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Department of Urology

Urinary Stone Disease

Presentation

Most urinary stones pass through the collecting system in an uneventful fashion. When a ureteral stone becomes obstructed it can result in severe pain with associated nausea and vomiting. Stones less than 5 mm in size have a 50% chance of spontaneous passage within a six-week period of time. If a patient has uncontrollable pain, persistent vomiting or a fever intervention is indicated. The imaging modality of choice is the non-contrast CT scan. All stone types except protease inhibitors (used in immuno-compromised patients) will be visualized. It eliminates the need for intravenous contrast, a skilled technician, and has the added benefit of imaging the entire abdomen and pelvis.

 

Intervention

If conservative observation while awaiting spontaneous passage is unsuccessful intervention is required. Ureteral stones can be approached in a variety of ways. The least invasive is with extracorporeal shock wave lithotripsy. Limitations include difficulty targeting small stones including those overlying the sacro-iliac joint. Additionally, after shock wave lithotripsy, patients have to pass stone fragments through the collecting system. If patients are away from immediate medical facilities, a double-J stent can be placed to assure urinary drainage. Successful treatment with shock wave lithotripsy is in the 60-80% range.

Distal ureteral stones in women of child-bearing age are best approached in an ureteroscopic fashion limiting potential damage (from SWL) to the ovaries. Stones can be retrieved with baskets or fragmented with a variety of lithotrites including ultrasonic, pneumatic, electrohydraulic, or laser lithotripsy. Smaller ureteroscopes have limited the need for routine balloon dilation of the ureteral orifice. Flexible ureteroscopes can be utilized to treat stones in the collecting system. Large stone burdens are best approached via a percutaneous route.

Percutaneous nephrolithotomy allows access to the entire upper tract. Urologists or interventional radiologists can successfully obtain percutaneous renal access. Lower pole renal access decreases postoperative morbidity but may increase the likelihood of a rare colonic injury, especially if the percutaneous puncture site is more than 1-2-finger breadths later to the paraspinous musculature. Superior pole punctures ease access into the ureter but typically require access above the costal margin, thus increasing potential injury to the pleura. The tract can be dilated with high pressure balloons, sequential Amplatz fascial dilators, or co-axial metal dilators. Contemporary series have reported blood transfusion rates less than 5-7%.

Rare anterior calyceal stones may best be approached in a laparoscopic fashion.

 

Metabolic Evaluation

After appropriate diagnosis and treatment a full metabolic evaluation is indicated to help reduce the recurrence of urinary stones. Eighty-five per cent of all stones are calcium based and are radio-dense as seen on plain abdominal radiographs. This excludes:

Magnesium-ammonium-phosphate stones

Magnesium-ammonium-phosphate stones, also referred to as infectious calculi, or struvite stones. These stones are found most frequently in women who present with recurrent urinary tract infections due to bacteria other than E. coli and typically grow urease-producing organisms such as Proteus, Providencia, or Pseudomonas. These urease-producing bacteria increase the urinary pH from a normal value of 5.8 to more than 7.2. Struvite stones will only precipitate in urine with a pH greater than 7.2. Struvite stones rarely present with ureteral colic.

Uric acid stones

Uric acid stones are relatively radiolucent on KUB radiographs. They typically occur in while males with a high recurrence rate. Uric acid stone will form in urine with an acidic melieu, < 5.5. Uric acid stones can be dissolved medically by increasing the urinary pH to 6.0-6.5 range with potassium citrate or potassium bicarbonate. Stones typically dissolve at a rate of one cm, as seen on KUB, per month with compliant urinary alkalization. Chronic urinary alkalization will drastically limit recurrent uric acid stones.

Cystine stones

Cystine stones are caused by abnormalities in amino acid pumps that effect cystine, ornithine, lysine and arginine (COLA). Patients frequently present with recurrent stones that have a ground-glass appearance on KUB. Intervention should be based on clinical symptoms or evidence of progressive obstruction. One should limit open surgical extraction as the vast majority of patients will develop many recurrent stones despite our best attempts to prevent them with disulfide binders (Thiola or Penicillamine) and urinary alkalization with potassium citrate. There are no known urinary inhibitors of cystine and thus patients should be encouraged to increase fluid intake (during the day and night) to decrease urinary supersaturation of cystine.

Calcium based stones

Calcium based stones can be evaluated based on complete 24-hour urine collections and can be divided into hypercalciuria, hyperuricosuria, hyperoxaluria and hypocitraturia. Patients may have one or multiple abnormalities.

Hypercalciuria is defined as > 4mg/kg of calcium in a 24-hour collection, or > 250-300 mg. There are three types of absorptive hypercalciuria. Type I absorptive hypercalciuria is dietary independent. Patients have elevated urinary calcium levels with a high or low calcium diet. One should not routinely recommend a reduced calcium diet for patients with calcium based stones. Such patients can be treated with calcium binders such a cellulose phosphate or alternatively with potassium citrate. Potassium citrate will be effective for a limited period of time (4-6 years) and as such repeat 24-hour urine collections are required to reassess values and ensure patient compliance. These patients, like other calcium stone formers need to be encouraged to have a low sodium diet. Where sodium goes, so does calcium. Additionally, patients are encouraged to reduce animal protein consumption by approximately 30%. That does not mean they need to be vegetarians. This reduced animal protein consumption will limit the post-prandial acid flux that will result in calcium being leached from bone. Finally, a generalized recommendation is to have patients drink adequate volumes so that they will void 1.5-2.0 liters per day. One should emphasize to the patient that it is the voided volume rather than the absolute volume consumed that is important. Type II absorptive hypercalciuria is dietary dependent and patients will have elevated urinary calcium levels only while consuming a high calcium diet. It is these patients that should be encouraged to reduce their calcium intake by about 50%. Type III absorptive hypercalciuria is secondary to a phosphate renal leak. The decreased phosphate results in a secondarily increased parathyroid hormone level and an increase in vitamin D production. The increased vitamin D results in increased phosphate AND increased calcium absorption, thus the name absorptive hypercalciuria. These patients can be successfully treated with phosphate supplements that are bio-available, such as with neutraphos.

Resorptive hypercalciuria is due to primary hyperparathyroidism. Such patients have elevated serum calcium and PTH levels, and the PTH values will not decrease after a one week HCTZ load; this an easy way to differentiate primary from secondary hyperparathyroidism in urinary stone patients. Such patients can not be effectively treated with medications and as such should undergo parathyroid surgery. Urinary and serum values will return to normal in 7-10 days.

Renal hypercalciuria is due to abnormal renal calcium pumps, resulting in increased urinary calcium and secondarily increased PTH. Unlike patients with primary hyperparathyroidism these patients have normal serum calcium levels. These patients can be effectively treated with potassium citrate.

Hyperuricosuria is the second major etiology of calcium-based stones. The most common etiology is dietary dependent and can be effectively treated by limiting purine intake. Those unresponsive to dietary recommendations should be treated with Allopurinol. Alternatively, they can be treated with potassium citrate.

Hyperoxaluria is most commonly found in those with gastrointestinal disorders such as short-gut syndrome or inflammatory bowel disease resulting in chronic diarrhea. The chronic diarrhea results in increased fat and bile contents in the stool. The fat and bile will bind with the intra-luminal calcium forming a soap-like compound. The oxalate in the gut is therefore unbound, as the calcium has been "consumed" and is freely available for absorption and subsequent increased urinary oxalate levels. The diarrheal states should be optimally treated. Typically, the diarrhea continues and these patients should be treated with oral calcium in the form of milk products or TUMS. This oral calcium will successfully bind the free oxalate. These medications must be taken with meals to bind to the dietary oxalate. There is a rare type of endogenous hyperoxaluria that results in oxalate precipitating in solid organs and frequently results in renal and liver failure. These rare patients can be successfully treated with a combined liver/kidney transplant.

Hypocitraturia is the last main subdivision of patients with calcium based stones. Hypocitraturia is defined as a 24-hour urinary citrate level < 320 mg. It is typically found in patients with a metabolic acidosis. Renal tubular acidosis (type I, distal) is a classic example. Other common causes include chronic diarrhea, chronic diuretic use, and chronic dehydration. These patients are best treated with potassium citrate supplementation. Potassium citrate can be delivered in a wax matrix tablet. Patients should be warned that these tablets can be seen in the stool, yet are typically well absorbed. Alternatively, potassium citrate crystals can be given when mixed in a glass of fluid. Oral formulations are cheap, yet may not be as convenient as the crystal and tablet formulations. Lemonade has been shown to increase quantitative urinary citrate levels by approximately 150 mg/day. In patients with mild hypocitraturia and intolerant or unwilling to take pharmacologic supplements, lemonade is a reasonable alternative.

 

 

Contents of This Page

Presentation
Intervention
Metabolic Evaluation
Magnesium-ammonium-phosphate stones
Uric acid stones
Cystine stones
Calcium based stones


Faculty

Marshall Stoller, MD
Maxwell Meng, MD

Appointments & Location

UCSF Medical Center, Parnassus Campus
400 Parnassus Avenue, Suite A-610
San Francisco, CA 94143-0330

Contact Number

To schedule an appointment please call us at 415/353-2200