 Introduction/Background Acute pyelonephritis (APN) is a severe urinary tract infection (UTI) that has the potential to cause sepsis, shock, and death [1]. The annual incidence of APN is 459,000 to 1,128,000 cases in the United States and 10.5 to 25.9 million cases globally [1,2]. The term pyelonephritis implies that there is inflammation of the renal pelvis and kidney. APN often presents with signs and symptoms of both systemic inflammation (eg, fever, chills, and fatigue) and bladder inflammation (eg, urgency, dysuria, and urinary frequency) [1]. There is a surprising lack of consensus regarding diagnostic criteria, and differentiation from infections of the lower urinary tract can be difficult [1]. Clinical presentation of APN can range from mild flank pain with low-grade or no fever to septic shock, and up to 20% of patients lack bladder symptoms. In patients with flank pain or tenderness, without or with voiding symptoms, without or with fever, and with a urinalysis showing pyuria and/or bacteriuria, APN is an appropriate presumptive diagnosis [1]. In this setting, urine cultures yielding >10,000 colony-forming units of a uropathogen per milliliter of urine is the fundamental confirmatory diagnostic test. Positive blood cultures may assist with the diagnosis. In young healthy women, Escherichia coli accounts for more than 90% of APN cases [1,3]. However, in men, elderly women, and urologically compromised and institutionalized patients, less-virulent E. coli strains, gram- negative bacilli, gram-positive organisms, and candida are also common [1,4]. Risk factors for cystitis predispose to APN and include sexual activity, new sexual partner, spermicide exposure, personal or maternal history of UTIs, genetic predisposition, and diabetes mellitus [1,5]. Fortunately, <3% of cases of cystitis and asymptomatic bacteriuria progress to APN [1,6].
Acute Pyelonephritis.  Introduction/Background Acute pyelonephritis (APN) is a severe urinary tract infection (UTI) that has the potential to cause sepsis, shock, and death [1]. The annual incidence of APN is 459,000 to 1,128,000 cases in the United States and 10.5 to 25.9 million cases globally [1,2]. The term pyelonephritis implies that there is inflammation of the renal pelvis and kidney. APN often presents with signs and symptoms of both systemic inflammation (eg, fever, chills, and fatigue) and bladder inflammation (eg, urgency, dysuria, and urinary frequency) [1]. There is a surprising lack of consensus regarding diagnostic criteria, and differentiation from infections of the lower urinary tract can be difficult [1]. Clinical presentation of APN can range from mild flank pain with low-grade or no fever to septic shock, and up to 20% of patients lack bladder symptoms. In patients with flank pain or tenderness, without or with voiding symptoms, without or with fever, and with a urinalysis showing pyuria and/or bacteriuria, APN is an appropriate presumptive diagnosis [1]. In this setting, urine cultures yielding >10,000 colony-forming units of a uropathogen per milliliter of urine is the fundamental confirmatory diagnostic test. Positive blood cultures may assist with the diagnosis. In young healthy women, Escherichia coli accounts for more than 90% of APN cases [1,3]. However, in men, elderly women, and urologically compromised and institutionalized patients, less-virulent E. coli strains, gram- negative bacilli, gram-positive organisms, and candida are also common [1,4]. Risk factors for cystitis predispose to APN and include sexual activity, new sexual partner, spermicide exposure, personal or maternal history of UTIs, genetic predisposition, and diabetes mellitus [1,5]. Fortunately, <3% of cases of cystitis and asymptomatic bacteriuria progress to APN [1,6].