The most important teaching point here is that the markedly elevated phosphate explains the increased anion gap. I have probably seen this about 4 times in the past 5 years.
I agree with the comments that the FeNa is very high, suggesting acute tubular necrosis. The rapid correction suggests that the patient was in the diuretic phase.
Another possibility is that the patient had extreme volume contraction, and had the urine lytes checked after receiving significant IV fluids. I do not know the exact time frame, but this is clearly a possibility.
The serum osms were 296 and the ethylene glycol level was negative. Calcium oxalate crystals in the urine are sensitive but not specific for ethylene glycol. Fortunately, fomipazole only costs ~$500 now (it is generic), and giving one dose is defensible.
I hope you enjoyed this complex presentation. One of the problems is that we do not always have good timing of our lab tests, making clinical interpretation much more difficult.
{ 3 comments… read them below or add one }
Lessons from this case:
Arterial blood gas abnormalities can have multiple different interpretations. (Why I don't like Board questions on ABGs)
There are primary disorders, secondary disorders and tertiary disorders.
Blood gases should be interpreted within clinical contexts, like any other lab result.
Blood gases and electrolyte disturbances are not static, the right explanation may not be apparent without observing trends and response to therapy, especially renal problems
I'm still not on board with ARF due to extreme volume contraction. The measured lactate level should be much higher. Basically, kidneys are failing in that situation due to hypoperfusion. Hypoperfusion triggers anaerobic metabolism leads to lactic acid.
I'm guessing the guy's CPKs were normal.
lurker:
In this case I don't know about ARF from volume contraction and I don't know his CPKs. But I am going to challenge kidneys failing from hypoperfusion. You won't like this but I think that is one of the most prevalent misconceptions in medicine. I submit renal failure form simple hypoperfusion is exceedingly uncommon.
The kidneys have their own regulatory mechanisms and with autoregulation are protected from most insults. People always see a decrease in renal function and assume it is hypotension/hypoperfusion even when it is not documented (as in this case, there is no mention of hypotension, why invoke it?). Many times we had patients in the ICU where the renal function went out and was unexplained and the nephrologists attributed it to hypotension. When I pointed out there was no documented hypotension they said it must have occurred on the ward and was undocumented. But then I would point out patients it happened to in the ICU who had arterial lines from admission with continuous tracings and there could not have been undocumented hypotension. They never wanted to change their theories. Theories must fit facts, not the other way around.
I will say two things- many people with hypotension develop renal failure – but usually there is a concomitant injury (muscle damage) or sometimes hypotension and renal failure exist due to a common cause, e.g. sepsis. But the same bllod pressure with an MI or hemorrhage does not cause renal failure. Look at all the young women with e coli urinary sepsis who present with mean BPs of 55 – renal failure is extremely uncommon if they are promptly treated.
One reason I do not believe that simple hypoperfusion from hypotension (and I'm not talking cardiac arrest obviously, I'm talking about mean BPs of 60-80) is the infrequency I saw it in two of the ICUs you would expect it most commonly- the trauma unit and the CCU. there is all sorts of subclinical hypoperfusion in those units, yet renal failure isn't all that common. Inthe trauma unit especially, young people bleed down to very low blood pressures but if they are resuscitated in a timely fashion, renal failure is unusual. People in those units got renal failure but the correlation with low blood pressure was not very close.