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1 Introduction CKD is a major global health burden, affecting roughly one in ten adults and substantially increasing premature mortality and cardiovascular complications ( Albuminuria is a robust predictor of kidney failure, cardiovascular events and all-cause mortality, and its reduction is an established therapeutic target in CKD ( High-throughput omics now enables systematic profiling of the genome, epigenome, transcriptome, proteome, and metabolome in blood, urine, and kidney tissue, providing a finer-grained view of early kidney injury ( 2 Pathophysiology of early-stage chronic kidney disease Even in the earliest stages defined by modest albuminuria and preserved eGFR, chronic kidney disease reflects the interaction of systemic haemodynamic and metabolic stress with intrinsic renal responses that together initiate glomerular, tubular, interstitial and microvascular injury ( As shown in Figure 1, at the glomerular level, increased transcapillary pressure and shear stress contribute to endothelial dysfunction, podocyte injury and expansion of the mesangial matrix ( FIGURE 1 Filtered albumin, lipids and glucose are reabsorbed by proximal tubular cells, where they can trigger oxidative stress, endoplasmic reticulum stress and activation of proinflammatory pathways, resulting in the production of chemokines and cytokines such as monocyte chemoattractant protein-1 and interleukin-6 ( Microvascular injury and capillary rarefaction are integral components of this process

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