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

Table 1 Acute factors during pancreatitis that may favor crystalluria without proving de novo stone formation

Metabolic factor	Likely acute effect	Interpretive implication
Intravascular volume depletion	Urine becomes concentrated, and supersaturation rises	Transient crystalluria may increase without establishing a new stable stone
Hypocitraturia or reduced inhibitors	Protective buffering against crystal aggregation decreases	Aggregation may be facilitated, but organized calculi still require time and retention
Transient hypercalcemia	Possible short-term increase in urinary calcium excretion if sustained	Serum calcium alone is insufficient evidence for stone causation without urine data
Inflammatory epithelial stress	Crystal adhesion and urothelial interaction may be altered	Acute illness may unmask a pre-existing crystal burden rather than generate a new calculus
Serial ultrasonography during recovery	Visibility of tiny echogenic foci may change with operator, body habitus, and acoustic windows	Apparent incidence may reflect detection bias instead of true lithogenesis