ABSTRACT
Iodinated Contrast Media (CM) has a plethora of applications in routine non-invasive or percutaneous invasive imaging examinations and therapeutic interventions. Unfortunately, the use of CM is not without complications, with contrast-induced acute kidney injury (CI-AKI) being among the most severe. CI-AKI is a syndrome defined as a rapid development of renal impairment after a few days of CM endovascular injection, without the presence of any other underlying related pathologies. Although mostly transient and reversible, for a subgroup of patients with comorbidities related to renal failure, CI-AKI is directly leading to longer hospitalization, elevated rates of morbidity and mortality, as well as the increased cost of funding. Thus, a need for classification in accordance with clinical and peri-procedural criteria is emerged. This would be very useful for CI-AKI patients in order to predict the ones who would have the greatest advantage from the application of preventive strategies. This article provides a practical review of the recent evidence concerning CI-AKI incidence, diagnosis, and sheds light on prevention methods for reducing contrast use and avoiding AKI during endovascular procedures. In conclusion, despite the lack of a specific treatment protocol, cautious screening, assessment, identification of the high-risk patients, and thus the application of simple interventions -concerning modifiable risk factors- can significantly reduce CI-AKI risk.
Subject(s)
Acute Kidney Injury/chemically induced , Acute Kidney Injury/prevention & control , Contrast Media/adverse effects , Endovascular Procedures/adverse effects , Humans , Incidence , Risk FactorsABSTRACT
Background: Ideal dosing for the preservative-free (PF) tafluprost/timolol fixed combination (TTFC) remains to be elucidated. Research design and methods: This study was a prospective, observer-masked, placebo-controlled, crossover, comparison in 42 consecutive open-angle glaucoma patients whose intraocular pressure (IOP) was insufficiently controlled with preserved latanoprost monotherapy (mean 24-h IOP >20 mmHg). Patients were randomized to either morning (08:00) or evening (20:00) PF TTFC for 3 months and then crossed over. After each treatment period, patients underwent habitual 24-h IOP monitoring with Goldmann tonometry in the sitting position (at 10:00, 14:00, 18:00, and 22:00) and Perkins tonometry in the supine position (at 02:00 and 06:00). Results: Mean 24-h IOP on latanoprost was 22.2±3.9 mmHg. Both PF TTFC dosing regimens obtained greater reduction in mean 24-h, daytime, nighttime, and peak 24-h IOP (P < 0.001). Evening dosing provided tighter 24-h IOP fluctuation versus latanoprost (P < 0.001). Evening dosing was superior to morning dosing at four time points (P < 0.01), for the mean daytime IOP (P < 0.001) and mean 24-h IOP fluctuation (P < 0.001). Hyperemia was more common with preserved latanoprost (21.4 vs. 7.1%; P = 0.031). Patients (n = 19; 45%) preferred evening dosing. Conclusions: PF TTFC provided greater 24-h IOP control and less hyperemia compared with preserved latanoprost. Evening administration of this novel medication offered superior 24-h efficacy. Trial registration: Clinicaltrials.gov (NCT03612817).