Delayed and slow graft function (DGF/SGF) in de novo kidney transplantation endanger outcomes of graft and patient, while predisposing the patient to acute rejection and lesser graft function. Causes and work-up of DGF/SGF are described in the present paper. Also, the epidemiology and pathophysiology of chronic renal failure both in kidney graft recipients and in recipients of other solid organs is discussed, especially in relation to calcineurin inhibitor (CNI) immunosuppression. An acute kidney injury event will have a greater and faster impact on impaired renal reserve in case of chronic renal failure. Major causes of acute kidney injury (AKI) of the native kidneys of solid organ recipients and of the transplanted kidney are: severe infections, acute toxic kidney injury caused by CNI treatment concomitant CYP450 3A4 inhibiting medication, toxic and infectious events inducing haemolytic uraemic syndrome, toxic rhabdomyolysis, acute interstitial nephritis, rapid IV immunoglobulin infusion and exposure to other well-known nephrotoxins, such as NSAIDs, amphotericin and aminoglycosides.