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Background: Acute kidney injury (AKI) is a common and often fatal disorder in dogs. Hypothesis: Urine neutrophil gelatinase-associated lipocalin (NGAL)/creatinine ratio is a sensitive and specific biomarker of AKI in dogs.Animals: Ninety-four dogs. Methods: Prospective study. Dogs were classified as follows: (1) healthy dogs, (2) dogs with lower urinary tract disorders, (3) dogs with chronic kidney disease (CKD), (4) dogs with azotemic International Renal Interest Society (IRIS) AKI Grades II-V, and (5) dogs with IRIS AKI Grade I (nonazotemic). Urinary NGAL was quantitated in each dog using an ELISA assay and concentrations were expressed as a ratio to urinary creatinine concentration from the same specimen, and designated the urinary NGAL/creatinine ratio (UNCR).Results: There was a significant difference in UNCR among the study groups (P < .001). Both the azotemic and nonazotemic AKI groups had higher UNCR when compared with all other groups (P < .001 for all pairs). There was a statistically significant difference in UNCR between dogs diagnosed with CKD compared with dogs with lower urinary tract diseases (P = .005) as well as between dogs with CKD and healthy dogs (P = .001). Receiver operator characteristics (ROC) analysis of UNCR as an indicator of azotemic and nonazotemic AKI had an area under the ROC curve of 0.94 and 0.96, respectively.Conclusions and Clinical Relevance: NGAL/creatinine ratio is a sensitive and specific marker of AKI. It can be used to screen patients at risk for AKI and can be utilized to diagnose milder forms of AKI potentially earlier in the course of the disease.

The Ace-1 xenograft is a useful model for investigating the pathogenesis of prostate cancer invasion and mixed osteoblastic/osteolytic bone metastases.

Human colorectal cancer (CRC) is one of the better-understood systems for studying the genetics of cancer initiation and progression. To develop a cross-species comparison strategy for identifying CRC causative gene or genomic alterations, we performed array comparative genomic hybridization (aCGH) to investigate copy number abnormalities (CNAs), one of the most prominent lesion types reported for human CRCs, in 10 spontaneously occurring canine CRCs. The results revealed for the first time a strong degree of genetic homology between sporadic canine and human CRCs. First, we saw that between 5% and 22% of the canine genome was amplified/deleted in these tumors, and that, reminiscent of human CRCs, the total altered sequences directly correlated to the tumor's progression stage, origin, and likely microsatellite instability status. Second, when mapping the identified CNAs onto syntenic regions of the human genome, we noted that the canine orthologs of genes participating in known human CRC pathways were recurrently disrupted, indicating that these pathways might be altered in the canine CRCs as well. Last, we observed a significant overlapping of CNAs between human and canine tumors, and tumors from the two species were clustered according to the tumor subtypes but not the species. Significantly, compared with the shared CNAs, we found that species-specific (especially human-specific) CNAs localize to evolutionarily unstable regions that harbor more segmental duplications and interspecies genomic rearrangement breakpoints. These findings indicate that CNAs recurrent between human and dog CRCs may have a higher probability of being cancer-causative, compared with CNAs found in one species only.

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