Models of kidney injury have classically concentrated on glomeruli as the primary site of injury leading to glomerulosclerosis or on tubules as the primary site of injury leading to tubulointerstitial fibrosis. However, current evidence on the mechanisms of progression of chronic kidney disease indicates that a complex interplay between glomeruli and tubules underlies progressive kidney injury. Primary glomerular injury can clearly lead to subsequent tubule injury. For example, damage to the glomerular filtration barrier can expose tubular cells to serum proteins, including complement and cytokines, that would not be present in physiological conditions and can promote the development of tubulointerstitial fibrosis and progressive decline in kidney function. In addition, although less well-studied, increasing evidence suggests that tubule injury, whether primary or secondary, can also promote glomerular damage. This feedback from the tubule to the glomerulus might be mediated by changes in the reabsorptive capacity of the tubule, which can affect the glomerular filtration rate, or by mediators released by injured proximal tubular cells that can induce damage in both podocytes and parietal epithelial cells. Examining the crosstalk between the various compartments of the kidney is important for understanding the mechanisms underlying kidney pathology and identifying potential therapeutic interventions.

肾损伤模型通常集中在肾小球是导致肾小球硬化的主要损伤部位，或小管是导致肾小管间质纤维化的主要损伤部位。然而，目前关于慢性肾病进展机制的证据表明，肾小球和肾小管之间复杂的相互作用是进行性肾损伤的基础。原发性肾小球损伤可明显导致随后的肾小管损伤。例如，肾小球滤过屏障的损伤会使肾小管细胞暴露于血清蛋白，包括补体和细胞因子，这些蛋白在生理条件下是不存在的，并且可以促进肾小管间质纤维化的发展和肾功能的进行性下降。此外，尽管研究较少，但越来越多的证据表明，肾小管损伤，无论是原发性还是继发性，也会促进肾小球损伤。这种从肾小管到肾小球的反馈可能是由肾小管重吸收能力的变化介导的，这可能会影响肾小球滤过率，或者由受伤的近端肾小管细胞释放的介质介导，这些介质可以诱导足细胞和壁上皮细胞的损伤。检查肾脏各个隔室之间的串扰对于了解肾脏病理学的潜在机制和确定潜在的治疗干预措施非常重要。