Chronic kidney disease (CKD) represents a major and widespread global health challenge. It affects over 800 million people worldwide, which is approximately 13% of the world’s population. Over the past 20 years, it has consistently ranked among the leading causes of death. As a result of its typically painless and asymptomatic presentation in the early stages of the disease, CKD is frequently diagnosed late, when the patient is already suffering from serious complications. In recent years, studies have identified novel biomarkers associated with the pathophysiology of CKD, including chronic inflammation, tubular injury, and CKD-related outcomes such as bone and mineral metabolism disorders, cardiovascular events, and all-cause mortality. Identifying and using these emerging biomarkers—like kidney injury molecule, N-acetyl–D-glucosaminidase, ficolins, the NLRP3 (nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3) inflammasome, soluble suppression of tumorigenicity-2, galectin-3, growth differentiation factor-15, soluble urokinase-type plasminogen activator receptor, sclerostin, the Dick-kopf proteins, and indexes such as the systemic inflammation response index—may lead to a significant advancement in early diagnosis, risk stratification, and personalized treatment strategies for CKD patients. Despite their potential, the routine clinical use of these novel biomarkers remains limited due to challenges such as high costs and the lack of standardized testing methods. There is still considerable room for advancement in both the diagnosis and management of CKD. Hopefully, increasingly more new biomarkers will become usable in clinical practice, ultimately improving care quality and outcomes for patients with CKD.

IgA nephropathy is the most common primary glomerulonephritis worldwide and a leading cause of chronic kidney disease and kidney failure in young and middle-aged adults, characterized by considerable ethnic differences in incidence and prognosis. This review summarises the evidence that these differences are, at least in part, genetically determined and maps the identified susceptibility loci onto the pathogenic sequence of the disease. Worldwide prevalence gradient increases with eastward and northward distance from Africa, while showing the significance of ancestry rather than environment in diaspora populations. Familial clustering provides support for an inherited component, while methylation differences between monozygotic twins discordant for IgAN point to an additional epigenetic layer. Genome-wide association studies (GWAS) in Han Chinese, European, and Korean cohorts have identified susceptibility loci implicated in antigen presentation, mucosal and intestinal IgA immunity, complement regulation, and innate immune signaling. Mapping these loci onto the four-hit hypothesis shows that inherited variation acts at distinct, potentially separable nodes. The MHC region contributes approximately half of the SNP-based heritability, while the CFH/CFHR locus provides the strongest signal outside the MHC. The complement arm has become the principal therapeutic target because it is currently the most pharmacologically tractable. We conclude by reviewing mechanism-directed therapies together with the safety questions and patient-selection issues that accompany them.