What are Kidney stones, How are they Formed and What are some Preventive Measures!

A kidney stone can be as small as the head of a pin, almost invisible to the naked eye but as every stone former knows, the pain resulting from this tiny crystal structure can be enormous.

Kidney stones or renal calculi are aggregates of crystals enclosed in a matrix that develop within the kidneys. They are classified according to the specific types of crystals they contain and fall into five major categories. These are Calcium oxalate, calcium phosphate, struvite, uric acid and cysteine. The most common is calcium oxalate.

How is a stone formed?  The first step is nucleation, ions such as calcium and oxalate that have been filtered into the urine by the kidney spontaneously joined together to form a solid crystal nidus, this is called nucleation.  There are two kinds of nucleation, in homogeneous nucleation crystals form around a nucleus with the same composition. Crystals of a different composition can also form around the nucleus. Organic materials, such as cell debris may be deposited between the crystals as a matrix. This is heterogeneous nucleation. The tiny crystal formations travel down the nephron and are usually deposited at the renal papilla where they undergo the next major phase “growth”.

Crystals that have already formed then begin to stick together forming large aggregates which can aggregate very quickly. New stones are retained in the kidney where they can continue to grow for an unspecified length of time until for reasons that are not well understood, they're displaced and travel through the kidney into the ureter.

Uncontroversial junctions 

If a stone continues to grow until it reaches a critical size, which can be as small as 4 to 5 millimeters in diameter, it may be too large to pass easily through the ureter. The edges of the stone may become wedged inside the ureter at the Ureteorpelvic junction (see picture), where the ureter crosses over the iliac atery or at the Ureterovesical junction. The result, pain and obstruction, until the stone slowly passes into the bladder and eventually passes out of the body in the urine stream.

In the U.S, it is estimated that 13 percent of men and 7 percent of women will develop a kidney stone during their lifetime. Fortunately, in about 78 percent of these patients, stones will be expelled spontaneously but stones that become lodged in the ureter may require lithotripsy, endoscopic removal or other treatments possible. It's important to note that nearly half of all first-time stone formers will have another stone episode within the next four years. Recurrent stone formers are at even greater risk and may form a new stone every two or three years. But what actually causes crystals to form? Why do some crystals develop into kidney stones and others do not?

One critical factor is super saturation of the urine with stone forming salts. Super saturation is the driving force for crystallization in under saturated urine, crystals cannot form.

The other important factor is a deficiency in substances called inhibitors. Inhibitors retard the nucleation, growth, and aggregation process by binding ions needed for crystal formation and growth. One of the most important inhibitors is citrate.

Urine saturation and inhibitor levels explain why in normal patients large crystals are not formed. Their urine is not as saturated and they have sufficient quantities of inhibitors present. But the urine of patients with kidney stones is more saturated it may also lack inhibitors that increase the propensity for crystallization of stone forming salts.

There are two reasons for this. First stone formers are known to suffer from a variety of metabolic disturbances that increase the amount of stone forming substances excreted in the urine and also decrease the excretion of inhibitors. Second, a number of common nutritional and environmental factors can cause abnormalities in the urine.

These factors may also exaggerate underlying abnormalities due to metabolic disturbances. Environmental stresses for example play a significant role in stone disease, especially factors that trigger excess water conservation in the kidney such as inadequate fluid intake. Dehydration is a major cause of kidney stones which is why people living in areas with high temperatures and humidity have a higher incidence of stone formation. A diet high in sodium is a double risk because it increases calcium excretion and reduces urinary levels of stone inhibiting citrate. Too much animal protein creates similar problems encouraging stone growth by increasing urinary uric acid and reducing urinary citrate. Certain medications are also known to encourage stone formation or growth in susceptible patients including common supplements such as vitamin C.

There is no cure for kidney stones but once an acute episode has been resolved, the key to therapy is simple, preventing recurrence. And fortunately, the most common stones calcium oxalate and calcium phosphate can be effectively managed with a combination of diet and lifestyle changes and medication. Compliance with proven management guidelines such as increasing fluid intake and avoiding stone promoting foods can significantly reduce stone recurrence. Medical therapies, such as thiazide diuretics and potassium citrate are also highly effective in appropriate patients and can reduce the need for expensive assisted stone removal procedures such as shock wave lithotripsy. The economic burden of kidney stones is significant with medical costs reaching billions of dollars annually.

Note: This article is not for any medico-legal purpose.