Acute Kidney Injury After Cardiac Surgery in Low‑ and Middle‑Income Countries

Incidence in High‑Income Countries

Large registry‑based and multicenter cohort studies from North America and Europe consistently report CSA‑AKI incidence rates between 20% and 35% when contemporary KDIGO or RIFLE criteria are applied [2,3,7]. Data from high‑volume centers demonstrate that while the overall incidence of AKI has remained relatively stable over time, the distribution is skewed toward milder stages, with only 1%–2% of patients progressing to dialysis‑requiring AKI [2,3]. In the Cleveland Clinic cohort of over 33,000 cardiac surgical patients, dialysis‑requiring CSA‑AKI occurred in approximately 1% overall, though risk varied markedly across predefined strata, reaching >20% in the highest‑risk patients [2].

Importantly, outcomes in HIC settings illustrate a dissociation between incidence and mortality. Despite stable AKI rates, AKI‑associated mortality has declined, reflecting improvements in perioperative monitoring, early detection, and timely access to advanced renal support, including continuous renal replacement therapy (CRRT) [2,7]. Nevertheless, even in these high‑resource environments, CSA‑AKI remains prognostically significant. Cohort data demonstrate a graded, stepwise increase in both short‑ and long‑term mortality across AKI severity, with excess mortality persisting even after apparent renal recovery [2,3]. These findings establish a critical benchmark: optimal detection and rescue reduce—but do not eliminate—the mortality burden of CSA‑AKI.

Incidence in Low‑ and Middle‑Income Countries

In contrast, studies from LMIC settings consistently report higher CSA‑AKI incidence, commonly ranging from 30% to over 40%, alongside a disproportionate burden of advanced disease at presentation [9–11,14–16]. Retrospective and prospective cohorts from Brazil, China, South Africa, India, and sub‑Saharan Africa demonstrate not only higher overall AKI rates, but also a greater representation of KDIGO stage 2 and 3 disease, suggesting delayed recognition and limited perioperative surveillance [9–11,14–16].

Data from public‑sector cardiac centers in South Africa and Brazil further highlight the downstream consequences of these patterns. Although rates of RRT remain low (approximately 1–3%), mortality among patients with severe CSA‑AKI is strikingly high, with stage 3 AKI associated with in‑hospital or 30‑day mortality exceeding 40–55% in several cohorts [10,11]. This mirrors the mortality observed in dialysis‑requiring AKI in HICs, but occurs in contexts where RRT access is constrained, initiation is delayed, and CRRT is often unavailable.

Direct comparisons between HIC and LMIC cohorts are complicated by heterogeneity in case mix, reporting practices, and monitoring intensity. However, a consistent epidemiologic signal emerges: patients in LMICs present later, with more severe renal injury, and experience substantially worse outcomes, even after accounting for comorbidity burden and surgical complexity [10,11]. Limited access to timely laboratory testing, reduced intraoperative hemodynamic monitoring, workforce constraints, and restricted critical care capacity likely contribute to both AKI progression and excess mortality.

Baseline renal reserve and comorbidity burden

Baseline renal vulnerability is a critical determinant of CSA‑AKI risk, and substantial differences exist between patients undergoing cardiac surgery in HICs and LMICs. In HIC settings, structured preoperative assessment—including routine estimation of glomerular filtration rate (eGFR), optimization of volume status, and medication review—allows identification and mitigation of renal risk prior to surgery [1,2]. In contrast, cohorts from LMICs consistently demonstrate a high prevalence of unrecognized or underdocumented chronic kidney disease (CKD), hypertension, and diabetes mellitus at the time of surgical admission, reflecting broader gaps in primary and secondary preventive care [11,17,18].

Data summarized in Table 1 illustrate that LMIC cardiac surgery cohorts report AKI incidences ranging from approximately 28% to over 40%, with a disproportionate burden of KDIGO stage 2–3 disease at diagnosis, compared with predominantly stage 1 presentations in HIC cohorts. Public‑sector studies from India and sub‑Saharan Africa further demonstrate that impaired baseline renal function is frequently identified only during preoperative admission rather than through longitudinal outpatient follow‑up [10]. This diminished renal reserve reduces physiological tolerance to perioperative hemodynamic stress and lowers the threshold for progression from transient creatinine elevation to established AKI. Importantly, these baseline differences are rarely captured in risk prediction models derived from HIC populations, contributing to systematic underestimation of AKI risk in LMIC patients.

Late surgical referral and advanced cardiac disease

Late referral for definitive cardiac surgery further compounds renal vulnerability in LMIC settings. Patients frequently present with advanced valvular disease, severe ventricular dysfunction, and chronic congestive states, all of which are independently associated with renal hypoperfusion and venous congestion [9,19,20]. Prolonged exposure to low cardiac output and elevated central venous pressure results in subclinical renal injury even before the operative insult occurs, effectively narrowing the margin for perioperative renal resilience.

Evidence from South African and Indian cardiac surgery cohorts demonstrates that many patients arrive for surgery already in a state of pre‑existing cardiorenal stress, rendering them particularly susceptible to CSA‑AKI despite technically successful procedures [10]. As reflected in Table 1, these cohorts not only exhibit higher AKI incidence but also markedly higher AKI‑associated mortality, especially among patients progressing to KDIGO stage 3 disease. In this context, postoperative AKI often represents the culmination of a chronic pathophysiological trajectory rather than an isolated perioperative complication.

Cardiopulmonary bypass exposure and perfusion strategies

CPB remains a central contributor to CSA‑AKI through mechanisms including non‑pulsatile flow, hemodilution, systemic inflammatory activation, and renal hypoperfusion. In HIC centers, advances in perfusion technology—such as goal‑directed perfusion, higher indexed pump flow targets, tighter hematocrit control, and near‑continuous monitoring of perfusion indices—have been increasingly adopted to mitigate renal risk during CPB [1,21]. Registry‑based and multicenter cohort data from these settings demonstrate that, despite stable AKI incidence over time, progression to severe AKI and dialysis‑requiring renal failure has declined in parallel with improvements in intraoperative perfusion and rescue strategies.

In contrast, data from LMIC cardiac surgery cohorts summarized in Table 1 consistently demonstrate higher proportions of moderate‑to‑severe AKI at diagnosis, suggesting greater cumulative intraoperative renal insult. Longer CPB times are commonly reported in these settings, reflecting greater disease complexity at presentation, workflow inefficiencies, and limited access to minimally invasive or off‑pump techniques [9,10,22]. Studies from Brazil, China, South Africa, and India report AKI incidences ranging from approximately 28% to over 40%, with KDIGO stage 2–3 disease accounting for a substantial proportion of cases—patterns that are closely aligned with prolonged CPB exposure and limited intraoperative renal protection. Additionally, constraints on disposables, perfusion equipment, and staffing may limit implementation of renal‑protective strategies that are routine in high‑resource environments, amplifying susceptibility to CPB‑related injury.

Intraoperative monitoring limitations

Continuous hemodynamic monitoring plays a critical role in preventing renal hypoperfusion during cardiac surgery. In HIC operating theatres, invasive arterial pressure monitoring, central venous pressure trend analysis, and—in selected centers—cerebral or renal near‑infrared spectroscopy (NIRS) are routinely used to guide perfusion and vasoactive therapy in real time [21,23]. These approaches facilitate early detection of occult hypotension, low cardiac output states, and perfusion–pressure mismatch, allowing timely corrective interventions that limit cumulative renal injury.

By contrast, intraoperative monitoring in many LMIC cardiac centers relies on intermittent measurements with limited physiological granularity. Advanced adjuncts such as renal oximetry are rarely available, and perfusion targets may be guided by population‑based norms rather than patient‑specific physiology. The tabled evidence demonstrates that LMIC cohorts not only experience higher AKI incidence but also a marked escalation in mortality once severe AKI develops, particularly among patients requiring RRT. This pattern is consistent with unrecognized or inadequately corrected episodes of intraoperative renal hypoperfusion, which accumulate over prolonged CPB runs and manifest postoperatively as advanced AKI.

Timing of AKI recognition

Early recognition of AKI is a cornerstone of renal‑protective care following cardiac surgery. In HIC cardiac ICUs, standardized postoperative pathways incorporating frequent serum creatinine measurement urine output monitoring, and implementation of KDIGO‑based care bundles enable timely diagnosis and early supportive intervention [2,24]. These protocols facilitate early hemodynamic optimization, avoidance of nephrotoxins, adjustment of fluid and vasoactive therapy, and early nephrology consultation, contributing to improved renal recovery and reduced progression to dialysis‑requiring AKI.

In contrast, data synthesized in Table 1 demonstrate that postoperative AKI in LMIC settings is frequently recognized later in its clinical course. Limited laboratory availability, reduced testing frequency, batching of samples, and staffing constraints commonly delay detection until overt oliguria or marked creatinine elevation has occurred [7,10]. This delayed recognition aligns with the consistently higher representation of KDIGO stage 2–3 disease and dialysis‑requiring AKI reported across LMIC cardiac surgery cohorts.

The tabled evidence further indicates that this delay in recognition is not merely diagnostic but translates directly into worse outcomes. LMIC studies consistently report higher AKI‑attributable mortality compared with HIC cohorts, even when overall AKI incidence is comparable. These findings suggest that the timing of detection—rather than AKI occurrence alone—is a critical determinant of prognosis following cardiac surgery.

Biomarkers and early detection tools

Novel biomarkers such as neutrophil gelatinase‑associated lipocalin (NGAL) and cystatin C have shown promise for early AKI detection in cardiac surgery populations, particularly in HIC research settings [25,26]. These biomarkers may identify renal injury hours to days before creatinine rises, theoretically expanding the window for preventive intervention.

However, as reflected in Table 2, these assays remain largely unavailable in LMIC clinical practice due to cost, infrastructure requirements, and limited laboratory capacity. As a result, clinicians in resource‑constrained environments continue to rely almost exclusively on serum creatinine—a late and insensitive marker of renal injury. This dependence reinforces diagnostic delay, particularly in the immediate postoperative period when renal injury may already be evolving despite preserved urine output.

The clinical consequence of this delay is a narrowing of the therapeutic window in which AKI may be reversible. By the time creatinine rises are detected, renal injury may already be established, limiting the effectiveness of supportive measures and increasing the likelihood of progression to dialysis‑requiring failure. This pattern is consistently reflected in the tabled LMIC cohorts, where delayed detection is closely coupled with higher rates of severe AKI, limited renal recovery, and excess mortality.

Availability of renal replacement therapy

Among patients who develop severe CSA‑AKI, access to timely RRT represents the single most important determinant of survival. In high‑income settings, escalation to RRT—most commonly in the form of CRRT—is routinely available within cardiac ICUs, supported by trained staff, dedicated machines, and established protocols for early initiation [1,2,27]. As reflected in the studies summarized in Table 1, this capacity allows for hemodynamic stabilization, controlled fluid balance, and metabolic support during periods of cardiac and renal instability, attenuating progression from severe AKI to irreversible multiorgan failure.

In contrast, Table 2 highlights that access to RRT in LMICs is frequently constrained by structural, logistical, and economic limitations. Public‑sector hospitals in sub‑Saharan Africa and South Asia report limited dialysis capacity that is often shared across multiple ICUs and medical wards, resulting in prioritization driven by bed availability, staffing, and affordability rather than clinical indication alone [10,11,18]. In this context, patients with CSA‑AKI may experience prolonged delays before dialysis initiation or may not receive RRT at all despite meeting accepted criteria.

The tabled evidence further demonstrates that modality availability differs substantially between settings. While CRRT is the dominant modality in HIC cardiac ICUs, LMIC centers rely predominantly on intermittent hemodialysis, often delivered in unstable postoperative patients due to infrastructure limitations. This mismatch between patient physiology and dialysis modality contributes to poor hemodynamic tolerance and limits the ability to provide sustained renal support during periods of vasoplegia or low cardiac output, as consistently noted across LMIC cohorts.

Crucially, outcome data summarized in Table 1 show that dialysis‑requiring CSA‑AKI in LMICs is associated with disproportionately high mortality, frequently exceeding 50%, particularly in public‑sector cardiac surgery programs [10]. These mortality rates contrast sharply with those reported in HIC cohorts, where earlier initiation, continuous modalities, and integrated critical care support mitigate—but do not eliminate—the lethality of severe AKI. The convergence of delayed initiation, intermittent therapy, and constrained rescue capacity positions dialysis‑requiring CSA‑AKI as a high‑mortality phenotype in LMIC settings.

Taken together, these findings indicate that differences in rescue capacity, rather than AKI incidence alone, drive much of the observed mortality gap between LMICs and HICs. Access to timely, appropriate RRT emerges from the tabulated data as the central determinant of survival once severe CSA‑AKI has developed, underscoring the role of AKI as a marker of health‑system performance rather than an isolated postoperative complication.

Timing and modality of RRT

Beyond availability, the timing and modality of RRT differ substantially between healthcare settings, with important implications for outcomes after cardiac surgery. In HIC cardiac ICUs, CRRT is favored for hemodynamically unstable postoperative patients, allowing gradual solute clearance, precise fluid balance, and avoidance of abrupt intravascular shifts [2,27]. Early initiation strategies—particularly in the context of fluid overload, refractory metabolic derangements, or evolving multiorgan dysfunction—are facilitated by protocolized care pathways and dedicated resources, and have been associated with improved hemodynamic tolerance and, in selected studies, better outcomes [14].

In LMICs, intermittent hemodialysis remains the predominant RRT modality due to lower cost and reduced infrastructure requirements. However, intermittent therapy is frequently poorly tolerated in vasoplegic or low‑output states common after cardiac surgery, resulting in intradialytic hypotension, treatment interruption, or suboptimal solute and fluid clearance [18]. These limitations are compounded by delayed initiation, as patients often reach thresholds for RRT only after marked metabolic derangement and established multiorgan dysfunction, by which time physiological reserve for recovery is substantially reduced.

The tabulated evidence highlights that differences in modality selection are closely linked to differences in timing. In HIC cohorts, continuous modalities permit earlier escalation of renal support during evolving injury, whereas in LMIC settings, initiation of RRT is frequently deferred until overt, late‑stage indications emerge, reflecting constrained capacity and prioritization pressures. As a result, dialysis initiation in LMIC cardiac ICUs commonly occurs later in the disease trajectory, when renal injury is less reversible and systemic complications are already established.

Critically, mortality differences between HIC and LMIC cardiac surgery populations appear to be driven less by how often AKI occurs and more by whether patients with severe AKI can be effectively rescued once injury has developed. The convergence of delayed initiation, reliance on intermittent modalities, and limited ability to deliver sustained renal support positions dialysis‑requiring CSA‑AKI as a disproportionately lethal complication in resource‑constrained settings.

AKI‑attributable mortality

Across all healthcare settings, CSA‑AKI is independently associated with increased mortality in a graded fashion according to severity. Large HIC cohorts consistently demonstrate stepwise increases in both in‑hospital and long‑term mortality with each advancing AKI stage, even after adjustment for baseline comorbidity burden and operative complexity [3,6,13]. Importantly, improvements in perioperative surveillance, hemodynamic management, and access to advanced critical care have translated into improved survival among patients with mild to moderate AKI in high‑resource environments over time.

In contrast, mortality associated with CSA‑AKI in LMIC settings remains substantially higher at comparable stages of renal injury. Cohort studies from Brazil, India, China, and South Africa consistently report elevated case‑fatality rates per AKI stage, with dialysis‑requiring AKI emerging as a particularly lethal phenotype [5,9–11,15]. Across these settings, mortality frequently exceeds 40–50% once RRT is required, a pattern that persists even when standardized definitions such as KDIGO are applied. This divergence highlights that outcome disparities are driven predominantly by post‑diagnostic care capacity—including delayed detection, limited monitoring, and restricted access to sustained renal support—rather than by differences in diagnostic classification alone.

The tabulated data further demonstrate that while AKI incidence may be broadly similar across income settings, progression to advanced stages and death occurs more frequently in LMIC cohorts. These findings support the concept of CSA‑AKI as a condition in which health‑system responsiveness, rather than biological susceptibility, is the dominant determinant of survival once injury has occurred.

Length of stay and opportunity cost

CSA‑AKI is also associated with prolonged ICU and hospital length of stay across all healthcare systems. In HICs, this increase in length of stay primarily translates into higher resource utilization and cost but is often accommodated within well‑resourced critical care infrastructures, supported by step‑down facilities and established discharge pathways [6,13]. Consequently, prolonged admission does not necessarily translate into system‑level congestion or access limitation.

In LMIC settings, however, prolonged ICU occupancy by patients with CSA‑AKI carries a substantial opportunity cost. Data from public‑sector hospitals demonstrate that delayed renal recovery, limited access to step‑down care, and slow escalation to definitive therapies—particularly RRT—result in disproportionately long ICU stays despite overall resource scarcity [10,18]. This paradox, whereby patients remain in high‑acuity beds longer despite fewer available resources, exacerbates existing bed shortages and constrains access for other critically ill surgical and medical patients.

The tabulated evidence underscores that prolonged length of stay in LMICs is not simply a marker of illness severity but reflects systemic inefficiencies in escalation, rescue, and recovery pathways. As a result, the burden of CSA‑AKI in resource‑limited settings extends beyond individual patient outcomes to exert a measurable strain on already constrained critical care systems.