I don't think it is presumptuous to say that, most care givers associate dietary magnesium with the formation of struvite crystals (magnesium ammonium phosphate) in the feline lower urinary tract - a most uncomfortable and even life threatening disease that can afflict cats. However, the fact is that, the actual magnesium content of a feline diet has little to do with the formation of struvite crystals in the urinary tract of cats, but several other factors play a much more important role in the potential formation of these magnesium containing crystals.

Magnesium and its Functions:
Magnesium is an essential mineral. It is involved in numerous functions of the body like energy production, formation of urea, in muscle relaxation, and neuromuscular transmission and activity. Magnesium also prevents tooth decay by binding calcium to tooth enamel, aids in bone growth, and is essential for proper function of the muscles - including the heart. It also helps to regulate the acid-alkaline balance in the body. Magnesium is the most bountiful cation (a positively-charged ion) in soft tissue next to potassium, and excessive loss leads to tissue breakdown and cell destruction. Magnesium promotes absorption and metabolism of other minerals like calcium, phosphorus, sodium, and potassium, and helps utilize vitamin E and vitamin B complex.

Deficiency:
Approximately 27% of the body's magnesium is contained within muscle tissue, and 60% is contained within the skeletal structure - providing a reservoir for adequate supply in times of need.
A deficiency of dietary magnesium severely affects cardiovascular, neuromuscular, and renal tissues, and contributes to calcium deposits in the kidneys (kidney stones), in blood vessels, and in the heart. It can also be the cause of gastro-intestinal disorders, irritability, irregular heart rhythm, lack of coordination, muscle twitch, tremors, and weakness. The symptom picture of long term dietary deficiency of magnesium is very similar to a deficiency in calcium, including muscle cramps, high blood pressure, and malformation of the bones.

Requirement:
Cats need magnesium as an essential part of their daily diet and a certain amount of it in relation to other minerals. Restricting dietary magnesium intake is not a means of preventing disease, but a cause of disease. The nutritional requirement of magnesium for cats, based on research published by the National Research Council, is about 38 mg per day for an adult cat of an average body weight of 6 kg. However, magnesium interacts with other minerals when absorbed by the body, and the diet needs to provide a specific ratio of these interactive minerals for optimal utilisation: Ca:P:Mg = 1.3:1:0.06.

Sources:
The major source of magnesium for the cat are the bones of her prey, or bone meal in the home prepared diet. Diets prepared using isolated calcium supplement - like calcium citrate, calcium gluconate, or calcium lactate - instead of bone meal, need to be supplement with magnesium respectably. Also, cooking removes magnesium from the foods.

Magnesium and Feline Urological Syndrome (FUS):
( also know as Feline Lower Urinary Tract Disease - FLUTD) The absolute level of magnesium in the feline diet by itself does not contribute to the formation of urinary struvite crystals, provided that it is present in the proper ratio to other minerals in the diet, and that other dietary factors support the maintenance of an acidic urinary pH. Experiments using supplemental magnesium chloride in the diet of cats have shown that, a high dietary magnesium intake does not result in any signs of FUS if an acidic urine is produced. However, if the urine pH is 7.5 or higher struvite crystals will form even in cats fed a diet low in magnesium. These facts emphasise the role of urinary pH in the development of FUS in the cat, who has been evolutionary adapted to produce acidic urine, and not total magnesium content.

The relationship of urine pH and Struvite crystals:
Wild living, prey eating cats produce a urine with a pH between 6.0 - 7.0. The cat evolved as a dessert dwelling animal and is capable of concentrating her urine in order to conserve water. The waste products in the cat's urine are very concentrated and include magnesium, ammonium, and phosphate ions that may crystallize in neutral and alkaline urine to form struvite. At a urine pH below 6.6 struvite remains largely soluble, whereas in a urinary pH above 7.1 crystallization may occur spontaneously.
Oxidation of sulfur amino acids during the process of catabolism (chemical breakdown: when the
body uses food for energy as part of the metabolism) of amino acids from proteins to urea, carbon dioxide, sulphate, and water has acid forming properties, influences the acid-base balance of the body and urine pH. This process does not take place when fats or carbohydrates are catabolized. Therefore, the carnivore cat - eating a largely all meat, high protein diet - will naturally produce a low, or acidic urine pH. Today, the carnivore cat as companion animal is largely condemned to eat cereal or vegetable-based commercially prepared foods that are convenient and inexpensive for the care giver. However, vegetable ingredients in the cat's diet result in the production of neutral or alkaline urine - predisposing the cat to crystalisation of mineral ions in the urine.

FUS and dry commercial cat food:
Clinical disorders of the lower urinary tract of cats are not a new phenomena, and have been observed as early as 1925. The frequency of its occurrence in the companion cat population is, however, on the rise and it is now considered to be a common feline disease. In the 1950s, clinical disorders of the lower urinary tract were considered rare in the veterinary practice. In the mid-70s a rise to 0.6% of cats in the companion cat population afflicted with FUS was recognized - a number that increased to 0.85% in the mid-80s. Today, more than 7 % of companion cats presented at veterinary clinics are diagnosed as having FUS. At the same pace, commercial dry cat foods are becoming increasingly popular, and are marketed to the cat owning population an the choice of veterinarians.
Cats need a high protein diet to maintain a low (acidic) urinary pH. Commercial dry cat foods are based on vegetable ingredients that make up 50% or more of the products weight, and vegetable ingredients result in the production of a high (alkaline) urinary pH. Also, the species of our domestic cat (Felis Silvestris Catus) has evolved as desert dwelling animals, capable of concentrating urine to a high degree and of relying entirely on the moisture content of prey, without the need for supplemental drinking water. Drinking is not natural for cats and they will do so only reluctantly. A cat eating 1 cup (85 g) of dry food would need to drink 8 oz. (225 ml) of water to prevent dehydration. However - most don't. The result is dehydration and a reduction in urine volume. Experiments have shown that crystal formation of mineral ions can be prevented by increasing urine output, and the occurrence of FUS in cats fed experimental dry diets has been abolished by hydrating the same diet to a moisture content of 80%.

FUS and modern treatments:
Pet food manufacturers literally exploit the high occurrence of disease in the modern companion cat population to market more expensive specialty diets that are supposed to address the disease cause. Numerous brands of cat foods are available that claim to prevent the occurrence of struvite crystals, most of which are - ironically - dry foods. Although the facts of how the majority of FUS cases could be prevented are clearly laid out, such commercial diets are not truly therapeutic. Pet food manufacturers are making use of a chemical substance called Ammonium chloride to artificially lower urine pH, while ignoring all dietary factors that could resolve the matter naturally. Ammonium chloride is a strong acid, and the veterinary community as since raised concern regarding its use as a means to lower urinary pH, because its acidifying affect can cause a condition called chronic acidosis. Repeated ingestion of this chemical compound, inducing acidosis, can lead to mobilisation of calcium from bone - meaning that calcium is leached from the skeletal structure and deposited in soft tissue. A combination of induced acidosis, leading to calcium loss from the bones, in combination with a reduced dietary intake of magnesium leads to formation of oxalate stones - a now common side effect of the treatment for struvite crystals.

Oxalate stones:
Formation of oxalate stones, which are commonly found as kidney stones, but also in the heart or lower urinary tract, is the result of free calcium ions binding to oxalic acid - a substance excreted in the urine - to form the less soluble salt called calcium oxalate. Over-supplementation with calcium, dietary intake of ammonium chloride leading to calcium loss from the bones, a magnesium deficiency, supplementation of vitamin C - which is metabolized to oxalic acid - and consumption of oxalic acid containing foods - like cabbage, spinach, beet tops, potatoes, or peas - can lead to formation of calcium oxalate and the possible formation of oxalate stones in soft tissue, or the upper or lower urinary tract.

Summary:

• Cats should eat a diet containing calcium, phosphorus, and magnesium in amounts as they are essential to maintain normal bodily functions and good health, and should be present in the proper ratio to one another. No single element should be increased or reduced, because a mineral imbalance will be the direct result, which in turn will interfere with normal functions of the body.
• Cats should eat a diet that reflects the lifestyle they have adapted to; a diet based on raw meat that is high in protein and has a sufficient moisture content to provide the cat with sufficient fluids through the meal, making supplemental water intake unnecessary.
• Cats should not be given vitamin C (unless the cats ability to synthesize vitamin C is disturbed due to disease) and should not be fed vegetable matter.

References:

• Nutrient Requirements of Cats - revised edition 1986, National Research Council
• The Journal of Nutrition, American Society for Nutritional Sciences, Vol. 128, 1998
• The Nutrition Desk Reference, 3rd. edition 1995, Robert Garrison, Jr.MA.,R.Ph. and Elizabeth Somer, MA., R.D., page158.
• Nutrition Almanac, 4th edition 1996, Gayla J. Kirschmann and John D. Kirschmann, page 120
• Prescription for Nutritional Healing, 2nd. edition 1997, James F. Balch, M.D., Phyllis A. Balch, C.N.C. page 359
• Food Chemistry - Naturally Occurring Toxins, an article by Stephen Gislason, M.D. 1999