Uric acid PEARL (thanks Chi!): Uric acid levels are often high in renal failure; we also often think about tumor lysis syndrome (in the right clinical context and appropriate other laboratory support) causing renal failure. A simple test to help us differentiate is the urine uric acid:Cr ratio!! A ratio >1 suggests tumor lysis; a ratio <1 suggests renal failure.
- Here is a 1978 article, thanks to Chi! http://www.ncbi.nlm.nih.gov/pubmed/637642
Molecular medicine imatinib PEARL (thanks Annie and Harry!): Imatinib is a tyrosine kinase inhibitor most notably used for Philadelphia chromosome positive CML, NOT for CLL. It is also used for refractory chronic GVHD (as for this patient). Here is some molecular medicine:
- Chronic GVHD: antibodies activating platelet-derived growth factor receptor pathway, which is inhibited by imatinib! This can slow progression.
- Here is one article in Blood: http://www.bloodjournal.org/content/114/3/709?sso-checked=true
TTP/HUS treatment PEARL: remember that if you are worried about TTP/HUS, treatment for TTP is emergent plasma exchange (and steroids as adjunct), and avoid platelet transfusions (increased risk of thrombotic complications)! HUS is often treated supportively, but assume TTP and treat as such.
- In general think about TTP/HUS whenever you see schistos + thrombocytopenia – usually with normal coags (as opposed to DIC where you see a coagulopathy)! LDH is often markedly elevated, in the 1000s. Here is an old UCSF chief cover sheet on this that I had referred to in the past and found helpful: http://medicine.ucsf.edu/education/resed/Chiefs_cover_sheets/thrombotic_microangiopathies.pdf
- Treatment: for TTP, need emergent plasma exchange (to get rid of the ADAMTS 13 Abs)! Adjunctive tx includes steroids, sometimes ritux if refractory. Avoid platelet transfusions unless life threatening bleed because of increased thrombotic complications!
- The mortality of TTP if untreated is >90% (goes down to 10-20% with treatment) and is characterized by low ADAMTS-13 function (from antibodies)
- Thank you to Sam for sharing this paper on “The clinical features, risk factors and outcome of TTP after BMT” – while the sample size was small (22), and most patients were dx’d with TTP 2 months after BMT (different from this patient), there was an 86% mortality.
- Check out this NEJM review article (2014) on TMAs: http://www.nejm.org/doi/full/10.1056/NEJMra1312353
High BUN:Cr ratios – a few PEARLS from Chi
- Cr may be very low in a pt with low muscle mass
- BUN may be high in UGIB
- When do you think about using uremia as an indication for dialysis?
- Typically, this is used more for patients with chronic renal failure with s/sx of uremic encephalopathy. Remember that young people can tolerate very high BUNs!
- Not commonly used as an indicator for acute renal failure!
- The uremic toxins themselves are not actually measured by BUN, particularly in acute renal failure
- For bleeding in the context of uremic platelets, think about using DDAVP (x3; after that, worry about tachyphylaxis)