The AKI Clinic for Fragile Patients T he recent terrorist attack in Manchester, England, at a pop "musical" concert 1 represents a somber reminder of the London Blitz-the "lightning war"-prosecuted by Hitler against Great Britain during World War II. The dome of the church on the cover illustration, provided by Guest Editor, Charuhas Thakar, represents the hope of the Londoners who survived the protracted bombing that lasted 9 months, and our own hope that an effective resolution to the abject, lawless acts of violence by fanatical and radical terrorists comes soon. Nephrologists are well acquainted with the physical repercussions of bombing. During the Blitz, muscle "crush" injuries from entrapment under the rubble of destroyed buildings led to oliguric kidney failure, eloquently described by Bywaters and Beall. 2 Without the extant technologies of kidney replacement that are commonplace in contemporary nephrology, those who did not experience rapid recovery of kidney function died a uremic death. From the clinical observations of the Blitzkrieg victims, Bywaters and Beall formulated the construct of myoglobin-induced acute kidney injury (AKI), Bywaters and colleagues subsequently developed 2 animal models of rhabdomyolysis-induced AKI that still serve as touchstones for all clinician scientists. One involved injection of crystalline myoglobin 3 and the other a controlled muscular crush injury. 4 Indeed, the scientific inquiry into pigmentary nephropathy via the subsequently developed rodent model of glycerol-induced rhabdomyolysis greatly advanced the knowledge base of AKI. These advances were followed by more comprehensive analyses of rhabdomyolysis-induced AKI and have elucidated that nearly all mechanisms of AKI are at play, including ischemic, toxic, cytokine mediated, among others. Despite advances in our understanding of AKI pathophysiology, we remain naïve in many areas, including even