Introduction - General Feline CKD Management

Medical management is the mainstay of treatment and can help patients cope with metabolic complications of the disease and improve quality of life. Typical complications that require identification and management include:

 Nutrition including appetite, nausea and body condition

 Hypertension

 Proteinuria

 Hypokalemia

 Hyperphosphatemia

 Hydration

 Anemia

 Urinary tract infections

Management of hypertension, hyperphosphatemia, hypokalemia and hydration will be the focus of this talk as other topics are covered in concurrent lectures in the series.

Hypertension

Elderly cats, particularly those with CKD, should be routinely screened both at initial CKD diagnosis, as well as throughout the course of the disease, as approximately 10% will develop hypertension at a later date. A variety of devices are available for evaluation of blood pressure in veterinary patients. At this time, no clear consensus on the most accurate and reliable methodology has been reached; however, Doppler and high-definition oscillometric devices appear to be most commonly recommended.

Unless blood pressure is >200 mm Hg and/or evidence of target organ damage is seen, blood pressure should be rechecked on two to three occasions to rule out white coat hypertension.

The patient should be classified according to their risk of target organ damage according to the International Renal Interest Society (IRIS) CKD blood pressure substaging system (Table 1).

Table 1

Once hypertension has been confirmed and classified, the decision to initiate therapy is based on the degree of hypertension and the animal's IRIS CKD stage. When blood pressure is >200 mm Hg and/or evidence of target organ damage is seen, therapy is immediately initiated. Patients with CKD stage 2 to 4 and blood pressure consistently over 160 mm Hg are candidates for treatment. Antihypertensive therapy should be considered for IRIS stage 1 patients with arterial blood pressure consistently greater than 180 mm Hg. A general guideline is to reduce the blood pressure to below 150 mm Hg.

Amlodipine is prescribed at an initial dose of 0.625 mg/cat <5kg and 1.25 mg in cats >5 kg. Alternative formulations of the drug have been explored including transdermal amlodipine and a chewable form which may provide some degree of efficacy. Blood pressure should be rechecked within 7–10 days after initiating therapy. In cats, if adequate blood pressure control has not been achieved the amlodipine dose is typically doubled.

Hyperphosphatemia

The kidneys are the main route of phosphorus excretion and as kidney function declines, hyperphosphatemia develops. Hyperphosphatemia is detrimental because it contributes to renal secondary hyperparathyroidism, tissue mineralization and progression of CKD. Thus, controlling phosphorus intake through diet and phosphate binders is an important part of CKD management.

If a renal diet is initiated and phosphorus is still elevated after 4–6 weeks, then a phosphate binder is recommended with the goal of keeping serum phosphorus in the low normal range if possible (Table 2). These medications bind the phosphorus in the food, making it less bioavailable, so it is critical that the medication is given with each meal. Several different phosphate binders are available including aluminum hydroxide, calcium carbonate, lanthanum carbonate; however, the main problem with administration is palatability.

Table 2. Recommended serum phosphorus concentrations at each IRIS stage²

Therapy is initiated with a starting dose of 30–100 mg/kg/day for aluminum hydroxide, 150 mg/kg/day for calcium carbonate and 30 mg/kg/day for lanthanum carbonate. Doses are to effect, and generally therapy begins at the lower end of the dose range and is increased every 4–6 weeks until serum phosphorus concentrations are within the desired range. Use of calcium-containing phosphate binders is associated with the development of hypercalcemia, particularly if calcitriol is also being administered. Serum calcium should be monitored during use.

Hypokalemia

Cats with CKD should be routinely screened for hypokalemia. Hypokalemia is a common finding in cats with stage 2 and 3 CKD with approximately 20–30% of cats affected. Mild hypokalemia may not be associated with clinical signs and clinically relevant hypokalemia can often be missed due to the lack of electrolyte readings on in-house chemistry analyzers. Moderate hypokalemia (2.5–3.0 mEq/L) may result in muscle weakness, lethargy, inappetence, and constipation. Severe hypokalemia (<2.5 mEq/L) may result in hypokalemic myopathy including cervical ventroflexion and plantigrade stance.

Potassium supplementation is recommended in hypokalemic animals and the oral route is the safest and preferred route in stable patients. Based on the possible renal effects of hypokalemia and how poorly representative serum potassium is in the face of metabolic acidosis, some clinicians advocate prophylactic supplementation even when serum potassium is in the low normal range, with a goal of maintaining serum potassium levels above 4 mg/dL. However, the value of prophylactic potassium supplementation has not yet been established. Potassium supplementation may be provided orally as potassium gluconate, (1–4 mEq per cat twice daily), or potassium citrate (40–75 mg/kg orally divided twice daily), to effect.

Potassium citrate has the added advantage of being an alkalinizing agent; however, the degree to which this is effective for metabolic acidosis has not been evaluated. In decompensated patients in hospital, potassium chloride is used to supplement intravenous fluids. Potassium chloride is not recommended as an oral supplement because it is acidifying and unpalatable, but may be added to subcutaneous fluids at concentration up to 30 mEq/L (higher concentrations can be associated with irritation). Serum potassium should be rechecked 7–10 days after initiating potassium supplementation and dosing titrated accordingly.

Fluid Balance

As CKD progresses, GFR decreases and azotemia worsens, yet the patient is not able to compensate by concentrating urine and maintaining hydration. Dehydration is therefore a common complication of CKD and can lead to inappetence, lethargy, weakness, constipation, and increased susceptibility to uremic crisis. Owners should be aware that concurrent illness, vomiting and diarrhea, household changes/stress or inadequate water sources promote dehydration and can have more serious effects in CKD patients, potentially precipitating a uremic crisis. Maintaining hydration by administering subcutaneous balanced electrolyte solutions appears to anecdotally improve appetite, activity and quality of life and reduce constipation in CKD patients, although no clinical trials have been performed.

Subcutaneous fluid administration is generally feasible in cats and small dogs and can be a very helpful tool for owners in management of disease, particularly in Stage 3 and 4. Additionally, feeding canned food instead of dry kibble, or adding water to food is another way to increase water consumption. Paying special attention to water sources in the house - fresh, accessible, water fountains for cats, etc. is also an important tip for owners.

References

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2.  Bijsmans ES, Jepson RE, Chang YM, et al. Changes in systolic blood pressure over time in healthy cats and cats with chronic kidney disease. J Vet Intern Med. 2015;29:855–861.

3.  Quimby JM, Smith ML, Lunn KF. Evaluation of the effects of hospital visit stress on physiologic parameters in the cat. J Feline Med Surg. 2011;13:733–737.

4.  Polzin DJ. Evidence-based step-wise approach to managing chronic kidney disease in dogs and cats. J Vet Emerg Crit Care (San Antonio). 2013;23:205–215.

5.  Huhtinen M, Derre G, Renoldi HJ, et al. Randomized placebo-controlled clinical trial of a chewable formulation of amlodipine for the treatment of hypertension in client-owned cats. J Vet Intern Med. 2015;29:786–793.

6.  Brown S, Atkins C, Bagley R, et al. Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. J Vet Intern Med. 2007;21:542–558.

7.  Polzin DJ. Chronic kidney disease in small animals. Vet Clin North Am Small Anim Pract. 2011;41:15–30.

8.  Jepson RE, Syme HM, Elliott J. Plasma renin activity and aldosterone concentrations in hypertensive cats with and without azotemia and in response to treatment with amlodipine besylate. J Vet Intern Med. 2014;28:144–153.

9.  Syme H. Hypertension in small animal kidney disease. Vet Clin North Am Small Anim Pract. 2011;41:63–89.

10. Kidder AC, Chew D. Treatment options for hyperphosphatemia in feline CKD: what's out there? J Feline Med Surg. 2009;11:913–924.