Myeloma kidney: advances in molecular mechanisms of acute kidney injury open novel therapeutic opportunities.

Renal impairment is a common complication of multiple myeloma (MM) and is supported in virtually all patients by a tubulointerstitial pathology that results from high serum concentrations of monoclonal free light chains (FLCs). The proteins involved in the kidney injury and the analysis of their binding interactions have been thoroughly investigated and the main pathogenic mechanisms are being elucidated. Early sustained reduction of circulating FLC leads to improved renal recovery rates that translate into improved quality of life and survival. The mainstay of therapy is presently the removal of aggravating factors (dehydration, hypercalcaemia, nephrotoxic drugs) and the prompt institution of rapidly acting novel chemotherapy combinations. This approach allows the rescue of kidney function in more than two-thirds of patients. High cut-off haemodialysis dialysers may potentially add clinical benefits and the outcomes of controlled trials are eagerly awaited. Basic research findings have led to the design of targeted drugs that prevented the functional manifestations of acute kidney injury in animal models. There is now hope to prevent the renal damage in patients with MM.