Chronic kidney disease (CKD) is a common condition in elderly cats. It is estimated that the overall prevalence rate for this population approaches 50%. Clinicians and cat owners focus on how to manage affected cats thru pharmacologic and dietary management of CKD, with the particular aims to slowing disease progression and improving quality of life. Poor or loss of appetite, nausea, vomiting or a combination of these signs is commonly associated with advanced CKD in cats.
In humans with end-stage kidney disease, gastric erosion and ulceration can occur leading to gastrointestinal bleeding for which acid suppression therapy is often recommended. There are few guidelines in cats for the use of acid suppression since gastric pH studies have not been done in cats with CKD. Gastric changes in cats have been characterized as mineralization, gland atrophy and hypergastrinemia but not ulcerative or erosive gastropathy.
There is no direct evidence to support the use of acid suppressants in these cases with CKD, yet acid suppressants such as famotidine and omeprazole are commonly prescribed for cats with CKD. One study reported that famotidine was one of the medications most frequently administered to cats with CKD (27% of 1089 cats).
Along with putting a “pill burden” on the cat owner to comply with treatment, prolonged administration of acid suppressants to cats with CKD may not be safe. Such prolonged use of these drugs has been associated with calcium and PTH derangements, osteoporosis and pathologic fractures in humans. A pilot study in healthy cats observed decreased bone mineral content and rebound serum hypergastrinemia with prolonged use in cats.
In this study, the authors wanted to determine if cats with CKD have decreased gastric pH compared to healthy cats. The study included 10 CKD cats ranging from IRIS stage 2 to 4 (50% of cases were IRIS stage 2) and 9 healthy control cats. In addition to baseline inclusion criteria, the cats had serum gastrin concentrations collected and measured along with 12-hour continuous gastric pH monitored such as mean pH and the percentage time that gastric pH was strongly acidic (pH <1 and <2).
The results showed there were no significant differences in serum gastrin concentrations or of any of the pH parameters between cats with CKD and healthy cats. The minimum pH was similar between the 2 groups; the group of CKD cats did not have gastric acidity compared to healthy control cats. The findings along with histopathologic studies show an absence of erosive and ulcerative disease in cats with CKD.
The authors conclude from the study that further evaluation is needed to determine if there is any benefit using acid suppressants to help manage GI signs in cats with CKD. This study suggests there may not be benefit for their use in cats with CKD. Additional study is advised to evaluate gastric pH in cats with later stages (IRIS stages 3 or 4) of CKD. (VT)
McLeland SM, Lunn KF, et al. Relationship among serum creatinine, serum gastrin, calcium-phosphorus and uremic gastropathy in cats with chronic kidney disease. J Vet Intern Med. 2014 May-Jun;28(3):827-37.