Dietary Management of Cats with CKD

• Diagnosis relies on biochemistry (urea, creatinine, SDMA, potassium, calcium, phosphate), urinalysis (USG, protein/UPC), blood pressure, haematology and imaging (ultrasound, radiography, occasionally advanced imaging), plus adjuncts such as FGF‑23, PTH or kidney biopsy/FNA in selected cases.
• IRIS staging standardises diagnosis and management: Stage 1 is non‑azotemic but with evidence of renal abnormality (e.g. inadequate USG, persistent proteinuria, imaging/biopsy changes), Stage 2–4 are defined by creatinine and SDMA cut‑offs, with substaging by UPC and systolic BP to reflect proteinuria and risk of target organ damage.

Important practical points: cats should be hydrated and fasted prior to staging, and when creatinine and SDMA stages differ, the higher stage guides therapy.

CKD causes phosphate retention, reduced calcitriol, hypocalcaemia and secondary hyperparathyroidism, leading to bone resorption, increased intracellular calcium, ATP disruption, neurotoxicity, immune dysfunction, anaemia and increased FGF‑23.

Over time, some cats develop hypercalcaemia within CKD‑MBD, with lower potassium and phosphate identified as independent risk factors for increasing total calcium; multiple parameters (creatinine, SDMA, phosphate, FGF‑23, ionised or total calcium) tend to increase in cats whose calcium status is “uptrend.”

Monitoring total and/or ionised calcium every 3–6 months is recommended rather than “set and forget” once a renal diet is started.

• Multiple trials show renal diets outperform conventional maintenance diets in CKD cats:
  • Elliot et al (JSAP 2000): cats on renal diets survived a median 21 months vs 8.8 months for those that refused the diet.
  • Plantinga et al (VR 2005): 321 cats, 175 on conventional diets vs 146 on seven renal diets, with median survival 16 months vs 7 months.
  • Ross et al (JAVMA 2006): in IRIS 2–3 cats, uraemic episodes and renal mortality were 26% and 22% on maintenance diets vs 0% on renal diets over two years.

For early CKD (including IRIS Stage 1), retrospective practice data show cats on renal diets are 41–46% less likely to progress to more advanced stages and live on average 5 months longer, with about a 30% reduction in all‑cause mortality and an adjusted hazard ratio for death around 0.70.

• Renal diets typically incorporate:
  • Phosphate restriction, which reduces histologic lesion severity and slows progression.
  • Modified protein levels to reduce nitrogenous waste while maintaining body weight and muscle mass via high energy density.
  • Supplementation with essential fatty acids, potassium, and often tailored sodium, vitamins and antioxidants.

The best‑supported mechanism is dietary phosphate restriction (with or without phosphate binders), which has excellent evidence for slowing CKD progression and attenuating histological damage.

• Suggested thresholds for initiating a renal diet include:
  • IRIS Stage 1 with phosphate >1.5 mmol/L or a rising phosphate trend, or rising FGF‑23.
  • Any IRIS Stage ≥2, provided the cat is stable and not acutely ill.
• Renal diets are generally not recommended in acute illness, IRIS Stage 4 (where intake may be limiting), IRIS Stage 1 cats with hypercalcaemia or in growing, pregnant or lactating cats.

Phosphate targets (derived from survival associations and histopathology) are roughly <1.5 mmol/L in Stage 1, 0.81–1.45 in Stage 2, 0.81–1.60 in Stage 3 and 0.81–1.90 in Stage 4, with FGF‑23 ≥400 pg/mL used as an indicator of phosphate overload and a >50% decrease suggesting improved control.

• Transitioning: gradual introduction over ~10 days (often longer), avoiding abrupt switches; 93% of cats in one series were successfully transitioned with this approach.
• If the cat refuses ≥2 meals within roughly 36 hours, revert to previous diet or offer acceptable alternatives, prioritising energy intake and body weight over “diet purity” in the short term.

Helpful techniques include mixing old and new foods (“SneakMix”), using appetite stimulants, offering variety, and avoiding introduction of new diets when the cat is sick.

Diet choice considerations:

• Prefer wet formulations to support hydration.
• Match texture and flavour to the cat’s preferences.
• Check Ca:P by dividing listed calcium % by phosphorus % (as‑fed or dry matter consistently), aiming for Ca:P about 1.1–1.4:1 and phosphorus around ≤1.3 g/1000 kcal for renal diets.

If total calcium exceeds ~3.0 mmol/L after starting a renal diet, ideally check ionised calcium and consider shifting to a higher‑phosphate/senior diet or mixing with maintenance to reduce Ca:P; supplements such as chia seeds (1–2 g/day) and diets with Ca:P <1.4:1 can help correct renal‑diet‑associated hypercalcaemia.

• Phosphate can be reduced by improved hydration, dietary phosphate restriction (effective up to IRIS Stage 3) and phosphate binding agents (usually required in IRIS Stage 4 or when diet alone is insufficient).
• Common binders include aluminium hydroxide, chitosan and calcium carbonate; lanthanum, sevelamer and lenziaren are additional agents, though some carry hypercalcaemia risk, especially with concurrent calcitriol.

Binders must be given with food to be effective, and acceptance can be poor, so owner education and palatability strategies are crucial.

• Inappetence is common: one study found 52% of CKD cats were inappetent 5–7 days per week.
• Appetite stimulants:
  • Mirtazapine (serotonin and presynaptic α2 antagonist) improves appetite and weight but can cause “serotonin syndrome” signs; dosing must be reduced in CKD.
  • Capromorelin (ghrelin receptor agonist) in a 55–56‑day trial of 176 CKD cats produced mean +5.2% body weight gain vs −1.6% in placebo, with >80% of treated cats gaining weight and hypersalivation as a notable adverse effect. This medication is not yet available in Australia.

Antiemetics:

• Maropitant reduces vomiting but did not significantly change appetite, activity, weight or creatinine in a short‑term trial.
• Mirtazapine, ondansetron (for refractory nausea), and metoclopramide (preferably CRI due to short half‑life, noting its effect on renal plasma flow) all play roles in controlling nausea and supporting intake.

Assisted enteral nutrition (feeding tubes) should be considered when oral intake remains inadequate to prevent malnutrition and support consistent delivery of renal diets and medications.

• Home monitoring focuses on body weight, food and water intake, urination behaviour and activity levels.
• Clinic monitoring ranges from minimum (history, body weight/score, PE, hydration, USG/dipstick, BP) to standard (plus PCV/TP, urea, creatinine, potassium, total calcium, phosphate, UA with sediment, UPC) to ideal (adding haematology, urine culture, FGF‑23, PTH, ionised calcium and blood gas).

Renal diets are central to progression and survival in feline CKD (including Stage 1), all causes of inappetence must be addressed, and ongoing monitoring plus strong owner communication and support will underpin successful long‑term management.