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Common Urological Problems

Urinary Stone Disease Prevention

  • - General Urology - Common Urological Problems - Urinary Stone Disease
  • Jul 25, 2010
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Tags: | absorptive hypercalciurics | alkalinizing ph agents | calcium nephrolithiasis | computed tomography |

3. Phosphate supplementation-
Renal phosphate leak is best treated by replacing phosphate. Phosphate absorption may be inhibited in the presence of aluminum-, magnesium-,  or calcium-containing antacids.  This treatment should be used with caution in digitalized patients and in those with severe renal failure, Addison disease, or severe hepatic dysfunction. It is generally well tolerated. Dosing can begin with 250 mg three to four times daily and may be doubled depending on follow-up serum electrolyte, calcium, and phosphorus levels.

4. Diuretics-
Thiazides can correct the renal calcium leak associated with renal hypercalciuria.  This prevents a secondary hyperparathyroid state and its associated elevated vitamin D synthesis and intestinal calcium absorption.  A rapid decrease in urinary calcium excretion is appreciated and is sustained long-term (>10 years). A starting dose of 25 mg may be titrated based on urinary calcium levels.  Side effects are usually well tolerated.  Potassium levels should be monitored. Hypokalemia induces a hypocitraturic state;  potassium replacement corrects the hypokalemia and its associated hypocitraturia.

Urinary Stone Disease

Urinary Stone Disease

Thiazides result in a transient decrease in urinary calcium excretion in absorptive hypercalciurics. Urinary calcium excretion rebounds to pretreatment values in 50% of such patients after 4–5 years of therapy.  Dietary changes are not believed to be responsible for this phenomenon.  Thiazides do not restore normal intestinal absorption of calcium.

5. Calcium supplementation-
Enteric   hyperoxaluric calcium nephrolithiasis is effectively treated with calcium supplements.  Calcium gluconate and calcium citrate are better absorbed and are more effective in increasing serum calcium availability than are other forms of calcium.

Calcium carbonate,  calcium phosphate,  and oyster shell are forms of calcium that are less efficiently absorbed;  they remain in the intestinal lumen, available to bind oxalate, thus reducing its absorption. These less efficiently absorbed forms of calcium are optimal to treat enteric hyperoxaluric calcium nephrolithiasis and must be given with meals to be effective.

6. Uric acid-lowering medications-
Allopurinol is used to treat hyperuricosuric calcium nephrolithiasis with or without hyperuricemia. Unlike uricosuric agents that reduce serum uric acid levels by increasing urinary uric acid excretion,  allopurinol is a xanthine-oxidase inhibitor and reduces both serum and urinary levels of uric acid. It has no impact on the biosynthesis of purines; rather, it acts exclusively on purine catabolism. Elevated levels of xanthine and hypoxanthine in the urine secondary to allopurinol have not been associated with nephrolithiasis. 

Allopurinol is a potentially dangerous drug and should be discontinued at the first appearance of a skin rash, which infrequently may be fatal.  Therapy can start at 300 mg/day.  It is tolerated best when taken after meals.

7. Urease inhibitor-
Acetohydroxamic acid is an effec-
tive adjunctive treatment in those with chronic urea-splitting urinary tract infections associated with struvite stones.

Acetohydroxamic acid reversibly inhibits bacterial urease, decreasing urinary ammonia levels, and will subsequently acidify urine.

It is best used as prophylaxis after removal of struvite stones.  It also may be used after unsuccessful attempts at curative surgical removal of calculi or culture-specific antibiotic therapy. Patients with serum creatinine >2.5 mg/dL are unable to achieve therapeutic urinary levels. Acetohydroxamic acid is not effective with non-urease-producing bacteria.  Long-term data (>7 years)  are unavailable. A significant number of patients complain of side effects,  including headaches that are usually shortlived and responsive to aspirin compounds.  Other frequent complaints include nausea, vomiting, anorexia, nervousness,  and depression.  A typical dosing regimen is 1 250 mg tablet three or four times daily (total dosage: 10– 15 mg/kg/day).

8. Prevention of cystine calculi -
Conservative   measures, including massive fluid intake and urinary alkalinization, are frequently inadequate to control cystine stone formation. Penicillamine, the same drug that is used to chelate excess copper in the treatment of Wilson disease, undergoes a thiol-disulfide exchange with cystine. 

This reduces the amount of urinary cystine that is relatively insoluble. Cystine solubility is pH-dependent (pH 5: 150–300 mg/L; pH 7:  200–400 mg/L;  pH 7.5:  220–500 mg/L).  D-Penicillamine is associated with numerous and frequent side effects, including rashes and hematologic, renal, and hepatic abnormalities.  An initial dosage of 250 mg daily in 3–4 divided doses may help reduce severe side effects. It may be increased gradually to 2 g/day.  Dosage should be titrated with quantitative urinary cystine values.  Penicillamine increases the requirement of pyridoxine (vitamin B6), which should be supplemented with 25–50 mg/day.

Mercaptopropionylglycine (Thiola)  is better tolerated by patients than is penicillamine.  Mercaptopropionylglycine, a reducing agent, binds to the sulfide portion of cystine, forming a mixed disulfide (Thiola-cysteine) water-soluble compound.  It may retard the rate of new stone formation.

The dosage should be titrated with repeat 24-hour urinary cystine values. An initial dosage may be 200–300 mg three times daily, either 1 hour before or 2 hours after each meal.  Side effects are not infrequent and may include drug fever; nausea, vomiting, and gastrointestinal upset; rash, wrinkling, or friable skin; lupuslike symptoms, decreased taste perception;  and a variety of hematologic disorders.

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Marshall L. Stoller, MD

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REFERENCES

  1. Ackermann D et al: Influence of calcium content in mineral water on chemistry and crystallization conditions in urine of calcium stone formers. Eur Urol 1988;14:305.
  2. Allie-Hamdulay S et al: Prophylactic and therapeutic properties of a sodium citrate preparation in the management of calcium oxalate urolithiasis:  Randomized,  placebo-controlled trial.  Urol Res 2005;33:116.
  3. Bilezikian JP et al:  Primary hyperparathyroidism:  New concepts in clinical,  densitometric and biochemical features.  J Intern Med 2005;257:6.
  4. Fellstrom B et al: Dietary habits in renal stone patients compared with healthy subjects. Br J Urol 1989;63:575.
  5. Gentle DL et al: Geriatric nephrolithiasis. J Urol 1997;158:2221.
  6. Heller HJ et al: Effect of dietary calcium on stone forming propensity. J Urol 2003;169:470.
  7. Langley SE, Fry CH: The influence of pH on urinary ionized [Ca2+]:

Full References  »

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