Fig. 1

Interaction of putative pathomechanisms in radiation nephropathy. Ionizing radiation induces DNA double-strand breaks (DSB) as well as renin–angiotensin–aldosterone system (RAAS) activation and vascular dysfunction. RAAS-activation and vascular dysfunction contribute to radiation nephropathy. DSB are induced directly through destruction of bonds and knock-out electrons and indirectly through oxidative stress. DSB trigger acute cell death, inflammation, and cellular senescence. Acute cell death and inflammation may enter a viscous cycle, although data on chronic inflammation in radiation nephropathy is conflicting. Cellular senescence promotes inflammation via the senescence associated secretory phenotype (SASP), which consists of pro-inflammatory cytokines. Cell death, possibly inflammation, and cellular senescence lead to loss of nephron mass and interstitial fibrosis, the hallmark of radiation nephropathy