FRII-14 THE CHRISTMAS CAROL DISEASE: THE KIDNEY DISEASE OF CHARLES DICKENS’ TINY TIM

Abstract

You have accessJournal of UrologyHistory of Urology: History Forum II1 Apr 2016FRII-14 THE CHRISTMAS CAROL DISEASE: THE KIDNEY DISEASE OF CHARLES DICKENS’ TINY TIM Daniel Marchalik Daniel MarchalikDaniel Marchalik More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.2935AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES It has long been proposed that all writing, at least partly, is autobiographical. Not immune to this tendency, Charles Dickens, who spent much of his adult life suffering from renal colic and ultimately died of renal failure, infused his personal struggles into his characters’ lives. His personal ailments, therefore, likely led Dickens to subject The Christmas Carol's Tiny Tim to renal disease, most closely resembling rickets or distal renal tubular acidosis (type I). METHODS Medical and literary databases, including MEDLINE and JSTOR, as well as primary texts were queried to chronicle Charles Dickens’ personal and medical history and the description of Tiny Tim's disease. RESULTS In “The Life of Charles Dickens” (1874), Dickens’ biographer and long-time friend, John Forster, describes Dickens’ ongoing struggle with renal colic which likely stemmed from nephrolithiasis. Familial in nature, Charles Dickens’ renal calculi are thought to have been inherited from his father who struggled with renal colic his entire life, ultimately dying from an open (and anesthesia-free) nephrolithotomy. A lifetime of renal complaints put the kidneys in Dickens’ forefront. As a result, Dickens, who often explored his personal life through the lives of his characters (e.g: David Copperfield), subjects Tiny Tim to a debilitating kidney dysfunction. Crippled and extremely small in stature, Tiny Tim, the son of Ebenezer Scrooger's clerk, Bob Cratchit, has been retrospectively diagnosed as suffering from both type I renal tubular acidosis (Lewis 1992) and rickets (Chesney 2012). Given the prevalence of rickets in half of 1820's pediatric population secondary to pollution and malnutrition, the deficiency in Vitamin D appears logical. At the same, the asymmetric bone deformity and intermittent muscle weakness has lead to the proposed diagnosis of RTA-I, which would have contributed to concomitant exacerbation of rickets in Tiny Tim. It is important to note that the Lewis's retrospective diagnosis spurred a series of comments and rebuttals, arguing that RTA was “an uncommon ‘zebra’-type diagnosis when the hoofbeats of Dickens’ time were more likely provided by the all-too-common rampant steeds of tuberculosis and rickets” (Petereson 1993). CONCLUSIONS Due to a personal history of nephrolithiasis and kidney disease, Charles Dickens incorporated such maladies into the life of Tiny Tim, giving the readers a glimpse into the 19th century understanding of the disease process. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e525 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Daniel Marchalik More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...