March 9th was World Kidney Day! After a one month rotation in the hemodialysis unit, I definitely appreciate my kidneys enough to give them a whole day. Filter the blood, regulate potassium, phosphate and calcium, promote red blood cell production, help activate vitamin D (so it can do its thing), indirectly keep calcium in my bones and not in my arteries….I think they deserve a week rather than a day next year. In all seriousness, the World Kidney Day is a global campaign for kidney health awareness and so I do digress. In terms of drug therapy and drug dosing, nephrology can be a whole other world. Nephrology, where uncommon drugs are used commonly and common drugs are used uncommonly. In hemodialysis (HD), vancomycin and gentamicin are relatively common empiric IV antibiotics. The dosing of these renally cleared medications is simplified as the extended half-life allows outpatients to be dosed each HD rather than daily. The target/accepted pre-HD gentamicin trough is also elevated at 2.5-5mg/L with the assumption that at least half of the drug is removed by hemodialysis (giving a post-HD trough of 1-2.5mg/L or less).
Decreasing or de-prescribing medications such as PPIs and H2RAs has required a little more investigation prior to a recommendation. A patient with polycystic kidney disease was taking rabeprazole 20mg PO bid for GERD caused by the pressure of her enlarged kidneys on the stomach (a fairly solid indication). The dose was reduced as her last flare was in the fall however until her kidneys are removed (hopefully during a transplant) she may require the high dose PPI in the future. Cases of severe GERD are not uncommon however re-evaluation and de-escalation of drug therapy is often warranted as conditions change. Terazosin, indicated for BPH, may act as a two-fer for the management of refractory hypertension. Heparin, replavite, alfacalcidol, IV iron, calcium carbonate (Tums), domperidone and quinine are seemingly the rule rather than the exception.
Management of disease states can differ as well. There have been three trials assessing the CV benefit of statins in HD patients. The 4-D, AURORA, and SHARP trials have failed to demonstrate a significant reduction in cardiovascular events despite reduction in LDL cholesterol. This may be secondary to the proposed mechanism of cardiovascular disease in these patients. Rather than atherosclerotic, vascular calcification is thought to be the predominant pathological change resulting in increased cardiovascular risk however, like osteoporosis and bone mineral disease, these two can co-exist. As a general rule, statins are not started in HD patients however they are continued if the statin preceded HD. A cardiology consult may change this when the harm of not treating may be substantial however questionably evidence based.
Stroke prevention in non-valvular atrial fibrillation (not to be confused with vavular atrial fibrillation or VTE treatment) is another good example. Warfarin appears to pose a greater bleed risk than stroke reduction in HD patients. It may even contribute to stroke risk. Warfarin inhibits the synthesis of vitamin K dependent clotting factors and it also inhibits the activation of matrix gla. Matrix gla is a protein which promotes bone calcification (rather than blood vessels). Hence the association of warfarin with calciphylaxis! Interestingly, in rat models, supplementation with vitamin K reduces warfarin associated vascular calcification. Could this benefit HD patients with atrial fibrillation and a mechanical valve??
I have to admit that I will miss the patients in the hemodialysis unit. They are truly inspiring individuals with a unique story and complicated, fascinating medication management needs.
For your enjoyment, I will leave you with this. You’re welcome 🙂