Acute pancreatitis, hypercalcemia, and kidney stones: True incidence or unveiled prevalence?

Recent study reported an association between hypercalcemia and nephrolithiasis in acute pancreatitis and proposed a striking rate of de novo stone formation during a 7-day hospitalization. Their work is valuable because it draws attention to the endocrine-metabolic dimension of acute pancreatic injury and to a potentially vulnerable subgroup of patients. However, the reported endpoint raises major biological and methodological concerns. Lithogenesis is a multistep process requiring urinary supersaturation, nucleation, aggregation, epithelial interaction, and retention; clinically meaningful stones generally evolve over weeks to months, not days. Moreover, although contrast-enhanced computed tomography was available at baseline and day 7, renal stone assessment relied on serial ultrasonography and on echogenic foci > 2 mm with posterior acoustic shadowing, a definition closer to microlithiasis than to established calculi. The absence of baseline non-contrast computed tomography analysis and 24-hour urinary biochemical profiling further weakens the inference of true incident nephrolithiasis. We therefore argue that the findings are more plausibly explained by the acute unmasking of prevalent, previously unrecognized microlithiasis under inflammatory-metabolic stress rather than by genuine de novo stone formation.