Background: Studies in dogs with experimental chronic kidney disease (CKD) have demonstrated that abnormalities of calcium-phosphorus (Ca-P) homeostasis occur frequently and have a negative effect on kidney function and survival. However, the prevalence of these alterations in dogs with naturally occurring CKD at different stages of severity has not yet been investigated.Hypothesis: Abnormalities of Ca-P metabolism occur early in the course of CKD with an increased prevalence in more severe stages.Animals: Fifty-four dogs with CKD and 22 healthy dogs.Methods: Blood and urine samples were obtained for a CBC, biochemistry, determination of parathyroid hormone (PTH), calcitriol, and ionized calcium concentrations and urinalysis. Based on urine protein/creatinine ratio and serum creatinine concentration, dogs were grouped according to the IRIS classification for CKD.Results: Hyperparathyroidism (HPTH) (PTH ! 48 pg/mL) was diagnosed in 41 (75.9%) dogs with CKD. Its prevalence increased from 36.4% (stage 1) to 100% (stage 4). Hyperphosphatemia (P 4 5.5 mg/dL) was present in 37 (68.5%) dogs; increasing in prevalence from 18% (stage 1) to 100% (stage 4). Receiver-operating characteristic curve analysis showed that serum phosphorus concentration in the 4.5-5.5 mg/dL range correctly identified the presence of HPTH in most dogs. Calcitriol concentration progressively decreased in dogs with CKD and differences became statistically significant by stage 3.Conclusion and Clinical Relevance: HPTH and hyperphosphatemia occur frequently in dogs with naturally occurring CKD, even at early stages of CKD in some dogs. These findings highlight the importance of monitoring these parameters early in the course of CKD.

An outbreak of a lethal morbillivirus infection of long-finned pilot whales occurred in the Mediterranean Sea from the end of October 2006 through April 2007. Sequence analysis of a 426-bp conserved fragment of the morbillivirus phosphoprotein gene indicates that the virus is more closely related to dolphin morbillivirus than to pilot whale morbillivirus.

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A prospective study was performed (November 1998 to December 2003) to determine the prevalence of systemic hypertension (SH) in dogs with glomerular disease secondary to leishmaniasis. One hundred and five dogs with leishmaniasis were screened and staged for the presence of renal disease (RD) and SH. For the purpose of the study, RD was defined as serum creatinine concentration > or = 1.4 mg/dL, a urine protein/creatinine ratio > or = 0.5, or both. SH was defined as a systolic blood pressure (SBP) > or =180 mm Hg or an SBP between 150 and 179 mm Hg in the presence of clinical manifestations of SH. Fifty-two (49.5%) of the dogs had some degree of RD, and 32 (61.5%) of these dogs were diagnosed with SH. Moreover, SH also was diagnosed in 3 dogs without RD. Left ventricular hypertrophy (LVH), estimated by echocardiography, was the most frequently observed systemic consequence of hypertension, being present in 32 (91.4%) of the hypertensive dogs. Echocardiographic abnormalities were not detected in any of the 33 dogs with leishmaniasis without RD, which were used as controls. Ocular consequences of SH were observed in only 2 (5.7%) of the dogs with hypertension. We conclude that SH is prevalent in dogs with RD secondary to leishmaniasis, not only in the more severe stages but also in the early course of the illness before azotemia becomes apparent. Canine leishmaniasis may be a useful natural model to study SH secondary to glomerular disease.

Opioid peptides derived from prodynorphin were localized immunocytochemically to dentate granule cells and mossy fibers of the rat hippocampus with antisera against dynorphin A(1-17) and dynorphin B. Extracts of microdissected hippocampal regions were resolved by reverse phase and molecular exclusion chromatography to identify the molecular forms of the dynorphin A immunoreactivity and to quantify regional contents. Results demonstrated that the relative concentration of dynorphin A within each dissected region of hippocampus agreed well with the distribution of dynorphin A detected by immunocytochemical methods. Immunostaining of proenkephalin-derived opioid peptides, [Leu5]enkephalin and bovine adrenal medullary peptide-22P, was concentrated in cell bodies of the entorhinal cortex, nerve fibers in the perforant pathway, and terminals in the outer molecular layer of the dentate gyrus. Light immunostaining of granule cells and mossy fibers with these antisera was also found. The relative concentration of [Leu5]enkephalin immunoreactivity in each microdissected region of the hippocampus also agreed well with the distribution of [Leu5]enkephalin immunostaining. Chromatography of hippocampal regional extracts demonstrated that the immunoreactivity measured was due to the presence of authentic [Leu5]enkephalin. The probable neurotransmitter function of both [Leu5]enkephalin and dynorphin A was shown by their calcium-dependent release after in vitro depolarization of hippocampal tissue. The reported presence of beta-endorphin in hippocampus was not verified. Comparison of the hippocampal distribution and content of prodynorphin and proenkephalin-derived opioids suggests that separate populations of neurons containing these two peptide families form distinct neurotransmitter systems of roughly equal concentration.