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

Figure 1 Acute pancreatitis may generate systemic inflammation and transient metabolic perturbations, including changes in serum calcium, parathyroid hormone dynamics, urine volume, and urinary inhibitors of crystallization. When serial ultrasonography is used without computed tomography-based renal endpoint confirmation, these acute changes can increase the visibility of pre-existing silent microlithiasis or transient crystal aggregates. Under this framework, apparent short-term “de novo nephrolithiasis” may represent an imaging-mediated unveiling of prevalent microlithiasis rather than biologically plausible new stone formation. PTH: Parathyroid hormone; CT: Computed tomography.