Page 773 - Small Animal Clinical Nutrition 5th Edition

Chronic Kidney Disease 801

appetite. The dog also had a lifelong history of polydipsia and polyuria.
Physical examination revealed 5% dehydration, thin body condition (body condition score 2/5, body weight 5.9 kg), pale mucous
VetBooks.ir membranes, poor coat quality, blood dripping from the penis and a small, irregular left kidney. Rectal examination revealed sym-
metric, nonpainful prostatomegaly and hematochezia.
Clinicopathologic abnormalities included nonregenerative anemia (hematocrit 15% [reference range 37 to 55%]), azotemia (urea
nitrogen 139 mg/dl [reference range 7 to 32 mg/dl], creatinine 3.3 mg/dl [reference range 0.5 to 1.5 mg/dl]) and hyperphos-
phatemia (8.3 mg/dl [reference range 2.2 to 7.9 mg/dl]). Examination of the blood smear revealed acanthocytosis (1+), poikilocy-
3
tosis (1+) and occasional schistocytes; spherocytes were not present. The platelet count was within normal limits (341 x 10 /µl).
Urinalysis revealed isosthenuria (specific gravity 1.012) and hematuria (too numerous to count red blood cells per high-power field).
Problems identified included CKD, nonregenerative anemia, prostatomegaly, hematemesis and hematochezia. Additional diag-
nostic procedures performed included fecal flotation, urine culture, bone marrow aspiration, indirect blood pressure measurement,
fundic examination, abdominal radiographs and ultrasound and ultrasound-guided fine-needle aspiration of the prostate gland.
Fecal flotation was negative for intestinal parasites. Aerobic urine culture yielded no bacterial growth. Cytologic examination of the
bone marrow aspirate revealed erythroid hypoplasia with adequate iron stores. Abdominal radiographs revealed prostatomegaly and
small irregular renal margins. Abdominal ultrasonography revealed that the kidneys were bilaterally hyperechoic with very thin renal
cortices (3 cm width). Considering the dog’s age and breed, these findings were consistent with congenital renal dysplasia.
Ultrasonography of the prostate gland revealed diffuse prostatomegaly with multiple small intraprostatic cysts. Cytologic examina-
tion of the prostatic aspirates revealed normal prostatic epithelial cells, numerous RBCs and small numbers of neutrophils and
macrophages.The ultrasonographic and cytologic findings were consistent with benign prostatic hyperplasia with intraprostatic cyst
formation. Aerobic culture of the prostatic aspirate yielded no bacterial growth. Results of indirect measurements of systemic blood
pressure were within normal limits. The fundic examination was normal.
Assess the Food and Feeding Method
Originally the dog had been fed a commercial dry dog food; after the diagnosis of CKD was made, a commercial veterinary ther-
a
apeutic renal food with controlled levels of protein, phosphorus and sodium was recommended. The dog continued to vomit and
refused to eat the food, however.The owner had switched to a moist commercial grocery brand dog food supplemented with com-
mercial treats.The moist food was fed twice daily and treats were given multiple times throughout the day to encourage the dog to
eat. The dog only ate small amounts of the moist food and some treats during the week before admission.

Questions
1. What are the most likely reasons for this dog’s anemia?
2. Why was the magnitude of increase in serum creatinine and urea nitrogen concentrations markedly different?
3. What nutritional recommendations should be made to optimize management of this dog’s problems?
4. What other therapies might improve nutritional management of this patient?

Answers and Discussion
1. There were multiple reasons for this dog’s anemia. Although the anemia was initially presumed to be an immune-mediated
hemolytic anemia, this diagnosis was unlikely at this time. The referring veterinarian submitted a sample to a commercial labo-
ratory for a Coombs test, and results were negative. Red blood cell morphologic examination revealed evidence of fragmentation
(which occurs with uremia) and no spherocytes. Likewise, the serum bilirubin concentration remained normal and bilirubinuria
was not present.The presumption of an immune-mediated process was based on the concurrent thrombocytopenia and progres-
sive anemia following trimethoprim-sulfamethoxazole therapy. The thrombocytopenia quickly resolved with discontinuation of
trimethoprim-sulfamethoxazole therapy and treatment with prednisone. However, anemia worsened progressively. Thrombo-
cytopenia was likely immune-mediated secondary to trimethoprim-sulfamethoxazole therapy; however, there was no evidence of
immune-mediated hemolytic anemia.
Results of bone marrow examination were interpreted to be consistent with a hypoproliferative anemia secondary to relative
erythropoietin deficiency. Dogs with moderate to severe CKD consistently have low erythropoietin concentrations relative to the
degree of anemia. Therefore, based on the bone marrow findings and concurrent diagnosis of CKD, it was likely that erythro-
poietin deficiency secondary to CKD was responsible for a major component of the anemia.
Another contributing factor to the anemia was gastrointestinal (GI) blood loss from uremic gastritis and concurrent prednisone
therapy.The dog had a history of hematemesis (fresh blood and vomitus that appeared like “coffee grounds”) and hematochezia.
Additionally, during hospitalization the dog had marked melena. Uremic gastritis may contribute to GI bleeding, vomiting and
anorexia as seen in this dog. Prednisone therapy probably contributed to some of the GI ulceration presumed to be present.
2. There are multiple reasons for the discrepancy in the magnitude of serum creatinine and urea nitrogen concentrations in this dog.
Creatinine enters the blood as a result of the nonenzymatic breakdown of phosphocreatine in skeletal muscle.Therefore, the rate
of entry of creatinine into the blood depends on muscle mass. Serum creatinine concentration will be lower than would be expect-
ed from the glomerular filtration rate (GFR) in a dog with decreased muscle mass. Therefore, the serum creatinine concentra-