The observations suggest that ONOO- and perhaps other reactive oxygen species are being produced in the sickle cell kidney. The mechanism may be ischemia/reperfusion due to intermittent vascular occlusion by sickle cells. The resulting hypoxia could result in iNOS activation, superoxide radical and peroxynitrite formation. Two consequences of these reactions appear to be nitration of tyrosine residues of some renal proteins and enhanced apoptosis.
These observations provide evidence that NO and/or ONOO- are responsible for initiating cell damage, which leads to apoptosis in sickle cell mouse kidneys.
Renal insufficiency is associated with high morbidity and mortality in multiple myeloma. One of the common causes for acute renal failure in multiple myeloma is cast nephropathy. It is important to reduce the levels of light chains to improve renal failure and also the overall outcome. Plasmapheresis has failed to show any significant improvement in renal failure due to cast nephropathy as demonstrated in a recent randomized control trial. Here, we present a case series of three patients who were treated with continuous venovenous hemofiltration as a modality to remove these free light chains. There was improvement in renal failure in these patients with decrease in the levels of free light chains. These patients remained off hemodialysis on follow-up and two of them were able to undergo hematopoietic stem cell transplantation.
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