The roentgen aspects of necrotizing renal papillitis.

Abstract

Acute necrosis of the renal papillae occurs most frequently as a complication in patients with diabetes mellitus and acute pyelonephritis (11, 12, 13). Less frequently it complicates the clinical picture of obstructive uropathy with super-imposed infection (10, 16, 17, 20). Because of the urgent measures necessary for treatment of papillary necrosis, it behooves the radiologist, as a consultant, to be aware of the clinical and laboratory findings as well as of the diverse Pyelographie changes that may take place. This paper includes a review of the roentgen observations recorded in the literature and a presentation of 8 cases of our own in which pyelography was performed. Acute necrosis of the renal papillae is known by a number of names: “necrotizing renal papillitis,” “renal papillary necrosis,” “renal medullary necrosis,” “necrotizing papillitis renis,” and “Günther's necrosis,” among others. Necrosis of the renal papillae was first reported by von Friedreich in 1877 (40). He described varying stages of papillary destruction, including complete separation of the papilla, in a seventy-year old, non-diabetic male suffering from obstructive uropathy. From 1877 to 1937, only occasional accounts appeared in the literature. In 1937, Günther emphasized the frequent association of diabetes mellitus with papillary necrosis (11, 12). In addition, he was probably the first to appreciate the full significance of the Pyelographie changes to be observed. Since 1937, reports of this important complication, which is found in 3 to 5 per cent of diabetics at autopsy (2, 4), have become increasingly frequent. Only an occasional publication, however, has appeared in the roentgenologic literature (5, 21). Clinical Findings Although a few cases have been recorded in which the occurrence of necrotizing renal papillitis was recognized in the patient's lifetime, the diagnosis is still usually established postmortem. This is because the onset of papillary necrosis is obscured by the more prominent signs and symptoms of the primary disease: usually diabetes mellitus, becoming uncontrollable, or progressive obstructive uropathy and, in either case, superimposed upper urinary tract infection. In the acute form of the condition, however, the urinary signs and symptoms become prominent with great rapidity, with costovertebral tenderness, pyuria, hematuria of varying degree, oliguria, azotemia, and prostration, proceeding to uremic coma and death. A smaller group of patients with either known or unsuspected chronic pyelonephritis may have a prolonged subacute course. Episodes of exacerbation are followed by remissions. Exacerbations may be related to heightened activity of the chronic pyelonephritis or to isolated episodes of papillary necrosis.