Medical prevention and treatment of urinary stones.

Despite revolutionary developments in minimally invasive methods for the removal of stones in the last 15 years, the medical prevention of urinary stones remains very rewarding, due to the continual increase in the prevalence of nephrolithiasis in western countries, the high recurrence rate of the disease, its complications, discomfort and the costs of lithotripsy. Medical prevention is highly effective (50-95% efficacy in different series) and cost-convenient; its basic elements are appropriate metabolic evaluation, adequate hydration, "common sense" diet, and, in selected cases, drugs of proven efficacy. Clinical-metabolic evaluation should aim at the recognition of specific types of nephrolithiasis, and sort out secondary and/or remediable cases, define urinary risk factors, assess patients' compliance and the side effects of any therapy during follow-up. Hydration has proved effective in clinical trials and population-based observational studies; "fluids" may consist of water (any kind), coffee (caffeinated or decaffeinated), tea, beer and wine; grapefruit juice appears to have an unexplained ill effect. Despite the lack of clinical demonstration that dietary manipulations reduce the recurrences of stones, biochemical and epidemiological data suggest that high sodium, animal protein and sucrose intake increase the risk. Undue reductions in Ca intake also appear to be detrimental both for stone recurrences and bone mineralisation: "adequate" Ca intake (800-1000 mg/day) should be encouraged, but only in food since supplemental Ca, as drugs, appears to increase the risk of stones. Effective drugs are available for cystine, uric acid, infected stones and several secondary causes of Ca nephrolithiasis; in "idiopathic" Ca nephrolithiasis, thiazides, allopurinol, K and K-Mg citrate and possibly neutral K phosphate have been shown to be effective, at least in specific metabolic contexts.

Calcium metabolism and calciotropic hormone levels in Gitelman's syndrome.

In 10 adult patients (5 females and 5 males, aged 13-57 years) with Gitelman's syndrome (GS, or hypocalciuric variant of Bartter's syndrome, characterized by chronic renal hypokalemia, metabolic alkalosis, hypomagnesemia and hypocalciuria), parameters of Ca metabolism and calciotropic hormone levels were evaluated. Hypocalciuria was associated with a marked reduction of fractional excretion of ionized Ca (as compared with 16 sex- and age-matched controls) and normal filtered Ca load, as indicated by serum ionized Ca; hypocalciuria was thus the result of increased tubular reapsorption of filtered Ca. Plasma levels of total Ca were increased in GS (p < 0.02) but ionized Ca was not different from controls; percent fraction of ionized to total Ca was reduced, indicating increased Ca complexation and/or protein binding, possibly related to a metabolic alkalosis-induced increase of plasma albumin affinity for Ca. Levels of plasma total protein and albumin were similar in GS and controls. Despite similar ionized Ca levels, PTH1-84 was lower in GS than in controls, indicating abnormal ionized Ca-PTH relationship, possibly related to hypomagnesemia. Plasma 1,25(OH)2D levels were not different in GS and in controls, and intestinal fractional Ca absorption (evaluated with a simplified method using stable Sr as a tracer) was not reduced in 4 patients. However, in 5 patients bone mineral density in the forearm (3 patients) or lumbar spine (2 patient) was normal. Thus, despite chronic hypocalciuria and normal 1,25(OH)2D levels, Ca 'thesaurosis' does not occur in bones of GS patients; a likely explanation is that, despite normal 'fractional' intestinal Ca absorption, 'net' intestinal absorption is reduced, due to increased intestinal Ca secretion.