CARDIOVASCULAR JOURNAL OF AFRICA • Volume 35, No 3, September – October 2024 AFRICA 163 Discussion The main finding of this study is that TRA did not decrease the incidence of post-PCI AKI compared to TFA in patients not complicated by major bleeding, acute heart failure or haemodynamic disturbance. This was further confirmed after PS matching of both groups. In addition to the conventional AKI definition (> 0.5 mg/dl or > 25% increase), different cut-off values for AKI yielded similar results in the matched population, although there was a trend towards less renal injury with TRA in the unmatched patients. Importantly, absolute and proportional changes in SCr level after intervention did not differ between TRA and TFA. Our analysis differs from previous ones in that it did not include patients with haemodynamic deterioration, acute heart failure and major bleeding. As these patients were extremely high risk, they were susceptible to deterioration in renal function, not only due to intervention, but also due to impaired renal haemodynamics. The majority of excluded patients during the study period developed AKI after the intervention. The pathophysiology of AKI after coronary interventions is multifactorial. It includes direct nephrotoxicity due to the contrast agent, systemic and renal haemodynamic conditions, and direct cholesterol/atheroma embolisation from the abdominal aorta.16 By excluding haemodynamic disturbances and major bleeding, and the fact that contrast volume in both access site groups was similar, we can conclude that the effect of cholesterol/ atherosclerotic embolism to the renal arteries on the development of AKI after transfemoral PCI was either minimal or absent. We found a 10.3% incidence of AKI post-PCI, according to the conventional definition. The rate of AKI was in line with published studies where the majority of patients had a normal pre-procedural renal function. The determinants of AKI were age, female gender, baseline SCr level, baseline eGFR and contrast volume. Female gender was not among the commonly reported determinants of AKI.17 Our analysis did not reveal other conventional risk factors such as diabetes or haemoglobin level. This might be related to the moderate size of the study. Some studies have reported a reduction in AKI with the TRA, however, the protective effect of TRA came from a reduction in bleeding events. A meta-analysis of six observational studies concluded that the TRA decreased incidence of post-PCI AKI (OR 0.51, 95% CI 0.39–0.67, p < 0.0001) compared to the TFA.10 The authors reported two co-variates: it was more pronounced in patients with STEMI, and the protective role of the TRA was associated with a reduction in access-site bleeding. AKI-MATRIX was a randomised, multi-centre study comparing TRA and TFA in patients with ACS. AKI was defined as 0.5 mg/dl or 25% increase in SCr level. The incidence of AKI was less with TRA (15.4 vs 17.3%). The authors reported TRA mainly reduced incidence of AKI by reducing bleeding events. When drop in haemoglobin level and blood transfusion were included in the multivariate analysis, the association of TRA with AKI was lost.11 In a PS-matched retrospective analysis of patients undergoing PCI for myocardial infarction, TRA was not found to be independently associated with AKI in both the non-matched and PS-matched cohorts.12 The authors concluded that the lower incidence of AKI in TRA might be influenced substantially by confounding factors, especially bleeding. Table 2. Multivariate logistic regression analysis of AKI Variables Overall study population (n = 339) Matched study population (n = 182) X2 p-value Odds ratio 95% CI X2 p-value Odds ratio 95% CI Age 5.648 0.017 1.055 1.01–1.103 4.379 0.036 1.075 1 005–1 151 Female gender 8.447 0.004 7.284 1.909–27.791 4.417 0.036 5.856 1 127–30 438 eGFR 10.296 0.001 1.065 1.025–1.107 8.683 0.003 1.051 1 017–1 087 Contrast volume 5.958 0.015 1.005 1.001–1.009 4.036 0.045 1.006 1.000–1.012 Baseline creatinine 4.254 0.039 21.212 1.164–386.617 CI: confidence intervals, eGFR: estimated glomerular filtration rate. Table 3. Secondary renal outcomes of TRA vs TFA in the overall study and PS-matched population Variables Overall study population (n = 339) PS-matched study population (n = 182) TRA TFA p-value TRA TFA p-value Post-PCI SCr 0.89 (0.79–1.01) 0.94 (0.78–1.10) 0.063 0.89 (0.79–1.01) 0.96 (0.79–1.12) 0.099 Change in SCr, mg/dl 0.04 (–0.02–0.09) 0.06 (–0.04–0.14) 0.212 0.02 (–0.04–0.07) 0.06 (–0.06–0.13) 0.199 Change in SCr, % 3.8 (–2.6–10.0) 6.0 (–5.0–14.7) 0.344 2.5 (–4.5–9.3) 5.5 (–6.0–13.5) 0.274 SCr increase > 0.3, mg/dl 4 (3.0) 16 (7.8) 0.097 4 (4.4) 6 (6.6) 0.747 SCr increase > 0.5, mg/dl 1 (0.7) 9 (4.4) 0.096 1 (1.1) 2 (2.2) 1.000 SCr increase > 25% 12 (9.0) 23 (11.2) 0.503 9 (9.9) 7 (7.7) 0.601 SCr increase > 50% 0 (0) 10 (4.9) 0.007 0 (0) 3 (3.3) 0.246 PCI: percutaneous coronary intervention, SCr: serum creatinine, TRA: transradial approach, TFA: transfemoral approach. Overall study PS-matched 9.0% p = 0.503 p = 0.601 11.2% 9.9% 7.7% TRA TFA Fig. 1. The incidence of AKI following PCI with the TRA versus TFA in the overall study and PS-matched patients.
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