Association of periprocedural phentolamine infusion with favorable outcome in patients with chronic kidney disease and chronic coronary syndrome undergoing coronary catheterization: a prospective randomized controlled pilot study

Mohamed Abo Hamila, Helmy El Ghawaby, Mohamed Zaki, Mohamed Soliman, Khaled Gabr, Mohamed Abo Hamila, Helmy El Ghawaby, Mohamed Zaki, Mohamed Soliman, Khaled Gabr

Abstract

Background: Chronic kidney disease (CKD) is a major risk factor for contrast induced acute kidney injury (CI-AKI) in chronic coronary syndrome (CCS) patients undergoing coronary catheterization. We aimed to evaluate the efficacy of phentolamine in prevention of CI-AKI in CKD and CCS patients undergoing percutaneous coronary catheterization for diagnostic angiography ± stenting.

Methods: Participants with CKD and CCS planned for percutaneous coronary catheterization were included, while participants with normal kidney functions were excluded. A consecutive sample of 107 participants (mean age 58.62 ± 8.96 years, 64.5% males) was selected, underwent diagnostic coronary angiography or percutaneous coronary intervention, and received either conventional CI-AKI prevention strategy (group 1) or periprocedural phentolamine and conventional CI-AKI prevention strategy (group 2).

Results: The percentages of study participants who had CI-AKI were 82.9% for group 1 and 17.1% for group 2, respectively. The incidence rate of CI-AKI was significantly lower in group 2 versus group 1 (p < 0.001). The urine output (ml/kg) and the urine output (ml/hour) within 72 hours post procedure was significantly higher in group 2 versus group 1 (t(105) = - 0.69, p < 0.001, t(105) = - 52.46, p < 0.001, respectively), the peak change in serum creatinine and the percentage of change relative to the baseline serum creatinine at 72 hours post procedure was significantly lower in group 2 versus group 1 (t(102) = 0.2, p 0.018, t(102) = 23.54, p < 0.001, respectively), and the incidence rate of major adverse cardiac and cerebrovascular events within 90 days post procedure was significantly lower in group 2 versus group 1 (t(102) = 1.168, P < 0.001), respectively. There was a statistically significant association of periprocedural phentolamine infusion with prevention of CI-AKI (OR = 0.041, 95% CI 0.0149-0.1128, P < 0.0001).

Conclusion: Our study highlights the potential role of phentolamine for protection of the kidney in CKD patients planned for coronary catheterization.

Trial registration: Pan African Clinical Trial Registry Number: PACTR202209493847741. Date of Trial Registration: 22/09/2022.

Keywords: Contrast induced acute kidney injury; Coronary catheterization; Phentolamine.

Conflict of interest statement

The authors have no conflicts and/or competing interests to disclose.

© 2022. The Author(s).

Figures

Fig. 1
Fig. 1
Case Screening and Processing Flow Chart showing case screening and processing
Fig. 2
Fig. 2
Histogram showing the change in urine output (ml/kg) in group 1 (mean urine output 0.64 ± 0.31 ml/kg) versus group 2 (mean urine output 1.33 ± 0.48 ml/kg) and the change in urine output (ml/hour) in group 1 (mean urine output 56.54 ± 28.14 ml/hr) versus group 2 (mean urine output 109.00 ± 39.20 ml/hr) within 72 hours post procedure
Fig. 3
Fig. 3
Line chart showing the percentage of change in serum creatinine relative to the baseline serum creatinine in group 1 at 72 hours post procedure (17.11 ± 15.93), 30 days post procedure (9.12 ± 23.06), and 90 days post procedure (9.10 ± 22.22) versus the percentage of change in serum creatinine relative to the baseline serum creatinine in group 2 at 72 hours post procedure (−6.43 ± 11.12), 30 days post procedure (−8.34 ± 15.83), and 90 days post procedure (−9.03 ± 15.59)
Fig. 4
Fig. 4
Line chart showing the percentage of change in eGFR relative to the baseline eGFR in group 1 at 72 hours post procedure (−11.41 ± 12.33), 30 days post procedure (− 8.23 ± 16.90), and 90 days post procedure (− 8.16 ± 17.07) versus the percentage of change in eGFR relative to the baseline eGFR in group 2 at 72 hours post procedure (7.93 ± 13.05), 30 days post procedure (8.28 ± 20.82), and 90 days post procedure (7.55 ± 24.93)

References

    1. Parfrey P. The clinical epidemiology of contrast-induced nephropathy. Cardiovasc Intervent Radiol. 2005;28(Suppl 2):S3–S11. doi: 10.1007/s00270-005-0196-8.
    1. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105(19):2259–2264. doi: 10.1161/01.cir.0000016043.87291.33.
    1. Chong E, Poh KK, Liang S, Tan HC. Risk factors and clinical outcomes for contrast-induced nephropathy after percutaneous coronary intervention in patients with normal serum creatinine. Ann Acad Med Singap. 2010;39(5):374–380.
    1. Bartholomew BA, Harjai KJ, Dukkipati S, et al. Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol. 2004;93(12):1515–1519. doi: 10.1016/j.amjcard.2004.03.008.
    1. Hall KA, Wong RW, Hunter GC, et al. Contrast-induced nephrotoxicity: the effects of vasodilator therapy. J Surg Res. 1992;53(4):317–320. doi: 10.1016/0022-4804(92)90054-4.
    1. Feldkamp T, Kribben A. Contrast media induced nephropathy: definition, incidence, outcome, pathophysiology, risk factors and prevention. Minerva Med. 2008;99(2):177–196.
    1. Nawa T, Nishigaki K, Kinomura Y, et al. Continuous intravenous infusion of nicorandil for 4 hours before and 24 hours after percutaneous coronary intervention protects against contrast-induced nephropathy in patients with poor renal function. Int J Cardiol. 2015;195:228–234. doi: 10.1016/j.ijcard.2015.05.078.
    1. Mahfoud F, Cremers B, Janker J, et al. Renal hemodynamics and renal function after catheter-based renal sympathetic denervation in patients with resistant hypertension. Hypertension. 2012;60(2):419–424. doi: 10.1161/HYPERTENSIONAHA.112.193870.
    1. Schlant RC, Adolph RJ, DiMarco JP, Dreifus LS, Dunn MI, Fisch C, Garson A, Jr, Haywood LJ, Levine HJ, Murray JA, et al. Guidelines for electrocardiography. A report of the American College of Cardiology/American Heart Association task force on assessment of diagnostic and therapeutic cardiovascular procedures (committee on electrocardiography) Circulation. 1992;85(3):1221–1228. doi: 10.1161/01.cir.85.3.1221.
    1. Ronco C, McCullough P, Anker SD, et al. Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative. Eur Heart J. 2010;31(6):703–711. doi: 10.1093/eurheartj/ehp507.
    1. Levey AS, de Jong PE, Coresh J, et al. The definition, classification and prognosis of chronic kidney disease: a KDIGO controversis conference report. Kidney Int. 2011;80:17-28.
    1. Chan YH. Biostatistics 102: quantitative data - Parametric & non-parametric Tests. Singap Med J. 2003;44(8):391–396.
    1. Chan YH. Biostatistics 103: qualitative data –tests of Independence. Singap Med J. 2003;44(10):498–503.
    1. Jager KJ, Zoccali C, Macleod A, et al. Confounding: what it is and how to deal with it. Kidney Int. 2008;73:256–260. doi: 10.1038/sj.ki.5002650.
    1. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med. 2006;354(26):2773–2782. doi: 10.1056/NEJMoa054209.
    1. Su X, Xie X, Liu L, et al. Comparative effectiveness of 12 treatment strategies for preventing contrast-induced acute kidney injury: a systematic review and Bayesian network Meta-analysis. Am J Kidney Dis. 2017;69(1):69–77. doi: 10.1053/j.ajkd.2016.07.033.
    1. Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after angiography with sodium bicarbonate and Acetylcysteine. N Engl J Med. 2018;378(7):603–614. doi: 10.1056/NEJMoa1710933.
    1. Xing K, Fu X, Wang Y, et al. Effect of rhBNP on renal function in STEMI-HF patients with mild renal insufficiency undergoing primary PCI. Heart Vessel. 2016;31(4):490–498. doi: 10.1007/s00380-015-0642-8.

Source: PubMed

Patrocinadores y Colaboradores

Condiciones médicas

Intervenciones de drogas

3
Suscribir