McLeland SM, Lunn KF, et al. Relationship among serum creatinine, serum gastrin, calcium-phosphorus product, and uremic gastropathy in cats with chronic kidney disease. J Vet Intern Med. 2014 May-Jun; 28(3):827-837.
In older cats, chronic kidney disease (CKD) is a common clinical diagnosis. As the disease progresses, uremia can develop and can be manifested clinically with such signs as weight loss, vomiting, and inappetence. Conventional belief is that these clinical signs are due to uremic gastritis, a condition caused by uremic toxins and excess stomach acid secondary to hypergastrinemia. This is the scenario documented in uremic humans and dogs, but much less is known about uremic gastropathy in cats.
The authors in this study evaluated uremic gastropathy in CKD cats with the goal to evaluate the best medical management in cats with gastrointestinal signs. 37 CKD cats (9 mildly azotemic, 9 moderately azotemic, 19 severely azotemic) and 12 non-azotemic cats were included in the study. Their stomachs were examined for lesions of uremic gastropathy. Histopathologic lesions were then compared with serum creatinine concentrations, calcium-phosphorus product (CPP), and serum gastrin concentrations.
Interestingly, the classic lesions (gastric ulceration, edema, and vascular fibrinoid change) found in humans and dogs with uremic gastritis were not found in cats in this study. In these CKD cats, they were more likely to have gastric mineralization and fibrosis present. Evidence of mineralization was observed only in cats with moderate to severe azotemia. CPP increased significantly with increased degree of azotemia and serum gastrin concentrations were also higher than in nonazotemic controls, but serum gastrin concentrations were not associated with gastric ulceration.
The results suggest that gastrointestinal signs noted in CKD cats may be more the result of uremic toxins and centrally acting emtogens than due to pathology within the stomach. The more common administration of antacids and gastroprotectants in cats may not be justified unless melena or hematemesis is noted. The increased level of gastric mineralization in CKD cats may emphasize a need for more focus and control of hyperphosphatemia and secondary hyperparathyroidism in these cases. Management of gastrointestinal signs by use of antiemetic and antinausea drugs may be more worthwhile in cats with CKD. Whether increased gastrin concentrations contribute to increased stomach acid levels remains unclear and should be evaluated with further studies. (VT)