Pre renal success is an interesting way to
think about increases in serum creatinine when overall the patient is improving
due to a therapy. Classically, this has been utilized when one uses ACEI/ARBs.
Too often the internists ( and even nephrologists) diagnose initial decline in
GFR following ACEI/ARB as “pre renal” AKI and reverse the beneficial effects of
these amazing therapies. Many times I
have seen such meds taken off due to an increase in creatinine. Long term
effects on mortality and CKD are more important than short term hardships of
elevated creatinine. In an article many
years ago in Kidney International, a term pre renal success was suggested rather
than renal failure for such cases to allow for non nephrologists to feel that
it’s a success from a patient stand point even though the serum creatinine
increased mild to moderately. We see
this a lot in HTN control as well. A
patient bp runs in 170/100 range and after few months of good therapy, you have
got it good control to 130-140 SBP range but serum creatinine increased from 1
to 1.3mg/dl—big deal! – This is PRE RENAL SUCCESS as long term- this bp control
is benefiting the patient from cardio vascular benefits.
A
recent article in AJN, this term is being re introduced.
Similarly, in CHF patients, aggressive diuresis also leads to the rise in creatining that scares the cardiologists and nephrologist to further diuresis the patients. A recent publication in Circulation confirms the assertion with use of tubular markers such as NGAL and KIM-1 that aggressive diuresis associated increases in creatinine are not bad. This is also pre renal success as overall, the patient benefits from being “less short of breath” and decreased hospitalizations. Levels of NAG and KIM-1 did not change with aggressive diuresis. Worsening renal function occurred in 21.2% of the population and was not associated with an increase in any marker of renal tubular injury: Interesting, these increases in NGAL, NAG, and KIM-1 were paradoxically associated with improved survival (adjusted HR: 0.80 per 10 percentile increase, 95% CI: 0.69-0.91; P=0.001)—again suggesting this concept of Pre renal success
These findings reinforce the notion that the small to
moderate deteriorations in renal function commonly encountered with aggressive
diuresis are dissimilar from traditional causes of acute kidney injury.
It’s about time we called the following situations Pre Renal Success(
this is personal opinion and there is room for debate)
1. Increases in creatinine 25-30%
after initiation of ACEI/ARB and perhaps we can add SGLT-2 inhibitors here as
well
2. Increase in creatinine 25-30%
after aggressive 2-4 months of blood pressure control in a patient with severe
HTN
3. Increases in creatinine 25-30%
after aggressive diuresis and a patient with severe CHF
Just some thoughts:
ReplyDelete1) the rise in creatinine after ACEI due to preferential dilation of the efferent arteriole results in decreased glomerular pressure, which is the goal in proteinuric renal disease for long-term nephroprotection, but it important to repeat the renal function again to make sure creatinine has stabilised. I suppose that could be like a “pre-renal success” or trade-off for the long term. Ensuring a patient is euvolemic is when titrating ACEI will paramount to avoid serious AKI.
2) Increase in creatinine after blood pressure reduction could be due to relative hypotension resulting in renal hypoperfusion. The medications may need to be relaxed a bit in this instance.
3) AKI can occur in overly aggressive diuresis before equilibration of fluid with the interstitial. Recheck renal function as striving for euvolemia. The rate of diuresis should be slower in cases of hypoalbuminemia and relative hypotension to decrease risk of precipitating AKI. In cases of AKi in CHF, improvement in cardiac output and volume status should improve creatinine (a marker of renal perfusion).
In "pre renal success" (first coined and explained in AJMed 2007: 120, 754-759) "success" requires that the BP not be too low, that the Creatinine re-equillibrate, and that the patient feels fine; otherwise, it is old-fashioned prerenal failure. Importantly, there is no reason to limit the rise in creatinine to 30% (see AJNephrology 36(5) 397-406 (2012) and the accompanying editorial by Dr Remuzzi)if successful treatment of HTN, proteinuria, and/or pulmonary edema leads to a greater rise. On the autoregulation curves relating GFR to BP (or sngfr to intraglomerular pressure) nothing specific happens at any 30% increase, it is just another point on the graph.
ReplyDeleteIs that 25% increase in creatinine or 25% decrease in eGFR?
ReplyDelete