Everything about Kidney Stones totally explained
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Kidney stones, also called
renal calculi, are solid concretions (crystal aggregations) of dissolved
minerals in
urine; calculi typically form inside the
kidneys or
bladder. The terms
nephrolithiasis and
urolithiasis refer to the presence of calculi in the kidneys and urinary tract, respectively.
Overview
The
kidneys are a pair of organs that are primarily responsible for filtering
metabolites and
minerals from the
circulatory system. These secretions are then passed to the
bladder and out of the body as
urine. Some of the substances found in urine are able to
crystalize, and in a concentrated form these
chemicals can
precipitate into a solid deposit attached to the kidney walls. These crystals can grow through a process of accretion to form a kidney stone. In
medical terminology these deposits are known as renal calculi (
Latin renal, "kidney" and
calculi, "pebbles").
Renal calculi can vary in size from as small as grains of sand to as large as a golf ball. Kidney stones typically leave the body by passage in the urine stream, and many stones are formed and passed without causing symptoms. If stones grow to sufficient size before passage—on the order of at least 2-3 millimeters—they can cause obstruction of the ureter. The resulting obstruction with dilation or stretching of the upper ureter and renal pelvis as well as spasm of muscle, trying to move the stone, can cause severe episodic
pain, most commonly felt in the
flank, lower abdomen and groin (a condition called
renal colic). Renal colic can be associated with nausea and vomiting due to the
embryological association of the kidneys with the intestinal tract.
Hematuria (bloody urine) is commonly present due to damage to the lining of the urinary tract.
Within the
United States, about 10–15% of adults will be diagnosed with a kidney stone, and the total cost for treating this condition was
US$2 billion in 2003. The incidence rate increases to 20–25% in the
Middle East, because of increased risk of dehydration in hot climates. Recurrence rates are estimated at about 10% per year, totalling 50% over a 5–10 year period and 75% over 20 years. Men are affected approximately 4 times more often than women.
History
The existence of kidney stones has been recorded since the beginning of civilization, and
lithotomy for the removal of stones is one of the earliest known surgical procedures. In 1901, a stone was discovered in the pelvis of an ancient egyptian
mummy, and was dated to 4,800 BCE. Medical
text from ancient
Mesopotamia,
India,
China,
Persia,
Greece and
Rome all mentioned calculous disease. Part of the
Hippocratic oath contains an admonition about the dangers of operating on the bladder for stones. The Roman medical treatise
De Medicina by
Cornelius Celsus contained a description of lithotomy, and this work served as the basis for this procedure up until the 18th century.
New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky. It was only after
Henry J. Bigelow popularized the technique of
litholopaxy in 1878 that the mortality rate dropped from about 24% down to 2.4%. However, other treatment techniques were developed that continued to produce a high level of mortality, especially among inexperienced urologists.
Among the famous leaders who were
kidney stone sufferers are Emperor
Napoleon Bonaparte, Emperor
Napoleon III,
Peter the Great,
Louis XIV,
George IV,
Oliver Cromwell, and former U.S. President
Lyndon B. Johnson. Other notable individuals who endured stones include
Benjamin Franklin, the philosopher
Sir Francis Bacon, the scientist
Sir Isaac Newton, the civil servant and diarist
Samuel Pepys, the physicians
William Harvey and
Herman Boerhaave, and the anatomist
Antonio Scarpa. Interestingly,
astronauts seem to have a higher risk of developing kidney stones during or after long duration
space flights.
Causes
Kidney stones can be due to underlying metabolic conditions, such as
renal tubular acidosis, and
medullary sponge kidney. Many health facilities will screen for such disorders in patients with recurrent kidney stones. This is typically done with a 24 hour urine collection that's chemically analyzed for deficiencies and excesses that promote stone formation.
There has been some evidence that
water fluoridation
may increase the risk of kidney stone formation. In one study,
patients with symptoms of
skeletal fluorosis were 4.6 times as likely to develop kidney stones. However,
flouride may also be an
inhibitor of urinary stone formation.
Calcium oxalate stones
The most common type of kidney stone is composed of
calcium oxalate crystals, occurring in about 80% of cases,
Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter and/or urethra.
Pyuria: pus in the urine.
Dysuria: burning on urination when passing stones (rare). More typical of infection.
Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra by stone, or extremely rarely, simultaneous obstruction of both ureters by a stone.
Abdominal distention.
Nausea/vomiting: embryological link with intestine—stimulates the vomiting center.
Fever and chills.
Diagnosis
Clinical 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). Pain in the back occurs when calculi produce an obstruction in the kidney.
Treatment
Temporizing
About 90% of stones 4 mm or less in size usually will pass spontaneously, however 99% of stones greater than 6 mm will require some form of intervention. There are various measures that can be used to encourage the passage of a stone. These can include increased hydration, medication for treating infection and reducing pain, and diuretics to encourage urine flow and prevent further stone formation. Eating starfruit can be effective at reducing pain and improving urination.
In most cases, a smaller stone that isn't symptomatic is often given up to four weeks
but it hasn't been felt warranted to change clinical practice at the clinic. The study reflects early experience with the original lithotripsy machine which had a very large blast path, much larger than what is used on modern machines. Further study is believed necessary to determine how much risk this treatment actually has using modern machines and treatment regimens.
More common complications related to ESWL are bleeding, pain related to passage of stone fragments, failure to fragment the stone, and the possible requirement for additional or alternative interventions.
Ureteral (double-J) stents
One modern medical technique uses a ureteral stent (a small tube between the bladder and the inside of the kidney) to provide immediate relief of a blocked kidney. This is especially useful in saving a failing kidney due to swelling and infection from the stone. Ureteral stents vary in length and width but most have the same shape usually called a "double-J or double pigtail". They are designed to allow urine to drain around any stone or obstruction. They can be retained for some length of time as infections recede and as stones are dissolved or fragmented with ESWL or other treatment. The stents will gently dilate or stretch the ureters which can facilitate instrumentation and that'll also provide a clear landmark to help surgeons see the stones on x-ray. Most stents can be removed easily during a final office visit. Discomfort levels from stents typically range from minimal associated pain to moderate discomfort.
Prevention
Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:
Avoidance of cola beverages.
For those patients interested in optimizing their kidney stone prevention options, it's essential to have a 24 hour urine test performed. This should be done with the patient on his or her regular diet and activities. The results can then be analyzed for abnormalities and appropriate treatment given.
Diuretics
Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stone 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 isn't the alcohol that creates a kidney stone but it's the alcohol drinker's associated behavior that sets it up.
One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretics. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property doesn't preclude their efficacy as stone preventive. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Though some have said that the effect probably fades after two years or so of therapy (tachyphylaxis), in fact it's only randomized controlled trials lasting 2 years or more that show the effect; there's really no good evidence from studies of calcium metabolism that the thiazide effect doesn't last indefinitely. Thiazides are the medical therapy of choice for most cases of hypercalciuria (excessive urinary calcium) but may not be suitable for all calcium stone formers; just those with high urinary calcium levels.
Allopurinol
Allopurinol (Zyloprim) is another drug with proven benefits in some calcium kidney stone formers. Allopurinol interferes with the liver's production of uric acid. Hyperuricosuria, too much uric acid in the urine, is a risk factor for calcium stones. Allopurinol reduces calcium stone formation in such patients. The drug is also used in patients with gout or hyperuricemia, but the latter isn't the critical feature of uric acid stones. Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion won't be associated with uric acid stone formation if the urine pH is alkaline. Therefore prevention of uric acid stones relies on alkalinization of the urine with citrate.
Allopurinol is reserved for patients in whom alkalinization is difficult. For patients with increased uric acid levels and calcium stones, alloprinol is one of the few treatments that has been shown in double-blinded placebo controlled studies to actually reduce kidney stone recurrences. Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/dL is often the goal of the drug's use in patients with gout or hyperuricemia.
Decreased protein diet
A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids, including uric acid. The most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering). The kidney filters the liberated calcium which may then form insoluble crystals (for example, stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions, depending on conditions. High protein intake is therefore associated with decreased bone density as well as stones. The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones.
In addition to increased fluid intake, one of the simplest fixes is to moderate animal protein consumption. However, despite epidemiologic data showing that greater protein intake is associated with more stones, randomized controlled trials of protein restriction have not shown reduced stone prevalence. In this regard, it isn't just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (for example, distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels; since citrates are normally present as potent inhibitors of stone formation, these patients are prone to frequent stone formation.
Other modifications
Potassium citrate is also used in kidney stone prevention. This is available as both a tablet and liquid preparation. The medication increases urinary pH (makes it more alkaline), as well as increases the urinary citrate level, which helps reduce calcium oxalate crystal aggregation. Optimal 24 hour urine levels of citrate are thought to be over 320 mg/liter of urine or over 600 mg per day. There are urinary dipsticks available that allow patients to monitor and measure urinary pH so patients can optimize their urinary citrate level.
Though caffeine does acutely increase urinary calcium excretion, several independent epidemiologic studies have shown that coffee intake overall is protective for stones.
Measurements of food oxalate content have been difficult and issues remain about the proportion of oxalate that's bio-available, versus a proportion that isn't absorbed by the intestine. Oxalate-rich foods are usually restricted to some degree, particularly in patients with high urinary oxalate levels, but no randomized controlled trial of oxalate restriction has been performed to test that hypothesis.
Calgranulin
Crystallization of calcium oxalate (CaOx) appears to be reduced by molecules in the urine that retard the formation, growth, aggregation, and renal cell adherence of calcium oxalate. By purifying urine using salt precipitation, preparative isoelectric focusing, and sizing chromatography, some researchers have found that the molecule calgranulin is able to inhibit calcium oxalate crystal growth. Calgranulin is a protein formed in the kidney. Given the large amounts of calcium oxalate in the urine, and considering its potency, calgranulin could become an important contribution to the normal urinary inhibition of crystal growth and aggregation. If so, it'll be an important tool in the renal defense against kidney stones.
Further Information
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