In short, egfr **increased ** while patients on treatment with retatrutide after 24 weeks or so. To my knowledge, there is currently is no drug that actually increases egfr, the current best in class ones only slow down the decrease.
Keep in mind that increasing GFR is not always a good thing. Depends on the mechanism. Hyperfiltration increases GFR but leads to long term nephron damage. Just an example.
Indeed, simply raising blood pressure will increase GFR, but lead to long term nephron damage. CKD naturally causes the kidney to emit Angiotensin II etc that raises blood pressure, to compensate for falling GFR. ARB and ACE class blood pressure medications were developed to block and reverse this natural effect, thus lowering GFR in the short term, to prevent long term damage from high blood pressure.
The important question is if Retatrutide improves GFR by a mechanism that does NOT lead to long term nephron damage.
As I understand it, high egfr with normal or falling uacr is good and doesn’t lead to nephron damage long term. The slides in the presentation above show that, although I didn’t link to them.
A low and slow approach may be enough to arrest a decline without leading to further damage. But low may do nothing. What are the advantages to deriving GFR from cystatin-c? Cost at Labcorp is $35 for a Cr-renal panel, $119 for cys-c.
The way I understand it is that the calculated one relies on creatinine levels which can be high after exercise, in athletes, and in people having a high protein diet.
The test relying on Cystatin c is a more direct measure of filtration function without the confounders that affect the one based on creatine.