Abstract
Monoclonal gammopathies (MG) encompass a variety of disorders related to clonal expansion and/or malignant transformation of B lymphocytes. Deposition of free immunoglobulin (Ig) components (light or heavy chains, LC/HC) within the kidney during MG may result over time in multiple types and degrees of injury, including acute kidney injury (AKI). AKI is generally a consequence of tubular obstruction by luminal aggregates of LC, a pattern known as “cast nephropathy”. Monoclonal Ig LC can also be found as intracellular crystals in glomerular podocytes or proximal tubular cells. Proliferative glomerulonephritis with monoclonal Ig deposits is another, less frequent form of kidney injury with a sizable impact on renal function. Hypercalcemia (in turn related to bone reabsorption triggered by proliferating plasmacytoid B cells) may lead to AKI via functional mechanisms. Pharmacologic treatment of MG may also result in additional renal injury due to local toxicity or the tumor lysis syndrome. The present review focuses on AKI complicating MG, evaluating predictors, risk factors, mechanisms of damage, prognosis, and options for treatment.
Highlights
An electrophoretically distinct, monoclonal β or γ globulin peak in serum [1,2] typifies monoclonal gammopathies Monoclonal gammopathies (MG))
It is of utmost importance to carefully evaluate renal function at the time of initiating treatment, both in order to choose a treatment regimen that could be well tolerated by patients with failing kidneys, and to avoid attributing acute kidney injury (AKI) to toxicity of drugs, when it rather results from the direct harmful effects of MC paraproteins over months of renal accumulation [18]
MG are an area in which the collaboration of hematologists and nephrologists is highly recommended and quite effective
Summary
Monoclonal β or γ globulin peak in serum [1,2] typifies monoclonal gammopathies MG). Often individuals with MGUS abnormality of serum electrophoresis have no evidence of a systemic hematological disease nor organ damage such as heart failure, liver dysfunction, bone/skeletal alterations, or renal dysfunction. The onset of proteinuria, a sudden decrease in renal function or worsening over a few days of a pre-existing renal failure may reveal ongoing kidney damage in the context of the so-called monoclonal gammopathies of renal significance (MGRS). This subfamily of MGUS or MM was first defined in 2012 in a report by the International Kidney and Monoclonal Gammopathy Research Group [5,6]. The present review, based on our 15-year clinical experience in this area, deals with the pathogenesis and treatment of AKI in MGRS, and the potential of tools such as the renal biopsy and high-cutoff hemodialysis membranes to support renal function while hematologic treatment becomes effective
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