Abstract
Background
Infectious complications remain the leading cause of morbidity and mortality in kidney transplant recipients (KTRs) across Africa, where immunosuppression is delivered amid endemic pathogens, resource constraints, and limited microbiological surveillance. These challenges are compounded by near-universal cytomegalovirus (CMV) seropositivity, high tuberculosis burden, and constrained access to standard prophylactic antivirals.
Objectives
To synthesize evidence on the epidemiology, microbiology, and management of infectious complications in African KTRs, with emphasis on context-adapted prophylaxis strategies and systemic gaps.
Methods
This scoping review searched PubMed and African Journals Online (2015–2025) for primary cohort studies, systematic reviews, and clinical trials published between 2015 and 2025 reporting infection outcomes in African KTRs, supplemented by global evidence on CMV prophylaxis in resource-limited settings. Foundational studies predating 2015 were included where no more recent equivalent existed. This review was conducted following the PRISMA Extension for Scoping Reviews (PRISMA-ScR). Studies were eligible if they reported infection outcomes in African kidney transplant recipients. Data were charted descriptively by infection type, country, and prophylaxis strategy.
Results
Bacterial urinary tract infections predominate early post-transplant, with Escherichia coli causing up to 54% of cases. CMV infection occurs in 13–63% of seropositive recipients despite prophylaxis, with rates varying by regimen and monitoring intensity; tissue-invasive disease is associated with acute rejection rates approaching 50%. Low-dose valacyclovir shows encouraging prophylactic efficacy comparable to valganciclovir at approximately one-sixth the cost, suggesting it may represent a pragmatic alternative in resource-limited African settings where valganciclovir is unavailable or unaffordable. Pediatric transplantation remains severely underdeveloped across sub-Saharan Africa, compounded by weight-based CMV dosing challenges and absent dedicated pediatric units. Critical systemic gaps, nephrology workforce deficits, and near-total absence of transplant infectious disease subspecialty training perpetuate high infectious morbidity after transplantation.
Conclusions
Improving outcomes will require evaluation of cost-effective prophylaxis protocols through prospective multicenter registries, alongside urgent investment in transplant infectious disease workforce capacity.
Supplementary Information
The online version contains supplementary material available at https://doi.org/10.1186/s12879-026-14052-5.
Keywords: Kidney transplantation, Infectious complications, Cytomegalovirus, Africa, Valacyclovir, Valganciclovir, Urinary tract infection, Resource-limited settings
Introduction
Kidney transplantation confers a significant survival advantage and superior health-related quality of life compared with chronic dialysis for patients with end-stage renal disease (ESRD) [1–3]. However, these benefits depend on the successful management of post-transplant complications, particularly infections. Globally, infectious complications affect an estimated 40–80% of kidney transplant recipients (KTRs) in the first post-transplant year and account for approximately 20–30% of post-transplant deaths [4–7]. In Africa, where the transplant recipient is immunosuppressed against a background of endemic tuberculosis (TB), human immunodeficiency virus (HIV), hepatitis B and C, and a high burden of multidrug-resistant organisms [4, 8, 9], the infectious risk is compounded by structural factors including limited microbiological surveillance, restricted access to prophylactic antivirals, and the limited availability of dedicated transplant infectious disease services [8, 10].
For this review, the term “infectious complications” is used broadly to encompass the full spectrum of infections encountered in the African transplant context, including classic transplant-associated opportunistic infections (CMV, BK virus, invasive fungi, Pneumocystis jirovecii pneumonia), endemic pathogens behaving opportunistically under immunosuppression (tuberculosis, strongyloidiasis, cryptosporidiosis), and common post-surgical and healthcare-associated infections (urinary tract infections, bacterial sepsis). This inclusive framing reflects the epidemiological reality of African transplant programmes, where the boundaries between these categories are frequently blurred by high background pathogen burden and limited diagnostic capacity.
Kidney transplantation in Africa has expanded substantially over the past two decades, yet access remains profoundly unequal. North Africa, led by Egypt, Morocco, and Tunisia, accounts for the majority of transplant activity on the continent, with Egypt’s Mansoura Urology and Nephrology Center performing more than 6,000 transplants since its establishment [11, 12]. Sub-Saharan Africa, by contrast, has relatively few established transplant programmes with South Africa, Nigeria, Tanzania, Ethiopia, and Zambia among the nations with documented services [13, 14]. This geographic and infrastructural disparity shapes the epidemiology of infections reported from African transplant centres, as transplant volume, immunosuppression protocols, prophylaxis access, and microbiological capacity vary enormously across the continent [15].
This scoping review synthesises the available evidence on infectious complications in African KTRs, drawing on primary data from Egyptian, Moroccan, and South African cohorts, and contextualises these findings within the global literature on CMV prophylaxis and bacterial infection management. We aim to identify actionable priorities for improving infection-related outcomes in this underserved population. The review question was framed using the PCC framework: Population = African kidney transplant recipients; Concept = infectious complications and prophylaxis strategies; Context = African transplant programmes.
Methods
We conducted a systematic search of PubMed/MEDLINE and African Journals Online (AJOL), for studies published between January 2015 and January 2025. Additional references were identified through manual screening of the bibliographies of included articles and relevant systematic reviews. Non-systematic searches of Google Scholar were conducted to identify grey literature, including WHO reports and conference abstracts, where primary data were otherwise unavailable.
Search terms included combinations of: “kidney transplant*”, “renal transplant*”, “Africa”, “infection*”, “cytomegalovirus”, “CMV”, “urinary tract infection”, “tuberculosis”, “prophylaxis”, “valacyclovir”, “valganciclovir”, and “resource-limited”. The full PubMed search string was: ((“kidney transplant“[tiab] OR “renal transplant“[tiab] OR “kidney transplantation“[MeSH Terms]) AND (“infect*“[tiab] OR “infection“[MeSH Terms]) AND (“Africa“[tiab] OR “African“[tiab] OR “sub-Saharan“[tiab] OR “North Africa“[tiab] OR “Egypt“[tiab] OR “Nigeria“[tiab] OR “South Africa“[tiab] OR “Kenya“[tiab] OR “Morocco“[tiab] OR “Tanzania“[tiab] OR “Ghana“[tiab] OR “Ethiopia“[tiab] OR “Sudan“[tiab] OR “Zambia“[tiab]) AND (“2015/01/01“[pdat] : “2025/01/31“[pdat])). AJOL was searched using two queries: (1) “kidney transplant” +infection and (2) “renal transplant” +infection. AJOL does not support Boolean MeSH-based searching; the +infection operator was used to require the term “infection” in all retrieved records. Studies were included if they reported original infection outcome data from African KTR cohorts, defined as kidney transplant recipients managed within transplant programmes located in Africa; eligibility was determined by the location of the transplant programme rather than the nationality or residency status of the recipient. None of the included studies explicitly reported recipient nationality, and transplant tourism to African centres is not documented in the published literature of these cohorts. Global evidence on CMV prophylaxis and antimicrobial management was incorporated as contextual background when no African-specific data were available; however, these studies were not counted as primary included sources and do not appear in the flow diagram. Studies were excluded if they did not report transplant-specific infection outcomes, were single case reports without epidemiological relevance, or were published in languages other than English or French. The 2015–2025 window was selected to capture contemporary African transplant programme data; foundational studies predating 2015 were retained where no more recent equivalent existed. No formal quality assessment or meta-analysis was performed, consistent with the scoping review methodology. The inherent limitations of this approach are acknowledged in the Limitations section. Conference abstracts (e.g. [16, 17]), were included where they represented the only available data from a given country or region; given the limited peer review of such sources, findings from conference abstracts are presented descriptively and are not used to draw quantitative conclusions. The selection process is summarized in the PRISMA-ScR flow diagram (Additional File 1). In total, 304 records were identified, 293 screened after duplicate removal, 28 assessed for full-text eligibility, and 7 primary African cohort studies were included.
The african transplant landscape: context for infectious risk
Epidemiology of ESRD and transplant activity
ESRD is a growing public health crisis across Africa, driven by hypertension, diabetic nephropathy, glomerulonephritis, and HIV-associated nephropathy. Despite this burden, access to renal replacement therapy remains catastrophically limited: a systematic review of dialysis outcomes in sub-Saharan Africa found that most patients with ESRD remain undiagnosed, untreated, and die without receiving any form of renal replacement therapy [18]. Kidney transplantation, the definitive treatment, is available in only a minority of African countries.
A 2023 scoping review of kidney transplantation across Africa identified fewer than 25 countries with any documented transplant activity, with outcomes data available from an even smaller subset [14]. A 2025 systematic review and meta-analysis confirmed that while transplant outcomes in African centres are broadly comparable to international benchmarks when programmes are well-resourced, infections remain the dominant driver of morbidity and graft loss [15]. In North Africa, Egypt leads transplant volume, with the Mansoura Urology and Nephrology Center reporting outcomes from over 6,000 procedures spanning nearly five decades [11]. Morocco has developed a growing programme centred at Ibn Sina University Hospital in Rabat, which has emerged as the country’s primary referral centre for kidney transplantation [12]. Tunisia has maintained a national transplant programme since 1986, with active centres in Tunis and Sfax, while Algeria has a smaller but established service [12].
Sub-Saharan Africa presents a starkly different picture. South Africa has the most mature programme (i.e., a well-established centre with high transplant volume, comprehensive services, and documented long-term outcomes), with Groote Schuur Hospital in Cape Town and Charlotte Maxeke Johannesburg Academic Hospital collectively accounting for the majority of transplants performed south of the Sahara [19, 20]. Tanzania’s programme at Muhimbili National Hospital, established in 2019, reported favourable one-year outcomes but identified infections as the principal post-transplant challenge [21]. Ethiopia’s first living-donor programme, established in 2016, demonstrated comparable early outcomes to international centres [22], while Nigeria’s programme remains fragmented across a small number of tertiary centres, with paediatric access described as negligible [23]. Zambia has recently described its nascent transplant experience, with preliminary data identifying infectious complications as the dominant post-operative concern [16, 17].
Table 1 summarises the key characteristics and infection outcomes of the primary African cohort studies included in this review.
Table 1.
Characteristics and infection outcomes of primary African kidney transplant cohort studies included in this review
| Study, Country | Study Design; Period; (N) | Population | Immunosuppression (Maintenance) | Antimicrobial/Antiviral Prophylaxis (Key Strategies Used) | Key Pathogens Isolated (% of infections) | Infection Types Reported |
|---|---|---|---|---|---|---|
| [24], Moroccoa | Retrospective; 1998–2023; (123) | Adults | CNI + MMF + steroids | Valacyclovir (CMV prophylaxis, majority); co-trimoxazole (PCP prophylaxis, NR) | E. coli (54% of UTIs)h; K. pneumoniae; BK virus | UTI (34.1%)b; pneumonia; BSI; fungal (6 episodes); parasitic (3 episodes)c |
| [25], Moroccoa | Retrospective; 2013–2017; (60) | CMV R+ adults | CNI + MMF + steroids | Valacyclovir 1500 mg q.i.d. ×6 months (80%); valganciclovir (minority) | CMV (dominant); BKV coinfection (higher in CMV disease group) | CMV DNAemia (63%); CMV disease (13%)d; UTI (NR) |
| [26], Egypte | RCT; 2015–2016; (80) | CMV R+ adults | CNI + MMF + steroids | Valacyclovir 2 g b.i.d. ×90 days vs. valganciclovir 450 mg q.d. ×90 days (randomised) | CMV (dominant); no bacterial isolates reported | CMV infection (13.75%); CMV pneumonitis (4 cases); CMV encephalitis (1 case)f |
| [27], South Africa | Retrospective; 2015–2019; (13) | Paediatric (≤ 16 years) | CNI + MMF + steroids | Not reported | Not specified | Not specified; 15.4% graft lossg |
| [11], Egypte | Retrospective editorial; 1976–2019; (> 6,000) | Adults | Varied by era | Varied by era; not reported by period | Not reported by pathogen | Infection (leading cause of death alongside CVD across all eras) |
| [16, 17], Zambia | Conference abstract; 2022–2024; (NR) | Adults | CNI + MMF + steroids | Not reported | Not specified | Infectious complications dominant post-operative concern; details NR |
aSuperscript ‘a’ applies to both [24]and [25], both conducted at Ibn Sina University Hospital, Rabat, Morocco
bRecurrent UTI in 15.4% of patients; female sex and prolonged catheterisation were independent risk factors (p < 0.001 each)
cCryptosporidiosis caused one death; miliary TB caused one death; COVID-19 caused four deaths (leading cause of infection-related mortality)
dOf 8 CMV disease cases, 6 (75%) were tissue-invasive; 2 (25%) were CMV syndrome. Acute rejection occurred in 50% of CMV disease patients vs. 0% of asymptomatic patients (p = 0.003)
eBoth studies from Mansoura Urology and Nephrology Center, Egypt
fOnly infection-related death was CMV encephalitis in the valganciclovir arm
g100% patient survival; 84.6% of recipients were Black African; cadaveric donor shortage identified as the principal barrier to programme expansion
h[24]is a 25-year retrospective cohort study of 123 kidney transplant recipients at Ibn Sina University Hospital, Rabat, Morocco. It provides data on infection episode frequency and timing (71.4% of early infections were bacterial), UTI incidence (127 episodes in 34.1% of patients), pathogen distribution (E. coli 54% of UTIs, followed by Klebsiella pneumoniae), recurrence rates (15.4%), and multivariate predictors (female sex, prolonged catheterisation). Resistance data for E. coli and Klebsiella isolates were not systematically reported; antimicrobial susceptibility testing results and ESBL rates were not provided. Readers should interpret pathogen frequency data in the absence of resistance profiling
CMV = cytomegalovirus; R+ = CMV-seropositive recipient; BKV = BK polyomavirus; UTI = urinary tract infection; BSI = bloodstream infection; CVD = cardiovascular disease; CNI = calcineurin inhibitor; MMF = mycophenolate mofetil; NR = not reported; RCT = randomised controlled trial; PCP = Pneumocystis jirovecii pneumonia
Structural determinants of infectious risk
Several structural features of African transplant programmes amplify infectious risk beyond what is observed in high-income settings.
First, living donors account for the overwhelming majority of kidney transplants across Africa, reflecting the near-absence of deceased-donor infrastructure and enabling legislation in most countries. A scoping review of kidney transplantation across Africa found that living-related donation dominates transplant activity in virtually all documented African programmes, with deceased-donor transplantation confined to a small number of centres in South Africa, Egypt, and Morocco [14]. In Nigeria, living donation is the exclusive source of transplant organs, with deceased-donor programmes non-existent at the national level [23]. Even in South Africa, the continent’s most mature programme, the number of deceased donors has declined over the past two decades, prompting expansion into donation after circulatory death as a strategy to sustain transplant volume [28]. This structural reliance on living donors concentrates transplant activity in younger recipients who may receive more intensive immunosuppression, and limits the overall scale of transplant programmes across the continent [14, 15]. Second, the background seroprevalence of CMV in African adult populations is near-universal (exceeding 90%), creating a prophylaxis environment that differs fundamentally from high-income settings where a meaningful proportion of recipients are CMV-seronegative [29–31]. This near-universal seropositivity, detailed in the CMV section below, means that the dominant risk profile in African programmes is D+/R+ (reactivation-driven) rather than the D+/R− category that drives the most severe disease in high-income settings. Similarly, EBV seroprevalence approaches universality by early adulthood [32], and HBsAg carriage rates substantially exceed those in Europe and North America, elevating the risk of donor-derived HBV transmission and reactivation under immunosuppression in African populations.
Third, exorbitant and unaffordable medication costs limit the extent of prophylaxis and treatment access by KTRs. For example, the cost of valganciclovir, the international standard for CMV prophylaxis, renders it inaccessible to the majority of patients in African health systems without comprehensive national health insurance, creating a cost barrier that has driven the adoption of valacyclovir as a pragmatic alternative in several African centres (detailed in the CMV Prophylaxis section below) [25, 26, 31].
Fourth, microbiological surveillance capacity across African health systems is substantially limited, with direct consequences for the detection and management of post-transplant infections. A systematic review of AMR surveillance systems across Africa found that only 23 of 54 African countries had any form of national AMR surveillance, and that data quality, laboratory capacity, and reporting consistency were severely constrained across the continent [33]. A 14-country analysis of bacteriology and AMR detection capacity in sub-Saharan Africa identified critical weaknesses at all tiers of national laboratory networks, including inadequate culture infrastructure, limited antimicrobial susceptibility testing panels, and absence of quality assurance programmes [34]. These deficiencies extend directly to transplant-relevant diagnostics: routine CMV quantitative PCR monitoring, antifungal susceptibility testing, BK virus surveillance, and multidrug-resistant organism screening require laboratory infrastructure that is unavailable or unaffordable in the majority of African transplant centres [35, 36].
Temporal distribution of infectious complications in African KTRs
The timing of infectious complications after kidney transplantation follows a broadly predictable pattern that reflects the intensity of immunosuppression, the nature of the pathogen, and the recipient’s pre-existing immunity. Table 2 summarises the temporal distribution of the major infectious complications reported in African KTR cohorts, organised by post-transplant period. This framework is adapted from the established transplant infectious disease timeline and contextualised with data from the African cohorts reviewed here.
Table 2.
Temporal distribution of infectious complications in kidney transplant recipients: African context
| Post-Transplant Period | Predominant Infection Type | Key Pathogens (African Cohort Data) | African Evidence Source | Typical Prophylaxis/Prevention Strategy |
|---|---|---|---|---|
| Early (< 1 month) | Bacterial (surgical site, UTI, BSI, pneumonia) | E. coli (54% of UTIs); K. pneumoniae; MDR Gram-negatives | [24]: 71.4% of early infections bacterial | Surgical antimicrobial prophylaxis (e.g., cefazolin); urinary catheter removal within 5 days; co-trimoxazole for PCP prophylaxis (3–6 months); antifungal prophylaxis (fluconazole) in high-risk patients |
| Intermediate (1–6 months) | Viral (CMV dominant); opportunistic fungal; TB reactivation | CMV (63% DNAemia, 13% disease); BK virus; Aspergillus spp.; M. tuberculosis | [25]: CMV 39% of intermediate infections; [24] | CMV prophylaxis: valacyclovir or valganciclovir (3–6 months); co-trimoxazole continuation; CMV QNAT monitoring where available; pre-emptive antiviral therapy for breakthrough DNAemia |
| Late (> 6 months) | Community-acquired; endemic pathogens; recurrent UTI; late CMV | CMV (late breakthrough); Cryptosporidium spp.; Strongyloides stercoralis; COVID-19 | [24]: fungal (6 episodes), parasitic (3 episodes) in late period; COVID-19 leading late mortality cause | Continued co-trimoxazole (lifelong in some protocols); targeted antimicrobial therapy for recurrent UTI; TB screening and isoniazid preventive therapy (IPT) in high-burden settings; COVID-19 vaccination |
| Any period | TB (reactivation or primary) | M. tuberculosis (including miliary TB); MDR-TB risk in high-burden settings |
[24]: miliary TB caused 1 death; SA incidence 427/100,000 vs. Morocco 92/100,000 vs. Egypt < 40/100,000 [37] (WHO GTB Report 2024) |
Pre-transplant TB screening (TST/IGRA); isoniazid preventive therapy (IPT) for LTBI; BCG vaccination status review; rifampicin–CNI interaction monitoring if active TB treatmenta |
MDR = multidrug-resistant; UTI = urinary tract infection; BSI = bloodstream infection; CMV = cytomegalovirus; TB = tuberculosis; SA = South Africa; KTR = kidney transplant recipient; GTB = Global Tuberculosis. Timing categories adapted from the standard transplant infectious disease timeline. African-specific data derived from cohort studies included in this review. aTB incidence varies substantially by region: South Africa 427/100,000, Morocco 92/100,000, Egypt <40/100,000 (WHO Global Tuberculosis Report 2024; available at: https://www.who.int/teams/global-programme-on-tuberculosis-and-lung-health/tb-reports). Rifampicin-based TB treatment can reduce tacrolimus and cyclosporine levels by up to 90% via CYP3A4 induction; close CNI monitoring is mandatory. LTBI = latent tuberculosis infection; TST = tuberculin skin test; IGRA = interferon-gamma release assay; IPT = isoniazid preventive therapy; QNAT = quantitative nucleic acid test
Bacterial infections: the dominant early threat
Epidemiology and microbiology
Bacterial infections are the most common infectious complication in the early post-transplant period (within the first month), accounting for 71.4% of all early infection episodes in a 25-year retrospective cohort of 123 KTRs at Ibn Sina University Hospital, Rabat, Morocco [24]. Urinary tract infections (UTIs) were the single most frequent infection across all post-transplant time periods, with 127 UTI episodes recorded in 42 of 123 patients (34.1%) in the same cohort. E. coli was the predominant uropathogen, accounting for 54% of all UTIs, followed by Klebsiella pneumoniae as secondary pathogens (specific proportions for these organisms were not reported in the source cohort). Recurrent UTIs affected 19 patients (15.4%), with female sex (p < 0.001) and prolonged catheterisation (p < 0.001) identified as independent predictors in multivariate analysis.
This predominance of bacterial infections, particularly UTIs caused by Gram-negative organisms, in the early post-transplant period is consistent with global data. Surgical site infections, pneumonia, and bloodstream infections also contribute to early post-transplant morbidity, with the latter increasingly driven by multidrug-resistant Gram-negative organisms in African centres where antibiotic stewardship programmes are limited. The Moroccan 25-year cohort documented infection-related acute kidney injury (AKI) in 34% of infection episodes, with persistent renal dysfunction in 49% of these cases and graft failure necessitating return to dialysis in 14.6% of the total cohort, underscoring the direct nephrotoxic consequences of uncontrolled infection [24]. In paediatric KTRs, UTIs are similarly the most common bacterial complication, with female sex, vesicoureteral reflux, and neurogenic bladder representing additional risk factors beyond those seen in adults; however, dedicated paediatric UTI outcome data from African transplant programmes are currently absent from the published literature.
Multidrug-resistant organisms (MROs) represent an escalating threat in African transplant centres. Extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae, predominantly E. coli and K. pneumoniae, are the dominant MRO pathogens in African KTRs, yet systematic resistance profiling is absent from the primary cohort studies included in this review: the Moroccan 25-year cohort (Kaouiri et al., 2025) [24] reported pathogen frequency data without ESBL rates or antimicrobial susceptibility testing results, a limitation explicitly noted in Table 1. Carbapenem-resistant organisms (CROs) are an emerging threat in African tertiary centres, driven by high antibiotic selection pressure and limited antimicrobial stewardship capacity [33, 38]. In the absence of local resistance data, empirical antibiotic selection for post-transplant infections in African centres must be guided by institutional antibiograms where available, with early escalation to carbapenem-sparing regimens in patients with risk factors for ESBL infection.
Tuberculosis and opportunistic bacterial pathogens
Transplant-specific TB incidence data from African cohorts are largely absent from the published literature; the following discussion therefore synthesises background burden data and the limited transplant-specific evidence available. TB deserves particular attention in the African context. Although TB incidence in KTRs is not systematically reported across African centres. Africa accounts for approximately 25% of global TB incidence [37], and the immunosuppressive state following transplantation is well established as a risk factor for TB reactivation in high-burden settings; transplant-specific incidence data from African programmes are not available to quantify this risk precisely. The Moroccan 25-year cohort recorded one death from miliary TB, and cryptosporidiosis caused a further death, reflecting the broader spectrum of infectious complications encountered in resource-limited settings [24].
The background population TB burden varies substantially across African regions, and this disparity is likely reflected in the infectious risk faced by transplant recipients, though transplant-specific incidence data stratified by region are unavailable. According to the WHO Global Tuberculosis Report 2024, South Africa has a TB incidence of 427 per 100,000 population, compared with 92 per 100,000 in Morocco; Egypt falls below the high-burden threshold of 40 per 100,000 [37]. BCG vaccination coverage and the availability of isoniazid preventive therapy (IPT) protocols likely differ between regions, though systematic comparative data from African transplant programmes are not available [37]. In South Africa, the high prevalence of latent TB infection in the general population means that most transplant candidates are likely to require pre-transplant TB screening and consideration of IPT, whereas in North African centres this is less uniformly practised [37]. The interaction between rifampicin-based TB treatment and calcineurin inhibitor (CNI) metabolism represents a critical management challenge in any African transplant programme encountering active TB post-transplant. Rifampicin is a potent inducer of CYP3A4 and can reduce tacrolimus and cyclosporine trough levels by up to 90%, necessitating CNI dose increases of two- to five-fold and close therapeutic drug monitoring to prevent acute rejection [37].
These findings reinforce the importance of pre-transplant TB screening and isoniazid prophylaxis protocols tailored to high-burden settings, though standardised African guidelines remain absent. Pre-transplant latent TB infection (LTBI) screening using tuberculin skin testing or interferon-gamma release assays (IGRAs), followed by isoniazid preventive therapy (IPT) for LTBI-positive candidates, is recommended by both WHO and Kidney Disease: Improving Global Outcomes (KDIGO) guidelines for transplant candidates in high-burden settings, and should be completed before transplantation where feasible [39, 40].
Cytomegalovirus: the dominant viral threat
Global burden and African context
CMV is the most clinically significant viral infection in KTRs worldwide. In the absence of prophylaxis, CMV disease affects up to 60% of transplant recipients; even with prophylaxis, CMV infection (detectable viral replication regardless of symptoms) remains common, and is associated with increased mortality, graft loss, and susceptibility to secondary opportunistic infections [39]. In the African context, CMV seroprevalence exceeds 90% in adult populations [29–31], meaning that virtually all African KTRs enter the post-transplant period as CMV-seropositive recipients (R+). The dominant risk profile in African programmes is therefore D+/R+ (intermediate risk, reactivation-driven), rather than the D+/R− category (primary infection, highest risk) that drives the most severe disease in high-income settings. This epidemiological reality should inform decisions on prophylaxis duration and monitoring intensity in African centres.
CMV epidemiology in African cohorts
The most detailed African data on CMV epidemiology in KTRs comes from a single-centre retrospective study at Ibn Sina University Hospital, Rabat, Morocco, enrolling 60 CMV-seropositive recipients transplanted between 2013 and 2017 [25]. Despite six months of antiviral prophylaxis (predominantly valacyclovir 1500 mg four times daily in 80% of patients), CMV infection (any DNAemia) occurred in 38 of 60 patients (63%), with CMV disease in 8 (13%), of whom 6 had tissue-invasive disease. The clinical consequences were severe: acute rejection occurred in 4 of 8 patients with CMV disease (50%) compared with 0 of 22 asymptomatic patients (p = 0.003), and coinfection was significantly more prevalent in the CMV disease group (75% vs. 23%; p = 0.028). Peak viral load was the strongest independent predictor of CMV disease (OR 3.39, 95% CI 1.21–9.53; p = 0.02).
In the same Moroccan centre, a 25-year retrospective analysis (1998–2023) of 123 KTRs confirmed that viral infections, predominantly CMV, were the leading infection category in the intermediate post-transplant period (1–6 months), accounting for 39% of all infections in that window, and remained the most frequent infection type beyond six months [24]. Infection-related mortality was 5.7%, with COVID-19 (four deaths), miliary TB (one death), and cryptosporidiosis (one death) as the leading causes, a distribution that reflects both the contemporary pandemic context and the endemic pathogen burden unique to African settings.
Published data on CMV prophylaxis from African transplant programmes remain sparse, with the Egyptian experience at Mansoura representing the only randomised controlled trial conducted on the continent to date. The international literature on CMV prophylaxis derives predominantly from high-income settings and should be interpreted with caution when applied to African contexts. In high-income settings, CMV infection rates in seropositive recipients receiving standard prophylaxis typically range from 10 to 20%, whereas the Moroccan cohort reported rates of 63% under valacyclovir prophylaxis [25], underscoring the amplified CMV burden in African programmes. The Egyptian RCT (detailed below) and the Moroccan observational cohort represent the entirety of African primary evidence on CMV prophylaxis, highlighting the urgent need for context-adapted strategies and larger multicentre trials.
CMV prophylaxis in resource-limited african settings: the valacyclovir question
The cost barrier to standard prophylaxis
International consensus guidelines recommend valganciclovir as the standard agent for CMV prophylaxis in KTRs, with a duration of three months for CMV-seropositive (R+) recipients and up to six months for those receiving lymphocyte-depleting induction therapy [40]. Throughout this review, ‘universal prophylaxis’ refers to antiviral therapy administered to all at-risk recipients regardless of viral load, whereas ‘pre-emptive therapy’ refers to antiviral therapy initiated upon detection of CMV viraemia above a defined threshold. However, valganciclovir is prohibitively expensive for the majority of patients in African health systems without comprehensive national health insurance. In the Egyptian RCT by Abdel-Rahman et al. [26], a 90-day course of low-dose valganciclovir cost 11,000 Egyptian pounds per patient, compared with 1,700 Egyptian pounds for low-dose valacyclovir, a 6.5-fold difference that is clinically decisive in a setting where out-of-pocket expenditure dominates healthcare financing [26]. In Morocco, valganciclovir is unavailable to patients not enrolled in national health insurance or medical assistance programmes, leading to the routine use of valacyclovir as the primary prophylactic agent [25]. Pharmacoeconomic analyses from other settings confirm that valacyclovir is consistently 40–50% less expensive than valganciclovir over a one-year post-transplant period [38], reinforcing the cost barrier to standard prophylaxis in low- and middle-income African countries.
Evidence for valacyclovir efficacy
The Egyptian RCT demonstrated equivalent efficacy between low-dose valacyclovir (2 g b.i.d.) and low-dose valganciclovir (450 mg q.d.) for CMV infection prevention (7/40 vs. 4/40; p = 0.348) and CMV disease (3/40 vs. 2/40; p = 0.61) over three years of follow-up, with comparable graft function and patient survival [26]. The Moroccan cohort similarly found no significant difference in CMV disease rates between valacyclovir and valganciclovir prophylaxis (p = 0.39) [25].
These African findings are broadly consistent with the global literature, though it should be noted that the international evidence base derives predominantly from high-income settings and may not fully reflect the pharmacokinetic, clinical, and resource contexts of African transplant programmes. A 2024 systematic review and meta-analysis of valacyclovir versus valganciclovir for CMV prophylaxis in KTRs found equivalent efficacy in preventing CMV infection and disease, with valacyclovir associated with a lower risk of bone marrow suppression [41]. A 2024 RCT in adult and paediatric KTRs found lower CMV infection rates with valacyclovir compared with valganciclovir (6% vs. 12%), though this did not reach statistical significance (OR 0.44, 95% CI 0.22–0.88; p = 0.23) [42].
A critical pharmacological consideration is the difference in dosing regimens across the two primary African studies: the Egyptian RCT employed valacyclovir 2 g twice daily (4 g/day) for 90 days, whereas the Moroccan cohort used 1,500 mg four times daily (6 g/day) for six months, a 50% higher total daily dose over a longer period, imposing a greater pill burden that may affect adherence. The 47% breakthrough DNAemia rate in the Moroccan cohort likely reflects the retrospective design, near-universal CMV seropositivity, adherence challenges with a q.i.d. regimen, and absence of systematic viral load monitoring. Both agents require dose adjustment for renal impairment (eGFR < 50 mL/min/1.73 m²), a threshold frequently crossed early post-transplant; in settings where eGFR monitoring is infrequent, both underdosing (prophylaxis failure) and overdosing (neurotoxicity or myelosuppression) are real hazards. The choice of dose and duration should be guided by local pharmacokinetic data, adherence capacity, and monitoring infrastructure rather than direct extrapolation from a single study.
Table 3 summarises the key evidence comparing valacyclovir and valganciclovir for CMV prophylaxis in KTRs, from both African and global studies.
Table 3.
Cytomegalovirus outcomes and prophylaxis strategies in kidney transplant recipients: African and global evidence
| Study, Setting | CMV Population (Risk) | Prophylaxis Regimen | CMV Infection / DNAemia (%) | CMV Disease (%) | CMV-Related Mortality | Notes |
|---|---|---|---|---|---|---|
| [25], Morocco | R+ adults | ValA 1,500 mg q.i.d. x6 months (80% of patients); ValG minority | 63% (any DNAemia); 50% quantifiable (≥ 1.49 log IU/mL) | 13% (8/60); 6/8 tissue-invasive (75%); 2/8 CMV syndrome | Not Reported | Ibn Sina University Hospital, Rabat. Breakthrough DNAemia in 47% during prophylaxis. Peak viral load strongest predictor of CMV disease (OR 3.39, 95% CI 1.21–9.53; p = 0.02). Acute rejection in 50% of CMV disease patients vs. 0% of asymptomatic patients (p = 0.003). |
| [26], Egypt | R+ adults (living donor RCT) | ValA 2 g b.i.d. vs. ValG 450 mg q.d. x90 days (randomised) | 17.5% vs. 10% (p = 0.348) | 7.5% vs. 5% (p = 0.61) | 1.25% (CMV encephalitis, ValG arm; only infection-related death) |
Mansoura Urology and Nephrology Center, Egypt. ValA 6.5x cheaper than ValG (1,700 vs. 11,000 Egyptian pounds/90 days). Drug interruption significantly higher with ValA (40% vs. 12.5%; p = 0.005), primarily elevated liver enzymes. |
| [43], USA | Adult and paediatric KTRs | ValA vs. ValG (standard dosing); RCT (n = 137) | 6% (4/71) ValA vs. 12% (8/67) ValG (p = 0.23) | Not separately reported | Not Reported | Verghese et al. (2024). Time to viraemia and AUC not significantly different. ValG participants more likely to require dose reduction due to leukopenia (21% vs. 2%; p = 0.0003). |
| [44], Global | Adult KTRs | ValA vs. ValG (various regimens); systematic review and meta-analysis of 6 studies (n = 888) | RR 0.70 (95% CI 0.31–1.57; p = 0.4) | RR 0.74 (95% CI 0.09–5.97; p = 0.8) | Not Reported | Acute rejection RR 0.97 (95% CI 0.50–1.91; p = 0.8). ValA associated with significantly lower leukopenia/neutropenia (RR 0.57; 95% CI 0.42–0.77; p < 0.01). No significant differences in BK viraemia or other herpesvirus infections. |
| [45], South Korea | Adult KTRs (n = 2,584) | ValA x3 months vs. no prophylaxis; nationwide cohort | Significantly reduced (p < 0.05) | Significantly reduced (p < 0.05) | Not Reported | ValA prophylaxis also significantly reduced acute rejection rates. |
| [46], Spain | CMV R+ adult KTRs (ATG-treated) | ValG prophylaxis; immunoguided discontinuation (QuantiFERON-CMV) vs. fixed duration | No significant difference in breakthrough CMV infection | No significant difference in CMV disease | Not Reported | Immune-guided discontinuation safely reduced prophylaxis duration without increasing CMV events. Approach may be relevant in African settings to minimise drug costs and toxicity; prospective validation in African cohorts required. |
ValA = valacyclovir; ValG = valganciclovir; CMV = cytomegalovirus; R+ = CMV-seropositive recipient; KTR = kidney transplant recipient; RCT = randomised controlled trial; NR = not reported; OR = odds ratio; RR = risk ratio; CI = confidence interval; AUC = area under the curve; ATG = antithymocyte globulin; q.i.d. = four times daily; b.i.d. = twice daily; q.d. = once daily
Safety profile and drug interruption
An important caveat from the Egyptian RCT is that valacyclovir was associated with a significantly higher rate of drug interruption than valganciclovir (40% vs. 12.5%; p = 0.005), primarily due to elevated liver enzymes. Drug interruption was associated with increased CMV infection risk, though this did not reach statistical significance. Valganciclovir, by contrast, was associated with leukopenia requiring granulocyte-colony stimulating factor in three patients [26]. The safety profiles of both agents require active management; programmes considering valacyclovir should implement regular liver function monitoring and structured adherence support, particularly given the multi-dose regimen.
Viral load monitoring as a complement to prophylaxis
The Moroccan data highlight the critical importance of quantitative CMV viral load monitoring as a complement to prophylaxis, particularly in the African context, where breakthrough infection during prophylaxis is common. In the cohort [25], 47% of patients with quantifiable DNAemia experienced active viral replication during the prophylactic period, and peak viral load was the strongest predictor of progression to CMV disease. Monthly QNAT monitoring during the first year post-transplantation is recommended, though this remains feasible only in centres with virology laboratory capacity [25].
Paediatric Considerations in CMV Prophylaxis: Paediatric KTRs in Africa face additional challenges, as weight-based valacyclovir dosing recommendations are extrapolated from adult or high-income country cohorts, with no validated pharmacokinetic data from African paediatric populations. The 2024 RCT by Verghese et al. [43] included paediatric recipients and found valacyclovir non-inferior to valganciclovir, providing some reassurance. Paediatric-specific pharmacokinetic studies in African children remain an important unmet research need.
Emerging and neglected infectious threats
The COVID-19 pandemic has had a disproportionate impact on KTRs globally, with a systematic review and meta-analysis of 28 studies reporting a mortality rate of approximately 20% in KTRs hospitalised with COVID-19, substantially higher than the general population [47]. In the Moroccan 25-year cohort, COVID-19 was the leading cause of infection-related mortality, accounting for four of six infection-related deaths [24]. This finding underscores the vulnerability of immunosuppressed transplant recipients to emerging respiratory pathogens and the importance of vaccination programmes in this population.
BK Polyomavirus (BKV) nephropathy (BKVaN) is an increasingly recognised cause of graft dysfunction in KTRs, driven by immunosuppression-induced viral reactivation, and represents the leading non-immunological cause of graft loss in the first two years post-transplant globally, affecting 1–10% of recipients [48]. Diagnosis requires plasma BKV PCR monitoring: a threshold of > 10,000 copies/mL warrants allograft biopsy to confirm BKVaN, and presumptive reduction of immunosuppression is recommended at > 1,000 copies/mL (BK viraemia) to prevent progression [48]. There is no approved antiviral therapy for BKVaN; management relies entirely on immunosuppression reduction, with the attendant risk of acute rejection requiring careful clinical judgement. In the Moroccan CMV cohort [25], BKV coinfection was more prevalent in patients with CMV disease than in those with asymptomatic CMV infection, suggesting CMV-BKV co-reactivation as a clinically important and recognised complication of intense immunosuppression [49, 50].
Routine BKV PCR surveillance data from African transplant programmes remain limited, raising concern that BKVaN may be substantially underdiagnosed and underreported in the region, an important evidence gap that should be addressed through prospective transplant registries [13, 15]. Limited access to specialised viral monitoring in some African transplant programmes may further contribute to delayed recognition.
HIV infection represents one of the most significant and most underreported intersections with kidney transplantation in Africa. HIV-associated nephropathy (HIVAN) has historically been a leading cause of end-stage renal disease in sub-Saharan Africa, driven by a high prevalence of APOL1 risk alleles in populations of African descent, and remains an important contributor in settings with incomplete antiretroviral therapy coverage [51, 52][58a, 58b]. South Africa, where HIV prevalence exceeds 13% in the adult population [53] [58c], has the largest number of people living with HIV globally, making HIV-positive individuals a numerically important potential transplant population [19, 19]. Despite this, none of the seven primary African cohort studies included in this review reported the HIV serostatus of transplant recipients, reflecting either the low HIV prevalence in North African transplant populations (Egypt, Morocco) or a systematic failure to report it, itself a critical evidence gap.
South Africa’s Groote Schuur Hospital pioneered the systematic transplantation of HIV-positive recipients, demonstrating that carefully selected HIV-positive patients, with CD4 counts > 200 cells/µL, undetectable viral load on stable antiretroviral therapy (ART), and no active opportunistic infections, can achieve graft and patient survival outcomes comparable to HIV-negative recipients [19, 54]. This programme established that HIV positivity is not a contraindication to kidney transplantation when ART is optimised and infectious risk is carefully managed. HIV-positive KTRs face a heightened risk of opportunistic infections post-transplant, including CMV disease, PCP, and cryptococcal disease, necessitating continued opportunistic infection prophylaxis alongside immunosuppression [54].
A critical pharmacological challenge in HIV-positive KTRs is the interaction between ART and calcineurin inhibitors. Protease inhibitor-based and cobicistat-boosted ART regimens are potent CYP3A4 inhibitors that can increase tacrolimus and cyclosporine exposure by 10- to 70-fold, requiring dramatic dose reductions (often to once-weekly or less) and intensive therapeutic drug monitoring [55]. Integrase inhibitor-based regimens, particularly dolutegravir and raltegravir, have substantially fewer pharmacokinetic interactions with CNIs and are the preferred ART backbone in transplant recipients where virological options permit [55]. The absence of systematic data on HIV-positive KTRs from African cohorts beyond South Africa represents a major evidence gap that future multicentre registries must address.
Opportunistic fungal infections (six cases) and parasitic infections (three cases) were documented in the late post-transplant period (> 6 months) in the Moroccan 25-year cohort, with cryptosporidiosis causing one death [24]. These pathogens, rarely encountered in high-income transplant programmes, reflect the endemic pathogen burden of North and sub-Saharan Africa and highlight the need for context-specific prophylaxis and surveillance protocols.
Infectious disease gaps in paediatric kidney transplantation
Infectious complications, while not the primary focus of this study, are a well-established driver of morbidity in paediatric KTRs globally, with CMV prophylaxis dosing in children presenting particular challenges due to weight-based pharmacokinetic variability [56]. As discussed in the CMV Prophylaxis section above, the absence of validated pharmacokinetic data from African paediatric populations means that weight-based dosing recommendations remain extrapolated from adult or high-income country cohorts, with the optimal regimen for African children undefined. Similarly, paediatric UTI management and TB screening protocols in African transplant programmes are not standardised, and the interaction between immunosuppression and endemic pathogens in growing children warrants a dedicated prospective study.
Equally critical is the near-total absence of transplant infectious disease (TID) as a recognised subspecialty in African transplant programmes. In high-income settings, dedicated TID physicians contribute to prophylaxis protocol design, donor risk assessment, and management of opportunistic infections, roles that demonstrably improve patient outcomes [10]. In Africa, this function is either absent or absorbed by generalist physicians without subspecialty training, a structural gap that likely contributes directly to the high infectious morbidity documented across African cohorts [57, 58]. Rather than calling for an immediate standalone TID subspecialty, premature in many African settings, we advocate for the integration of transplant infectious disease competencies into existing infectious disease and nephrology training curricula. This competency-based approach does not require mature transplant infrastructure as a prerequisite; it is designed to grow alongside emerging programmes, ensuring that infectious disease expertise is embedded from the outset rather than acquired after preventable morbidity has occurred [10, 57, 58].
Expert-informed recommendations for context-adapted infection management in african KTRs
The following recommendations are grounded primarily in evidence from two African cohort studies (the Egyptian RCT [26] and the Moroccan observational cohort [24, 25]) and are supplemented, where African data are absent, by international literature and the authors’ expert interpretation. Readers should note that the African primary evidence base is limited in scope and geographic diversity, and that recommendations drawing on international data represent informed extrapolation rather than direct evidence from African settings. The evidence reviewed here supports several actionable recommendations for improving infection outcomes in African KTRs.
First, based on the available African evidence, a single RCT and one observational cohort, valacyclovir may be considered a pragmatic, cost-effective alternative to valganciclovir for CMV prophylaxis in resource-limited African settings where valganciclovir is inaccessible. This recommendation is supported by encouraging but limited data; formal adoption as a standard-of-care alternative will require larger, multicentre African trials. The critical caveat is that drug interruption, more common with valacyclovir, must be actively prevented through close monitoring of liver function and patient education.
Second, quantitative CMV viral load monitoring during the first-year post-transplantation should be a minimum standard for all African transplant programmes with virology laboratory capacity.
Third, UTI prevention should be operationalised through centre-level protocols, given the dominant contribution of UTIs to post-transplant infection-related morbidity across African cohorts. Key measures include: (i) early urinary catheter removal and timely ureteric stent removal, as prolonged catheterisation and stenting were identified as independent predictors of UTI and recurrence in the Moroccan cohort [24]; (ii) enhanced surveillance of high-risk recipients, particularly women, who demonstrated significantly higher UTI rates across several cohorts; and (iii) targeted antimicrobial prophylaxis for selected high-risk patients, guided by local susceptibility data rather than routine empirical use, particularly important given the high prevalence of ESBL-producing organisms in African settings. Recurrent UTI should prompt urological evaluation to identify correctable anatomical abnormalities.
Fourth, pre-transplant TB screening and isoniazid prophylaxis protocols adapted to high-burden African settings are essential. The Moroccan 25-year cohort documented miliary TB as a cause of post-transplant death, and background TB incidence across sub-Saharan Africa is among the highest globally [37]. The critical management challenge is the interaction between rifampicin-based TB treatment and calcineurin inhibitors, which can reduce tacrolimus and cyclosporine levels by up to 90% via CYP3A4 induction, precipitating acute rejection if not closely monitored [37]. KDIGO and WHO guidelines recommend LTBI screening of all transplant candidates in high-burden settings, with completion of isoniazid preventive therapy before transplantation where feasible [39, 40].
Fifth, the development of prospective multicentre transplant registries across Africa, analogous to the European Renal Association registry, is urgently needed to generate the epidemiological data required to develop evidence-based, context-adapted infection management guidelines.
No existing African-specific consensus guidelines currently formalise a tiered approach to CMV prophylaxis and monitoring; the ISN Global Kidney Health Atlas and AFROSN represent potential platforms for guideline development and dissemination [59, 60]. Recognising this gap, we propose the following tiered framework as an expert-informed, consensus-derived starting point for African transplant programmes and professional societies, explicitly not a formal evidence-based guideline, but an informed proposal pending the development of African-specific consensus. At the basic level (limited laboratory capacity): oral valacyclovir (dose-adjusted for renal function), monthly clinical review, and empirical pre-emptive therapy for symptomatic patients. At the intermediate level (virology capacity available): the above, plus quantitative CMV QNAT monitoring at one, three, and six months, with pre-emptive therapy guided by viral load thresholds. At the advanced level (national referral centre): the above, plus CMV-specific cell-mediated immunity testing, antifungal and BKV surveillance, and registry participation.
Figure 1 presents a visual synthesis of the temporal distribution of infectious complications, comparative CMV prophylaxis outcomes between African and high-income cohorts, and the proposed expert-informed tiered framework for infection prevention in African kidney transplant programmes.
Fig. 1.

Infectious complications in African kidney transplant recipients: temporal burden, CMV prophylaxis outcomes, and an expert-informed tiered framework for infection prevention. (A) Relative proportion of infectious complications by pathogen category across the three canonical post-transplant periods, based on data from [24] and [25]. Proportions are illustrative of manuscript-reported data and are not derived from a formal meta-analysis. (B) CMV infection rates by study cohort and prophylactic regimen. Orange circles and squares represent African cohorts [25, 26]; blue symbols represent a high-income country cohort (Verghese et al., 2024). Circles denote valacyclovir (ValA) arms; squares denote valganciclovir (ValG) arms. The shaded band represents the high-income country (HIC) benchmark range (10–20%). Valacyclovir is approximately 6.5 times less expensive than valganciclovir in African settings (1,700 vs. 11,000 Egyptian pounds per 90-day course; [26]. (C) Expert-informed, context-adapted tiered prophylaxis and monitoring framework proposed for African transplant programmes, stratified by laboratory and clinical capacity. This framework is intended as a conceptual proposal rather than an evidence-based clinical guideline. BSI = bloodstream infection; CMV = cytomegalovirus; eGFR = estimated glomerular filtration rate; QNAT = quantitative nucleic acid test; SSI = surgical site infection; UTI = urinary tract infection; ValA = valacyclovir; ValG = valganciclovir
Limitations
This review has several limitations that should be acknowledged. First, as a scoping review, it does not employ systematic meta-analytic methods, and the findings cannot be pooled to generate summary estimates of infection incidence or prophylaxis efficacy across African settings. Second, the included studies are highly heterogeneous in design (retrospective cohorts, a single RCT, conference abstracts), population characteristics, immunosuppression protocols, prophylaxis regimens, and follow-up duration, limiting direct comparability. Third, the evidence base is geographically skewed: the majority of primary data derive from North African centres (Egypt and Morocco), with very limited data from sub-Saharan Africa and virtually no data from West or Central Africa. This geographic imbalance limits the generalisability of conclusions to the full African continent. Fourth, publication bias is a significant concern: transplant programmes with high infectious morbidity or poor outcomes may be less likely to publish their data, potentially leading to an underestimate of the true infectious burden across the continent. Fifth, the absence of standardised outcome definitions across studies (e.g., varying thresholds for CMV DNAemia, differing definitions of CMV disease) complicates cross-study comparisons. Sixth, while this review documents the occurrence of opportunistic fungal and parasitic infections in African KTR cohorts, the evidence base for antifungal and anti-parasitic prophylaxis practices across African transplant programmes is extremely sparse; no African centre has published systematic data on antifungal prophylaxis protocols, and the optimal approach to endemic parasitic infections (e.g., strongyloidiasis, cryptosporidiosis) in immunosuppressed African recipients remains undefined. Lastly, title and abstract screening and data charting were performed primarily by a single reviewer, without full dual independent screening. Although a second reviewer independently verified a random 20% sample of screened records, the absence of complete dual screening is a methodological limitation that may have introduced selection bias. Future scoping reviews in this area should employ dual independent screening with formal inter-rater reliability assessment.
Several clinically important pathogens are not addressed in depth in this review, including malaria, schistosomiasis, hepatitis B and C, and mpox. The absence of these pathogens from the primary inclusion data reflects a genuine evidence gap in the African transplant literature, particularly notable given the high background prevalence of HBV in sub-Saharan Africa [61] and the well-documented impact of HBV on transplant outcomes in other settings [62]. The absence of these pathogens from the primary included studies reflects the published literature: our search strategy employed broad infection terms (‘infect*’) and did not restrict by pathogen type; the absence of HBV, HCV, malaria, and mpox from the primary data therefore reflects the published literature rather than a search limitation.
These limitations underscore the urgent need for prospective, multicentre, registry-based data collection using harmonised outcome definitions across African transplant programmes.
Conclusions
Infectious complications are the dominant driver of morbidity and a leading cause of mortality in kidney transplant recipients across Africa. The epidemiological profile is shaped by a unique convergence of high endemic pathogen burden, near-universal CMV seropositivity, limited access to standard prophylactic antivirals, and constrained microbiological surveillance capacity. Bacterial UTIs dominate the early post-transplant period, while CMV, despite prophylaxis, remains a major threat in the intermediate period, with tissue-invasive disease conferring a 50% acute rejection rate in affected patients. Valacyclovir shows promise as a cost-effective alternative to valganciclovir for CMV prophylaxis in African settings, with encouraging efficacy data from a single Egyptian RCT and a Moroccan observational cohort; however, the evidence base remains limited in scope and geographic diversity, and larger multicentre African trials are needed before formal guideline adoption. Addressing the infectious burden in African KTRs requires not only context-adapted prophylaxis protocols but also investment in transplant registries, microbiological infrastructure, and healthcare financing mechanisms that make life-saving medications accessible to all patients. Critically, sustainable progress will also require investment in nephrology and transplant infectious disease workforce capacity, through regional training programmes, international partnerships, and the development of Africa-specific clinical guidelines, to ensure that the specialist expertise needed to prevent, diagnose, and manage infectious complications is embedded within African transplant programmes themselves.
Electronic Supplementary Material
Below is the link to the electronic supplementary material.
Supplementary Material 1: PRISMA-ScR Flow diagram
Acknowledgements
The authors thank the staff at the Medical and Scientific Research Centre, University of Ghana Medical Centre Limited, Accra, Ghana.
Abbreviations
- AMR
Antimicrobial resistance
- AJOL
African journals online
- BKV
BK polyomavirus
- CMV
Cytomegalovirus
- CKD
Chronic kidney disease
- ESKD
End-stage kidney disease
- HBV
Hepatitis B virus
- HCV
Hepatitis C virus
- HIV
Human immunodeficiency virus
- HPV
Human papillomavirus
- KTR
Kidney transplant recipient(s)
- KDIGO
Kidney disease: improving global outcomes
- LMIC
Low- and middle-income country/countries
- MDR
Multidrug-resistant
- PRISMA-ScR
Preferred reporting items for systematic reviews and meta-analyses extension for scoping reviews
- QNAT
Quantitative nucleic acid test
- RRT
Renal replacement therapy
- SOT
Solid organ transplant(ation)
- SSA
Sub-saharan africa
- TB
Tuberculosis
- TID
Transplant infectious disease
- UTI
Urinary tract infection
- VGC
Valganciclovir
- VAC
Valacyclovir
Author contributions
S.E.A: Conceptualization, Writing–original draft, Writing–review & editing. A.S. & M.N.A.A.L: Writing–original draft, Writing–review & editing. R.O: Writing–original draft. J.O.A., C.L.O & G.B.K: Writing–review & editing.
Funding
No funding was received for this review.
Data availability
All data supporting the findings of this review are derived from published studies cited in the reference list. No primary datasets were generated or analysed. The charted data underpinning all findings are presented in full in Table 1 of the manuscript. Requests for further information regarding the data sources or review methodology may be directed to the corresponding author, Dr. Sabastine Eugene Arthur, Medical and Scientific Research Centre, University of Ghana Medical Centre, Accra, Ghana (email: sarthur@ugmc.ug.edu.gh).
Declarations
Ethics approval and consent to participate
Not applicable. This scoping review is based entirely on previously published studies and did not involve the collection of primary data from human participants. No ethics approval or participant consent was required.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Supplementary Material 1: PRISMA-ScR Flow diagram
Data Availability Statement
All data supporting the findings of this review are derived from published studies cited in the reference list. No primary datasets were generated or analysed. The charted data underpinning all findings are presented in full in Table 1 of the manuscript. Requests for further information regarding the data sources or review methodology may be directed to the corresponding author, Dr. Sabastine Eugene Arthur, Medical and Scientific Research Centre, University of Ghana Medical Centre, Accra, Ghana (email: sarthur@ugmc.ug.edu.gh).
