This article provides a thorough overview of the biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI) and acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical applications. This review also highlights the links between renal injury and the pathophysiological mechanisms underlying AKI and AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and the cellular senescence of renal cells. Key signaling pathways, such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The renin–angiotensin–aldosterone system (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating the oxidative stress and cellular changes that promote fibrosis. The clinical evidence suggests that RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

This article provides a thorough overview of biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI), acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical application. The pathophysiological mechanisms underlying AKI, AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses, with the impact on renal injury. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and cellular senescence of renal cell. Key signaling pathways, such as Wnt/β-Catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The Renin-Angiotensin-Aldosterone System (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating oxidative stress and cellular changes that promote fibrosis. Clinical evidence suggests RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

Backgrounds: Sacubitril/valsartan (angiotensin receptor neprilysin inhibitor [ARNi]) effectively treats heart failure with reduced ejection fraction. Its impact on advanced chronic kidney disease (CKD) or end-stage renal disease (ESRD) remains unclear due to their exclusion from major trials. We aimed to evaluate ARNi’s effectiveness and safety in these populations. Methods: We systematically searched PubMed, Cochrane, Embase, and ClinicalTrials.gov for observational studies of ARNi use in adults with advanced CKD or ESRD requiring maintenance dialysis. Primary outcomes were all-cause mortality and heart failure hospitalization (HHF), with secondary outcomes focusing on left ventricular ejection fraction (LVEF), blood pressure, and biomarkers. A random-effects model was used to derive pooled estimates, and study quality was assessed using the Newcastle-Ottawa scale. Results: Ten observational studies included 4329 patients with advanced CKD or ESRD. The pooled odds ratio (OR) for mortality plus HHF was 0.54 (95% confidence interval [CI]: 0.25–1.18, P = .12). Subgroup analysis showed ORs of 0.67 (95% CI: 0.17–2.70) for ESRD and 0.64 (95% CI: 0.25–1.66) for CKD. The pooled OR for mortality alone was 0.86 (95% CI: 0.50–1.46, P = .57). In ESRD, ARNi was linked to significant LVEF improvement (+4.20%, P < .001) and reduced systolic blood pressure (−7.13 mm Hg, P = .008), without increased risk of hyperkalemia or hypotension. Conclusion: In advanced CKD and ESRD with heart failure with reduced ejection fraction, ARNi did not significantly reduce mortality or HHF but showed potential benefit in LVEF improvement. Larger randomized trials are required to confirm its efficacy and safety in this high-risk population.

Background: Pulmonary cryptococcosis is an important opportunistic fungal infection in immunocompromised individuals, including those with an infection of the human immunodeficiency virus (HIV) but it can be increasingly seen in non‐HIV patients. Methods: We retrospectively reviewed the medical records of 58 non‐HIV‐infected patients with International Classification of Diseases, Ninth Revision, Clinical Modification Code B45.0 (pulmonary cryptococcosis) who were admitted to the Chi‐Mei Hospital, Taiwan from January 2016 to April 2022. Results: Of the enrolled 58 cases, 56 patients had no evidence of disease outside the lungs, and only two patients (3.4%) had disseminated diseases. Thirty‐nine patients had pathologically confirmed pulmonary cryptococcosis, and 19 patients had clinically confirmed disease. Pulmonary cryptococcus patients with cancer had a nonsignificant numerically higher rate of ICU use (14.29% vs. 5.13%; p = 0.348). There were similar mortality rates in both cancer and noncancer patients with pulmonary cryptococcosis (4.76% vs. 2.70%; p = 0.581). Patients in the cancer and noncancer groups had a similar duration of hospital stay (7 vs. 6 days, p = 0.799) and low mortality rates (4.76% vs. 2.70%, p = 0.581) on standard antifungal therapy. Conclusions: Cancer and noncancer patients had similar good outcomes after receiving appropriate standard antifungal treatment. Asymptomatic patients with pulmonary cryptococcosis diagnosed incidentally are self‐limited and require no antifungal therapy. Trial Registration: IRB number: 11111‐004.