology and roles in knee pain and OA progression are not fully clear. Experimental treatments for knee disorders that are successful in animal models often produce unsatisfactory results in humans due to species differences or the inability to fully replicate disease progression in experimental animals. The use of animals with spontaneous knee pathologies, such as dogs, can significantly help addressing this issue. As microscopic and macroscopic anatomy of the canine and human menisci are similar, spontaneous meniscal pathologies in canine patients are thought to be highly relevant for translational medicine. However, it is not clear whether the biomolecular mechanisms of pain, degradation of extracellular matrix, and inflammatory responses are species dependent. The aims of this review are (1) to provide an overview of the anatomy, physiology, and pathology of the human and canine meniscus, (2) to compare the known signaling pathways involved in spontaneous meniscus pathology between both species, and (3) to assess the relevance of dogs with spontaneous meniscal pathology as a translational model. Understanding these mechanisms in human and canine meniscus can help to advance diagnostic and therapeutic strategies for painful knee disorders and improve clinical decision making. KW - meniscus KW - inflammation KW - oxidative stress KW - pain KW - dog Y1 - 2018 U6 - https://doi.org/10.3389/fvets.2018.00073 SN - 2297-1769 VL - 5 PB - Frontiers Research Foundation CY - Lausanne ER - TY - GEN A1 - Krupkova, Olga A1 - Smolders, Lucas A1 - Wuertz-Kozak, Karin A1 - Cook, James A1 - Pozzi, Antonio T1 - The pathobiology of the meniscus BT - a comparison between the human and dog T2 - Frontiers in Veterinary Science N2 - Serious knee pain and related disability have an annual prevalence of approximately 25% on those over the age of 55 years. As curative treatments for the common knee problems are not available to date, knee pathologies typically progress and often lead to osteoarthritis (OA). While the roles that the meniscus plays in knee biomechanics are well characterized, biological mechanisms underlying meniscus pathophysiology and roles in knee pain and OA progression are not fully clear. Experimental treatments for knee disorders that are successful in animal models often produce unsatisfactory results in humans due to species differences or the inability to fully replicate disease progression in experimental animals. The use of animals with spontaneous knee pathologies, such as dogs, can significantly help addressing this issue. As microscopic and macroscopic anatomy of the canine and human menisci are similar, spontaneous meniscal pathologies in canine patients are thought to be highly relevant for translational medicine. However, it is not clear whether the biomolecular mechanisms of pain, degradation of extracellular matrix, and inflammatory responses are species dependent. The aims of this review are (1) to provide an overview of the anatomy, physiology, and pathology of the human and canine meniscus, (2) to compare the known signaling pathways involved in spontaneous meniscus pathology between both species, and (3) to assess the relevance of dogs with spontaneous meniscal pathology as a translational model. Understanding these mechanisms in human and canine meniscus can help to advance diagnostic and therapeutic strategies for painful knee disorders and improve clinical decision making. T3 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe - 677 KW - meniscus KW - inflammation KW - oxidative stress KW - pain KW - dog Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-460868 SN - 1866-8364 IS - 677 ER -