- Email: [email protected]
Uremic gastropathy in cats
PAGE 8
A D V A N C E S
Results
UREMIC GASTROPATHY IN CATS Background Chronic kidney disease (CKD) is a common clinical problem in many older cats. Progression of CKD typically results in uremia, a syndrome that manifests clinically as a variety of signs, including weight loss, vomiting, and poor appetite. These clinical signs frequently are ascribed to uremic gastritis, a condition attributed to the presence of uremic toxins and gastric hyperacidity secondary to hypergastrinemia. Although complications of uremia such as gastritis, ulceration, and hemorrhage are common in humans with CKD, they appear to be less common and less severe in dogs. The prevalence of uremic gastritis has not been well evaluated in cats. Cats with CDK have been shown to have high serum concentrations of gastrin that increase with the severity of renal failure, but the relationship among gastrin, gastric acid secretion, and gastric pathology has not been investigated. Gastrin is secreted by G cells in the gastric antrum and stimulates the secretion of gastric acid by the parietal cells. In humans, the development of hyperacidity in association with CKD appears to be inconsistent and may be related to the presence of Helicobacter spp. infection. Gastrin secretion has not been studied in cats with CDK. Thus, there is very little available evidence on which to base recommendations for the use of aciddecreasing medications, such as H2 blockers, proton pump inhibitors, or sucralfate in the cats with uremia.
Objectives To evaluate uremic gastropathy in CKD cats in order to facilitate refinement of medical management for gastrointestinal signs.
Procedure Stomachs of 37 CKD cats and 12 nonazotemic cats were evaluated for the presence of classic uremic gastropathy lesions. Histopathologic lesions were compared with serum creatinine concentrations, calciumphosphorus 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 significantly more likely to have gastric fibrosis and mineralization than nonazotemic controls. Only cats with moderate and severe azotemia had gastric mineralization. CPP was correlated with disease severity. Severely azotemic CKD cats had significantly higher CPP compared with nonazotemic controls, and to mildly and moderately azotemic cats. Serum gastrin concentrations were significantly higher in CKD cats compared with nonazotemic controls, but increased concentrations were not associated with gastric ulceration.
Journals Monitored s !MERICAN *OURNAL OF 6ETERINARY Research s !USTRALIAN 6ETERINARY *OURNAL s !USTRALIAN 6ETERINARY 0RACTITIONER s !VIAN $ISEASES s "RITISH 6ETERINARY *OURNAL s #ANADIAN *OURNAL OF 6ETERINARY Research s #ANADIAN 6ETERINARY *OURNAL s *OURNAL OF !VIAN -EDICINE AND Surgery s *OURNAL OF THE !MERICAN Animal Hospital Association s *OURNAL OF THE !MERICAN Veterinary Medical Association s *OURNAL OF 3MALL !NIMAL 0RACTICE
Author Conclusion Uremic gastropathy in CKD cats differs from that described in other species, and this difference should be considered when prescribing medical management.
Inclusions
s *OURNAL OF 3MALL %XOTIC !NIMAL Medicine s *OURNAL OF 6ETERINARY $ENTISTRY s *OURNAL OF 6ETERINARY %MERGENCY and Critical Care
Six figures, 3 tables, 26 references.
s *OURNAL OF 6ETERINARY )NTERNAL Medicine
Editor Annotation
s *OURNAL OF 6ETERINARY Pharmacology and Therapeutics
Cats with CKD often have GI signs and therefore are prescribed acid-decreasing medications. However, the prevalence of uremic gastritis in cats has not been systemically evaluated in cats. The results of this study demonstrated that cats with CKD appear to have gastric mineralization and fibrosis rather than ulceration, which is common in dogs and humans with CKD. Therefore, gastric protectants may not be necessary. Rather, the chemoreceptor trigger zone may be affected by circulating uremic toxins, and antiemetic and antinausea drugs may be more appropriate. Lastly, the role of hypergastrinemia and gastric lesions in cats with CKD remains unclear. Clinicians may want to rethink their medications used for gastrointestinal problems in CKD cats. (MM) McLeland SM, Lunn KF, Duncan CG, 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;28:827-837.
s *OURNAL OF :OO AND 7ILDLIFE Medicine s .EW :EALAND 6ETERINARY *OURNAL s 2ESEARCH IN 6ETERINARY 3CIENCE s 6ETERINARY AND #OMPARATIVE Orthopaedics and Traumatology s 6ETERINARY $ERMATOLOGY s 6ETERINARY )MMUNOLOGY AND Immunopathology s 6ETERINARY 0ATHOLOGY s 6ETERINARY 2ADIOLOGY Ultrasound s 6ETERINARY 2ECORD s 6ETERINARY 2ESEARCH Communications s 6ETERINARY 3URGERY ... and more than 20 others
A D V A N C E S
Results
UREMIC GASTROPATHY IN CATS Background Chronic kidney disease (CKD) is a common clinical problem in many older cats. Progression of CKD typically results in uremia, a syndrome that manifests clinically as a variety of signs, including weight loss, vomiting, and poor appetite. These clinical signs frequently are ascribed to uremic gastritis, a condition attributed to the presence of uremic toxins and gastric hyperacidity secondary to hypergastrinemia. Although complications of uremia such as gastritis, ulceration, and hemorrhage are common in humans with CKD, they appear to be less common and less severe in dogs. The prevalence of uremic gastritis has not been well evaluated in cats. Cats with CDK have been shown to have high serum concentrations of gastrin that increase with the severity of renal failure, but the relationship among gastrin, gastric acid secretion, and gastric pathology has not been investigated. Gastrin is secreted by G cells in the gastric antrum and stimulates the secretion of gastric acid by the parietal cells. In humans, the development of hyperacidity in association with CKD appears to be inconsistent and may be related to the presence of Helicobacter spp. infection. Gastrin secretion has not been studied in cats with CDK. Thus, there is very little available evidence on which to base recommendations for the use of aciddecreasing medications, such as H2 blockers, proton pump inhibitors, or sucralfate in the cats with uremia.
Objectives To evaluate uremic gastropathy in CKD cats in order to facilitate refinement of medical management for gastrointestinal signs.
Procedure Stomachs of 37 CKD cats and 12 nonazotemic cats were evaluated for the presence of classic uremic gastropathy lesions. Histopathologic lesions were compared with serum creatinine concentrations, calciumphosphorus 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 significantly more likely to have gastric fibrosis and mineralization than nonazotemic controls. Only cats with moderate and severe azotemia had gastric mineralization. CPP was correlated with disease severity. Severely azotemic CKD cats had significantly higher CPP compared with nonazotemic controls, and to mildly and moderately azotemic cats. Serum gastrin concentrations were significantly higher in CKD cats compared with nonazotemic controls, but increased concentrations were not associated with gastric ulceration.
Journals Monitored s !MERICAN *OURNAL OF 6ETERINARY Research s !USTRALIAN 6ETERINARY *OURNAL s !USTRALIAN 6ETERINARY 0RACTITIONER s !VIAN $ISEASES s "RITISH 6ETERINARY *OURNAL s #ANADIAN *OURNAL OF 6ETERINARY Research s #ANADIAN 6ETERINARY *OURNAL s *OURNAL OF !VIAN -EDICINE AND Surgery s *OURNAL OF THE !MERICAN Animal Hospital Association s *OURNAL OF THE !MERICAN Veterinary Medical Association s *OURNAL OF 3MALL !NIMAL 0RACTICE
Author Conclusion Uremic gastropathy in CKD cats differs from that described in other species, and this difference should be considered when prescribing medical management.
Inclusions
s *OURNAL OF 3MALL %XOTIC !NIMAL Medicine s *OURNAL OF 6ETERINARY $ENTISTRY s *OURNAL OF 6ETERINARY %MERGENCY and Critical Care
Six figures, 3 tables, 26 references.
s *OURNAL OF 6ETERINARY )NTERNAL Medicine
Editor Annotation
s *OURNAL OF 6ETERINARY Pharmacology and Therapeutics
Cats with CKD often have GI signs and therefore are prescribed acid-decreasing medications. However, the prevalence of uremic gastritis in cats has not been systemically evaluated in cats. The results of this study demonstrated that cats with CKD appear to have gastric mineralization and fibrosis rather than ulceration, which is common in dogs and humans with CKD. Therefore, gastric protectants may not be necessary. Rather, the chemoreceptor trigger zone may be affected by circulating uremic toxins, and antiemetic and antinausea drugs may be more appropriate. Lastly, the role of hypergastrinemia and gastric lesions in cats with CKD remains unclear. Clinicians may want to rethink their medications used for gastrointestinal problems in CKD cats. (MM) McLeland SM, Lunn KF, Duncan CG, 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;28:827-837.
s *OURNAL OF :OO AND 7ILDLIFE Medicine s .EW :EALAND 6ETERINARY *OURNAL s 2ESEARCH IN 6ETERINARY 3CIENCE s 6ETERINARY AND #OMPARATIVE Orthopaedics and Traumatology s 6ETERINARY $ERMATOLOGY s 6ETERINARY )MMUNOLOGY AND Immunopathology s 6ETERINARY 0ATHOLOGY s 6ETERINARY 2ADIOLOGY Ultrasound s 6ETERINARY 2ECORD s 6ETERINARY 2ESEARCH Communications s 6ETERINARY 3URGERY ... and more than 20 others