The development of renal insufficiency after percutaneous coronary intervention (PCI) is associated with increases in morbidity and mortality. Recent studies have reported that hyperuricemia (HU) results in hypertension, intrarenal vascular disease, and renal injury. We postulated that HU contributes to progressive renal disease after PCI. We studied 139 patients with chronic kidney disease (CKD) undergoing elective PCI including 59 HU patients. We assessed the relationship between HU and the development of renal insufficiency after PCI by estimating traditional contrast-induced nephropathy (CIN) and persistent postprocedural nephropathy (PPN) defined as an increase in creatinine ≥0.2 mg/dl of the baseline value 2 weeks after procedure. CIN and PPN were seen in 6.5 and 28.8% respectively. The incidence of PPN was higher in HU patients than in non-HU patients (p < 0.001) although the incidence of CIN was not significantly different between the two groups. PPN was more frequently observed in hyperuricemic patients irrespective of association with hypertension (with and without hypertension, p < 0.001 and p = 0.034, respectively). By univariate analysis, HU and hypertension are associated with PPN although there was no significant predictor of CIN in this study. Multivariate analysis showed HU and hypertension were independent predictors of PPN. HU is a predictor of slow and mild development of renal insufficiency after PCI in patients with CKD.
Female sex, secondary prevention, and experience of ICD shock therapy are important risk factors affecting shock anxiety in Japanese patients. Attention should be paid to the after-effects of ICD shock in these patients, regardless of the shock type, with particular attention to women and patients who require secondary prevention.
In revascularized patients with severe LV dysfunction, the presence of a large amount of perfusionmetabolic mismatch evaluated by Tl-201 and BMIPP imaging identifies patients with the best prognosis.
OBJECTIVE
Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes.
RESEARCH DESIGN AND METHODS
Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to <75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c <7.5% (58 mmol/mol) or ≥7.5%.
RESULTS
Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c <7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia.
CONCLUSIONS
Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.
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