Short-term dietary restriction (DR) may prevent organ damage from ischemic or toxic insults in animals, but clear evidence in humans is missing. While especially intraarterial administration of contrast media represents a cause of hospital-acquired acute kidney injury (AKi), targeted preventive strategies are not available. This trial investigated the feasibility and effectiveness of pre-interventional DR for preventing AKi in patients undergoing percutaneous coronary intervention (pci). patients were randomized to receive a formula diet containing 60% of daily energy requirement (DR group) or ad-libitum food during the 4-day-interval before PCI. Primary endpoint was change of serum creatinine 48 h after PCI (Δcreatinine). further analyses included incidence of AKi and safety evaluation. Δcreatinine post PCI in the DR group vs. the control group did not show any difference (DR: 0.03(−0.15,0.14)mg/dL vs. control: 0.09(−0.03,0.22)mg/dL;p = 0.797). Subgroup analyses revealed a significant beneficial impact of DR in patients that received ≤100 ml of contrast agent (DR n = 26: Δcreatinine −0.03(−0.20,0.08) mg/dL vs. control n = 24: Δcreatinine 0.10(−0.08,0.24)mg/dL; p = 0.041) and in patients with ≤2 risk factors for AKi (DR: n = 27; Δcreatinine −0.01(−0.18,0.07)mg/dL vs. control n = 31: Δcreatinine 0.09(−0.03,0.16)mg/dl; p = 0.030). Although the primary endpoint was not met, the results of this trial suggest a beneficial impact of DR in low-to-moderate risk patients. Dietary restriction (DR) is characterized by reduced food intake without inducing poor nutrition and subsumes numerous interventions including general calorie restriction (CR), protein restriction (PR) and various fasting protocols. Short-term DR-usually excercised for several days to weeks-has an extraordinary power to reduce cellular damage susceptibility by promoting resistance towards ischemic insults in rodent models of injury to the liver, 1,2 kidney 3,4 brain, 5 and heart. 6 Furthermore, DR has also been proven highly effective in preventing or ameliorating chemotoxic injury to the heart (secondary to doxorubicin) 7 and the kidney (secondary to cisplatinum) 8 and successfully improved survival in a murine chemotoxic stress model. 9 Possible mechanisms contributing to this phenomenon are versatile and include improvement of insulin sensitivity and reduction of oxidative stress and free radical induced damage, as well as modification of DNA repair. Alterations in the mechanistic target-of-rapamycin(mTOR)-signaling and other pathways, such as 5′ adenosine monophosphate-activated