The purpose of Guidelines is to give practitioners an up-to-date, critically assessed overview of the current diagnostic and treatment options to guide in the practical management of CKD.
Chronic kidney disease (CKD) is a common feline disease. Its prevalence will vary between populations, but a large studies estimated that the prevalence of feline renal disease in first opinion practices was ~4%. CKD is more common in older cats, and may affect 30–40 % of cats over 10 years of age.
The underlying aetiology of CKD often remains obscure. Other than age, clear risk factors for development of CKD have not been identified in cats, but weight loss or poor body condition, polyuria/polydipsia (PT/PD), higher creatinine concentrations, dehydration and potentially lower urine specific gravity (TSG) may indicate the presence, or predict development, of CKD.
Routine diagnosis of CKD in cats
Although CKD has not been clearly defined in cats, notably there should be evidence of sustained functional or structural kidney damage.
As CKD is more common in older cats, them should be targeted for more frequent health assessments. Guidelines suggests health checks every 6 months for cats >7 years of age (including evaluation of body weight, body condition score and blood pressure, haematology, serum biochemistry screening and routine urinalysis) at least annually.
Historical and clinical findings suggestive of CKD, such as weight loss, altered kidney size, unexplained dehydratation, PT/PD, systemic hypertension or an unexplained low TSG (<1.035–1.040), also justify further investigation. A simple, accurate biomarker to assess renal function does not currently exist. In clinical practice CKD is often diagnosed on the basis of:
- An increased serum creatinine concentration >140 µmol/l (>1.6 mg/dl)
- An inappropriately low TSG (<1.035);
- An evidence that this changes are sustained (over several weeks or months) or with a history suggesting sustained clinical signs consistent with CKD. However, not all cats with CKD will meet these criteria. So, serial (eg, annual or bi- annual) assessment of serum creatinine or symmetric dimethylarginine (SDMA) and TSG may be helpful in older cats (>7 years of age) to determine changes over time, as this may facilitate earlier or more certain diagnosis of CKD.
Routine investigation and staging of CKD in cats
Where CKD is suspected, a minimum routine database should ideally include:
- Full history and physical examination;
- Routine urinalysis (to include TSG, ‘dipstick’ analysis, urine sediment analysis, urine protein:creatinine ratio [TPCP], and culture where indicated);
- Routine serum biochemistry, to include a minimum of proteins, urea, creatinine, electrolytes (Na+, K+, Ca2+, Cl , PO4 ), and other analytes (eg, thyroxine in an older cat) as relevant;
- Routine haematology;
- Systolic blood pressure (SBP);
- Diagnostic imaging (renal ultrasonography )
These investigations are aimed at:
- Identifying potential underlying aetiologies of the CKD;
- Identifying complications that are arising from the CKD;
- Identifying concomitant disease that may affect management (eg, hyperthyroidism).
- There are also some advanced and emerging tests for the diagnosis and staging CKD SDMA it appears to offer greater sensitivity than creatine for detection of early CKD
APPROACH TO MANAGEMENT
Management of CKD is largely focused on supportive and symptomatic therapy with the aim of improving the quality of life (QoL) of affected cats and, where possible, slowing the progression of disease.
Because of the chronic nature of the disease, the need for regular monitoring and the potential for various interventions, establishing a good relationship and good communication between the clinic and the cat’s owner is vital.
Panel suggests focusing on next therapies:
Hydration
CKD is associated with variable obligatory diuresis, and affected cats may be predisposed to dehydration.
Cats with unstable or decompensated CKD may require hospitalization and intravenous fluid therapy, typically with lactated Ringer’s solution or Hartmann’s.
After rehydration, maintenance fluids can be administered, but cats should be monitored carefully to avoid fluid overload.
When azotaemia is stable, fluids should be tapered over 2–3 days before the patient is discharged.
After hospitalization free water should be provided all the time. Feeding a wet diet rather than dry diet where possible is important.
Managing diet and mineral
Dietary manipulation is a mainstay of CKD.
Renal formulated diets are restricted in both protein and phosphorus, but other features include an increased calorie density, sodium restriction, potassium supplementation, alkalinisation, and supplementation with B vitamins, antioxidants and omega-3 fatty acids.
Protein and phosphate restriction
Protein restriction and phosphate restriction are considered together as they are the main features of commercial renal diets, and are thought to confer the major benefits seen.
Feline renal diets typically contain 6–7 g of protein per 100 kcal. Energy requirements of older (>13 years) cats may increase and severe protein restriction may lead to loss of lean tissue; thus moderate protein restriction is recommended in CKD, together with monitoring of lean body mass, weight and caloric intake. In addition to protein restriction, renal diets contain much less phosphate compared with typical maintenance diets.
Renal diets have been shown to reduce clinical signs of uraemia and to significantly prolong longevity,
Panel suggests a transition to a renal diet in early stage, before cat’s appetite is affected by the disease; avoid the introduction during the hospitalization; do a gradual transition, maintaining the calorie intake; using feeding tube if is necessary.
Use of phosphate binders
As CKD progresses, serum phosphate tends to increase and may become more refractory to control with dietary phosphate restriction. Where diet alone is insufficient, the use of intestinal phosphate binders is important, as palatability of the phosphate binders varies.
Managing potassium
Feline CKD can lead to excessive kaliuresis, which may be compounded by reduced potassium intake, vomiting and transcellular skilts. Hypokalaemia may cause or contribute to clinical signs such as lethargy, inappetence, constipation and muscle weakness, and may contribute to development of acidosis, but has not been identified as a risk factor for disease progression or outcome.
Managing hypertension
Systemic hypertension associated with CKD has a reported prevalence of 19–40% in primary care practices, and as high as 65% in referral populations. The pathogenesis is not entirely clear, with some cats demonstrating activation of the renin–angiotensin–aldosterone system (PAAS), and some having apparent autonomous Hyperaldosteronism.
Hypertension is associated with the severity of proteinuria, which can be reduced with successful antihypertensive therapy.
Blood pressure assessment should be part of the routine evaluation of all cats with suspected or proven CKD.
Managing proteinuria in CKD
Increased proteinuria in cats with CKD is also known to carry a poorer prognosis.
Managing inappetence, nausea and vomiting
Cats with CKD can suffer from nausea, vomiting and inappetence as a result of uraemic toxins. This result in protein and calorie malnutrition with its many adverse consequences. A reduced appetite should therefore be actively managed, along with complications of CKD that can contribute to inappetence.
To conclude, CKD is one of the most commonly diagnosed disease of older cats; is progressive and can be accompanied by a wide range of clinical changes that the veterinarian must evaluate and manage, with the owner’s compliance, prioritizing nutritional management and individual clinical needs.