Metabolic Acidosis

Quick Answer: Metabolic acidosis in CKD cats happens when failing kidneys can no longer remove excess acid from the blood or retain enough bicarbonate to buffer it. It is diagnosed via blood gas analysis or TCO2 measurement, and treatment typically begins with a renal diet, moving to potassium citrate or sodium bicarbonate if bicarbonate or TCO2 remains below 16 mmol/L. The IRIS 2023 guidelines recommend maintaining blood bicarbonate or TCO2 between 16 and 24 mmol/L.

The body maintains a delicate acid-base equilibrium measured as blood pH. Normal feline blood pH sits at around 7.40, slightly alkaline. A reading below 7.35 indicates acidosis, meaning the blood has become too acidic.

In healthy cats, the kidneys regulate acid-base balance through two mechanisms. First, bicarbonate ions held in kidney tissue act as a buffer against acid accumulation. Second, the kidneys actively flush excess acids from the body through urine. When CKD damages kidney tissue, both mechanisms fail. Excessive urine output washes bicarbonate out of the system before it can do its buffering work, and the damaged kidneys lose their ability to excrete acids efficiently. The result is rising acidity throughout the body, a condition called metabolic acidosis.

The term “metabolic” distinguishes this condition from respiratory acidosis, which arises from lung dysfunction and impaired carbon dioxide clearance. The two have different causes and different treatments, so the distinction matters.

It is also worth clarifying that metabolic acidosis is not the same as gastric hyperacidity, which involves excess stomach acid stimulated by the hormone gastrin. CKD can impair gastrin excretion, leading to gastric hyperacidity as a separate problem, and the two conditions can coexist in the same cat. If your cat is being treated for stomach acid issues, that treatment will not address metabolic acidosis, which is a whole-body acid-base problem measured in the blood.

Metabolic acidosis becomes increasingly prevalent as CKD progresses through IRIS stages. Research published in the Journal of Small Animal Practice found metabolic acidosis present in around 15% of IRIS Stage 3 cats, rising to over 52% in cats at the upper end of Stage 3 and into Stage 4. A 2025 retrospective study evaluating bicarbonate deficiency across 618 cats with kidney disease found that nearly half of all cats with CKD, acute kidney injury, or acute-on-chronic kidney disease had measurable bicarbonate deficiency.

Earlier-stage cats are not immune. Metabolic acidosis can occur even in cats with relatively modest rises in creatinine, and IRIS recommends monitoring for it from Stage 2 onward. It is also worth noting that in cats with CKD, blood pH may remain within normal limits for some time at the expense of bone health, with the skeleton acting as a buffer by releasing calcium into the circulation. This means overt acidosis on bloodwork can underrepresent how long the body has been managing excess acid load.

The systemic effects of metabolic acidosis are wide-ranging because blood pH touches virtually every organ system.

Muscle and protein metabolism are among the most clinically significant concerns for CKD cats. Metabolic acidosis triggers accelerated protein catabolism, meaning the body breaks down lean muscle tissue faster than it can be replaced. This drives the visible muscle wasting, weight loss, and the bony spine that owners of CKD cats often notice. Research confirms that sodium bicarbonate supplementation in humans with CKD improves lean body mass and nutritional markers, and the same mechanisms apply in cats. The 2023 IRIS treatment recommendations cite correcting metabolic acidosis as a means of minimising protein catabolism alongside slowing CKD progression.

Bone health is affected because the body draws calcium from bone tissue to help buffer excess acid. A 2025 retrospective feline study found that cats with elevated calcium-phosphate products were significantly more likely to develop acidosis, reinforcing the link between metabolic acidosis and CKD-mineral bone disorder. This demineralisation is rarely visible on examination but contributes to the broader picture of renal osteodystrophy seen in advanced CKD.

Appetite, nausea, and general wellbeing are affected too. Metabolic acidosis contributes to anorexia, nausea, vomiting, lethargy, and weakness. Correcting acidosis often produces a noticeable improvement in how a cat feels, even when kidney values themselves do not change. This is one of the reasons treatment is worth pursuing even in cats where CKD is not reversible.

Respiratory changes may be observed in some cats. Because metabolic acidosis leads to excess carbon dioxide in the body, the respiratory system compensates by increasing breathing rate and depth in an attempt to expel more CO2. This compensatory breathing pattern, known as Kussmaul breathing, can look like breathlessness or laboured breathing.

Potassium balance is also implicated. Metabolic acidosis can cause potassium to shift out of cells and into the bloodstream, making serum potassium appear normal or even elevated when the cat may actually be potassium-depleted at the cellular level. After treatment begins, potassium levels should be monitored closely, as they can fall.

Diagnosing metabolic acidosis accurately requires more than a standard chemistry panel. The definitive test is blood gas analysis, either arterial or venous. Arterial blood gas analysis is more precise, particularly for evaluating respiratory compensation, but requires sedation and specialised equipment not universally available in general practice. Venous blood gas analysis, ideally drawn from the jugular vein, is sufficient for most CKD cats and is the practical standard.

One important caveat with blood gas samples is that exposure to air allows dissolved gases to escape, which can artificially lower readings. Samples should be collected carefully and processed promptly.

Key values to look for:

Blood pH below 7.35 indicates acidosis. A pH above 7.45 indicates the opposite problem, metabolic alkalosis. For CKD cats, the treatment target is a blood pH between 7.2 and 7.4.

TCO2 (total carbon dioxide) appears on most standard chemistry panels and serves as a useful proxy for bicarbonate. A TCO2 below 16 mmol/L is the threshold at which IRIS 2023 recommends initiating treatment. TCO2 readings can be falsely low if blood collection tubes are underfilled, so a result just below the threshold should be confirmed with blood gas analysis before starting treatment.

The bicarbonate value (HCO3) from blood gas analysis is the most direct measure. Normal range is approximately 16 to 24 mmol/L. Values below 16, particularly in combination with low pH, confirm metabolic acidosis requiring treatment.

The anion gap is a calculated value representing the difference between measured cations and anions in the blood: sodium plus potassium, minus chloride and bicarbonate. In CKD-related metabolic acidosis the anion gap is typically elevated, though it has limitations. A cat with severe diarrhoea, for example, may have metabolic acidosis with a normal anion gap because chloride rises to compensate for bicarbonate loss. An elevated anion gap should always be interpreted alongside blood pH to distinguish metabolic acidosis from metabolic alkalosis, both of which can raise the anion gap.

BUN can also rise in metabolic acidosis because accelerated protein catabolism generates additional urea, contributing to a high BUN-to-creatinine ratio independent of further kidney deterioration.

The IRIS 2023 treatment guidelines, the ISFM consensus guidelines, and the broader veterinary nephrology consensus align on the same targets: blood bicarbonate or TCO2 maintained between 16 and 24 mmol/L, and blood pH between 7.2 and 7.4. Once treatment begins and targets are reached, reassessment every three to four months is recommended to confirm ongoing stability.

It is worth setting realistic expectations. Treating metabolic acidosis is unlikely to produce an improvement in creatinine or other kidney function markers. The goals are to slow CKD progression, preserve muscle mass, and help the cat feel better, all of which are meaningful and achievable.

Treatment is stepped, starting with dietary management and escalating to supplementation if bloodwork targets are not met.

Diet

Most veterinary therapeutic renal diets are formulated to be pH-neutral or mildly alkalinising, and many contain potassium citrate as a built-in alkalinising agent. Transitioning to a renal diet is the first line of intervention for mild metabolic acidosis. The ISFM guidelines state that cats fed a renal diet and kept adequately hydrated often require no additional treatment. Urinary tract diets, which are acidified to reduce struvite crystal formation, are contraindicated in CKD cats and particularly harmful in cats with metabolic acidosis.

Lactated Ringer’s Solution

Cats on subcutaneous fluid therapy using Lactated Ringer’s Solution (LRS) may receive some benefit from the lactate content, which the liver converts to bicarbonate. This is generally not sufficient to correct established acidosis on its own, but it is one reason LRS is preferred over normal saline for CKD cats. Sodium chloride fluids may actually worsen metabolic acidosis and should be discussed with your vet if they are currently in use.

Potassium Citrate

Potassium citrate is the preferred choice for cats who have both metabolic acidosis and low potassium levels, as it addresses both problems simultaneously. It is also a reasonable first-line alkalinising agent for cats with normal potassium, since it is generally well tolerated. The ISFM guidelines recommend a starting dose of 40 to 75 mg/kg twice daily, titrated to maintain bicarbonate or TCO2 between 16 and 24 mmol/L. NC State’s College of Veterinary Medicine has an active clinical trial evaluating potassium citrate specifically for metabolic acidosis in CKD cats, reflecting ongoing interest in refining its evidence base in feline patients. Potassium citrate should not be used in cats with high potassium levels. It should also be given at least two hours apart from aluminium-containing phosphorus binders, as citrate can increase aluminium absorption.

Sodium Bicarbonate

Sodium bicarbonate (baking soda) is the most commonly used alkalinising agent for CKD-related metabolic acidosis when dietary management and potassium citrate are insufficient, or when potassium levels make potassium citrate unsuitable. It works by directly replenishing the bicarbonate that damaged kidneys can no longer retain. A 2025 systematic review of nine randomised controlled trials in humans with CKD found that sodium bicarbonate supplementation improved serum bicarbonate levels, and several trials reported preserved kidney function and improved lean body mass as additional benefits, though results were not entirely consistent across studies. Typical starting doses in cats are 8 to 12 mg/kg given every 8 to 12 hours, with the dose individualised based on the cat’s response and blood monitoring. Because the amounts involved are very small and the margin between a therapeutic dose and too much is not wide, dosing should always be guided by your vet, and the cat’s acid-base status should be rechecked within a few weeks of starting treatment. Sodium bicarbonate should not be given to cats who do not have confirmed metabolic acidosis, and it is not appropriate for cats with low potassium levels, as it can reduce potassium further. Overdosing risks producing the opposite problem of metabolic alkalosis, which can itself be dangerous. Potassium citrate is the better choice for cats with concurrent hypokalaemia.

Can a cat in early-stage CKD have metabolic acidosis?
Yes. Although metabolic acidosis becomes more common as CKD progresses, it can occur in earlier stages. IRIS 2023 recommends monitoring for it from Stage 2 onward. Blood pH may also remain normal for a period while the body buffers excess acid load at the expense of bone mineral, so monitoring TCO2 on routine bloodwork is worthwhile even before overt acidosis appears.

Will treating metabolic acidosis improve my cat’s kidney values?
Probably not directly. Creatinine and BUN are unlikely to fall as a result of treating acidosis. What treatment does is slow ongoing kidney injury, reduce protein catabolism that contributes to muscle loss, and help the cat feel better day to day. These are significant benefits even without improvements in the numbers.

My vet doesn’t want to treat the metabolic acidosis yet. Is that reasonable?
In some cases, yes. If acidosis is mild and the cat has just been transitioned to a renal diet, monitoring for a few weeks before adding supplementation is a reasonable approach, since dietary change alone sometimes resolves mild acidosis. The body also produces its own compensatory response. However, if bicarbonate or TCO2 remains below 16 mmol/L after dietary stabilisation, the IRIS 2023 guidelines, the ISFM guidelines, and the Merck Veterinary Manual all recommend treatment. It may help to share those references with your vet.

Is baking soda the same as the sodium bicarbonate used to treat metabolic acidosis?
Yes, in the US baking soda and sodium bicarbonate are the same compound. Baking powder is not the same thing and should not be used, as it contains additional ingredients. The doses involved for cats are extremely small, so accurate measurement and veterinary guidance on dosing are important.

How often should we monitor after starting treatment?
IRIS guidelines suggest reassessing every three to four months once targets are stable. Your vet may want to recheck sooner after a dose change to confirm the adjustment is working as intended.

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