Kidney Stones

The following was taken from an article on the Wikipedia website.

Kidney stones, also known as nephrolithiases, urolithiases or renal calculi, are solid accretions (crystals) of dissolved minerals in urine found inside the kidneys or ureters. They vary in size from as small as a grain of sand to as large as a golf ball. Kidney stones typically leave the body in the urine stream; if they grow relatively large before passing (on the order of millimeters), obstruction of a ureter and distention with urine can cause severe pain most commonly felt in the flank, lower abdomen and groin. Kidney stones are unrelated to gallstones.

Etiology
Conventional wisdom has held that consumption of too much calcium can aggravate the development of kidney stones, since the most common type of stone is calcium oxalate. However, strong evidence has accumulated demonstrating that low-calcium diets are associated with higher stone risk and vice-versa for the typical stone former.

Other examples of kidney stones include struvite (magnesium, ammonium and phosphate), uric acid, calcium phosphate, or cystine (found only in people suffering from cystinuria). The formation of struvite stones is associated with the presence of urea-splitting bacteria, most commonly Proteus mirabilis (also Klebsiella, Serratia, Providencia species) which can split urea into ammonia, resulting in favorable conditions for the formation of struvite. A lack of the protein calgranulin is blamed by some for the appearance of calcium oxalate stones.

Symptoms
Kidney stones are usually asymptomatic until they obstruct the flow of urine. Symptoms can include acute flank pain (renal colic), nausea and vomiting, restlessness, dull pain, hematuria, and possibly fever if infection is present. Acute renal colic is described as one of the worst types of pain that a patient can suffer. Note that the pain is generally due to the stone's presence in the ureter, and not—as is commonly believed—the urethra and lower genitals.

Some patients have no symptoms until their urine turns bloody—this may be the first symptom of a kidney stone. The amount of blood may not be sufficient to be seen, and thus the first warning can be microscopic hematuria, when red blood cells are found in the microscopic study of a urine sample, during a routine medical test.

Diagnosis & Investigation
Diagnosis is usually made on the basis of the location and severity of the pain, which is typically colic in nature (comes and goes in spasmodic waves). Radiological imaging is used to confirm the diagnosis and a number of other tests can be undertaken to help establish both the possible cause and consequences of the stone. Ultrasound imaging is also useful as it will give details about the presence of hydronephrosis (swelling of the kidney - suggesting the stone is blocking the outflow of urine). It will also show the 10% of stones that do not have enough calcium to be seen on x-rays (radiolucent stones).

The relatively dense calcium renders these stones radio-opaque and they can be detected by a traditional X-ray of the abdomen that includes Kidneys, Ureters and Bladder—KUB. This may be followed by an IVP (Intravenous Pyelogram; IntraVenous Urogram (IVU) is the same test by another name) which requires about 50ml of a special dye to be injected into the bloodstream that is excreted by the kidneys and by its density helps outline any stone on a repeated X-ray. These can also be detected by a Retrograde pyelogram where similar "dye" is injected directly into the ureteral opening in the bladder by a surgeon. Computed tomography (CT or CAT scan), a specialized X-ray, is considered the gold-standard diagnostic test for the detection of kidney stones, and in this setting does not require the use of intravenous contrast, which carries some risk in certain people (eg, allergy, kidney damage). All stones are detectable by CT except very rare stones composed of certain drug residues in urine.

Investigations typically carried out include:

• Microscopic study of urine, which may show proteins, red blood cells, pus cells, cellular casts and crystals.
• Culture of a urine sample to exclude urine infection (either as a differential cause of the patient's pain, or secondary to the presence of a stone)
• Blood tests: Full blood count for the presence of a raised white cell count (Neutrophilia) suggestive of infection, a check of renal function and if raised blood calcium blood levels (hypercalcaemia).
• 24 hour urine collection to measure total daily urinary calcium, oxalate and phosphate

Treatment
Stones less than 5 mm in size usually will pass spontaneously, however the majority of stones greater than 6 mm will require some form of intervention, especially so if the stone is stuck causing persistent obstruction and/or infection of the urinary tract. Management of pain from kidney stones varies from country to country and even from physician to physician, but may require intravenous medication (eg, narcotic or nonsteroidal antiinflammatories) in acute situations or similar classes of drugs may be effectve orally in an outpatient setting for less severe discomfort. In many cases non-invasive Extracorporeal Shock Wave Lithotripsy may be used. Otherwise some form of invasive procedure is required; with approaches including ureteroscopic fragmentation (or simple basket extraction if feasible) using laser, ultrasonic or mechanical (pneumatic, shock-wave) forms of energy to fragment stones. percutaneous nephrolithotomy or open surgery may ultimately be necessary for large or complicated stones or stones which fail other less invasive attempts at treatment.

A single study in the USA, at the Mayo Clinic, has suggested that Lithotripsy may increase subsequent incidence of diabetes and hypertension, but it has not been felt warranted to change clinical practice at the clinic.

Secondary Prevention
Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:

• Drinking enough water to make 2 to 2.5 litres of urine per day.
•A diet low in protein, nitrogen and sodium intake.
• Restriction of oxalate-rich foods and maintaining an adequate intake of dietary calcium is recommended. There is equivocal evidence that calcium supplements increase the risk of stone formation, though calcium citrate appears to carries the lowest, if any, risk
• Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol depending on the cause of stone formation.
• Depending on the stone formation disease, vitamin B-6 and orthophosphate supplements (such as IP-6) may be helpful, although these treatments are generally reserved for those with Primary Hyperoxaluria. Cellulose supplements have also shown potential for reducing kidney stones caused by certain conditions, although, again, not much research has been completed on this treatment.

Certain foods may increase the risk of stones: spinach, rhubarb, chocolate, peanuts, cocoa, tomato juice, grapefruit juice, apple juice, soda (acidic and contains phosphorus), all types of tea, and berries (high levels of oxalate). In the United States, the South has the highest incidence of kidney stones, a region where sweet tea consumption is very common. Other drinks are associated with decreased risk of stones, including wine, lemonade and orange juice, the latter two of which are rich in citrate, a stone inhibitor.

A note on alcohol: Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stones sufferers to avoid, there are no conclusive data demonstrating any cause and effect regarding kidney stones. However, some have theorized that frequent and binge drinkers create situations that set up dehydration, (alcohol consumption, hangovers, and poor sleep and stress habits). In this view, it is not the alcohol that creates a kidney stone but it is the alcohol drinker's associated behavior that sets it up. [citation needed]

One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretic. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property does not preclude their efficacy as stone preventive. Though caffeine does acutely increase urinary calcium excretion, coffee has a high oxalate content which has been known to cause stones in some patients and should be used sparingly. Sodium restiction is necessary for clinical effect, as sodium excess promotes calcium excretion. In addition, the effect probably fades after two years or so of therapy (tachyphylaxis).
A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids. The most available alkaline base to balance the acid from protein is calcium carbonates and phosphates from the bones (buffering). The kidney filters the liberated calcium which may then form insoluble crystals (ie, stones)in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions depending on conditions. One of the simplest fixes in addition to increased fluid intake is to moderate animal protein consumption. In this regard, it is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (eg, distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels, which is a potent inhibitor of stone formation, and these patients are prone to frequent stone formation.