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The roles of calcium and phosphorus

01 November 2014, at 12:00am

Lee Danks in this latest in a series of columns from Royal Canin focusing on innovations in small animal nutrition, looks at the roles of macronutrients calcium and phosphorus in veterinary diets.

IN terms of food, minerals are simply the inorganic elements that we nd listed collectively as “ash” after removal of all organic matter.

They are naturally occurring substances which aren’t produced by the body but quite a number are used and even essential to everyday function.

They may form the components of bodily structures and fluids (think electrolytes) or be involved in the biochemical reactions which happen in both normal physiological and pathological states.

Given their important and often essential roles, minerals are kept in close homoeostatic check which quite often involves significant mineral interactions. The macronutrients are a select group definitively required by the animal and therefore need to be included in the diet within specific reference ranges, which are established by the regulatory and research authorities in small animal feeding, in the case of dogs and cats.

Two macronutrients which are in close balance with one another are calcium and phosphorus.

The mineral element found in the greatest abundance in mammals is calcium. It is vital for healthy bones and teeth (where 90% of this mineral is found) where along with phosphorus it brings rigidity and shape to these structures.

Calcium also plays a fundamental role in the transfer of information between cells and in the transmission of nerve impulses. For example, it plays essential roles in blood coagulation and muscular contraction as well as serving as a second messenger in a host of intracellular reactions.

Similar to calcium, a large proportion of phosphorus (over 80%) is retained in the bones and teeth. Other roles include its presence in cell membranes (as phospholipids) and the provision of energy at a cellular level. Phosphorus is also a structural component of DNA and RNA, the molecules that carry the cell’s genetic code.


Bodily calcium homoeostasis is a complex process, involving several organs. Concentration of free calcium in the blood is the major initiator of calcium regulatory mechanisms which involves the interplay of parathyroid hormone and calcitonin.

These stimulate a number of metabolic cascades which alters the body’s selective uptake, absorption, resorption or excretion of calcium which happens wherever it’s present or processed (namely from skeletal stores, intestinal contents and throughout the renal system).

To add further complexity, calcium requirements change during growth, pregnancy and lactation.

Everything working as it should, calcium should be in equilibrium with 50% present in the body in its free or ionised state, 40-45% in a protein- bound state and 5-10% in a chelated state, bound to other ions.

Diet, of course, plays a role in calcium balance by way of affecting intestinal availability. If de ciencies are present, the pet becomes susceptible to skeletal abnormalities, particularly while in growth or lactation, when calcium demands are greatest.

Achieving a nutritional balance between calcium, phosphorus (described below) and energy in accordance with the recommendations made by regulating authorities (such as NRC, AAFCO and FEDIAF) is of key importance. Some companies go one step beyond and assess the macronutrient requirements of pets according to their expected adult bodyweight. This is one hallmark of a “tailored nutrition” approach.

Where calcium is in excess in the bloodstream and phosphorus is equally high, soft tissue mineralisation is likely. Any organ where an extensive microvascular network is present is more at risk of damage should calcium and phosphorus come together to form an insoluble molecule. Hypercalcaemia and the resultant sequelae can occur in renal failure and mineralisation can, of course, affect the kidney.

Signs of hypercalcaemia include anorexia, lethargy and weakness but individuals can display remarkable differences in their symptoms. They are usually insidious and often not noticed by owners and, being non-specific, the electrolyte imbalance can sometimes be difficult to elucidate.

Some signs may be referable to the urinary system (e.g. PU/PD, dehydration, haematuria/pollakiuria/ dysuria associated with urolithiasis), the gastrointestinal system (e.g. vomiting, constipation), neuromuscular system (e.g. seizures, weakness) or cardiac system (arrhythmias).

The differential diagnoses for hypercalcaemia are many in number and beyond the scope of this article but further reading is in the reference list below.

Moving to phosphorus, regulation also requires the co- ordinated efforts of the kidneys and intestine. Under conditions of low dietary phosphorus intake, the intestine increases its absorptive efficiency and the kidneys increase phosphorus transport to minimise urinary losses.

Conversely, under conditions of dietary excess, the kidneys increase excretion of minerals. These processes are very much due to the influence of the homoeostatic mechanisms which regulate calcium.

Given their close homoeostatic relationship, dietary phosphorus content is usually governed by calcium levels with a focus on achieving precisely the right Ca:P ratio for each species, size and life-stage. That said, ageing pets may demonstrate sub-clinical renal insufficiency and consequently be more susceptible to the effects of excess phosphorus.

Here, ideal ratios can change and senior diets are often formulated with phosphorus levels at the lower end of the reference range. When we get to the point of CKD diagnosis, avoiding dietary phosphorus to the best of our ability will help to slow the progress of kidney disease.

Of all of the macronutrient groups, calcium and phosphorus interact with one another more than most. It’s imperative to get the nutritional balance right and consider the requirements of the individual dog or cat which depends on many a physiological or pathological process. 

  • For further reading go to vet portal. (or for Ireland).

References and further reading:

  • Elliott, D. (2012) Nutritional considerations for optimal puppy growth. Veterinary Focus 22 (2): 2-10. Galvao, J., (2011) Hypercalcaemia: diagnosis and treatment options in the dog and cat. Veterinary Focus 21 (1): 27-34. 
  • Grandjean, D. and Butterwick, R. [eds] (2009) Waltham pocket handbook of essential nutrition for dogs and cats: Waltham-on-the- Wolds, UK.
  • Hand, M., Thatcher, C., Remillard, R. and Roudebush, P. [eds] (2000) Small Animal Clinical Nutrition: Mark Morris Institute, Kansas, USA.
  • Kallfelz, F. (2004) Calcium and phosphorus requirements of puppies and kittens. Veterinary Focus 14 (3): 4-9. Martin, L. (2004) Classic pitfalls in puppy nutrition. Veterinary Focus 14 (3): 23-27. Nutrient Requirements of Dogs and Cats (2006): National Academies Press, Washington, USA.
  • Wills, J. and Simpson, K. [eds] (1994) The Waltham Book of Clinical Nutrition of the Dog and Cat: Kidlington, UK. 
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