Evidence over reviews — drugs and supplements sorted by research, track record and real usage in this app.
Clearly worth starting when phosphorus exceeds the stage target. The first card to play when renal diet alone falls short.
Binders grab dietary phosphorus in the gut before it is absorbed and send it out in stool. There are several kinds — calcium carbonate (cheap, watch calcium), lanthanum carbonate (potent, calcium-free), sevelamer. Adding one when renal diet alone cannot reach the phosphorus target is the standard IRIS sequence, and phosphorus control changing CKD progression is about the least-disputed fact in this field.
A well-evidenced binder in an easy-to-mix powder. One stick is a full dose close to the studied amount — start at 1/3–1/2 stick and step up once it is eaten well. Judge the effect by blood phosphorus after 4–6 weeks.
A phosphate binder developed by Porus GmbH (trademark and EU authorisation), made in Germany and sold by Dechra. The single active is lanthanum carbonate octahydrate — the same compound as Lantharenol and Renalzin, which were studied in cats in Europe. Read the label in three steps. 457 mg of the 520 mg of granules (distributor label) is lanthanum carbonate octahydrate, and 46% of that — about 210 mg (up to about 250 mg by specification) — is the elemental lanthanum that actually binds phosphorus. Fosrenol is labelled as elemental lanthanum, so Fosrenol 500 mg ≈ 2.0–2.4 Catney One sticks. The amount used in feline clinical studies (400–600 mg octahydrate a day) is about 0.9–1.3 sticks, and the Fosrenol starting dose for a 5 kg cat (12.5–25 mg/kg) is 0.3–0.6 stick. Measured in people, lanthanum binds roughly 80–155 mg of phosphorus per gram, so one stick blocks about 15–40 mg a day — a slice of a CKD cat's daily 150–300 mg intake. Diet comes first; the binder is a correction on top.
The reference lanthanum binder. If you still have some, keep using it at the elemental dose — but it is now hard to obtain in Korea, so plan the switch to the same compound (Catney One) before it runs out.
Fosrenol is the brand name for lanthanum carbonate (developed by Shire, Takeda since 2020). It treats hyperphosphataemia in human dialysis patients; in Korea JW Pharmaceutical imported 500 and 750 mg chewable tablets and a 1000 mg oral powder, and vets split them for cats. When the supply contract with Takeda ended, all three approvals were voluntarily withdrawn on 5 December 2024 (the 500 mg stopped shipping in November 2024). So unless a clinic still has stock or it comes from abroad, it is now hard to get. The label is elemental lanthanum, so one 500 mg tablet equals 2.0–2.4 Catney One sticks (about 210–250 mg elemental each). The feline starting dose is 12.5–25 mg/kg a day (1/8–1/4 tablet for a 5 kg cat), and 35–50 mg/kg is often needed when phosphorus is high. The simplest switch is to Catney One, matching the elemental amount. Among human drugs, sevelamer (Renvela, Invela) is still sold in Korea — per gram it binds about 1/2.7 as much as elemental lanthanum, but the amount of powder to feed is similar to Catney One.
A realistic option when calcium is too high for calcium binders and lanthanum is hard to get. Split the powder over 2–3 meals a day and judge by blood phosphorus after 4–6 weeks.
Renvela (Sanofi, the original) and Invela (SK Chemicals, a 2015 generic) are brand names for the same compound, sevelamer carbonate. Both come as 800 mg tablets and 0.8 g / 2.4 g oral powder. A non-absorbed polymer with no calcium or aluminium binds phosphorus in the gut and leaves in the stool. Since Fosrenol left Korea in December 2024, it is effectively the only calcium-free binder available as a human drug there. The feline dose is extrapolated from paediatric dosing: start at 100–120 mg/kg a day, titrating to 130–160 mg/kg, split over three meals (Kidder & Chew 2009). For a 5 kg cat that is about 0.5–0.8 g a day — 2/3 to one 0.8 g sachet. Per gram it binds about 1/2.7 as much as elemental lanthanum, but comparing product weights is more practical: one Catney One stick (520 mg, about 210–250 mg elemental) binds roughly as much phosphorus as 0.56–0.67 g of sevelamer (human binding coefficients). So the amount of powder to feed is not very different from Catney One. The older hydrochloride form (Renagel) could worsen acidosis; today's carbonate form fixes that.
Clearly worth starting when systolic stays above 160. Top-tier evidence for protecting the eyes, brain, heart and kidneys.
Hypertension has no symptoms, which makes "symptomatic treatment" a misnomer — unmeasured, it silently damages the eyes (acute blindness), brain, heart and kidneys. Amlodipine dilates vessels directly and lowers pressure reliably; telmisartan adds proteinuria reduction, a bonus in CKD. Both are solidly evidenced in cats. The raw material for the decision is home blood-pressure records — your Care Companion trend chart.
Clearly worth discussing for a cat persistently above UPC 0.4. The liquid form makes dosing easier, too.
Proteinuria independently accelerates CKD by damaging the tubules directly. Telmisartan blocks RAAS to lower glomerular pressure and reduce the leak — one of the few drugs formally licensed for feline proteinuria (liquid Semintra). Trials proved UPC reduction; benazepril, in the same family, is the alternative. For cats with concurrent hypertension, one drug covers both problems — see the BP-meds entry for that side of the story.
For a cat whose intake has collapsed, this drug builds the platform for everything else. Far better evidenced than the "just a stopgap" reputation suggests.
CKD inappetence is not pickiness — it is where the uremia-nausea spiral begins: not eating costs muscle, and muscle loss accelerates the disease. Mirtazapine acts on serotonin and histamine receptors in the brain, raising appetite and easing nausea. In a placebo-controlled trial in CKD cats (Quimby 2013), 1.88 mg (1/8 of a 15 mg tablet) every other day for 3 weeks increased appetite and weight and reduced vomiting — rare direct feline evidence. Because poor kidneys clear it slowly, every other day rather than daily is the norm; vocalising or agitation after a dose means the dose is too high. The same drug as an ear ointment is Mirataz; a stimulant with a different mechanism is capromorelin (Elura) — see those cards.
First choice for cats who fight pills or are nauseous. Nothing goes in the mouth, so the cat never learns that food and mouth mean something unpleasant.
Same drug as mirtazapine tablets, but applied to the hairless skin inside the ear instead of swallowed. Dose is 0.1 g once daily (2 mg mirtazapine, about a 3.8 cm strip of ointment); the licensed course is 14 days. In a randomised trial of 177 cats with poor appetite and weight loss (Poole 2019), body weight rose 3.9% on average in 14 days (placebo 0.4%) and appetite improved. Same drug, so the benefits and side effects (vocalising, agitation — serotonin signs) are in the same family as the tablet. The difference is zero pilling stress — for a sick cat that is not a small thing. Whether to continue past 14 days can be judged from how weight and food intake moved over those two weeks.
The drug for holding weight over months, not a few days. For a CKD cat that keeps losing weight, it has the longest-running evidence of any option.
Capromorelin directly stimulates the receptor for ghrelin, the hunger hormone released when the stomach is empty, creating a genuine hunger signal in the brain. Its mechanism is completely different from mirtazapine (serotonin/histamine), so one can be the alternative when the other does not suit. Dose is 2 mg per kg once daily as an oral liquid. In a trial of 176 CKD cats that had lost at least 5% of body weight (Wofford 2025), weight rose 5.2% on average over 56 days while the placebo group lost 1.6%; gains were already visible at days 15 and 27. Unlike Mirataz (licensed for 14 days), it is designed for long-term use, which fits when steady weight loss is the problem. The trade-offs: vomiting in about 30% is the most common side effect, and a brief drop in heart rate and blood pressure means caution in cats with heart disease.
Not a first-line drug. A fallback to agree with your vet when mirtazapine, Mirataz or capromorelin do not suit or are unavailable. Never use it together with mirtazapine.
An antihistamine that blocks serotonin and histamine receptors in the brain, dulling the feeling of fullness. Never licensed for cats, it has been used as an appetite stimulant for decades; the 2022 ISFM guidelines list 1–4 mg per cat every 12–24 hours. Its efficacy rests on experience rather than controlled trials, so it sits a step below mirtazapine (Quimby 2013), Mirataz (Poole 2019) and capromorelin (Wofford 2025), which all have feline trial evidence. The Trestan capsule common in Korea is a human combination product: each capsule holds 1.5 mg cyproheptadine salt (about 0.9 mg of the drug itself) plus carnitine, lysine and vitamin B12. Only the cyproheptadine stimulates appetite; the rest has weak or no feline appetite evidence (see Types & ingredients). The key caution is mirtazapine — cyproheptadine is the antidote for mirtazapine overdose, so giving both cancels each other out.
A clearly evidenced choice for a vomiting cat. But the hope that it will also restore eating is not backed by the data — that job belongs to appetite stimulants.
Uremic toxins stimulate the brain's vomiting center directly — CKD nausea is not an upset stomach. Maropitant (Cerenia), an NK-1 blocker, proved it reduces vomiting in a placebo-controlled CKD-cat trial. The honest limit: in that same trial, appetite and weight did not improve. Hence the practical combo — an antiemetic to switch off nausea, plus an appetite stimulant to restart eating. And remember: invisible nausea (lip-licking, hovering over food) deserves treatment too.
Life-quality-changing for stage 3–4 cats with recurring dehydration. But cats with concurrent heart disease risk fluid overload — set volume and frequency with your vet.
As CKD advances, drinking cannot keep up with urinary water loss, and chronic dehydration sets in — fueling the spiral of poorer appetite and reduced renal blood flow. Sub-Q fluids break that loop at home. No controlled study proves longer survival, but hydration and well-being benefits are broad clinical consensus, and IRIS recommends them from stage 3. In cats with concurrent heart disease (HCM), fluids can overload the lungs — volume must be designed with your vet.
Generally worth feeding — it is already in renal diets for a reason. Dose and freshness decide whether it does anything.
It works by lowering inflammation and glomerular pressure. In cats the evidence is retrospective (cats on higher-EPA diets lived longer); in dogs, controlled trials show renal protection. No direct feline trial yet — hence the yellow grade — but few supplements come close to this. Human single-ingredient products (iHerb-style) are fine; dose by combined EPA+DHA, and refrigerate to prevent rancidity.
For a cat below the treatment line (HCT under 25%), this is the de-facto first-line therapy — the drug that stops "just old age" from being the answer.
CKD anemia is fundamentally an EPO-production problem, and ESA injections replace the missing hormone directly. The current standard is darbepoetin (off-label human drug, starting weekly subcutaneous) — it has effectively replaced older epoetin thanks to fewer antibody reactions. Feline retrospective studies confirm HCT rises and reduced transfusion need, and when a cat responds, the quality-of-life change is visible. Red-cell production needs iron, so iron assessment and supplementation come as a set (see the iron entry), and blood pressure is monitored as a known side effect.
A meaningful new option for cats stressed by injections or responding poorly to darbepoetin. But "conditional" approval means exactly that — the data is still accumulating.
It mimics the body's low-oxygen signal (the HIF pathway), switching the remaining kidney and liver back into making their own EPO. Unlike ESA injections, it is an oral syrup — developed specifically for cats and conditionally approved in the US (Varenzin-CA1). Trials showed HCT rises, but conditional approval is not the same as large-scale proof — a drug to hold with both hope and caution. The "New treatments" article covers the background.
For suspected pyelonephritis, antibiotics are kidney-saving treatment. Conversely, "preventive" use for symptomless bacteriuria is exactly what current guidelines advise against.
CKD cats are a UTI risk group — dilute urine washes bacteria away poorly. Pyelonephritis, where infection climbs into the kidney itself, is a *reversible* cause of deterioration: when values suddenly spike and appetite crashes, finding and treating a hidden kidney infection can bring the numbers back. Worth checking before concluding "the disease just progressed."
The opposite trap exists too — bacteria in urine without symptoms (subclinical bacteriuria) should generally NOT be treated, per current guidelines. Antibiotics belong with culture and sensitivity results, taken for the full prescribed course. Amoxicillin-clavulanate is a common first choice; pyelonephritis needs longer courses (weeks).
For cats with low blood B12 this is a real fix — appetite and energy can change. Not a give-it-blind supplement.
CKD cats lose B12 in urine while eating less of it, so hypocobalaminemia is common. Low B12 compounds inappetence, anemia and lethargy, and some cats improve visibly with supplementation. The key is the order — measure blood cobalamin first, supplement when low. Extra B12 for a cat with normal levels has no demonstrated benefit.
May be worth trying for uremic-symptom relief, but the evidence for improving values or slowing progression is weak.
It adsorbs uremic-toxin precursors (indoles) in the gut, charcoal-style, and passes them in stool. The theory is plausible and it has decades of human use in Japan — yet the large EPPIC trials failed to delay dialysis. Feline data remains small-scale. Many "creatinine dropped" reviews likely reflect hydration changes. The honest expectation: an adjunct for uremic-symptom management, not a value-fixer.
Preliminary evidence that lab markers like uremic toxins and proteinuria fall — but every study is small and maker- or distributor-supported. No evidence it slows progression: optional either way, and drop it first if it puts the cat off food.
Spherical carbon granules (Renaltec) adsorb uremic-toxin precursors (indoles) in the gut and pass them in stool. The brand belongs to Porus GmbH (Germany); Dechra distributes it (in the US since 2021). Same family as Kremezin (AST-120), with more feline research — but all three studies are linked to the maker or the distributor. (1) 2019 congress abstract (maker-linked): 12 healthy senior cats vs 6 controls, indoxyl sulfate (IS) down more than 60% at 8 weeks. (2) 2024, 13 cats with experimental CKD (non-randomised; funded by a Dechra donation to the research fund, one author a Dechra consultant): at 56 days IS fell 8.5% (once daily) and 30% (twice daily), p-cresyl sulfate 16.5% and 47%. (3) 2026 JFMS randomised pilot (LMU Munich, IRIS 2–3, Renaltec 10 vs control 9, 6 months): at the end IS (P=0.045), UPC (P=0.001) and the faecal dysbiosis index (P=0.009) were lower than controls; SDMA did not differ and 2 cats progressed in each group. The maker supplied product and paid for lab tests (stated to have no role in analysis or writing); there was no placebo, so everyone knew who was treated, and the Renaltec group also received Add One treats, so the microbiome change cannot be pinned on either. In short: preliminary evidence that lab markers fall; whether it slows progression or extends life is unknown. At most 19 cats, mostly stage 2, no stage 4 data.
Evidence that it lowers values is weak. Not harmful, but no reason to rank it above phosphorus control and hydration.
The product rides on the "enteric dialysis" hypothesis — gut bacteria degrading uremic toxins. Early small studies were manufacturer-affiliated, and an independent feline double-blind trial failed to reproduce the effect. It has survived 18 years because it is safe and gives caregivers the sense of doing something. On a limited budget, binders, hydration and diet come first.
"Designed with AIM in mind" is not "an AIM drug." The real AIM therapeutic is still in trials; this product is an amino-acid/antioxidant blend borrowing the name.
AIM-protein research (Prof. Toru Miyazaki) — implicating AIM in feline kidney disease — is the most anticipated science in this field. But the actual AIM therapeutic born of that research is still in clinical trials, not on sale. Dr. Toru is a supplement: an amino-acid complex "designed with the AIM mechanism in mind," plus resveratrol and CoQ10. There is no clinical evidence this blend activates AIM or changes renal outcomes. Curious about AIM itself? Read our "New treatments" article — it draws the line between the science and the marketing.
Some ingredients point the right way, but whether the amounts reach studied doses is the question. Its real value is convenience — one product standing in for several.
A one-jar blend of probiotics, prebiotics, chitosan (a phosphate binder) and B vitamins. Products like this must be judged by ingredient evidence, not product marketing — and by whether per-ingredient amounts reach studied doses. Buying single ingredients separately is usually surer on dosing; blends are a practical compromise to reduce pill count. ※ Ingredient list to be verified against the product label.
The theory and human data are interesting, but there is not yet evidence of benefit in cats. Safety appears good.
A component of cellular energy production and an antioxidant. Some positive human heart-failure data made it popular for cardiac and senior support, but feline clinical evidence does not exist. In a senior cat already juggling pills, "adding one more harmless thing" is not always the right answer — pill stress is a cost too.
Yes, hospitals use it — but that is the emergency-antidote story. As a daily antioxidant supplement, it remains unproven.
NAC is a precursor of glutathione (the cell's flagship antioxidant) and has a solid record as the standard antidote for acetaminophen toxicity in cats. The catch: that record does not translate into "daily use protects kidneys" — feline evidence for chronic supplementation is absent. The fact-check article covers the mechanism and the judgment call.
For a cat with confirmed low potassium, this is clearly effective, test-driven supplementation. There is no basis for "preventive" use at normal levels.
CKD leaks potassium as urine volume rises, making hypokalemia a common companion. Low potassium brings lethargy, a drooping head and weak hind legs — and supplementation reverses it, a rare case of clear cause and clear fix. Two forms: potassium gluconate (mild taste, the default) and potassium citrate (which also corrects metabolic acidosis — see the acidosis entry). The order is everything: confirm low on bloodwork, start, and recheck to confirm correction.
Clearly worth correcting when HCO3 (or tCO2) stays below 16. Potassium citrate can fix low potassium in the same stroke.
The kidney is the body's acid-exporter, so failing kidneys let the body drift acidic (metabolic acidosis) — an invisible war of attrition that wastes muscle, weakens bone and dulls appetite further. Human nephrology has controlled trials showing correction slows progression; for cats, IRIS recommends holding HCO3 at 16–24. Two tools: potassium citrate (two birds when hypokalemia coexists) and sodium bicarbonate (for hyperkalemic cats; mind the sodium load). Read alongside the HCO3 card in Care Companion.
Clear value for an anemic cat with low iron status. No basis for "preventive" use in a non-anemic cat — excess iron is harmful.
CKD anemia is primarily an EPO problem, so iron alone does not fix it. But once darbepoetin starts and red-cell production ramps up, iron demand surges — that is when supplementation becomes standard. Order matters: confirm anemia → assess iron status → supplement if needed. "Preemptive" iron for a cat with normal HCT has no evidence and real risks.
The SOD your cat's body makes matters greatly — but there is no evidence the SOD you feed does that job. A textbook case of marketing borrowing science's name.
SOD is the cell's first-line enzyme against free radicals — its role inside the body is genuine, important science. The problem is *eating* it: SOD is a protein enzyme, and swallowed proteins get broken down by stomach acid and digestive enzymes into amino acids. It never reaches the bloodstream as a working enzyme. Coated products (GliSODin etc.) try to dodge this, but the evidence is rodent-and-small-human-study level — and zero in cats.
One principle to keep: this applies to "edible enzymes" in general, with one exception — digestive enzymes (pancreatin etc.) are *meant* to work inside the gut, no bloodstream required. Those are the enzymes worth swallowing.
Not an evidence-based choice for CKD management. The stomatitis/immune context is a different story — but even that rests on small studies.
An iron-binding protein from milk and colostrum, popular in the human market for antimicrobial and immune-modulating claims. In cats, evidence amounts to a few small studies of topical use in stomatitis; nothing relates to CKD progression or values. If uremic mouth ulcers are why you're considering it — remember the real levers there are uremia control and pain management.
Worth trying for a cat with concurrent GI trouble. Feeding it "for kidney values" shares the same evidence problem as Azodyl.
Probiotics must be judged strain by strain. Evidence for specific strains in feline GI disease is accumulating, but the kidney pathway — gut bacteria reducing uremic toxins — remains hypothesis-stage. Since CKD cats often have concurrent gut trouble, indirect help is plausible; where you place your expectations is the point. See the fact-check article for a strain-by-strain breakdown.
This compendium summarizes published research and anonymous app statistics for reference. Always discuss starting, stopping or dosing with your vet.
