Acute kidney injury (AKI) is a common clinical syndrome characterized by a sudden decline in or loss of kidney function. AKI is not only associated with substantial morbidity and mortality but also with increased risk of chronic kidney disease (CKD). AKI is classically defined and staged based on serum creatinine concentration and urine output rates. The etiology of AKI is conceptually classified into three general categories: prerenal, intrarenal, and postrenal. Although this classification may be useful for establishing a differential diagnosis, AKI has mostly multifactorial, and pathophysiologic features that can be divided into different categories. Acute tubular necrosis, caused by either ischemia or nephrotoxicity, is common in the setting of AKI. The timely and accurate identification of AKI and a better understanding of the pathophysiological mechanisms that cause kidney dysfunction are essential. In this review, we consider various medical causes of AKI and summarize the most recent updates in the pathogenesis of AKI.

Hyperglycaemia is directly involved in causing long-term diabetic complications. The non-enzymatic glycation of proteins, yielding irreversible advanced glycation end products and advanced glycation end products-derived protein crosslinking, participates in the development of diabetic complications, such as diabetic nephropathy. Diabetic nephropathy is becoming a major medical problem with increasing numbers of these patients progressing to end stage renal disease, thus requiring renal replacement therapy. While several interventions may slow the development and progression of diabetic nephropathy, there is no effective treatment to prevent or reverse the disease. Pimagedine (aminoguanidine HCl) has been shown to be an effective agent in reducing the severity of the structural and functional alterations associated with experimental diabetic nephropathy. Preliminary studies suggest a beneficial effect of pimagedine in treating patients with diabetic nephropathy. In summary, these observations support a rol...

Along with the increase in aging of our population, the proportion of older patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) is on the rise as a result of the accumulation of comorbidities as well as biological processes associated with aging. Older patients with acute kidney injury (AKI) comprise an increasing proportion of patients with CKD/ESRD as well. In this review, we will discuss biological processes of aging that predispose patients to AKI and CKD.

Nonsteroidal mineralocorticoid receptor antagonists (MRAs) present a promising therapeutic option in cardiorenal diseases, mitigating the limitations of steroidal MRAs. Finerenone, a third-generation nonsteroidal MRA, has demonstrated beneficial effects in heart failure (HF) and chronic kidney disease (CKD). Clinical trials, including FIDELIO-DKD and FIGARO-DKD, revealed finerenone’s efficacy in improving kidney and cardiovascular (CV) outcomes. Patients with CKD and type 2 diabetes (T2DM) on finerenone experienced reduced rates of cardiovascular events, including hospitalization for HF. However, these trials excluded symptomatic HF patients, focusing on asymptomatic or early-stage HF. The ongoing FINEARTS-HF trial evaluates finerenone in HF with preserved ejection fraction (HFpEF). Additionally, studies exploring finerenone and sodium-glucose cotransporter 2 (SGLT2) inhibitors’ (Empagliflozin) combination effects in CKD and T2DM (CONFIDENCE) and the selective MR modulator AZD9977 with another SGLT2 inhibitor (dapagliflozin) in HF and CKD (MIRACLE) aim to expand treatment options. While SGLT-2 inhibitors were shown to reduce hyperkalemia risk in FIDELIO-DKD and potentially lower new-onset HF incidence in FIGARO-DKD, further research is essential. So far, the evidence for the beneficial effect of finerenone in the spectrum of cardiorenal diseases is based only on the results of studies conducted in patients with T2DM, and clinical trials of finerenone in patients with nondiabetic kidney disease are ongoing. Nonsteroidal MRAs hold significant potential as pivotal treatment targets across the cardiorenal disease spectrum. This review will focus on the effects of finerenone on cardiorenal disease.

The incidence of acute kidney injury (AKI) in hospitalized patients is increasing. Many of these patients survive the immediate post-AKI period and may be prone to developing long-term complications of AKI. This study aimed to determine whether complete recovery following an episode of AKI is associated with a lower risk of long-term major adverse cardiovascular events (MACE). Retrospective cohort study. Adults admitted to the University of Virginia Medical Center between January 1, 2002 and December 31, 2012 who developed hospital-acquired AKI. AKI was defined as an increase in serum creatinine (SCr) by ≥ 0.3 mg/dL from the baseline and or requirement for acute dialysis during index hospitalization. Complete recovery was defined as a return of SCr to less than 1.25 times the baseline value and not dialysis dependent. Outcome and measurement: MACE was defined as subsequent admission for myocardial infarction, stroke or transient ischemic attach and heart failure using ICD- 9-CM codes. Overall, 11,538 patients survived beyond 90 days of AKI and had data available for analysis. Of the 9,673 survivors of AKI in whom recovery could be assessed, 7170 (74.12%) had complete renal recovery. MACE occurred in 27.28% of our study population over a median follow-up period of 399 days. 28.19% of patients who completely recovered renal function developed MACE, while only 32.48% did in those who did not recover completely. Patients who had complete recovery had a lower risk of long-term MACE when compared with those without complete recovery (adjusted hazard ratio 95% confidence interval (CI): 0.774 (0.713, 0.842)). Measurement of albuminuria was not available. Complete renal recovery after an episode of AKI in patients with normal baseline kidney function is associated with a lower risk of long-term MACE when compared with those who did not fully recover.