Page 774 - Small Animal Clinical Nutrition 5th Edition

802 Small Animal Clinical Nutrition

tion was probably low in this dog relative to serum urea nitrogen concentration, thereby overestimating relative GFR and under-
VetBooks.ir estimating the severity of renal dysfunction.
The urea nitrogen concentration was probably higher relative to the GFR in this dog.The rate of urea production depends on
dietary protein intake, rate of production by the liver and catabolism of endogenous body protein stores. This dog was currently
being fed relatively high levels of dietary protein, which would contribute to greater production of nitrogenous waste products
such as urea. GI hemorrhage mimics a high-protein meal resulting in an increased rate of urea synthesis by the liver. Also, admin-
istration of corticosteroids results in catabolism of body proteins, which releases nitrogen-containing amino acids. Urea is pro-
duced when these amino acids are catabolized for energy.Therefore,the rate of urea production in this dog was probably increased
from GI bleeding and catabolism induced by prednisone therapy. The net result is that the urea nitrogen concentration was
increased relative to the serum creatinine concentration and actual GFR. Increased production of potentially toxic nitrogenous
breakdown products (represented by urea) probably worsened uremic signs in this dog.
3. This dog was classified as having CKD, most likely stage 3; however, final staging should be based on a stable serum creatinine
a
concentration obtained after correction of dehydration. Feeding a veterinary therapeutic renal food to dogs with stage 2 to 3
CKD has been associated with prolonged survival time, decreased uremic episodes and improved quality of life compared with
feeding a maintenance food that contains higher amounts of protein, phosphorus and sodium. Avoiding excessive protein intake
is important in advanced stages of CKD to control clinical signs of uremia. However, attempting to immediately feed any food
to a patient with anorexia and vomiting from severe uremic gastritis is likely to fail. Therefore, our recommendation was to treat
the uremic crisis first, and then reintroduce an appropriate food after the GI signs were controlled. To avoid food aversion asso-
ciated with hospitalization or nausea in some patients (especially cats and small dogs), it may be more appropriate to feed a food
for mature adult dogs during hospitalization and then have the owner gradually transition to the therapeutic renal food at home.
4. Other therapies to treat the consequences of the uremic syndrome are indicated when a dog has moderate to advanced CKD
(late stage 3 and stage 4). Therapy should be aimed at controlling uremic gastritis, secondary renal hyperparathyroidism, anemia
and hypertension (if present). Uremic gastritis is thought to occur secondary to hypergastrinemia in dogs with advanced stages
of CKD. Therapy designed to minimize uremic gastritis and gastric and duodenal ulceration includes H -receptor antagonists
2
(i.e., cimetidine, famotidine, etc.), misoprostol, omeprazole and sucralfate.Therapy designed to minimize secondary renal hyper-
parathyroidism includes avoiding excessive phosphorus intake, intestinal phosphate-binding agents and potentially low-dose cal-
citriol therapy after correction of hyperphosphatemia. The most effective method of treating the anemia of CKD is to adminis-
ter recombinant human erythropoietin (r-HuEPO).Therapy with r-HuEPO is reserved for patients with moderately severe ane-
mia (i.e., hematocrit values <20 to 25% in dogs).

Therapy Including Feeding Plan
b c d
The dog was initially treated with intravenous fluid therapy, intravenous cimetidine and oral misoprostol and sucralfate. Food
was withheld for 48 hours until the vomiting ceased. The dog was then offered a food for mature adults with controlled levels of
protein, phosphorus and sodium, divided into four small meals per day. The amount of food was initially calculated to meet the
resting energy requirement for an ideal body weight of 7.5 kg.

Progress Notes
The vomiting, hematemesis, hematochezia and melena resolved. Azotemia improved with intravenous fluid therapy; serum urea
nitrogen concentration decreased to 58 mg/dl and serum creatinine decreased to 2.1 mg/dl. However, hematocrit decreased to 11%.
These findings are consistent with stage 3 CKD. The dog was discharged after five days of hospitalization while the owners con-
a
sidered castration. Nutritional recommendations were to gradually transition to a veterinary therapeutic renal food or a homemade
food that avoided excessive levels of protein and phosphorus. Therapy was continued at home including oral famotidine, oral alu-
e
minum hydroxide and subcutaneous injections of r-HuEPO three times per week.
Reevaluation nine days after discharge from the hospital revealed the dog’s attitude and appetite had improved.The dog had been
chewing its tail for two days; however, and the distal 4 cm of the tail were dark blue to black, had several scabs and lacked pain sen-
sation.The tail lesions were thought to be due to ischemic necrosis related to uremic vasculitis. Serum creatinine concentration was
3.1 mg/dl and urea nitrogen concentration was 111 mg/dl. Hematocrit had improved to 19%.The dog was given intravenous fluid
therapy in preparation for surgical amputation of the distal tail. Castration was also recommended to treat the benign prostatic
hyperplasia with intraprostatic cysts. The serum urea nitrogen and creatinine concentrations decreased with fluid therapy and sur-
gery was performed for tail amputation and castration (Figure 1). The dog was discharged with similar treatment recommenda-
f
tions to those listed above. In addition, a combination of amoxicillin and clavulanic acid was administered for two weeks as a pro-
g
phylactic antibiotic for the tail amputation, and low-dose calcitriol therapy was initiated. Calcitriol was administered to decrease
serum parathyroid hormone concentration associated with renal secondary hyperparathyroidism.
The dog’s condition remained stable with this combination of nutritional and medical therapy for several months. The dog con-
tinued to eat the veterinary therapeutic renal food well and gained weight (body weight 7.5 kg).The coat returned to normal qual-
ity (Figure 2). The anemia resolved and the r-HuEPO was decreased to a maintenance dose twice weekly. The magnitude of