Environmental factors can affect CKD development and progression. Individual risk for CKD development and prognosis may be determined by insurance systems, neighborhoods, and occupational environments (6). Wu et al. observed that patients with stage 3b to 5 CKD are exposed long-term to air pollutants [particles measuring <2.5 μm in diameter, PM2.5 level ≥ 31.44 μg/m³ or nitrogen dioxide (NO2) ≥ 15.00 ppb] may be associated with higher risks of first-hitting renal function deterioration. It is worth noting that both ranges are more elevated than WHO Air Quality Guidelines (15 μg/m³ and 13.3 ppb, respectively) (7). This highlights that governments need to pay more attention to health equity, especially regarding environmental threats to kidney health.

Although there are varying scales of CKD screening in different countries, timely identification of the risk of CKD progression in a community is challenging. Chu et al.'s study defined overweight as a body mass index ≥ 24 kg/m² and metabolically unhealthy as a Homeostasis Model Assessment of Insulin resistance score ≥ 2.5 in one community cohort. They discovered that metabolically unhealthy people, regardless of body weight, compared to those with metabolically healthy normal weight, increased the incident intensity to a 15% decline in the estimated glomerular filtration rate (eGFR) in the elderly, indicating that other metabolic disorders in addition to body weight should be considered to intervene to prevent renal function decline. Tsai et al. used 10-year screening survey data to establish CKD state transition risk functions by common screening items to improve existing CKD screening practices. It is anticipated that these study findings could inspire more longitudinal community-based studies to offer more evidence based on the natural course of CKD.

The mortality risk, especially caused by cardiovascular disease, is higher than the dialysis risk in the early CKD phase. Vascular calcification may be an early sign of CKD prognosis. Wang et al. surveyed cardiovascular events, including non-fatal myocardial infarction, unstable angina, cerebrovascular events (intraparenchymal hemorrhage, subarachnoid hemorrhage, cerebral infarction), hospitalization for congestive heart failure, serious cardiac arrhythmia (resuscitated cardiac arrest, ventricular fibrillation, sustained ventricular tachycardia, paroxysmal ventricular tachycardia, an initial episode of atrial fibrillation or flutter, severe bradycardia or heart block) and peripheral arterial disease in patients with CKD stages 1–4. Their study found that cardiac valvular calcifications were only associated with cardiovascular events in patients with an eGFR ≥45 ml/min/1.73 m². However, abdominal aortic calcifications were associated with an increased risk of all-cause mortality; thus, more research is needed to explore the roles of valvular calcification sites and their clinical significance in CKD.

In conclusion, CKD is a global public health matter. This research article does not attempt to incur all relevant research in such a short period, but it is the start of a continuous process to bring more evidence, attention, and actions on CKD prevention and care.

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The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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