© Springer International Publishing Switzerland 2015David A. Schulsinger (ed.)Kidney Stone Disease10.1007/978-3-319-12105-5_19
19. Medical Therapy: Mind Your Medicines
Department of Urology, Stony Brook Medicine, Stony Brook, NY, USA
David A. Schulsinger (Corresponding author)
Medical Management Facts
Medical management of stone disease has been shown to reduce stone recurrence.
Hydrochlorothiazide (HCTZ) decreases urinary calcium.
Potassium Citrate replenishes urinary citrate, increases urine pH and complexes urinary calcium.
Thiopronin makes stone-forming cystine into soluble cysteine.
High-resolution fiber-optic scopes, powerful Holmium yttrium aluminum garnet (Ho:YAG) lasers, tandem and broad-focused shock wave lithotripters, intricately versatile surgical and endoscopic instruments, and other advances offer minimally invasive and efficacious treatment of urinary tract stones. Even these interventions have a modicum of invasiveness that subjects patients to possible complications. An ideal method for achieving and maintaining stone-free status would rely more on hydration, medicine, and nutrition than on state-of-the-art surgical instrumentation. In this chapter, tailored medical strategies for treatment and prevention of stone disease are discussed.
To develop a kidney stone management strategy that is best tailored to a patient’s individual metabolic nuances, tests of the blood, urine, and any previous kidney stones are extremely helpful. Depending on the results of these tests, the urine pH and the concentration of certain electrolytes – most notably calcium, oxalate, citrate, and urate – can be determined. Based on these concentrations, the metabolic cause for stone precipitation can be identified and targeted with specific medical and nutritional therapy. The most common identifiable abnormality in urinary tract calcium stone formers is excess calcium in the urine (hypercalciuria, 62 %), followed by deficient urinary citrate (hypocitraturia, 41 %), excess urinary urate (hyperuricosuria, 35 %), excess urinary oxalate (hyperoxaluria, 8 %) and decreased urinary magnesium (hypomagnesiuria, <5 %). For non-calcium stone formers, the common causes for these stones are infection (struvite, 15 %), low urine pH (uric acid stones, 5 %) and finally increased urine levels of the amino acid cystine (cystinuria, 1 %) (These factors are expressed as percentage of the total, and since some patients have multiple factors, the percentage total exceeds 100 %).
Medical management for stone disease is a critical approach in the treatment process. New guidelines for the Medical management of renal stones have just been established and presented at the American Urological Association Meeting AUA (2014); these strategies were developed jointly between the American Society of Nephrology and the Endourological Society. There is good evidence that dietary and medical therapy of stone disease can significantly reduce the risk of stone recurrence. This chapter will address the medical management of stone disease to make the urine’s composition less conducive to stone formation.
As discussed in Chap. 8, there are three types of hypercalciuria: absorptive, renal and resorptive hypercalciuria. Chapter 27 discussed the dietary management of hypercalciuria, including maintaining adequate hydration, maintaining normal calcium intake in most patients (restrict calcium with absorptive hypercalciuria), limit dietary sodium and animal protein intake. Medical therapy for hypercalciuria include:
Hydrochlorothiazide (HCTZ) (25 mg twice/day) decreases calcium excretion into urine by increasing the kidney’s ability to reabsorb calcium. By helping the kidneys reabsorb calcium, HCTZ keeps calcium out of the urine and prevents it from forming urinary tract stones. As such, HCTZ is most useful in cases of hypercalciuria. When taken over a period of many years, HCTZ may become less effective. In addition, excess sodium can blunt the effects of HCTZ. Side effects of HCTZ include dizziness, upset stomach, lightheadedness, headache, and muscle cramps.
Chlorthaladone (25 mg/day) is similar the HCTZ and has a longer half-life.
Citrate is the most commonly recognized inhibitor of calcium oxalate stone formation and the lack of citrate in the urine can produce hypocitraturia. As a solitary abnormality, hypocitraturia is responsible for 5–10 % of stones, however, as a mixed abnormality, it is accountable for up to 50 % of stones. Some of the causes for hypocitraturia include distal renal tubular acidosis (RTA Type I), chronic diarrhea, physical exercise (i.e., lactic acidosis), acid-ash rich diet and depletion of potassium (excess use of HCTZ). The treatment for hypocitraturia is alkalinization therapy.
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