Every Cat Logo

Sodium nutritional needs for cats

Nguyen P, Reynolds B, et al. Sodium in feline nutrition.  J Anim Physiol Anim Nutr2017;101:403-420.

Major concerns regarding sodium intake and its impact on human health have been discussed and investigated for decades in both scientific and popular media.  Are there similar issues pertaining to dietary sodium in feline health and nutrition?  This review article evaluates current evidence regarding the risks, safety, and benefits of various sodium levels in feline diets, and recommends a safe upper limit (SUL) for sodium intake in cats, based on this evidence.

Sodium, chloride, and potassium are the key electrolytes in bodily fluids.  The article begins with a discussion of the physiological and biochemical functions of sodium, mechanisms of sodium homeostasis, absorption of dietary sodium, and sodium urinary output.  As the kidneys are the major controllers of sodium homeostasis in the body, sodium urinary output is strongly correlated with sodium intake in cats and other animals.  Also, while many herbivorous and omnivorous animals have an innate appetite for sodium and will seek or choose sodium solutions over fresh water or prefer salted foods, no such appetites have been identified in cats and dogs, even those in which a sodium deficiency is identified or induced.

In humans, chronic high dietary sodium intake has been associated with the development of hypertension and hypertension-related cardiovascular diseases, renal diseases, gastric mucosal damage, and even gastric neoplasia.  However, the evidence is equivocal and controversial regarding the effects of dietary sodium restriction on reducing blood pressure, in both hypertensive and normotensive people.  Sodium content in cat foods varies widely; many calculolytic feline diets contain high levels of sodium, while diets designed for cats with renal or cardiac disease often have low sodium content.

In humans, high-salt diets may promote calcium oxalate nephrolithiasis, as high sodium intake promotes calciuria, but the exact mechanism is unknown, and the importance of this phenomenon in the formation of calcium oxalate uroliths is uncertain and controversial.  In cats, the effects of dietary sodium intake on calcium oxalate urolith formation are likewise unclear and controversial.  Several studies have shown that cats fed diets with high sodium levels are actually less likely to develop calcium oxalate uroliths.  Water intake and urine production are also increased, while urine specific gravity is decreased, in cats eating diets with high sodium content, so it is possible that the effects of sodium in promoting increased water intake and production of more dilute urine are greater than those of sodium enhancing calciuria.  High sodium levels are also used in some feline prescription dietary foods designed to cause struvite dissolution.  In this case the sodium promotes the desired effect by causing an increase in water intake and urine volume. The specific effects of dietary sodium levels on the dissolution and prevention of feline struvite uroliths have not been reported, however, even though some cat foods that have been found effective for struvite dissolution have high sodium content.

Hypertension is now known to be a common problem in feline patients; only about 20% of feline hypertension is considered to be idiopathic.  Most feline hypertension is secondary to chronic kidney disease or hyperthyroidism.  Low-sodium diets have historically been recommended for hypertensive cats based on data from studies in laboratory animals and humans.  All of the studies reviewed in this report demonstrated no association between increased dietary sodium intake and increased blood pressure in cats, regardless of whether the cats were healthy young adults, healthy aged animals, or subjects with impaired renal function.  Nonetheless, the 2007 consensus statement of the American College of Veterinary Internal Medicine on systemic hypertension in dogs and cats recommended avoiding high dietary sodium-chloride intake in such patients, even though it also affirmed that there was no clear rationale for dietary sodium restriction in hypertensive cats and dogs.

High sodium intake in humans has also been associated with higher risks of hypertension-associated cardiovascular diseases such as stroke, left ventricular hypertrophy, and aortic stiffness.  Cardiac diseases, particularly hypertrophic cardiomyopathy, are relatively common in cats, and may affect up to 20% of the feline population.  In the few studies published that evaluated cardiac functional and anatomical parameters in cats without heart disease fed different amounts of dietary sodium, no changes in these parameters were identified in cats fed high levels of dietary sodium over a period of months.  No studies have addressed the effect of dietary sodium levels on feline patients with cardiac disease, or the effect of sodium intake on the progression of cardiac disease in cats.

Most of the studies reviewed regarding the effects of dietary sodium intake on kidney health in healthy cats showed no correlation between high dietary sodium and adverse impacts on renal function and health.  Adverse effects of higher dietary sodium levels on renal function are considered to be mediated by hypertension, which in turn leads to increased glomerular capillary pressure, resulting in glomerular sclerosis and escalation of proteinuria.  At this time, there are still no published studies that evaluate the effects of different levels of dietary sodium on disease progression in cats with naturally occurring chronic kidney disease.

In humans, treatments that inhibit activity of the renin-angiotensin-aldosterone system (RAAS) are found to be renoprotective and may slow or stop progression of chronic nephropathies.  In cats, the role of the RAAS in progression of renal disease is under investigation. Based on the few studies currently available, high dietary sodium intake does not appear to adversely affect renal function in young healthy cats or older cats over the medium and long terms. In contrast to humans with chronic kidney disease, in whom RAAS blockade occurs with moderate dietary sodium restriction, increased dietary sodium intake in cats with kidney disease actually suppressed kaliuresis and RAAS stimulation. Both kaliuresis and RAAS activation are likely to be detrimental to renal function in patients with chronic kidney disease, and higher dietary sodium levels may therefore be renoprotective in these animals.

The National Research Council has established the safe upper limit (SUL) as the maximum concentration or amount of a nutrient in animal feed that is not associated with adverse effects. Based on a long-term (24 month) study of aged healthy cats, the recommended SUL of sodium in feline diets is 740 mg/mJ (megajoule) of metabolizable energy (ME), or 1.25 g/kg in 4000 kcal ME/kg diets), including diets for aged cats.

The authors conclude that blood pressure and hypertensive status in cats are not sodium-sensitive. Even though there is insufficient data available to determine a recommended amount of sodium in diets for feline patients with cardiac or renal disease, the current evidence indicates that higher dietary sodium intake does not lead to increases in blood pressure. [PJS]

See also:

Chetboul V, Reynolds BS, et al.  Cardiovascular effects of dietary salt intake in aged healthy cats:  a 2-year prospective randomized, blinded, and controlled study.  PLoS One2014;9:e97862.