Relationship among Serum Creatinine, Serum Gastrin, Calcium-phosphorus Product, and Uremic Gastropathy in Cats with Chronic Kidney Disease
Article first published online: 14 MAR 2014
Copyright © 2014 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 28, Issue 3, pages 827–837, May/June 2014
How to Cite
McLeland, S.M., Lunn, K.F., Duncan, C.G., Refsal, K.R. and Quimby, J.M. (2014), Relationship among Serum Creatinine, Serum Gastrin, Calcium-phosphorus Product, and Uremic Gastropathy in Cats with Chronic Kidney Disease. Journal of Veterinary Internal Medicine, 28: 827–837. doi: 10.1111/jvim.12342
- Issue published online: 28 APR 2014
- Article first published online: 14 MAR 2014
- Manuscript Accepted: 3 FEB 2014
- Manuscript Revised: 15 DEC 2013
- Manuscript Received: 17 SEP 2013
- Colorado State University College of Veterinary Medicine and Biomedical Sciences College Research Council
- Chronic renal failure;
Chronic kidney disease (CKD) in cats is associated with gastrointestinal signs commonly attributed to uremic gastropathy. Consequently, patients often are treated with antacids and gastrointestinal protectants. This therapeutic regimen is based on documented gastric lesions in uremic humans and dogs, but the nature and incidence of uremic gastropathy in cats are unknown.
Evaluate uremic gastropathy in CKD cats to facilitate refinement of medical management for gastrointestinal signs.
Thirty-seven CKD cats; 12 nonazotemic cats
Stomachs were evaluated for the presence of classic uremic gastropathy lesions. Histopathologic lesions were compared with serum creatinine concentrations, calcium-phosphorus product (CPP), and serum gastrin concentrations.
Gastric ulceration, edema, and vascular fibrinoid change were not observed. The most important gastric lesions in CKD cats were fibrosis and mineralization. Sixteen CKD cats (43%) had evidence of gastric fibrosis of varying severity and 14 CKD cats (38%) had gastric mineralization. CKD cats were more likely to have gastric fibrosis and mineralization than nonazotemic controls (P = .005 and P = .021, respectively). Only cats with moderate and severe azotemia had gastric mineralization. CPP was correlated with disease severity; severely azotemic CKD cats had significantly higher CPP when compared with nonazotemic controls, and to mildly and moderately azotemic cats (P < .05). Gastrin concentrations were significantly higher in CKD cats when compared with nonazotemic controls (P = .003), but increased concentrations were not associated with gastric ulceration.
Conclusions and Clinical Importance
Uremic gastropathy in CKD cats differs from that described in other species and this difference should be considered when devising medical management.