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The first order of business for today’s Renal Fellow Network is to welcome another regular contributor to the mix: nephrology fellow Albert Lam, of Brigham & Women’s Hospital. Fresh off the Nephrology boards, Albert will be periodically posting his renal pearls of wisdom for the benefit of renal fellows everywhere.

Today’s post is on hemoperfusion. If you’ve never had experience with hemoperfusion, you’re not alone: according to this 2008 Kidney International paper by Tyagi et al, use of hemoperfusion has sharply declined over the past several years, and the indications for its use are infrequent.

What is it, exactly? The hemoperfusion procedure is employed in the treatment of specific intoxications and consists of running a patient’s blood through a column containing adsorbent particles to which the toxin binds and are removed from the circulation. These adsorbent particles can either be charcoal (which binds water-soluble drugs) or various polystyrene resins (which bind lipid-soluble molecules). Since dialysis is generally successful at removing most low molecular weight, water-soluble molecules which are not protein-bound, it makes sense that hemoperfusion would be considered only when dialysis is not effective (e.g., high molecular weight, highly-protein bound, large VOD drugs). Some of the drugs traditionally removed via hemoperfusion are theophylline and barbiturates, both of which have fallen out of favor (and thus may account some for the decline in the use of hemoperfusion). Valproic acid compounds can also be effectively removed via hemoperfusion, though dialysis is marginally effective as well. Other factors which have contributed to lower hemoperfusion usage include improvements in dialysis technology (e.g., use of continuous therapies and high-flux membranes) as well as the high expense associated with hemoperfusion cartridges, which cannot be reused. Complications of hemoperfusion include thrombocytopenia, leukopenia, and hypocalcemia.

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