A new form of XXXX "kidney": shortened hemofilter survival and implications for membrane filtration plasmapheresis.

@entity1 @entity295 @entity1581 @entity2264 @entity1792 @entity1582 @entity810
BACKGROUND: Despite rigorous focus on extracorporeal CRRT parameters such as access, blood flow, hemoconcentration, and anticoagulation, some @entity1 have unexpected repetitive hemofilter clotting. We instead explored @entity1 or disease-related factors that could be responsible, and present a case of @entity1581 in which paraproteins caused hollow fiber failure. METHODS: A patient with IgG kappa chain multiple @entity1582 complicated by @entity295 and @entity810 was started on CVVH with a regional @entity1792 anticoagulation protocol that typically yields filter life of >50 h. @entity2264 hemofilters repetitively clotted every 2-4 h, even after excluding circuit-related problems. Failed filters were examined by light, electron (EM), and immunofluorescence (IF) microscopy. RESULTS: Imaging of the hemofilters revealed several ultrastructural features typical for @entity1582 -associated alterations in native @entity1 tissue. Red cell rouleaux formation occurred within the hollow fibers. There was extensive protein layering on the luminal surface of the fibers with some extension into their walls: these deposits were IF+ for IgG kappa, and had a fibrillary substructure on EM. CONCLUSION: Extracorporeal hollow fiber phenomena recapitulate many intra-corporeal paraprotein effects such as those described in the kidney with @entity1581 . Rapid protein layering suggests fouling of the membrane, decreased solute clearance before total device failure, and raises the theoretical concern that this might also occur during filtration plasmapheresis: we thus suggest serial serum free light chain levels to confirm their removal when using that technique. These findings emphasize the importance of disease rather than circuit-related factors that are under-appreciated causes of premature hemofilter failure.
