The natural history of post-extracorporeal shock wave lithotripsy residual stone fragments (clearance, growth and aggregation) is incompletely known, even though they are believed to constitute a risk in terms of new stone formation and persistent infection of the urinary tract. We addressed this issue and the hypothesis that alkaline citrate therapy improves residual stone fragment clearance in a 12-month followup study. There were 40 sterile calcium and 30 struvite stone patients with residual fragments after extracorporeal shock wave lithotripsy (diameter less than 5 mm.) consecutively enrolled and randomly assigned to a citrate therapy (6 to 8 gm. per day) or control (hygienic measures only) group. Infection stone patients also received adequate antibiotic therapy throughout the study. Among the patients in the untreated sterile group 21% and 32% were stone-free at 6 and 12 months, respectively. In the infection group these figures were 27% and 40%, respectively. Among the untreated sterile calcium stone patients in whom clearance was not achieved a high percentage experienced residual fragment growth or reaggregation. Citrate therapy significantly improved the stone clearance rate in the sterile (at 6 and 12 months 65% and 74% were stone-free, respectively) and infection (71% and 86%, respectively) stone patients, and prevented residual fragment growth or reaggregation in subjects in whom clearance was not achieved. The data show that growth and persistence are common in the natural history of residual stone fragments. Citrate ameliorated the outcome of these residual fragments by reducing the growth or agglomeration, and by increasing the clearance rate in calcium oxalate and in infection stone patients.

We measured the rate of oxalate flux across the red-cell membrane in the steady state in 114 patients with a history of calcium oxalate kidney stones and in 25 controls. Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria. Oxalate exchange was significantly higher in the 98 patients with idiopathic stone formation than in the controls (-1.10 +/- 0.95 [SD] X 10(-2) min-1 vs. -0.31 +/- 0.12 X 10(-2); P less than 0.001); it was above the upper limits of normal in 78 of these patients. All 8 patients with hyperparathyroidism and the patient with primary hyperoxaluria had values in the normal range; 2 of the patients with renal or urinary tract malformation had values at the upper normal limit. A study of five families indicated that the abnormality is an autosomal monogenic dominant trait with complete penetrance and variable expressivity. Oxalate-tolerance tests were carried out in five pairs of brothers. One brother in each pair had the abnormality in oxalate flux, and had a significantly higher percentage of oxalate excretion at two hours after oxalate loading (18.09 +/- 3.07 [SD] vs. 10.37 +/- 3.08 percent; t = 3.97; P less than 0.005) and four hours (14.87 +/- 2.91 vs. 9.89 +/- 2.93 percent; t = 2.70; P less than 0.05). Treatment with oral hydrochlorothiazide (50 mg per day) or amiloride (5 mg per day) or both restored normal or nearly normal red-cell oxalate exchange in all of 33 patients who initially had increased rates. We conclude that an inherited cellular defect in oxalate transport may be a factor in "primary" calcium oxalate stone formation and that this defect may be corrected with diuretics.

Uric acid nephrolithiasis appears to increase in prevalence. While a relationship between uric acid stones and low urinary pH has been for long known, additional association with various metabolic conditions and pathophysiological basis has recently been elucidated. Some conditions such as diabetes and metabolic syndrome disease, excessive dietary intake, and increased endogenous uric acid production and/or defect in ammoniagenesis are associated with low urinary pH. In addition, the phenomenon of global warming could result in an increase in areas with greater climate risk for uric acid stone formation. There are three therapeutic steps to be taken for management of uric acid stones: identification of urinary pH profiles, assessment of urinary volume status, and identification of disorders leading to excessive uric acid production. However, the most important factor for uric acid stone formation is acid urinary pH, which is a prerequisite for uric acid precipitation. This article reviews recent insights into the pathophysiology of uric acid stones and their management.

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Urinary excretion of glycosaminoglycans (GAGS) and sialic acid (SA), as well as the activity of two renal enzymes related to glycoprotein metabolism, N-acetyl-β-D-glucosaminidase (NAG) and β-galactosidase (GAL), and two others unrelated to glycosaminoglycans and glycoprotein metabolism, γ-glutamyltranspeptidase (γ-Gt) and angiotensin-I-converting enzyme (ACE), were evaluated in 40 insulin-dependent diabetic patients with normal range albuminuria, 21 patients with mesangial glomerulonephritis, and 30 control subjects. Diabetic and glomerulonephritic patients excreted a significantly higher amount of GAGS and SA, and showed greater NAG and GAL activities; γ-Gt and ACE levels were within normal ranges. No correlation could be demonstrated between diabetes duration and GAGS, SA, NAG and GAL findings. Moreover, no correspondence between degree of metabolic control, as reflected by glycosylated hemoglobin (HbA_1a._c) and GAGS, SA, NAG and GAL emerged.