Welcome back to the tasty morsels of critical care podcast.
This is a somewhat basic and general episode, even for this podcast which indulges in frequent generalisation and summaries of pre existing summaries.
It covers Oh’s Manual Chapter 47 looking at Acute Kidney Injury. While hardly the most exciting topic in the world, there a few important pearls here perhaps worth emphasising.
Oh leads with KDIGO as the AKI classification of choice. The KDIGO classification splits you into 3 stages based on changes in creatinine and urine output over specified time periods. When you compare it with older definitions like AKIN and RIFLE you can see that not a great deal has changed. KDIGO maintains its importance as the one used in most of the recent CRRT trials.
The old pre renal, intrinsic and post renal classification still seems to work in terms of classifying the causes, however the vast majority of what we see is boring old pre renal septic AKI. The pathophys is challenging to study but one animal model we do have suggested renal blood flow actually increases initially with the hyperdynamic state of sepsis without histological signs of injury. This seems to me to be the opposite of what we would intuit might happen. Most of the changes resulting in reduced function are probably at a micro vascular level and remain slightly opaque at least to arm chair renal hobbyists like myself.
Parenchymal diseases are often those that nephrologists who like to
taste spin their own urine get very excited about. They are rare but often have specific treatment beyond a spin on the big green machine. These are better dealt with in a different post altogether.
Excluding obstruction in AKI with some imaging like an ultrasound is a common recommendation but incredibly low yield. While iI hear it is technically possible to get someone admitted to hospital without a CT, it seems that most people I find in the ICU the next day will have had some imaging done (which I really don’t complain about). But in those who have sneaked into the unit without a run through the doughnut of truth then it is worth putting the probe on and look for some hydro as now and again you’ll come out like a rockstar for picking it up.
There’s a reminder in Oh that none of the “nephroprotective drugs” have panned out. Renal dose dopamine has gone the way of ventilating people with a Vt of 12ml/kg. Oh phrases this generously saying “a phase III clinical trial in critically ill patients showed that low dose dopamine was as effective as placebo in the prevention of renal dysfunction in ICU patients.”
There’s also a useful reminder here that urea and creatinine only rise after ~50% of GFR lost which begs the question of “why haven’t we invented a better biomarker yet. There are indeed a few out there with names like cystatin c and my personal favourite neutrophil gelatinase associated lipocalin (NGAL) which sounds to me like some form of experimental ice cream. Thankfully none are ready for clinical use so it would seem unfair to more about them than this for an exam.