Renal stones are common, with a prevalence of 5 to 10% worldwide. Acute stone passage almost always produces the severe pain of renal colic, but stones are often asymptomatic and discovered incidentally on imaging. Prevalence of both symptomatic and asymptomatic disease appears to be rising, although the relative contributions of increasing use of more sensitive imaging modalities and real changes relating to diet and lifestyle are debated. The initial evaluation of patients with renal colic optimally includes noncontrast CT to accurately visualize the size and location of stones in the urinary tract. Initial management of stones less than 5 mm in diameter in patients without anatomical abnormalities of the urinary tract is to provide adequate analgesia coupled with α-blockade, followed by watchful waiting to allow time for stone passage. The presence of urinary tract infection, inability to take oral fluids, or obstruction of a single functioning kidney requires hospitalization and active management. Once the acute episode of stone passage or removal is over, thought should be given to diagnosis of the underlying causes and steps taken towards prevention. Since stone analysis is the cornerstone of diagnosis, the patient should be encouraged to collect any stones passed and retain them for analysis. Most stones (66–76%) are formed of calcium oxalate: other types include calcium phosphate (12–17%), uric acid (7–11%), struvite (magnesium ammonium phosphate, 2–3%), and cystine (1–2%). They form because urine becomes supersaturated with respect to the solute, and treatment to lower its concentration can prevent recurrence. This chapter describes the aetiology, pathogenesis, diagnosis and treatment of calcium oxalate stones, calcium phosphate stones, uric acid stones, struvite stones, cystine stones, and nephrocalcinosis.
Citrate inhibits growth of residual fragments in an in vitro model of calcium oxalate renal stones