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Urinary tract infection in autosomal dominant polycystic kidney disease

INTRODUCTION

Approximately 30 to 50 percent of patients with autosomal dominant polycystic kidney disease (ADPKD) will have a urinary tract infection (UTI) during their lifetime. Cyst infections responsible for hospitalization occur much less frequently, approximately 9 percent [1]. An infected cyst and acute pyelonephritis are the most common kidney infections, although complications such as a perinephric abscess and bacteremia can occur [2,3]. Cyst infection incidence rates are approximately 0.01 episode per patient per year [1]. Even nonfunctional end-stage polycystic kidneys may be a source of infection [4]. After transplantation, special attention needs to be paid to the native kidneys in patients who present with sepsis, fever, or flank or abdominal tenderness.

By convention, UTI is defined either as a lower tract (acute cystitis) or upper tract (acute pyelonephritis) infection. This topic will review issues related to UTIs, particularly upper tract infections, in patients with ADPKD. Discussions related to UTI in patients without ADPKD as well as the therapy of ADPKD and other renal manifestations of ADPKD can be found separately. (See "Course and treatment of autosomal dominant polycystic kidney disease" and "Renal manifestations of autosomal dominant polycystic kidney disease" and "Acute uncomplicated cystitis and pyelonephritis in women" and "Acute complicated cystitis and pyelonephritis", section on 'Pyelonephritis'.)

SOURCE OF INFECTION

As with UTIs in the general population, UTIs in patients with ADPKD are more likely to occur in women [2,5-7]. The infections are typically caused by Gram-negative enteric organisms.

With respect to upper tract infections:

Gram-negative enteric organisms ascend from the bladder among patients with pyelonephritis [2,5-7]. Such infections may be associated with dysuria and frequency due to bladder infection.

      

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Literature review current through: Aug 2014. | This topic last updated: Mar 28, 2014.
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