Abstract: SA-PO0586
The Stone Feast: Exploration of Dietary, Genetic, and Metabolic Drivers of the Fatal Nephrolithiasis of Samuel Pepys, 1633-1703
Session Information
- Bones, Stones, and Mineral Metabolism: Research and Cases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 502 Bone and Mineral Metabolism: Clinical
Author
- Reisinger, Nathaniel, Saint Louis Kidney Consultants, Kirkwood, Missouri, United States
Introduction
Samuel Pepys was a 17th-century naval administrator, diarist, and lifelong stone-former. From 1660 to 1669 he kept the most celebrated personal diary in the English language. A vivid microcosm of Restoration life, it records everything from world-shaking events like the Great Plague, the Dutch raid on the Medway, and the Great Fire of London to the monotonous details of his profoundly lithogenic diet. To the practicing nephrologist it is the mother lode of stone pathogenesis, giving us insight into both the etiology of his nephrolithiasis and the psychology of his abortive attempts at reform, culminating in post-mortem-confirmed fatal obstructive nephropathy.
Case Description
First symptomatic at age 21, Pepys underwent an anesthesia-free perineal lithotomy in 1658. His diary documents a "constant succession" of 35 subsequent episodes triggered by cold exposure, alcohol, and dietary excess. The diet he records is absurdly lithogenic: daily venison pasty, organ meats, oysters, lobster, anchovies, and salt-preserved meats washed down with Rhenish wine, sack, claret, and ale. Fresh fruit, vegetables, and water are nearly absent across nine years. His physician presciently identified alcohol as the primary modifiable risk factor in 1661. Pepys undertook at least six abstinence oaths over the following four years, none sustained beyond two weeks. He also constructs a compelling pedigree: a mother who voided a calculus, a maternal aunt who died of stone disease, and a brother with hematuria at onset, supporting a possible heritable metabolic diathesis.
Discussion
The convergence of high animal protein, high purine, high sodium, and low citrate intake with chronic alcohol-driven hyperuricemia, absent hydration, and likely familial hypercalciuria or primary hyperoxaluria created near-ideal conditions for mixed uric acid and calcium oxalate lithogenesis. No metabolic evaluation was ever performed. Post-mortem revealed seven calculi (130 g) in the left kidney with complete parenchymal ulceration and gangrenous bladder. Pepys celebrated his lithotomy anniversary each year with a feast of venison and oysters, and preserved his stone in a bespoke carrying case costing 24 shillings. A Fellow of the Royal Society who once directed an anatomy lecture toward the urinary tract, Pepys would have found the pathogenesis of his own demise a matter of keen scientific interest.