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Urinary tract infection in kidney transplant recipients

Urinary tract infection in kidney transplant recipients
Literature review current through: Jun 2023.
This topic last updated: Sep 28, 2022.

INTRODUCTION — Urinary tract infection (UTI) is the most common infection after kidney transplantation. UTI is associated with the development of bacteremia, acute T cell-mediated rejection, impaired allograft function, and allograft loss, with increased risk of hospitalization and death. Morbidity and mortality from UTI can be caused by recurrent and/or severe sepsis.

This topic reviews the definitions, epidemiology, microbiology, clinical manifestations, diagnosis, treatment, and prevention of bacterial UTI in kidney transplant recipients. UTI in the general population and among patients with end-stage kidney disease is discussed elsewhere.

(See "Acute simple cystitis in females".)

(See "Acute simple cystitis in adult males".)

(See "Asymptomatic bacteriuria in adults".)

(See "Recurrent simple cystitis in women".)

(See "Non-access-related infections in patients on chronic dialysis", section on 'Genitourinary infection'.)

TERMINOLOGY — We use the following terminology when discussing asymptomatic bacteriuria and UTI in kidney transplant recipients [1]:

Asymptomatic bacteriuria – In the transplant population, this is defined by the presence of >105 bacterial colony-forming units per milliliter (CFU/mL) on urine culture with no local or systemic symptoms of UTI.

Simple cystitis – The presence of >105 CFU/mL on urine culture with local urinary symptoms, such as dysuria, frequency, or urgency, but no systemic symptoms, such as fever or allograft pain, and no indwelling device (eg, ureteral stent, nephrostomy tube, or chronic urinary catheter).

Complicated UTI – The presence of >105 CFU/mL on urine culture with fever, allograft pain, chills, malaise, or bacteremia with the same organism in urine, or a biopsy with findings consistent with pyelonephritis.

Recurrent UTI – Two or more episodes of UTI in six months, or three or more episodes of UTI in one year.

EPIDEMIOLOGY AND RISK FACTORS — The reported prevalence of UTI among kidney transplant recipients varies widely, ranging from 7 to 80 percent [2]. This variability may be explained by differences in the definition of UTI, geographical location, duration of follow-up, and prophylactic antibiotic regimens among studies. UTIs can occur at any time after transplantation but are most common in the first year posttransplant. In one study of 101 transplant recipients with bacteriuria, asymptomatic bacteriuria, uncomplicated UTI, complicated UTI, and recurrent UTI comprised 44, 32, 24, and 14 percent of cases, respectively [3,4].

Risk factors have been studied in several epidemiologic studies and include [3,5,6]:

Female sex

Advanced age

Recurrent UTI prior to transplant

Vesicoureteral reflux

Urethral catheterization

Ureteral stent placement

Deceased-donor kidney transplant

History of autosomal dominant polycystic kidney disease (ADPKD) [7,8]

Delayed graft function

MICROBIOLOGY — UTI after kidney transplantation is usually caused by gram-negative organisms (56 to 90 percent), with Escherichia coli as the dominant causative organism [3,4,9-11]. Other commonly found gram-negative uropathogens include Pseudomonas aeruginosa, Enterobacter cloacae, Klebsiella pneumoniae, and Klebsiella oxytoca.

The widespread use of antibiotic prophylaxis among kidney transplant recipients has led to an increased rate of resistance to ciprofloxacin and trimethoprim-sulfamethoxazole [9,11,12]. Enterococcus species has emerged as an important pathogen and now accounts for 24 to 33 percent of UTIs [3,4,6,9,12,13]. Gram-positive bacteria such as Staphylococcus saprophyticus, Streptococcus species, and Corynebacterium urealyticum can rarely cause UTI [14].

PATHOGENESIS — The pathogenesis of UTI typically begins with uropathogenic bacteria ascending to the bladder from the urethra. Pathologic invasion of the urothelium can then occur and is aided by bacterial virulence structures, such as P fimbriae, that promote adhesion [15]. The absence of a sphincter between the transplanted ureter and the native bladder can predispose kidney transplant recipients to developing allograft pyelonephritis. Ureteral stents placed during transplantation and kidney cysts in patients with polycystic kidney disease can serve as reservoirs for bacteria and predispose patients to developing recurrent UTIs [3,5,6,16]. Transplant pyelonephritis can occasionally occur by seeding of the kidney from bloodstream infection or surgical site infection.

CLINICAL MANIFESTATIONS — UTI can present as either simple cystitis or complicated UTI [3,4,6].

Simple cystitis – Classically, simple cystitis presents with dysuria, urinary frequency, urinary urgency, hematuria, and suprapubic pain. However, not all patients present with classic symptoms; in some, presenting symptoms are nonspecific and include low-grade fever, nausea, diarrhea, and leukocytosis. (See "Acute simple cystitis in females", section on 'Clinical manifestations' and "Acute simple cystitis in adult males", section on 'Clinical manifestations'.)

Complicated UTI – Patients with complicated UTI may present with fever, allograft pain, chills, and/or malaise. Patients may also have more subtle symptoms including nausea, diarrhea, and fatigue. Acute elevations in serum creatinine may also be seen.

It may be difficult to distinguish complicated UTI from acute rejection. Fever tends to be more commonly associated with UTI and is rarely seen during allograft rejection unless the patient has been nonadherent with their immunosuppressive therapy. Tenderness directly over the allograft is also more commonly observed with complicated UTI. (See 'Differential diagnosis' below.)

DIAGNOSTIC EVALUATION

Initial evaluation — Patients with suspected UTI should undergo testing with a urine dipstick, urine microscopy, and urine culture. In addition, blood cultures should be obtained in those with symptoms suggestive of a complicated UTI (eg, fever or other systemic symptoms and/or allograft tenderness). (See 'Clinical manifestations' above.)

In patients with compatible clinical features, the diagnosis of UTI requires the following:

Evidence of inflammation on urine dipstick (ie, positive leukocyte esterase) and/or pyuria on urine microscopy (≥10 white blood cells per high-power field of unspun urine). In addition, urine dipstick may be positive for nitrites (produced by certain bacteria), blood, and protein.

Culture of >105 colony-forming units (CFU)/mL of a urinary pathogen.

Among kidney transplant recipients with UTI, 9 percent have positive blood cultures [3].

For patients who present with signs and symptoms of UTI and have a positive urinalysis but negative urine culture, infection is not definitely ruled out. Pathogens that are not typically isolated on routine culture, including yeast, acid-fast bacilli, and C. urealyticum, should be considered in the differential diagnosis. C. urealyticum is a slow-growing organism with potent urease activity that requires selective media for isolation [17]. C. urealyticum can cause UTI and should be suspected in patients with chronic UTI symptoms with negative conventional urine cultures, alkaline urine (pH >7), pyuria or microscopic hematuria with no other explanation, presence of struvite crystals, obstructive uropathy, and encrusting cystitis or pyelitis [14]. It is resistant to the oral antibiotics that are most commonly prescribed for UTI and requires treatment with vancomycin [14,17].

Imaging/urologic evaluation in selected patients — Once the diagnosis of UTI is established, selected patients may require imaging to exclude potentially correctable structural or functional abnormalities of the urinary tract [18]. We perform an ultrasound of the kidney allograft, native kidney, and postvoid bladder for patients who:

Are within one month of transplant (ie, the early postoperative period), or

Have a history of nephrolithiasis, or

Have a history of recurrent UTI (≥2 episodes within six months or ≥3 episodes within one year), or

Have persistent acute elevation in serum creatinine.

Ultrasonography of the urinary system with measurement of a postvoid residual is a reasonable first step for most patients, given its ease and lack of side effects.

In patients with recurrent UTI who have unrevealing ultrasonography, we perform a noncontrast computed tomography (CT) scan of the urinary tract. Although the absence of contrast reduces the sensitivity of the CT scan, we avoid contrast to prevent nephrotoxicity. These imaging studies can identify urinary tract strictures, stones, and complex cysts. If the CT is also unrevealing, measurement of urine flow rate and urodynamic studies can be performed to identify bladder dysfunction or outflow tract obstruction, in consultation with urology. Flexible cystoscopy may be required to detect abnormalities in the urethra or bladder [18].

Patients who have autosomal dominant polycystic disease (ADPKD) may require additional imaging if an infected cyst involving the native kidney is suspected. Suspected infection of kidney cysts in patients with polycystic kidney disease should be further investigated using CT-positron emission tomography scan [16,19]. The interpretation of imaging for patients with ADPKD and recurrent UTIs is challenging. Such patients typically have innumerable cysts of different sizes and image densities; thus, identifying a definitively infected cyst can be difficult. (See "Autosomal dominant polycystic kidney disease (ADPKD): Evaluation and management of complicated urinary tract infections", section on 'Diagnosis'.)

DIFFERENTIAL DIAGNOSIS — The major differential diagnosis among patients who present with complicated UTI is acute allograft rejection. Fever and allograft tenderness are suggestive of UTI, whereas increased serum creatinine in the presence of new or worsening proteinuria and hypertension suggest acute rejection. Among patients who have characteristics of acute rejection, we generally perform a kidney biopsy for a definitive diagnosis. (See "Kidney transplantation in adults: Clinical features and diagnosis of acute renal allograft rejection".)

Among patients with polycystic kidney disease, infected or hemorrhagic cysts may mimic pyelonephritis of the native kidney. Such patients generally have symptoms referable to the native kidney (ie, flank pain and costovertebral angle tenderness) rather than the allograft. (See "Autosomal dominant polycystic kidney disease (ADPKD): Evaluation and management of complicated urinary tract infections", section on 'Clinical features'.)

PREVENTION

Antimicrobial prophylaxis — UTIs are associated with significant morbidity among transplant recipients, especially if they occur early after transplantation. To prevent UTIs, kidney transplant recipients generally receive prophylactic antibiotics in the early posttransplant period.

Most patients receive trimethoprim-sulfamethoxazole (TMP-SMX), which is universally given to transplant recipients without sulfa allergies to prevent Pneumocystis pneumonia (PCP) but is also effective at preventing UTIs [20,21]. Prophylaxis with TMP-SMX can be administered as one double-strength tablet (160 mg of the trimethoprim component) daily or three times per week or one single-strength tablet daily and continued for six months to one year posttransplant; some experts continue TMP-SMX prophylaxis indefinitely [22]. (See "Prophylaxis of infections in solid organ transplantation", section on 'Pneumocystis pneumonia'.)

For patients who are reported to be allergic to TMP-SMX, we carefully assess reported adverse events to determine if patients are truly allergic and offer desensitization to those with true allergies. For those who are still unable to take TMP-SMX, an alternative agent for PCP prophylaxis (eg, atovaquone) is given. The need to give an additional agent for UTI prophylaxis is determined by the transplant center. Alternative agents for UTI prophylaxis include nitrofurantoin (100 mg orally twice daily, provided that estimated glomerular filtration rate [eGFR] is >30 mL/min/1.73 m2) and cephalexin (500 mg orally twice daily). If either of these agents is used, some experts recommend limiting the duration of prophylaxis to the first posttransplant month (when the risk of UTI is thought to be highest) [1] since data on long-term prophylaxis with these agents in transplant recipients are limited [20]. Fluoroquinolones should generally be avoided for prophylaxis due to the risk of promoting fluoroquinolone resistance.

Evidence in support of antimicrobial prophylaxis to prevent UTI is provided by a meta-analysis of six randomized trials in 545 kidney transplant recipients, which demonstrated that antibiotic prophylaxis (mostly with TMP-SMX) reduced the risk of sepsis and bloodstream infection (relative risk [RR] 0.13, 95% CI 0.2-0.7) and bacteriuria (RR 0.41, 95% CI 0.31-0.56) [20]. Prophylaxis did not reduce graft loss or mortality, and effects on the risk of symptomatic UTI or pyelonephritis were not reported.

Concerns have been raised that TMP-SMX prophylaxis has become less effective as uropathogens have become more resistant to this regimen [11,13]. However, there is no consensus among transplant clinicians regarding the optimal preventive strategy for UTI in the era of increasing antibiotic resistance. One trial that randomly assigned kidney transplant recipients to TMP-SMX plus either a single dose of intravenous fosfomycin or placebo peritransplant found a lower incidence of symptomatic UTIs during the first seven weeks posttransplant in the fosfomycin group (7 versus 37 percent) [23]. However, another trial comparing TMP-SMX plus oral fosfomycin with TMP-SMX alone found no difference in the incidence of UTI during the first six months posttransplant [24].

Early ureteral stent removal — Early ureteral stent removal within four weeks of transplant may help to prevent UTI after kidney transplantation.

Ureteral stents, which are commonly placed across the ureteral-vesicular anastomosis during kidney transplant surgery, reduce the risk of urologic complications such as urinary leak or ureteral stenosis but also appear to increase the risk of UTI. In a Cochrane systematic review of randomized trials comparing routine intraoperative ureteral stent placement with no stent placement, the risk of UTI was higher among patients who received routine stent placement (hazard ratio [HR] 1.49, 95% CI 1.04-2.15) although this excess risk was no longer statistically significant when the definition of UTI was restricted to symptomatic UTI (HR 1.23, 95% CI 0.80-1.90) [25]. Another Cochrane analysis found that the risk of UTI could be reduced with early (within two weeks) stent removal compared with late stent removal (RR 0.49, 95% 0.30-0.81), particularly if a bladder indwelling stent was used [26].

Monitoring for asymptomatic bacteriuria — Whether monitoring and treating asymptomatic bacteriuria in the early posttransplant period improves clinical outcomes is uncertain. In the past, monitoring with routine urine cultures was frequently performed because of concerns about the association between untreated UTI and an increased risk of allograft rejection [6]. However, many transplant centers have moved away from routine monitoring for asymptomatic bacteriuria since there are no high-quality data showing that either monitoring or treating asymptomatic UTIs prevents symptomatic UTIs. Most patients who are observed without antibiotic treatment will spontaneously clear bacteriuria [27].

If monitoring is performed (with routine urine cultures), it should be limited to the first one to two months posttransplant [1,6]. The detection of asymptomatic bacteriuria should prompt a second urine culture to confirm persistent bacteriuria with the same pathogen before treatment decisions are made. If the patient has two consecutive cultures that yield >105 colony-forming units (CFU)/mL of the same pathogen, antibiotic treatment for five days may be reasonable, with antibiotic selection based upon the susceptibility pattern of the microorganism. If the second urine culture shows clearance of the initial bacteriuria or if a different organism is identified, antibiotic treatment should not be initiated. Similarly, asymptomatic candiduria should generally not be treated unless the patient is at risk for complications or progression of infection (eg, patients who are undergoing a urologic procedure or are neutropenic) [1,28-30]. (See "Candida infections of the bladder and kidneys", section on 'Asymptomatic candiduria'.)

Monitoring for asymptomatic bacteriuria after two months should not be performed since treatment beyond this time has not been shown to be effective in preventing symptomatic UTI, pyelonephritis, bloodstream infection, or allograft rejection [27,31-33] and can lead to unnecessary antibiotic administration [34].

MANAGEMENT OF SYMPTOMATIC INFECTIONS

Simple cystitis — In all transplant recipients who present with signs and symptoms of simple cystitis, we treat with antibiotics. A urinalysis and urine culture should be obtained prior to initiation of therapy. The initial selection of antibiotic is based upon knowledge of local antibiotic resistance patterns and the patient's past causative organisms and antibiotic exposure. Definitive treatment is administered once the species and antibiotic susceptibilities of the micro-organism are identified. If the urine culture reveals candiduria, treatment should be tailored according to the identified Candida species and according to whether localized or disseminated infection is present [29]. This is discussed in more detail elsewhere. (See "Candida infections of the bladder and kidneys", section on 'Symptomatic candiduria'.)

Antibiotic selection – Preferred oral agents for empiric therapy of simple cystitis in transplant recipients include the following [1]:

An oral fluoroquinolone (ciprofloxacin 250 mg twice daily or levofloxacin 500 mg once daily, with dose adjustments based on estimated glomerular filtration rate [eGFR]), or

A third-generation cephalosporin (eg, cefpodoxime 100 mg twice daily or cefdinir 300 mg twice daily), or

Amoxicillin-clavulanate (500 mg twice daily).

Nitrofurantoin (100 mg twice daily) is another option for patients with an eGFR >30 mL/min/1.73 m2. Although nitrofurantoin was previously contraindicated in patients with creatinine clearance <60 mL/min, studies in nontransplant patients have found that it can be safely and effectively used in patients with a creatinine clearance of ≥30 mL/min [35-38]. Multiple randomized trials have demonstrated the efficacy of these agents for treatment of acute cystitis in the general population. (See "Acute simple cystitis in females", section on 'Management'.)

Fosfomycin and trimethoprim-sulfamethoxazole (TMP-SMX), which are considered first-line agents for empiric therapy of simple cystitis in nontransplant patients, should not be routinely used for empiric therapy in kidney transplant recipients. Transplant recipients who have recently been given TMP-SMX (eg, for prophylaxis) should be assumed to be infected with an organism that is resistant to TMP-SMX. Use of fosfomycin should be limited to patients with multidrug-resistant cystitis [1].

Duration of therapy The optimal duration of antibiotic therapy for simple cystitis among kidney transplant recipients is unclear. Our approach depends upon the timing after transplantation. For simple cystitis that occurs earlier than six months posttransplant, we treat for 10 to 14 days. For simple cystitis that occurs more than six months posttransplant, we treat for five to seven days.

Complicated UTI — In transplant recipients who present with signs and symptoms of a complicated UTI, we typically treat with intravenous (IV) antibiotics that cover both gram-negative and gram-positive bacteria initially, unless signs and symptoms are mild enough such that outpatient oral antibiotics with high bioavailability can be started. We obtain urine and blood cultures prior to initiating antibiotics. As with simple cystitis, empiric treatment should be followed by definitive treatment once the identity and antibiotic susceptibilities of the causative organism are known. If the urine culture reveals candiduria, treatment should be tailored according to the identified Candida species and according to whether localized or disseminated infection is present. This is discussed in more detail elsewhere [29]. (See "Candida infections of the bladder and kidneys", section on 'Symptomatic candiduria'.)

Antibiotic selection – Empiric antibiotics should have adequate coverage against P. aeruginosa, enteric gram-negative organisms, and Enterococcus species. Commonly prescribed treatment regimens include [1]:

Piperacillin-tazobactam 4.5 g IV every six hours, or

Meropenem 1 g IV every eight hours, or

Combination therapy with vancomycin (table 1) plus cefepime 1 g IV every eight hours.

Antibiotic dosing must be adjusted according to kidney function.

Duration of therapy – The optimal duration of treatment is not known. We treat all patients with complicated UTI with 14 to 21 days of antibiotic therapy [39]. Oral agents may be substituted for IV therapy once the patient is free of symptoms and antibiotic susceptibilities are known. However, if the causative pathogen is susceptible to a fluoroquinolone (eg, ciprofloxacin), then it is reasonable to switch from IV to oral therapy once the patient is able to take oral medications since fluoroquinolones are highly bioavailable and achieve high concentrations in the urinary tract. Fluoroquinolone-calcineurin inhibitor drug interactions, especially with the higher dose of ciprofloxacin typically used for treatment of pyelonephritis, should be anticipated, and dose reduction of the calcineurin inhibitor is often necessary to prevent calcineurin inhibitor toxicity.

Recurrent UTI — Prevention and treatment of recurrent UTI in kidney transplant recipients are important given that recurrent UTI has been associated with an increased risk of allograft loss and death in this population [40].

Approach to prevention — In kidney transplant recipients with recurrent UTI, we take the following approach to prevention:

All patients should be evaluated for anatomic or functional abnormalities of the urinary tract, which may increase the risk of infection. This is frequently done in consultation with a urologist. (See 'Imaging/urologic evaluation in selected patients' above.)

All patients should be counseled on the risk factors for recurrent UTI and behavioral changes that might reduce the risk. Such behavioral changes are similar to those for nontransplant patients with recurrent UTI and include increased fluid intake, frequent voiding, postcoital voiding, contraception modification (in sexually active patients), and wiping from front to back (in females). (See "Recurrent simple cystitis in women", section on 'Changes in behavior' and "Recurrent simple cystitis in women", section on 'Risk factors'.)

Some experts administer prophylactic antibiotics to selected patients with recurrent UTI. The decision to administer long-term antibiotic prophylaxis should be individualized. The choice of prophylactic antibiotics is discussed elsewhere in this topic. (See 'Antimicrobial prophylaxis' above.)

For postmenopausal females, topical estrogen may prevent recurrence of UTIs. (See "Recurrent simple cystitis in women", section on 'Topical estrogen for postmenopausal women'.)

Some transplant programs use methenamine hippurate (1000 mg twice daily) with or without ascorbic acid (1000 mg twice daily) for prevention of recurrent UTI. (See "Recurrent simple cystitis in women", section on 'Methenamine'.)

A retrospective study of 38 kidney transplant recipients found that use of methenamine alone was associated with a 45 percent reduction in the frequency of UTI, 42 percent reduction in the length of antibiotic use for UTI treatment, and 59 percent reduction in UTI-related hospitalizations [41]. Similar findings were reported in a second study of 30 kidney transplant recipients treated with the combination of methenamine and ascorbic acid; the benefit was greatest in female patients and patients with diabetes, especially those with a glycated hemoglobin (A1C) ≥8 percent [42]. Patients with an eGFR <30 mL/min/1.73 m2 are less likely to benefit from this intervention.

We do not routinely use strategies such as cranberry juice or probiotics due to the lack of clear data supporting their use in transplant recipients. While we avoid probiotics in immunocompromised patients, we do not discourage the use of cranberry tablets or unsweetened cranberry juice for patients who are interested or find them helpful. (See "Recurrent simple cystitis in women", section on 'Optional strategies of uncertain benefit'.)

Treatment of recurrent episodes — Each episode of simple cystitis or complicated UTI should be treated with an appropriate duration of antibiotic therapy, as detailed above (see 'Simple cystitis' above and 'Complicated UTI' above). In some situations, a longer course may be necessary for patients with persistent/recurrent UTI with the same organism. As an example, recurrent UTIs associated with an indwelling source (such as infected cysts in native kidneys) can require up to four to six weeks of therapy. In other situations, therapy for recurrent UTIs can be discontinued after a shorter period, and the patient can be transitioned to prophylactic antibiotics. (See 'Antimicrobial prophylaxis' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Urinary tract infections in solid organ transplant recipients".)

SUMMARY AND RECOMMENDATIONS

Clinical manifestations – We use the following terminology for the presenting clinical syndromes in kidney transplant recipients (see 'Terminology' above and 'Clinical manifestations' above):

Asymptomatic bacteriuria is the presence of >105 bacterial colony-forming units per milliliter (CFU/mL) on urine culture with no local or systemic symptoms of urinary tract infection (UTI).

Simple cystitis is the presence of >105 CFU/mL on urine culture with local urinary symptoms, such as dysuria, frequency, or urgency, but no systemic symptoms, such as fever or allograft pain, and no indwelling device (eg, ureteral stent, nephrostomy tube, or chronic urinary catheter).

Complicated UTI is the presence of >105 CFU/mL on urine culture with fever, allograft pain, chills, malaise, or bacteremia with the same organism in urine, or a biopsy with findings consistent with pyelonephritis.

Recurrent UTI is two or more episodes of UTI in six months, or three or more episodes of UTI in one year.

Diagnostic evaluation – Patients with suspected UTI should undergo testing with a urine dipstick, urine microscopy, and urine culture. Blood cultures should be obtained in those with symptoms suggestive of a complicated UTI. Once the diagnosis of UTI is established, selected patients may require imaging to exclude potentially correctable structural or functional abnormalities of the urinary tract. (See 'Diagnostic evaluation' above.)

Prevention

Antimicrobial prophylaxis – Nearly all kidney transplant recipients receive trimethoprim-sulfamethoxazole (TMP-SMX) to prevent Pneumocystis pneumonia (PCP); this is also effective at preventing UTIs. For rare patients who are unable to take TMP-SMX (eg, due to allergy), an alternative agent for PCP prophylaxis (eg, atovaquone) is given, and the need to give an additional agent for UTI prophylaxis is determined by the transplant center. (See 'Antimicrobial prophylaxis' above.)

Monitoring for asymptomatic bacteriuria – Many transplant centers, including our centers, have moved away from routine monitoring for asymptomatic bacteruria since there are no high-quality data showing that either screening or treating asymptomatic UTIs prevents symptomatic UTIs. If screening is performed (with routine urine cultures), it should be limited to the first one to two months posttransplant. (See 'Monitoring for asymptomatic bacteriuria' above.)

Management of symptomatic infections – We treat all symptomatic UTIs in transplant recipients with antibiotics, first with empiric therapy followed by definitive treatment once the identity and antibiotic susceptibilities of the causative organism are known.

Simple cystitis – For transplant recipients with simple cystitis, we suggest empiric therapy with a fluoroquinolone (ciprofloxacin or levofloxacin), a third-generation cephalosporin (eg, cefpodoxime or cefdinir), or amoxicillin-clavulanate rather than first-line agents used in nontransplant patients (eg, fosfomycin, trimethoprim-sulfamethoxazole) (Grade 2C). Nitrofurantoin is another option for patients with an estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m2. The choice of antibiotic is based upon knowledge of local antibiotic resistance patterns and the patient's past causative organisms and antibiotic exposure. We tailor the duration of treatment according to the time since transplant. (See 'Simple cystitis' above.)

Complicated UTI – For transplant recipients with a complicated UTI, we suggest empiric therapy with piperacillin-tazobactam, meropenem, or combination therapy with vancomycin plus cefepime rather than other agents used in nontransplant patients (eg, fluoroquinolone, ceftriaxone) (Grade 2C). We treat all patients with complicated UTI for 14 to 21 days. Oral agents may be substituted for intravenous (IV) therapy once the patient is free of symptoms and antibiotic susceptibilities are known. (See 'Complicated UTI' above.)

Recurrent UTI – Recurrent UTI is treated similarly to initial episodes of UTI. All patients should be evaluated for anatomic and functional abnormalities and counseled about behavioral modifications. The decision to give prophylactic antibiotics is generally individualized. (See 'Recurrent UTI' above.)

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Topic 7298 Version 31.0

References

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