In the pie-chart located on the Overview page, Calcium Oxalate stones occupy the majority of the space, as they are the most common stone type.
Calcium Oxalate crystals form when calcium combines with oxalic acid. Oxalic acid (illustrated above), is a dead-end waste product that the kidneys remove, which contains two carbon atoms (black spheres), four oxygen atoms (red spheres), and two hydrogen atoms (Silver spheres).
At a pH of 6 (acidity of urine), the positively charged hydrogen atoms leave the negatively charged oxygen atoms. This leaves the oxalate molecule with two negative charges. In the illustration below, one of the negatively charged oxygen atoms attracts the hydrogen of a nearby water molecule (H —O -H), while another attracts a positively charged calcium atom.
It isn’t hard to imagine how another oxalate ion could attract the same calcium, or another calcium atom attract the bottom oxygen on the oxalate molecule so the chain extends and makes a crystal. In essence, the calcium atoms and oxalate molecules combine by the attraction of their opposite charges.
A little known fact is that Calcium Oxalate stones come in two varieties: Calcium Oxalate Monohydrate and Calcium Oxalate Dihydrate. Monohydrate stones are harder and thus more resistant to fragmentation by lithotripsy. Additionally, Monohydrate stones appear more often when oxalate levels in the urine are elevated.
Sometimes this kidney stone arises from a systemic cause, like bowel disease, primary Hyperparathyroidism, or primary Hyperoxaluria. Only physicians can establish that a known disease – like bowel disease – is the cause of stones. Only physicians can discover underlying primary Hyperparathyroidism as a cause of stones. Patients cannot do much for themselves except provide as complete a medical record as possible.
Most of the time this kidney stone arises simply from the interplay between inheritance, diet, and aspects of daily living. Such people are referred to as idiopathic Calcium Oxalate stone formers, from the Greek words “idios” (one’s own) and “pathos” (suffering).
Even though physicians can discover the links between daily living and stone production, and select those changes that can prevent new stones, patients themselves must create and maintain those changes. When changes in daily life are not enough, physicians add medications, so even then, patients remain active therapists for their own disease.
*For a comprehensive list of oxalate containing foods, please click HERE.
About one million nephron units make up a normal adult kidney. The Calcium Oxalate kidney stone type does not grow in the tubules of the nephrons but “outside” of them, on the surfaces of the renal pelvis where final urine collects and drains through the ureter to the bladder.
Calcium Phosphate crystals form when calcium atoms combine with phosphoric acid instead of oxalic acid. The below illustration outlines the construction of phosphoric acid.
Phosphoric acid is simply a phosphorus atom (P) with 4 oxygen atoms bound to it. The bond between one of the oxygen atoms has two lines to illustrate its bond to phosphorus; this oxygen atom cannot provide any charge with which to bond to calcium atoms in order to form a crystal. The other three oxygen atoms have ordinary bonds and are shown by a line, a dashed arrow, and a solid arrow. The two arrows signify that the oxygens lie above and below the plane on paper.
One of the three negatively charged oxygens almost never has a hydrogen on it in urine (however, rare instance have been found only in exceedingly acidic solutions). A second charged oxygen is always occupied by a hydrogen atom in urine. This makes the third oxygen, variably occupied by a hydrogen in urine, a tie breaker.
In a urine of average/normal acidity (pH around 6), most of the tie breaker oxygens have their hydrogen leaving the phosphate ion only one negative charge, which is not enough to make a crystal. However, when the urine is abnormally alkaline (pH above 6.3 or 6.5), the variable oxygen becomes charged so the ion has two negative charges, which can combine with calcium to make crystals. For this reason the Calcium Phosphate kidney stone tends to occur in people who produce a more alkaline urine than those who produce Calcium Oxalate kidney stones.
Like Calcium Oxalate stones, Calcium Phosphate crystals begin as a one to one pairing of doubly negative phosphate ions with doubly positive calcium atoms. The initial crystal that forms is called Brushite.
Brushite is an equal mix of calcium and phosphate ions which can convert to hydroxyapatite (HA). Hydroxyapatite crystals have a more unbalanced proportion of calcium to phosphate. The resulting unbalance makes bones hard. Hydroxyapatite crystals, being less soluble than Brushite, cannabalize brushite crystals. The organic molecules in urine tend to modify this process.
Primary Hyperparathyroidism and renal tubular acidosis raise average urine alkalinity (higher urine pH) and foster Calcium Phosphate kidney stones. Many uncommon genetic diseases do the same.
Idiopathic Calcium Phosphate stone formers share a common set of tradings. Perhaps, because urine contains far more phosphate than oxalate, they form more frequent and larger stones than idiopathic Calcium Oxalate stone formers. Often the stones originate as crystal plugs at the terminal ends of the kidney tubules. More crystals deposit over the end of the plug open to the urine, to make the final stone. Crystal plugs damage the cells that line the tubules and cause local scarring.
*Source: Dr. Frederic Coe - University of Chicago
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