Urolithiasis

Medical Therapy and New Approaches to Urolithiasis

The introduction of extracorporeal shock-wave lithotripsy (ESWL) has revolutionized the urologic practice in urolithiasis. [1] This technology has reduced considerably the morbidity of stone disease, by allowing relatively noninvasive removal of stones.  Unfortunately, the facilitated removal of stones by ESWL has led some urologists to abandon or disparage the medical approach to stone management. This development is unfortunate, because the need for medical diagnosis and prevention has not diminished. Renal stone disease is characterized by a high rate of recurrence. [3] The propensity for stone recurrence is not altered by removal of stones with ESWL. [5] Ample evidence has accumulated, however, showing that a variety of medical treatments can prevent recurrence of stones. [9]

There have been notable advances in the medical management of urolithiasis. A method for the analysis of urinary-stone risk factors in a 24-hour urine sample was described in 1985. [14] A graphic display of stone risk factors is now available commercially. A step-by-step approach to diagnosis and treatment of different causes of urolithiasis was described in 1996. [15] A simplified, nonselective treatment program was recommended in 1997. [11] Despite this progress, many urologists are confused by current guidelines on medical diagnosis and prevention.
It is the objective of this article to offer practical guidelines in medical management of urolithiasis. Although borrowing from prior recommendations, [11] [14] [15] the current guidelines represent a simpler version directed at a practicing urologist.
Described here in stepwise fashion is the approach that a practicing urologist might take in medically diagnosing and managing patients with stones, summarized as follows:

Step 1. History and minimum diagnostic tests

Step 2. 24-hour urinary stone risk profile(cstomary diet)

Identification of abnormal dietary risk factors

Short-term dietary modification

Step 3. Repeat stone risk profile after dietary modification

Step 4. Elucidation of causes and construction of treatment options for abnormal risk factors

Relevant history and minimum diagnostic test results first are obtained. A full 24-hour stone risk profile is measured on a random diet and fluid intake. Another stone risk profile is obtained after a short-term dietary modification. From these simplified tests, potential causes are discerned and treatment options are constructed for each abnormal stone-risk factor and combined derangements.

SIMPLE DIAGNOSTIC APPROACH

Initial Visit

The first step, to be undertaken during the initial visit, is to take a careful history and conduct minimum diagnostic tests:

History

Secondary causes

Dietary aberrations

Stone-provoking drugs

Minimum diagnostic tests

Abdominal radiograph of the kidneys,ureter, and bladder

Urinary sediment (crystals)

Serum calcium, potassium, electrolytes,and uric-acid levels

History
In all patients with stones, a careful history should be taken. The history should include prior stone occurrences, family history of stones, and history of gout, bowel disease, fluid loss, or urinary-tract infection; dietary aberrations; and use of stone-provoking medications. Gout, bowel disease, urinary-tract infection, and excessive fluid loss represent potential secondary causes of stones. Dietary aberrations include low intake of fluids or citrus fruits and a high intake of calcium, oxalate, sodium or animal proteins. Drugs that can cause stones include those that can increase urinary calcium (acetazolamide, calcium-channel blockers, calcium or vitamin D preparations, phosphorus-binding antacids, furosemide, and theophylline), oxalate (vitamin C), uric acid (uricosuric agents), and those than can enhance urinary excretion of poorly soluble substances (triamterene).
Minimum Diagnostic Tests
The following tests should be obtained in any patient presenting with stones, for the first time or after prior stone episodes: Urinalysis and culture; radiograph of kidneys, ureter, and bladder; stone analysis; and measurement of serum calcium, phosphorus, electrolyte, uric-acid, and creatinine levels.
The finding of calcium oxalate crystals is not overly useful, because they can be found in normal urine. The detection of cystine or struvite (magnesium-ammonium phosphate) crystals, however, is diagnostic of cystinuria or infection stones, respectively. A positive culture for urea-splitting organisms is indicative of infection stones. Radioopaque stones imply the presence of calcium oxalate, calcium phosphate, struvite, or cystine. Radiolucency suggests that stones might be composed of uric acid.
The finding of cystine and struvite on stone analysis is diagnostic of cystinuria and infection stones, respectively. Uric-acid stones are indicative of conditions that cause low urinary pH (e.g., such as gout or chronic diarrheal states) or marked hyperuricosuria. Stones composed largely of calcium phosphate (hydroxyapatite) are suggestive of primary hyperparathyroidism, renal tubular acidosis, and sodium alkali therapy. Of lesser diagnostic importance are common stones of calcium oxalate. They are encountered with hypercalciuria, hyperoxaluria, hypocitraturia, hypomagnesiuria, or low urine volume.
Presence of hypercalcemia and hypophosphatemia is indicative of primary hyperparathyroidism. Hypokalemia and high serum bicarbonate concentration are suggestive of renal tubular acidosis. Hyperuricemia indicates gouty diathesis.

Twenty-four-hour Urinary Stone Risk Profile on the Customary Diet

The second step, to be undertaken in recurrent stone formers and first-time stone formers with increased risk (i.e., family history of stones, bone or bowel disease, gout, chronic urinary-tract infection, or nephrocalcinosis), is to obtain a 24-hour urine sample, while patients maintain their customary diets and fluid intakes, for the analysis of full stone risk profile. [14] The metabolic factors include calcium, oxalate, uric acid, citrate, and pH. Environmental factors comprise total volume, sodium, sulfate, phosphorus, and magnesium. Physicochemical factors are urinary saturation of calcium oxalate, brushite (CaHPO4 2H2 O), monosodium urate, and uric acid, expressed relative to mean values in normal subjects without stones.
Identification of Abnormal Dietary Risk Factors
Aberrations in diet and fluids can produce abnormal environmental factors cited previously. They also could exaggerate disturbances in metabolic factors. From the stone risk profile, it is important to identify aberrant environmental risk factors and try to correct them with dietary modification.
Short-term Dietary Modification
If urinary total volume is less than 2 L/d, patients should increase fluid intake. If urinary sodium exceeds 200 mEq/d, sodium intake should be restricted. In general, this goal may be achieved by avoidance of salt shakers and obviously salty foods. If urinary oxalate exceeds 45 mg/d, one should impose dietary oxalate restriction, that is, limitation or avoidance of tea, spinach, and other dark roughage; nuts; and chocolate. Vitamin C in excess of 500 mg/d is not advisable because it can be converted to oxalate.
If urinary calcium exceeds 250 mg/d in a patient taking a high-calcium diet, a moderate calcium restriction might be imposed, for example, 1 glass of milk and a small serving of another dairy product per day. If urinary uric-acid and sulfate levels exceed 700 mg/d and 30 mmol/d, respectively, one should restrict animal proteins by limiting the intake of beef, poultry, and fish to two servings per day. If urinary pH, citrate, and potassium are low, patients should be told to increase the intake of potassium-rich citrus fruits (e.g., orange, grapefruit, and cranberry).

Repeat 24-hour Profile After Short-term Dietary Modification: Identification of Abnormal Environmental and Metabolic Risk Factors

In the third step, another 24-hour urine is to be collected for a stone risk profile, after the dietary modification described previously for 1 week. From a stone risk profile so obtained it is important to identify abnormal environmental and metabolic risk factors.
The stone risk profile obtained following dietary modification is compared with that measured on a random diet. The correction of aberrant risk factors by dietary modification suggests that such abnormalities are environmental in origin. If risk factors considered to be clearly environmental remain abnormal (e.g., low urine volume or high urinary sodium level), the dietary modification may have been inadequate or poorly followed. In contrast, the persistence of abnormal metabolic stone risk factors would confirm that the derangements were metabolic in origin.
In the fourth step, potential causes are discerned and treatment guidelines are constructed, for each abnormal urinary risk factor and combination of deranged risk factors. This task is aided by history, minimum diagnostic tests, and stone risk profiles.

CAUSES AND TREATMENT OF INDIVIDUAL ABNORMAL STONE RISK FACTORS

Long-term Dietary Modification

In all patients with stones, dietary modification should be continued in the long term:

High fluid intake: At least ten 10-oz glasses per day

Sodium restriction: Avoidance of salt shakers and salty foods

Oxalate restriction: Avoidance of nuts, dark roughage, chocolate, tea, vitamin C

Restriction of animal proteins: Limited servings of meat products

Increased citrus fruits: Potassium-rich products preferable

The high fluid intake and restriction of sodium and oxalate should be maintained, without fear of adverse effects on health. In most patients, purine restriction is difficult to maintain. Adequate intake of fruits and vegetables to balance the intake of animal proteins should be encouraged. Potassium-rich citrus fruits, such as orange, grapefruit and cranberry, are preferable to low-potassium citrus fruits, such as lime and lemon. Orange juice, for example, represents a natural form of potassium citrate and possesses alkalinizing and citraturic action. [24] Lime juice, on the other hand, is composed largely of citric acid, and does not affect acid-base balance appreciably. [20] Thus, it does not alter urinary pH and only modestly increases urinary citrate (from the renal clearance of a small amount of absorbed citrate that escapes oxidation in vivo).

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