28 Sept 2015
Kit Sturgess
Job Title
Figure 1. Cat with advanced chronic kidney disease.
Optimising the management of feline chronic kidney disease (CKD; Figure 1) can significantly impact on the patient’s quality and quantity of life, but can be challenging as it requires the cooperation of both the cat and its owner, making both clinical and communication skills important.
Two key elements are needed to optimise treatment.
This article will focus on taking the patient’s clinical data and forming it into a long and short-term treatment plan.
Key elements of that treatment plan would include:
CKD is for the rest of the patient’s life, so it is worth investing in as accurate a diagnosis as possible and as a minimum sufficient to stage the case using the International Renal Interest Society (IRIS) staging (Tables 1a to 1c) together with potassium and calcium status.
Where patient and owner finances allow, complete investigation would include:
Having obtained as much information as possible the cat can be assigned to an IRIS classification and treatment can be prioritised based on:
A monitoring plan can also be implemented. No studies have looked at the optimum monitoring, but it is important not to over-monitor, particularly in the early stages, as this risks loss of client confidence and cooperation for when more intensive monitoring is likely to be useful in later stage disease.
The author generally advises monitoring blood pressure USG, UPCR, urine culture, PCV and biochemistry, including electrolytes, proteins, calcium and phosphorus:
Therapeutic goals should:
There is clear evidence of increased survival times with dietary management of cats in IRIS stage three and four (Elliott, 2006) and some evidence to support dietary management of cats in stage two, especially late stage.
Dietary benefit seems to be driven primarily by control of phosphate. Renal diets tend to have lower protein, but this is as much a function of reduced phosphorus as a deliberate goal, although in later stage disease lower protein levels are associated with reduced urea and, therefore, ameliorate some of the effects of uraemia. In addition, renal diets tend to have an increased potassium: protein ratio, increased levels of water soluble vitamins and omega-3 fatty acids.
A range of formulations of veterinary renal diets are available and different cats may prefer one type or another so, as the potential benefit is great – median survival 633 days versus 250 days (Figure 3; Elliott et al, 2000) – if initial attempts to introduce a kidney diet fail it is definitely worth trying other diets. With the survival benefits in mind, owner support and encouragement is critical for them to persevere with dietary therapy.
Timing a change to kidney diets is important and this should not be attempted when a cat is in crisis or feeling nauseated as this risks the cat associating that food with feeling unwell. Generally, the author would not try to change a cat on to a renal diet while it is hospitalised. Diet is not an acute therapy and other issues such as nausea, hypertension, anaemia and dehydration are better addressed first.
Diet is a crucial first step, but as disease progresses it may be insufficient. IRIS targets for serum phosphorus levels are given in Table 2.
There is a relatively poor correlation between total and ionised calcium; the latter should be used where possible to drive therapeutic decisions. Where diet fails phosphate binders are appropriate.
A variety of options exist (Table 3) and choice should be based on ease of administration and clinical effect. It is essential phosphate binders are given with feeding. If the patient is not eating, phosphate binders will not help. They act principally to make dietary phosphate into insoluble salts that are not absorbed.
In later stages of CKD, maintaining calorie intake and hydration can become a major issue and, ultimately, negative nitrogen balance and dehydration is the most common cause of euthanasia in cats with CKD. Many cats will derive a significant amount of fluid through eating wet food so maintaining caloric intake will have a significant benefit. A variety of options are available, but need to be tailored to the owner-cat partnership and would include:
Although widely used (including by the author) there is limited evidence cats truly develop uraemic gastritis, with one study suggesting that while gastric calcification was common, gastritis and ulceration was rare (McLeland et al, 2014).
Studies in humans and dogs have suggested use of ACEi may ameliorate some of the effects of CKD. A study correlated the immunoreactivity to angiotensin II in the tubules and interstitium to the degree of CKD (Mitani et al, 2013).
Anaemia can result from reduced production secondary to protein-calorie malnutrition, decreased red cell life span, chronic gastrointestinal haemorrhage with secondary iron deficiency as well as a failure of erythropoietin production.
Appropriate therapy will therefore depend on understanding the cause of the anaemia. In those cases where erythropoietin levels are low, recombinant human erythropoietin or better synthetic poietins such as darbopoietin can be highly effective. Generally, therapy should be started when clinical signs associated with anaemia are present (PCV less than 15% to 18%).
A variety of supplements are marketed as “supporting” renal function, including Pronefra (Virbac); Azodyl (Vétoquinol) and Rubenal (Vétoquinol).
These products contain different components aimed at managing uraemia. The true impact of these products on the progression of CKD is unknown, but they may provide some additional benefits in management (Hanzlicek et al, 2014; Rishniw and Wynn, 2011).
Therapy of CKD in cats can markedly impact on the quality of life of both the patient and the owner as well as considerably extending survival times. However, it is important the owner understands there is not a “one size fits all” treatment.
Best management is based on understanding the owner and the cat, accurate and complete diagnosis, continued support and encouragement and regular monitoring of what is a dynamic and progressive disease.
