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Year : 2020  |  Volume : 14  |  Issue : 4  |  Page : 283-287

Urinary tract infections in kidney transplantation: An emerging crisis of drug resistance

Department of Nephrology and Renal Transplantation, Virinchi Hospitals and Max Superspeciality Medical Centre, Hyderabad, Telangana, India

Date of Submission20-Jun-2020
Date of Acceptance25-Nov-2020
Date of Web Publication30-Dec-2020

Correspondence Address:
Dr. Praveen Kumar Etta
Department of Nephrology and Renal Transplantation, Virinchi Hospitals and Max Superspeciality Medical Centre, Hyderabad - 500 034, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_60_20

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How to cite this article:
Etta PK. Urinary tract infections in kidney transplantation: An emerging crisis of drug resistance. Indian J Transplant 2020;14:283-7

How to cite this URL:
Etta PK. Urinary tract infections in kidney transplantation: An emerging crisis of drug resistance. Indian J Transplant [serial online] 2020 [cited 2021 May 10];14:283-7. Available from: https://www.ijtonline.in/text.asp?2020/14/4/283/305428

Urinary tract infections (UTIs) are the most common infections after kidney transplantation (KT).[1] The prevalence of UTIs in KT recipients (KTRs) varied considerably due to differences in the definition, diagnostic criteria, study design, follow-up periods, geographical location, immunosuppression, and prophylactic regimen used. UTIs contribute to 35%–72% of all infections and up to 30% of all hospitalizations for sepsis in KTRs.[2] They are most often seen during the 1st year, especially the first few months after KT. According to Rubin's timetable, UTIs predominate in the 1st month due to health care-related causes such as surgical injury, urinary tract stents, bladder catheterization, and intensive immunosuppression.[3]

  Spectrum of Urinary Tract Infections Top

UTIs in KTRs may present as asymptomatic bacteriuria (ASB), symptomatic UTI (cystitis or pyelonephritis [PN]), or asymptomatic graft dysfunction. Recent updated 2019 guidelines from the American Society of Transplantation Infectious Diseases Community of Practice have attempted to unify definitions for all UTI syndromes in solid organ transplant recipients.[4] ASB is defined as the presence of bacteriuria (≥105 CFU/mL) without any local or systemic signs or symptoms of UTI. For the diagnosis of ASB, two consecutive positive tests (ideally within 2 weeks) are needed in women compared to one single positive test in men. Uncomplicated UTI (cystitis and prostatitis) presents with local urinary symptoms such as dysuria, frequency, urgency, or suprapubic pain with no indwelling device and no systemic symptoms such as fever, allograft pain, or hemodynamic compromise. Complicated UTI, including graft PN or upper tract UTI, presents with fever and either one of the following: allograft pain, chills, malaise, bacteremia, hemodynamic instability, leukocytosis, or biopsy consistent with PN. Because the transplanted kidney is not innervated, pain may not always be present in cases of PN. Many a times, UTI can be clinically asymptomatic due to concomitant use of immunosuppressive drugs and denervated graft. Many clinicians consider all forms of UTIs among KTRs as complicated UTIs because of the altered anatomy of the urinary tract and the immunocompromised status.[5] UTI may also be associated with the development of bacteremia, cytomegalovirus (CMV) infection, acute rejection (AR), graft dysfunction or loss, and patient's death. The absence of a sphincter between the transplanted ureter and the native bladder increases the risk of vesicoureteral reflux (VUR) predisposing to PN. Graft PN can mimic AR. Fever and graft tenderness are usually suggestive of PN, whereas graft dysfunction in the presence of proteinuria and hypertension usually suggest AR.[6] Recurrent UTI (rUTI) is three or more episodes of UTI in 1 year or two or more episodes of UTI in a 6-month period. Emphysematous PN is characterized by severe necrotizing infection which results in the formation of gas within the renal parenchyma, collecting system, or perinephric tissues.[7]

With the widespread use of antibiotics, including the routine use of antimicrobial prophylaxis, the prevalence of multidrug resistance (MDR) among uropathogenic bacteria is increasing in KTRs. MDR-UTI is defined as an infection caused by a uropathogen resistant to at least one agent in three or more classes of drugs normally active against the isolated bacteria. Extensively drug resistant (XDR) is resistance to at least one agent in all but two or fewer antimicrobial categories. The risk factors for MDR-UTIs in KTRs include female gender, elderly age, history of rUTI, urinary tract abnormality or obstruction, VUR, polycystic kidney disease (PKD), deceased donor, delayed graft function, frequent ARs, greater immunosuppression, diabetes mellitus, or new-onset diabetes after transplantation, CMV infection, previous antibiotic exposure or prophylaxis, repeated urologic instrumentation, ureteral stent placement, prolonged catheterization, and hospital stay.[8],[9] Several studies have noted that UTI with MDR pathogens was more frequently associated with rUTI.[10] A recent randomized study comparing early ureteral stent removal at 1 week to routine stent removal at 4 weeks found that early removal can reduce the risk of UTIs.[11]

  Uropathogens and their Pathogenetic Factors Top

Gram-negative organisms contribute up to 60%–90% of UTIs; important pathogens include Escherichia coli (commonest), Pseudomonas, Enterobacter, Klebsiella, and Proteus. In a recent Indian study, authors have observed the common organisms associated with the UTIs in KTRs as E. coli, followed by Klebsiella.[12] In another study, UTI was diagnosed 33.6% of KTRs, and Gram-negative bacteria were most prevalent with E. coli (43.53%), followed by Enterobacter spp. (35.37%) as the major organisms. The rate of resistance to all tested antibiotics was highest in Enterobacter spp.[13] Several prior studies demonstrated that MDR isolates were responsible for the majority of symptomatic UTIs in KTRs.[8],[14] In a recent study on MDR/XDR UTIs in KTRs, Gram-negative infections accounted for 66% of all bacterial UTI episodes and the most frequent MDR/XDR Gram-negative organism was E. coli (62.5%).[8] E. coli ST131 is the predominant multilocus sequence type found worldwide as the cause of MDR-UTIs. In a study, rUTI due to drug-resistant organisms was caused by extended-spectrum β-lactamase (ESBL) producing Klebsiella pneumoniae, followed by E. coli and MDR-Pseudomonas aeruginosa.[10] Gram-positive organisms (e.g., Enterococcus) account for few cases, especially in the first posttransplant month; fungal (e.g., Candida), mycobacterial, and viral infections (CMV, BK virus, and adenovirus) can also occur.[15] MDR pathogens, such as ESBL-producing and carbapenem-resistant enterobacteriaceae (CRE), MDR-Pseudomonas, and vancomycin-resistant enterococcus (VRE) causing UTIs are now occurring at increasing frequency in KTRs. Enterococcus faecium accounts for most VRE isolates. The term “ESKAPE” has been proposed to denote nosocomial resistant pathogens, including E. faecium, Staphylococcus aureus, K. pneumoniae, Acinetobacter baumannii, P. aeruginosa, and Enterobacter species.

Various pathogenetic mechanisms such as immune evasion, toxin production, iron acquisition, adherence, bacterial motility, and ascent are involved in UTIs. Various virulence structures of bacteria (e.g., P fimbriae in E. coli) are involved in urothelial adhesion and invasion. About 80% of E. coli isolates from patients with UTI belong to a subset of O-serotype including O1, O2, O4, O6, O7, O16, O18, and O75. Some strains of E. coli encode the proteins SisA and SisB, which suppress the host inflammatory response; produce hemolysin, which induces the formation of pores in the cell membrane, and aerobactin, a siderophore necessary for iron uptake in the iron-poor environment of the urinary tract. Nonsecretors of histo-blood group antigens are more likely to have rUTI. Some of the uropathogenic bacteria (e.g., E. coli, K. pneumoniae) can enter the cytosol and rapidly multiply, forming a biofilm-like assembly known as the intracellular bacterial community (IBC). This is determined by its fimbrial adhesins, called type 1 pilus. These IBC bacteria become a reservoir that will periodically resurge and cause rUTI.[16] Few bacteria (e.g., Proteus mirabilis, Corynebacterium urealyticum) produce urease, which leads to alkalinization of urine and predisposes to the formation of stones and persistence of infection. All these pathogenic factors are also important in precipitating MDR-UTIs.

Microbial drug resistance can be a result of sporadic chromosomal mutations that may allow organisms to change the drug target site, increase drug efflux, limit drug entry, or shift to an alternative metabolic pathway. Resistance can also be carried on foreign DNA through transposons and plasmids, which can be transferred between organisms of the same species or across species. Plasmids may also concurrently carry genes for resistance to multiple antibiotics. Hence, MDR pathogens can arise even among patients exposed to only one class of antimicrobials. Gram-negative organisms achieve resistance to β-lactam antibiotics through the expression of β-lactamase enzymes, which are carried on chromosomes or exist as transferable genes. Ambler classification separates β-lactamases into 4 classes: classes A, C, and D of serine-β-lactamases and the class B of metallo-β-lactamases (MBLs). Amp C β-lactamases (Ambler class C) are carried chromosomally and infer inducible resistance to penicillins, narrow-spectrum cephalosporins, and cephamycins. ESBLs (Ambler class A), a class of plasmid-based enzymes, have the ability to inactivate all cephalosporins. Enterobacteriaceae that produce CTX-M β-lactamases also carry concurrent resistance genes to fluoroquinolones, aminoglycosides, and sulphonamides. CTX-M-15 is probably the most prevalent type of ESBL produced by resistant uropathogens (such as E. coli ST131) in India.[17] Carbapenems are resistant to Amp C β-lactamases and ESBLs. Carbapenemases infer the ability to neutralize carbapenems in addition to penicillins and cephalosporins. They belong to Ambler class A, B, or D β-lactamases. Some of the most common carbapenemases include KPC (Klebsiella pneumoniae carbapenemase, Ambler class A), NDM (New Delhi MBL), IMP-type MBL, VIM (Verona integron-encoded MBL) and OXA (oxacillinase, Ambler class D). Carbapenemases are encountered in CRE isolates and some strains of P. aeruginosa. Recent case reports have noticed the emergence of K. pneumoniae NDM-1 strain in KTRs and they are resistant to almost all antibiotics, including carbapenems.[18] Enterococci are intrinsically resistant to cephalosporins, antistaphylococcal penicillins, trimethoprim, and low concentrations of clindamycin and aminoglycosides. Enterococci are now noted to have developed resistance to high concentrations of aminoglycosides, β-lactams, and most notably, glycopeptides such as vancomycin.

  Screening and Prophylaxis Top

The role of routine screening and treating ASB to prevent symptomatic UTI in KTRs is controversial. However, untreated ASB that occurs within 3 months posttransplant is associated with an increased risk of acute cellular rejection.[19] Although few centers recommend screening for ASB in the first few months after transplantation, the infectious disease society of America currently recommends against testing for ASB in KTRs after 1 month of KT.[20] The optimal strategy, antibiotic regimen, and duration of prophylaxis are not known. Few guidelines recommended perioperative antimicrobial prophylaxis with cefazolin to reduce surgical site infections in KTRs.[21] One study found a reduction in the incidence of early UTIs after KT when adding gentamycin to the usual prophylaxis. However, the use of aminoglycosides in the early posttransplant period is not desirable due to their potential nephrotoxicity.[22] A recent study found that perioperative antimicrobial prophylaxis with a single dose of ertapenem in KTRs reduced the incidence of early infections due to ESBL-producing Enterobacteriaceae without increasing the incidence of other MDR microorganisms or Clostridium difficile.[23] A systematic review and meta-analysis of randomized controlled trials (RCTs) concluded that antibiotic prophylaxis during the first 6 months posttransplant was associated with a reduced risk of sepsis and bacteriuria, although no significant reduction in all-cause mortality and graft loss was detected.[24] Most centers continue antibiotic prophylaxis for at least 6 months to 1 year posttransplant. Co-trimoxazole (TMP-SMX) is the most commonly prescribed drug based on its experience in KTRs and it also prevents opportunistic infections, such as Pneumocystis carinii and Nocardia. Few studies have shown that using ciprofloxacin in addition to TMP-SMX further reduces the incidence of UTI compared to TMP-SMX alone.[25] Several studies have shown a rising prevalence of resistant uropathogens while on antimicrobial prophylaxis.[24] Secondary antimicrobial prophylaxis for the prevention of rUTI in KTRs has not been well studied.

  Management Top

In recent years, many transplant centers have noted an increase in the incidence of UTIs caused by MDR microorganisms, making it difficult to treat and also limiting the choice of empirical and specific antimicrobial therapy. The choice of antimicrobial agent, the dose, and the duration of therapy depends on the site of infection, the presence or absence of complicating factors, and local resistance patterns. Beside this, the treatment of ASB is controversial in KTRs. ASB represents colonization rather than infection and it may be considered a risk factor for symptomatic UTI, but treatment does not reduce the frequency of symptomatic UTI or recurrent ASB. One retrospective study concluded that evolution to symptomatic UTI was similar between treated and untreated ASB. Persistent ASB occurred in 46% of treated episodes, with the selection of resistant pathogen in 78% of cases. Spontaneous bacterial clearance occurred in 59% of untreated episodes.[26] Another retrospective study showed that the risk of developing symptomatic UTI and hospitalization were significantly higher in the treated group.[27] A recent single-center RCT concluded that the treatment of ASB made no difference in the incidence of any of the outcomes in 2-year follow-up.[28] A retrospective study showed that between 2 and 5 and >5, ASB episodes were independent risk factors associated with PN, whereas >5 episodes was also a risk factor associated with AR. Despite the treatment, the incidence of PN was much higher in the group of patients with ASB.[29] Hence, most guidelines do not advise to treat ASB episodes unless the patient is undergoing a urologic procedure or is neutropenic. The American Society of Transplantation Infectious Diseases Community of Practice advises not to treat ASB occurring more than 3 months after RT unless there is an increase in serum creatinine.[5] It is more complex if the ASB is caused by drug-resistant organisms.[30]

It is challenging to treat UTIs in KTRs as they are immunocompromised and are at risk of serious complications and drug resistance. They are also prone to graft dysfunction and loss. They can have serious adverse drug interactions due to the concomitant use of immunosuppressive drugs. Antimicrobial therapy is based on the severity of UTI, local resistance pattern, previous infection, and antibiotic exposure. Fluoroquinolones have good oral bioavailability and achieve high concentrations in the urinary tract, hence they are most preferred. Once susceptibility data are available, the initial therapy should be deescalated and the most narrow-spectrum antibiotic should be used to complete the course of therapy. Complicated UTI/PN with renal or perinephric abscess or emphysematous PN may occur and usually requires a multidisciplinary approach for percutaneous or surgical drainage of abscesses. The optimal duration of treatment is not known. It is generally recommended to treat complicated UTI with 14–21 days of therapy and should be extended until adequate drainage of abscesses and clinical resolution of infection has been achieved. A prolonged therapy up to 4–6 weeks may be required in special cases such as infected cysts in PKD and in cases of rUTI. Few authors suggest a prolonged duration or indefinite treatment as secondary prophylaxis in selected cases of rUTI.[31],[32]

The bacterial resistance to antibiotics is an evolving problem. The evaluation of patients with graft PN, rUTIs, and MDR-UTIs includes identifying any anatomical or functional abnormalities in the urinary tract, postvoid residual volume, or persistent focus of infection like prostatitis/cyst infection using various imaging modalities directed to transplanted and native kidneys, ureters, and bladder; few may require uroflowmetry, voiding cystourethrogram, urodynamic studies, and cystoscopy. Since most patients on dialysis are oliguric or anuric, urinary tract obstruction may become evident only after KT with the restoration of diuresis. Repeated antibiotic exposure in patients with rUTI can predispose to drug resistance. A recent study analyzed antimicrobial susceptibility of Gram-negative urinary pathogens in KTRs and found antimicrobial resistance of Klebsiella spp. increased significantly compared to E. coli and P. aeruginosa isolates.[33]

Many MDR-uropathogens retain susceptibility to two old antibiotics, nitrofurantoin, and fosfomycin trometamol. They share some specific advantages over newer drugs such as achieving high urinary concentrations, lower rates of “collateral damage” on the gastrointestinal flora, lower propensity for resistance, minimal toxicity, and can be administered orally. As both these drugs achieve high therapeutic drug concentrations in the urinary tract, they are useful for the treatment of uncomplicated UTI. As low serum concentrations lead to treatment failures, these are not appropriate for patients with bacteremia or upper tract UTIs such as PN. Serratia, Acinetobacter, Morganella, Proteus, and Pseudomonas are usually resistant to nitrofurantoin; and Morganella and Acinetobacter are typically resistant to fosfomycin. Nitrofurantoin has 80% oral bioavailability, and approximately 25% is excreted unchanged in the urine. It became a preferred drug in the international consensus guidelines for UTI.[34] In a study published in IJT, the authors reported a case of MDR-ASB, within the 1st month of KT, treated successfully with a single dose of oral fosfomycin, with long-term remission.[35] An intravenous formulation is also available for fosfomycin.

The emergence of ESBL-producing or carbapenemase-producing pathogens has been the important threat in KTRs in recent years. A major contributing factor is the acquisition of plasmids that can encode resistance factors for multiple drug classes. Carbapenems are still preferred for infections due to ESBL-producing bacteria; less severe infections can be treated with cephamycins, cefepime, and β lactam-β lactamase inhibitors (e.g., piperacillin-tazobactam). Other options in the case of proven susceptibility include tigecycline, TMP-SMX, fluoroquinolones, and aminoglycosides. For uncomplicated cystitis secondary to ESBL-producing organisms, UTI-specific antibiotics, such as fosfomycin and nitrofurantoin can be used. Pivmecillinam is also effective but not available in India. The combination of antibiotic therapy is a standard of care for CRE infections. Polymyxins (colistin) are the most active agent against these strains and should be considered the basis of the treatment in most patients. Other options for the use of combination antibiotic therapy include aminoglycosides, fosfomycin, tigecycline, or even high-dose carbapenems. P. aeruginosa is intrinsically resistant to tigecycline. Tigecycline and polymyxin B do not have good clearance in the urine and they are not approved for the treatment of UTIs. Several novel β-lactamase inhibitors such as avibactam are active against carbapenemases and showed promising results when used in combination with β-lactam agents.[36] Some novel drugs such as ceftolozane/tazobactam and plazomicin are approved recently to treat UTIs due to MDR-pathogens.[37]

In cases of severe infection with systemic sepsis or shock, the option of reduction or discontinuation of one or more immunosuppressive drugs (especially antimetabolites) together with urological intervention should be considered. In a recent Indian study, about 46.6% and 33.3% of the UTI isolates were found to be ESBL producers and carbapenem-resistant, respectively; carbapenem-resistance was observed in 62.5% of E. coli isolates overall and 100% of E. coli in the 1st month posttransplant.[38] Another recent Indian study showed that MDR was highest in K. pneumoniae (100%).[12] Among VRE, Enterococcus faecalis isolates remain sensitive to ampicillin, amoxicillin, nitrofurantoin, fosfomycin, and fluoroquinolones. Doxycycline has low levels of urine clearance despite showing activity against VRE and hence may be of limited utility for treating UTIs. Severe infections can be treated with a combination of ampicillin and gentamycin, linezolid, daptomycin, tigecycline, and quinupristin/dalfopristin (E. faecium only).

Shortening the duration of antibiotics uses to reduce antibiotic-related selective pressures could be an important prophylactic step to avoid infection with MDR organisms. Other measures such as hand hygiene, environmental cleaning, contact precautions, and stringent infection control practices are helpful to reduce the occurrence and spread of MDR organisms during hospitalization. The antimicrobial stewardship programs recommend the reduction of antibiotic exposure, use of rational antibiotics with the narrowest spectrum possible, and to limit the duration of therapy as much as possible. However, antimicrobial prophylaxis is crucial to prevent life-threatening infections immediately after KT. Hence, a balance has to be maintained between antimicrobial exposure and prevention of resistance to drugs. In patients with symptomatic UTI, removal (preferred) or replacement of urinary tract instruments such as urethral catheters and urologic stents is recommended for resolution of UTI as they may be covered with bacterial biofilm.[39]

  Conclusions Top

MDR-ASB and UTIs are very common among KTRs and remain a major cause of morbidity and mortality. The current data do not show a beneficial effect of treating ASB. UTIs should be treated with the narrowest spectrum antibiotic to minimize the emergence of resistance. MDR-UTIs and rUTIs should be evaluated for any potentially reversible causes. Future studies and interventions should focus on optimal prevention and treatment of MDR-UTIs.

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