Traditional Kidney Stone Treatments
About 90% of stones 4 mm or less in size usually will pass spontaneously, however the majority of stones greater than 6 mm will require some form of intervention. In most cases, a smaller stone that is not symptomatic is often given up to 30 days to move or pass before consideration is given to any surgical intervention as it has been found that waiting longer tends to lead to additional complications. Immediate surgery may be required in certain situations such as in people with only one working kidney, intractable pain or in the presence of an infected kidney blocked by a stone which can rapidly cause severe sepsis and toxic shock.
Analgesia
Management of pain from kidney stones varies from country to country and even from physician to physician, but usally requires intravenous administration of narcotics in an emergency room setting for acute situations. "Old school" physicians know that narcotics (morphine, demerol or dilaudid) are usually the only effective and expedient means of analgesia for acute kidney stone pain. Narcotics relax the ureter enough to facilitate passing of smaller stones within 24-48 hours of treatment, therefore, analgesia actually is the treatment of the condition.
Similar classes of drugs may be effective orally in an outpatient setting for less severe discomfort where nonsteroidal anti-inflammatories or narcotics like codeine can be prescribed. Some doctors will give patients with recurring passing small stones a small supply [one effective dose] prescription for hydrocodone to avoid a future visit to the ER when the next episode occurs.
Taken at the first sign of pain, hydrocodone can eliminate the acute pain which necessitates the midnight ER visit and a needless ambulance trip, and still facilitate stone passage. An immediate follow-up with your personal physician during business hours after an event goes without saying in these situations.
The current standard of care for acute ureteral colic caused by stone in patients who are not allergic to aspirin, is intramuscular or intravenous injection of the non-steroidal medication Ketorolac, which acts by reducing renal blood flow. Patients who are to be treated non-surgically, may also be started on an alpha adrenergic blocking agent, which acts to reduce the muscle tone of the ureter and facilitate stone passage.
After treatment, the pain seldom returns and patients are encouraged by their follow-up physicians to strain their urine so they can collect the stone when it eventually passes and send it for chemical composition analysis which will be used to establish preventative options.
Urologic interventions
In many cases non-invasive Extracorporeal Shock Wave Lithotripsy or (ESWL) 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 the 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.
One modern medical technique uses a ureter stent (a small tube between the bladder and the inside of the kidney) to provide some relief of a blocked kidney. This is especially useful in saving a failing kidney due to swelling and infection from the stone. This tubing allows urine to drain from kidney and in some cases medicine to be injected directly. Ureter stents vary in shape and size, but most are designed to allow urine to drain and be retained for some length of time as infections reside and as stones are dissolved or sonar blasted. Most stents can be removed during a final office visit. This can range from little associated pain to extreme pain.
Possible lithotripsy complications
A single retrospective 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. 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 requirement for additional or alternative interventions.
Prevention
Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:[3]
- Drinking enough water to make 2 to 2.5 liters of urine per day.
- A diet low in protein, nitrogen and sodium intake.
- Avoiding excess Vitamin C, especially Vitamin C supplements.
- Restriction of oxalate-rich foods and maintenance of an adequate intake of dietary calcium. There is equivocal evidence that calcium supplements increase the risk of stone formation, though calcium citrate appears to carry the lowest, if any, risk.
- Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol, depending on the cause of stone formation.
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 is not the alcohol that creates a kidney stone but it is 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 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.
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 is only randomized controlled trials lasting 2 years or more that show the effect; there is really no good evidence from studies of calcium metabolism that the thiazide effect does not 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 hyperuricosuria is not the critical feature of uric acid stones.
Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion will not 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 (i.e., 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 is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (e.g., 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 is bio-available, versus a proportion that is not 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.[6] 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 will be an important tool in the renal defense against kidney stones.
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