| Abstract|| |
Since the initial times of renal transplantation in the 1950s, understanding various aspects influencing graft survival and outcome have been progressively improving. However, infections especially urinary tract infections (UTIs), are an important factor leading to an increase in morbidity and graft failure. UTI degrades the health-related quality of life and can potentially impair graft function. UTI occurs in 25% of kidney transplant recipients within one year of transplant and accounts for 45% of infectious complications. Asymptomatic bacteriuria (ASB), uncomplicated UTI, and complicated UTI comprise 44%, 32%, and 24% of cases, respectively. This article reviews important aspects regarding posttransplant UTI, including definition, incidence, predisposing factors, recommendations, ASB, and controversies in management. UTI after renal transplantation is still an under-estimated aspect, despite its degrading effects on allograft and recipient health.
|How to cite this article:|
Meena P, Bhargava V, Rana DS, Bhalla AK. Urinary tract infection in renal transplant recipient: A clinical comprehensive review. Saudi J Kidney Dis Transpl 2021;32:307-17
|How to cite this URL:|
Meena P, Bhargava V, Rana DS, Bhalla AK. Urinary tract infection in renal transplant recipient: A clinical comprehensive review. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jan 25];32:307-17. Available from: https://www.sjkdt.org/text.asp?2021/32/2/307/335441
| Introduction|| |
Following kidney transplantation, urinary tract infection (UTI) is the most common infection and the incidence varies from 35% to 60%. It accounts for approximately 44%–47% of all infectious complications. This considerable variation in the incidence of UTI could be due to variability in the local epidemiology, local outbreaks and difference in the definitions and diagnostic criteria used in the studies. The risk of UTI is highest in the 1st-month post- transplantation and continues up to three months; following which this risk reduces. UTI in the post transplant patient is attributed to factors associated with the host and the causative organisms. Various predisposing factors for UTI are shown in [Figure 1] and are divided into preoperative, intraoperative, and postoperative factors.
|Figure 1: Predisposing factors for urinary tract infection after renal transplantation.|
UTI: Urinary tract infection, AR: Acute rejection, SLE: Systemic lupus erythematosus, CMV: Cytomegalovirus.
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Acute, uncomplicated UTIs in adults include episodes of acute cystitis and acute pyelonephritis in otherwise healthy individuals. These UTIs are seen mostly in women without structural and functional abnormalities within the urinary tract, kidney diseases, or comorbidity. These could result in more severe outcomes and therefore need attention.
A complicated UTI is an infection associated with a structural or functional abnormality of the genitourinary tract or in the presence of an underlying disease, which increases the risks of an infection or resistance to therapy.
| Host Factors|| |
Some of the risk factors predisposing to UTI in postrenal transplant patients are common to the general population. As compared to males, females are at higher risk due to a shorter urethra and proximity to the anus. Multiple studies have shown that the immunosuppressant dose and depleting antibody agents used for induction like anti-thymocyte globulin significantly contribute to increasing UTI and risk for other infections. The insertion of Foley’s catheter is a routine practice during renal transplantation surgery, which is a common cause of UTI in the early post-transplantation period. As the number of days with the urethral catheter in situ increases, the risk of UTI increases. In the general population, as the number of days with the catheter in situ increases the risk of bacteriuria increases by approximately 5% per day. It is advisable to keep catheter for as short as two days to prevent UTI.
| Genetic Factors|| |
Innate immunity is the first line of defense that provides a barrier to pathogen invasion and is responsible for host resistance against UTI. Cells of innate immunity such as neutrophils, macrophages, and natural killer cells, limit penetration and damage by the pathogen. Numerous studies have established the association of polymorphism in genes like toll-like receptors (TLR4) and C-X-C Motif Chemokine Receptor 1 (CXCR1) with asymptomatic bacteriuria (ASB) and acute pyelonephritis (APN). CXCR1 was the first identified human UTI susceptibility locus, followed by polymorphisms in other genes such as interferon regulatory factor 3 and TLR4. Genetic variants lead to impaired antibacterial defense by the host and allowbacteria to establish infection in individual hosts but not in others.
| Microbiological Factors|| |
UTI in posttransplant patients can be caused by viruses, bacteria, fungi and parasites. Gram-negative bacteria, including Escherichia coli (E. coli), Enterococcus sp., are the most common organisms accounting for more than 70% of UTIs. The strain of bacteria varies between centers as it depends on local epidemiology, immunosuppressive regimen, and antimicrobial protocol. Pathogenicity of E. coli in urothelium increases with P. fimbriae expressed on its surface to facilitate its adherence to the urothelium. Patients with diabetes are predisposed to fungal UTIs. Candida albicans is the most common organism causing fungal UTIs. The fungus can aggregate as fungal balls to obstruct and lead to hydronephrosis. Common viruses causing UTIs are the BK virus and cytomegalovirus (CMV) virus. In countries like Africa, Schistosoma hematobium is endemic. Its infection is often associated with renal stones and ureteric stricture. In developing countries, tuberculosis (TB) mycobacteria is also a cause of UTI (reactivated by immunosuppressive medication).
| Allograft Factors|| |
There is inconclusive evidence that as compared to living kidney transplantation, transplantation from deceased donors is at high risk of postoperative UTI. The most likely cause of lower incidence of UTI in kidneys from a living donor could be due to shorter periods of cold ischemia and less severe ischemia-reperfusion as compared to cadaveric transplants. In patients of autosomal dominant polycystic kidneys, the native kidney serves as a reservoir for microorganisms and can cause recurrent UTI.
Some studies have found that because of the use of more intense immunosuppression, acute rejection (AR) episodes are linked to higher episodes of UTIs.
| Ureteral Stents and Other Urinary Tract Manipulations|| |
History of instrumentation of the urinary tract also predisposes transplant patients to UTI., Foreign material in the urinary tract, like stents and Foley’s catheters can cause UTI. Loss of glycosaminoglycans from the urothelium leads to the invasion of pathogens into the cells of the urothelium. Wilson et al have shown that ureteric stents inserted during transplantation surgery are associated with an increase in relative risk of UTI up to 1.5-times. In a study by Kamath et al, the odds ratio of ureteric stents for UTI was as high as 4.6.
| Anatomical Factors|| |
In the renal transplant population, development of urinary stasis due to urethral disease, pelviureteric obstruction, vesicoureteric junctions, dysfunction of bladder or outflow obstruction, and neurogenic bladder can lead to the development of UTI. In renal transplantation surgeries, the ureter is generally anastomosed to the bladder by using an extravesical technique. In this anastomosis, secondary reflux occurs, which can affect both transplanted and native kidneys. Unsterile infected urine, if present, causes UTI and predisposes to graft pyelonephritis. In the pediatric population disorders like prune-belly syndrome, posterior urethral valves, spina bifida, or any other urogenital sinus abnormalities lead to any structural changes or neurogenic bladder., Regular posttransplant follow-up, and evaluation and treatment of neurogenic bladder before kidney transplantation is vital in these patients.
| Immunosuppression|| |
Theoretically, the immunosuppression regimen should impact UTI incidence and spectrum, but there is insufficient evidence about the association of any specific immunosuppressant with increased risk of UTI. However, anti-CD3 use as induction treatment has been seen to increase UTI incidence in numerous studies.
Hence, multiple factors such as catheterization, manipulation of the urinary tract, lower urinary tract dysfunction, and the impact of antibody depleting agents are responsible for UTI in the posttransplant period.
| Clinical Presentation|| |
As compared to the general population, transplant patients with UTI are often asymptomatic as symptoms and signs of UTI can be masked by immunosuppressive therapy. Especially pain over the renal allograft is often absent because of the denervated transplanted kidney. Symptomatic patients can present as acute cystitis or graft pyelonephritis, sometimes with native pyelonephritis. Symptoms depend on the involvement of the upper urinary tract or lower urinary tract, ranging from mild lower tract irritative symptoms, for example, frequency, urgency, dysuria, suprapubic tenderness, and incontinence. However, there can be severe systemic manifestations, such as bacteremia, sepsis, and shock. Fever with costovertebral angle pain and graft site tenderness are the manifestations of APN. Sometimes, patients can also complain of cloudy or foul-smelling urine. Characteristic symptoms of UTI are summarized in [Table 1]. A study by Valera et al on 172 transplant patients showed that uncomplicated acute bacterial cystitis is the most common presentation and accounted for 77% of UTIs. Another study on 189 renal transplant patients reported APN in 10% of cases the study showed that more than five episodes of ASB after transplantation was as independent predictors for APN. Infections with TB manifest as low-grade prolonged fever and renal impairment. BK virus infection can present as symptomatic graft failure, urethral stricture, and stenosis.
| Site of Infection|| |
The most common site of involvement is the urinary bladder (>95%), followed by renal allo-graft. Occasionally, an infection of the native kidneys can develop. Symptoms and signs of UTI can be masked by immunosuppressive therapy, especially pain over the graft is often absent because of the denervated transplanted kidney. Nevertheless, other atypical forms must also be considered in a transplant recipient. Prostatitis due to Cryptococcus, Aspergillus, or Salmonella and epididymitis with Klebsiella, Mycobacterium haemophilum, CMV or TB have also been reported. Furthermore, orchitis due to salmonellosis and CMV ureteritis have been described in the context of renal transplantation. Recipients of a combined pancreas-kidney transplant with drainage of the exocrine pancreas to the bladder might also develop (nonbacterial) urethritis.
| Pathogenesis|| |
The pathogenesis of UTI typically begins with uropathogenic bacteria ascending to the bladder from the urethra. Pathologic invasion of the urothelium is aided by bacterial virulence structures, such as P. fimbriae, which promote adhesion to the urothelium. Type 1 pili get attached to mannose receptors on uroepithelial cells lining the urinary tract. The absence of a sphincter between the transplanted ureter and the native bladder can predispose kidney transplant recipients to develop transplant pyelonephritis. Transplant pyelonephritis can occasionally occur by seeding of the kidney from bloodstream infection or surgical site infection.
| Acute Effects of Urinary Tract Infection on Graft Kidney|| |
The acute effects of UTI on renal graft are complex. Colonization of virulent microorganisms in the renal pelvis can cause direct cellular injury. Indirect damage can also occur from inflammatory mediators. Sometimes metastatic infection leads to renal infection, which presents as cortical abscesses. Elevation of inflammatory mediators and acute phase reactants such as erythrocyte sedimentation rate and C-reactive protein (CRP) may be found. Increased levels of serum interleukin-6 (IL-6) and IL-8 are responsible for fever. The secretion of tubular proteins in urine such as a2-macroglobulin and N-acetyl-b-D-glucosaminidase reflect tissue damage.
Bacteria can induce a serological immune response to its various antigenic components leading to damage to the renal parenchyma and promote more permanent structural and functional impairment.
| Asymptomatic Bacteriuria|| |
The definition of ASB in patients without indwelling catheters is ≥105 colony-forming units (CFU)/mL in a voided urine specimen without signs or symptoms attributable to UTI. For women, two consecutive samples should be obtained, within two weeks, to confirm persistent bacteriuria. For men, a single urine specimen meeting these quantitative criteria is sufficient for diagnosis. Patients with indwelling devices often have multiple organisms isolated from the urine, some of which are present at lower quantitative counts.
ASB is a common finding in renal transplantation patients. Risk factors for ASB are similar to symptomatic UTI, such as female sex, comorbidities, urologic abnormalities, and immunosuppression. A retrospective analysis of 189 renal transplant patients on 36 months follow-up showed that 51% of patients had one or more episodes of ASB among these, 19% of patients had one episode, 24% of patients had 2–5 episodes whereas 8% of patients had >5 episodes of ASB.All episodes of bacteriuria in these patients were consistently treated with anti-microbials. More than two episodes of ASB were reported as an independent risk factor for APN. However, this finding was not supported by other studies. In a study done by Green et al analyzing a single episode of ASB diagnosed in 112 patients following one year after transplantation; antimicrobial treatment for ASB was given to 19.6% of patients, no difference was found in the increase in serum creatinine, graft loss, pyelonephritis, or urosepsis in treated and untreated patients. In various other studies also no benefit of the treatment of ASB was proved. Concern about the treatment of ASB with antimicrobials is increasing the risk of antimicrobial-resistant organisms, and these resistant organisms are difficult to treat. There are high chances of promotion of reinfection with organisms with the treatment of ASB. High-quality evidence also suggests that antimicrobial therapies are associated with adverse effects.
In renal transplant recipients who have had renal transplant surgery > 1 month prior, recommendations are against screening or treating ASB.
| Importance of First Three Months Post-transplantation|| |
Säemann and Hörl established that most UTIs are diagnosed after renal transplantation occurred within the first three months. A retrospective cohort analysis involving 29,000 transplant patients reported a 17% cumulative incidence of UTI during the initial three months. So, it is essential to detect UTIs as early as possible among transplant recipients, particularly those who are within three months of transplantation. According to Giral et al, APN in the first three-month post-renal transplant negatively affects graft survival.
| Diagnosis|| |
Lower UTI present as burning micturition, frequency, urgency, fever, allograft site pain, and fatigue-like symptoms of systemic inflammation. These are also common symptoms of pyelonephritis. Careful clinical history is essential to distinguish between ASB and UTIs, more importantly, APN.
Patients presenting with UTI should be examined for loin pain, suprapubic tenderness, prostatomegaly, and atrophic vaginitis.
As urine culture is crucial for the diagnosis of UTI, accurate specimen collection is essential to reduce the chances of contamination. A specimen should be collected before the administration of antibiotics. The Infectious Diseases Society of America (IDSA) recommends cleaning of perineum or glans with antiseptic wipes and then collects mid-stream clean catch urine in a sterile container. Indwelling catheters increase the propensity of colonizing flora due to biofilm formation; therefore, specimens from urinary catheters in place for >2 weeks are strongly discouraged, but if necessary, the sample must be taken from the sampling port of a newly inserted device. The diagnostic recommendations by the IDSA are presented in [Table 2].
|Table 2: Classification of urinary tract infection in renal transplant recipients.|
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Pyuria (>10 white blood cells/mL in the urine) is the usual finding in UTIs. Its absence prompts for consideration of an alternative diagnosis. The presence of a positive dipstick test for leukocyte esterase and nitrite increases the likelihood of a positive culture, but their usefulness in renal transplant patients is limited. The role of urine culture in the diagnosis of UTI is indispensable. Typically, for symptomatic UTI significant quantitative count of bacteria (≥105 CFU/mL) is necessary. Definitions of different UTIs according to urine culture are given in [Table 3].
|Table 3: Diagnostic recommendations by the Infectious Diseases Society of America.|
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In case of suspicion of pyelonephritis, blood cultures should be sent before antibiotic initiation. Raised CRP and leukocyte count indicates systemic infection. To detect CMV and BK virus, urine and blood polymerase chain reaction and urine cytology for decoy cells must be done. Suspected cases of TB should be screened with the polymerase chain reaction of early morning urine.
Role of different imaging modalities is as follows:
- Ultrasound of transplanted kidney, native kidney and bladder: Dilated pelvicocalyceal system, stones
- Plain X-ray/computed tomography (CT) kidney, ureter, and bladder: Stones in transplanted or native kidneys, pyelonephritis,
- CT–positron emission tomography: Localized infection of polycystic kidneys,
- Micturatingcystogram: Suspected reflux,
- Urodynamics: Bladder dysfunction and outflow obstruction,
- Static renogram (DMSA scan): Renal scarring.
| Prophylaxis and Challenges in Treatment of Urinary Tract Infection|| |
Although there is no consensual universal statement regarding posttransplant UTI prophylaxis, however, most centers prescribe antimicrobial therapy for three to six months but follow variable regimens. Antimicrobial therapy prophylaxis for the long term is effective in reducing the incidence of UTIs, but its benefit in the improvement of patient and graft survival is not established. A meta-analysis by Green et al showed that antimicrobial prophylaxis therapy lowered the risk of developing bacteriuria by 60%. Trimethoprim/sulfamethoxazole (TMP/ SMX) was well tolerated, and a daily dose of 320/1600 mg provided optimal benefit. TMP/ SMX is the first-line recommended therapy for prophylaxis against Pneumocystis jirovecii pneumonia (PJP) for the first 6–12 months posttransplant. In a prospective, double-blinded randomized control trial by Khosroshahi et al, done on 95 renal allograft recipients, two groups were analyzed. Group 1 (n = 63) received low-to-moderate doses of TMP/SMX (either 80/400 mg or 160/800 mg, daily) and group 2 (n = 32), high doses of TMP/SMX (320/1600 mg, daily in two divided doses). The high dose group had UTI in about 25% of patients, whereas UTI was found in 49.2% in low- to moderate-dose group. An increase in serum creatinine and hyperkalemia are two important side effects of TMP/SMX.
In numerous studies, fluoroquinolones were also used as prophylaxis for renal transplant recipients, but their use has been linked to surges in fluoroquinolone-resistant Pseudomonas aeruginosa. Other agents that can be used as an alternative to TMP-SMX are nitrofurantoin (only if estimated GFR >60 mL/min), cephalosporins (e.g., cephalexin) or fluoroquinolones.
TMP-SMX prophylaxis for six months is recommended for PJP prophylaxis, and it decreases UTI and bacteremia in renal allograft recipients (evidence: strong, high).
If TMP-SMX cannot be used for primary prophylaxis of UTI after renal transplant, alternative agents with limited data include nitrofurantoin (avoid if GFR <60 mL/min), cephalexin, or fluoroquinolones.
For secondary prophylaxis of UTI in renal allograft recipients with recurrent UTI, non- antimicrobial prevention strategies are preferred. Antimicrobial prophylaxis may be appropriate for selected patients who have severe episodes of recurrent UTIs such as pyelonephritis (evidence: weak, low).
| Ureteral Stent Removal|| |
Ureteral stents are placed at ureteral-vesicular anastomosis to prevent complications such as urine leak, ureteral necrosis, and uretero-vesical obstruction or stenosis. A Cochrane review revealed that indwelling stents increase the risk for UTI by 49%, but at the same time reduce urological complications by as much as 76%. It highlighted that indwelling stent increases UTI risk if kept for >2 weeks.
In renal transplant recipients, limiting the duration of catheters and stents to <4 weeks following transplant surgery is suggested. If severe UTI occurs in the period from two to four weeks after the transplant, consider early stent removal while balancing the risk of urologic complications (evidence: strong, moderate).
Challenges in the treatment
Antibiotic-resistant micro-organism: With unrestricted use of antibiotics in transplant recipients, microorganism resistance to multiple drugs has become the major concern in the treatment of UTIs. The emergence of multi- drug resistance (MDR), including organisms producing extended-spectrum beta-lactamase or carbapenemase, is associated with a poorer outcome and increased risk of recurrent UTI.
Drugs such as colistin used may be nephrotoxic and are associated with high mortality rates.
Prolonged use of antibiotic therapy predisposes for fungal infections. Candiduria may complicate UTI by forming a “fungus ball” within the bladder and kidney.
| Recommendations for Treatment of Urinary Tract Infection in Post-Transplant Patients|| |
For simple cystitis in renal allograft recipients, it is reasonable to limit therapy to 5–10 days. Single-dose or three-day treatment courses are not recommended.
For pyelonephritis/complicated UTI in renal allograft recipients, an antibiotic with narrow-spectrum should be used to complete 14–21 days of therapy based on susceptibility data.
| Short- and Long-term Outcome|| |
The effect of UTI on graft survival in transplant patients is still controversial. So far, no consensus has been established about short- term and long-term impact on UTI. Previously UTI was considered innocuous, but now there are emerging shreds of evidence that UTI in kidney transplant patients can cause severe morbidity and increase in mortality affecting long-term effects on graft function. Depending on the pathogen virulence factor and its interaction with host factors, it can result in urosepsis, bacteremia, and devastating condition of septic shock. In some studies, APN was not associated with a decrease in graft or patient survival, but as compared to patients with uncomplicated UTIs, patients with APN are found to exhibit an increase in serum creatinine after one year that persisted four years after transplantation. Papasotiriou et al analysis showed no alteration in long-term renal function with the occurrence of UTIs in transplanted patients; nevertheless, APN may be associated with an abiding decrease in renal graft function. Other researchers have confirmed that there are no differences in graft survival rates between the patients without UTIs and those who had a single episode; however, a reduction of renal function might be observed in patients during UTI episodes. Although there is a lack of literature regarding the association of AR and UTI, few studies report that UTI can trigger acute rejection (AR)., Intensive immunosuppressive treatment of AR may predispose UTIs. A study by Kamath et al proved this observation, and it showed that AR preceded APN in 41% of cases and APN episodes followed 28% of cases of AR.
The following are the impact of recurrent UTIs on short and long-term outcomes after renal transplantation:
- Recurrent hospitalization
- Acute graft dysfunction
- Chronic rejection
- Urosepsis, bacteremia
- Septicemia, death.
| Future Areas for Investigation|| |
There is a constant need for studies to establish duration and drug of choice for antimicrobial prophylaxis in renal allograft recipients during this era of high prevalence of MDR organisms.
New and reliable biomarkers are required to confirm the diagnosis of UTI and distinguish UTI from graft rejection. The optimal timing of stent removal is yet to be explored. Treatment and screening of ASB are still controversial. Further RCTs are required to guide prophylaxis and preventive therapies. Discovery of new antibiotics with fewer side effect profiles is required. Research of non antibiotic and vaccine approaches to the prevention of recurrent UTI is warranted and recommended. An appropriate immunosuppressive regimen/protocol to reduce the incidence of UTI should be developed.
Conflicts of interest: None declared
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Department of Nephrology, Institute of Renal Science, Sir Gangaram Hospital, New Delhi
[Table 1], [Table 2], [Table 3]