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Diabetic Cystopathy with Bilateral Hydronephrosis

Computerized tomography of the abdomen and pelvis, revealing massive distention of the urinary bladder* (A) sagittal view; and hydronephrosis* (B) axial view; (C) coronal view.

Computerized tomography of the abdomen and pelvis, revealing massive distention of the urinary bladder* (A) sagittal view; and hydronephrosis* (B) axial view; (C) coronal view.

A 40-year-old man with poorly controlled diabetes mellitus (glycated hemoglobin 19%) with related peripheral neuropathy, nephropathy, and proliferative retinopathy presented with epigastric discomfort, anorexia, polyuria, polydipsia, nausea, and diminished urine output. His longstanding use of insulin was halted in the preceding month owing to termination of employment and loss of health insurance coverage. Examination revealed an afebrile and fully oriented thin man who was hypertensive. He had a distended and diffusely tender abdomen. Laboratory studies identified a serum glucose of 1061 mg/dL. Serum sodium was 121 mmol/L; potassium was 5.0 mmol/L, bicarbonate 23 mmol/L, and serum creatinine was 2.9 mg/dL. Computerized tomography of the abdomen and pelvis revealed massive distention of the urinary bladder, extending 7 cm above the umbilicus with diffuse bladder wall thickening (Figure, panel A), together with moderate bilateral hydronephrosis (Figure, panels B and C) and hydroureter. A diagnosis of diabetic cystopathy with bilateral hydronephrosis was made. A urethral catheter was inserted into our patient’s bladder, draining 2 L of urine. Clean intermittent catheterization was advised, with consideration to potential placement of a suprapubic catheter.

Involvement of the autonomic nervous system is common in diabetes mellitus and can cause significant disability to patients. Histologic studies suggest that autonomic neuropathy is likely a result of metabolic changes of the Schwann cell, leading to demyelination and impaired nerve conduction.1 Impaired voiding, as seen in diabetic cystopathy, is one of the most frequent sequelae from damage to innervation of the lower urinary tract. In studies evaluating the urinary function of diabetic patients with routine urodynamic assessments, the incidence of diabetic cystopathy ranged from 27% to 85%.23 Diabetic cystopathy is insidious in onset and characterized by the triad of decreased bladder sensation, increased postvoid residual volume, and impaired detrusor contractility.45Dysfunction of bladder sensation typically develops first and is likely a consequence of damage to the visceral afferent fibers of the bladder wall.6

Cystopathy and proximal genitourinary tract impairment can result in hydroureter and hydronephrosis, as well as renal infections, including pyelonephritis, which occur at a higher rate in diabetics than in the nondiabetic population.7 The mainstay of treatment in symptomatic individuals is intermittent bladder catheterization.8

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Jacqueline M. Schulman, MD
Aliki Medical Service, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD
Massachusetts General Hospital and Brigham and Women’s Hospital, Harvard Medical School, Boston, MA

Allan C. Gelber,  Aliki Medical Service, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD

This article originally appeared in the June issue  of The American Journal of Medicine.

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