Oral sodium bicarbonate is the most commonly used alkalinizing agent for patients with metabolic acidosis of chronic renal
insufficiency or failure. Because the effects of gastric acid on oral sodium bicarbonate are unpredictable, the dosage should
be individualized for each patient. A suggested initial dose is 8 to 12 mg/kg given every eight to 12 hours. Unfortunately,
many dogs and cats find sodium bicarbonate distasteful unless given as tablets. Sodium bicarbonate is available as 5-and 10-grain
Potassium citrate may offer the advantage, especially in cats, of allowing for the simultaneous treatment of both hypokalemia
and acidosis with a single drug. Metabolic acidosis when accompanied by potassium or magnesium depletion may respond poorly
to alkali therapy alone. However, since potassium doses required for adequate correction of hypokalemia may exceed the citrate
dose required to correct acidosis, there is a risk of excessive alkalinization. Starting doses of 40 to 60 mg/kg given orally
every eight to 12 hours are recommended.
Once therapeutic targets have been attained, re-evaluate dogs and cats receiving alkalinizing therapy every three to four
months to ensure continued compliance and therapeutic success at maintaining the target.
#6 Maintain hydration. Intervention to correct and prevent dehydration is indicated in dogs and cats with chronic kidney disease stages 2 through
4 with clinical evidence of dehydration. Maintaining hydration in patients with chronic kidney disease depends on adequate
compensatory polydipsia. Cats with chronic kidney disease appear to be particularly susceptible to chronic dehydration, perhaps
because the magnitude of compensatory polydipsia is inadequate. However, lack of adequate access to good quality drinking
water, certain environmental conditions, and intercurrent illnesses that limit fluid intake or promote fluid losses (e.g. pyrexia, vomiting, diarrhea) may lead to dehydration.
The clinical consequences of chronic dehydration include decreased appetite, lethargy, weakness, constipation, prerenal azotemia,
and predisposition to acute kidney injury. Additional loss of kidney function due to acute kidney injury is a potentially
important cause of progression of chronic kidney disease. The goal of therapy is to correct and prevent dehydration and its
In patients with signs consistent with chronic or recurrent dehydration, long-term subcutaneous fluid therapy may be considered
(evidence grade 4). Typically, a balanced electrolyte solution (e.g. lactated Ringer's solution) is administered subcutaneously every one to three days as needed. The volume administered depends
on the patient's size, with a typical cat receiving about 75 to 100 ml per dose. If the patient's clinical response is suboptimal,
the dose can cautiously be increased. However, it is possible to induce fluid overload with excessive fluid administration.
In addition, sodium-containing fluids used for subcutaneous therapy do not provide electrolyte-free water. A more physiologically
appropriate approach is to provide water through a feeding tube. This approach may also be easier for clients. Because recent
evidence suggests excessive sodium intake may harm the kidneys, recommendations for long-term sodium administration in any
form should be carefully considered.9,10
AMELIORATE THE EFFECTS OF CHRONIC KIDNEY DISEASE
#7 Correct clinically apparent anemia. Treating anemia is indicated in a patient with chronic kidney disease stages 3 and 4 when the hematocrit declines below 20%
and the patient has clinical signs attributable to anemia. The goal of treatment is increasing the hematocrit to about 30%
to 40% in cats and 38% to 48% in dogs. Signs attributable to anemia may include impaired appetite, lethargy, weakness, and
decreased social interaction. Administering erythropoietin, either as recombinant human erythropoietin (Epogen—Amgen, Procrit—Ortho
Biotech) or darbepoetin alfa (Aranesp—Amgen), is the only effective means of correcting anemia of chronic kidney disease.
However, other factors that may exacerbate anemia, including blood loss, iron deficiency, poor nutrition, hyperparathyroidism,
and infections, should be ruled out first.
Anti-erythropoietin antibodies may develop in some patients, rendering them unresponsive to further recombinant human erythropoietin
treatment. Immediately terminate therapy if antibody -associated anemia is suspected. Since canine and feline species-specific
erythropoietin is not available, closely monitor patients treated with recombinant human erythropoietin for recurrence of
anemia, which may herald the onset of anti-erythropoietin antibodies. A newer, longer-acting erythropoietin, darbepoetin,
may be less likely to induce anti-erythropoietin antibodies, but experience with darbepoetin in dogs and cats is limited.
Monitor dogs and cats treated with erythropoietin weekly until treatment targets have been achieved. Once therapeutic targets
have been attained, the packed cell volume should be monitored at least monthly to detect development of anti-erythropoietin
antibodies and to adjust dosages or provide supplemental iron as needed.