Lots of creatine kinase in the blood, two days after taking a large dose of Rapamycin?

Two days after a dose of around 20 mg rapamycin + grapefruit seed extract + 500mg metformin, I had
CK-MM (creatine kinase muscular) 3948 (reference range <171)
CK-MB (myocardial CK) 44 (<25)
AST 164 (0-35)
ALT 66 (0-45)
LDH 498 (230-416)

38, male. Full results here:
Taken almost daily: metformin or acarbose with the two meals, depending on what I’m eating.

Should I worry? Anyone has had a similar experience? What should I do next, on top of retesting after two weeks? Note that I’ve always had high CK, yet never at this level:

I suspect there’s no liver damage since GGT was fine.

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Hmmn. Something wasn’t well.

What is your BMI?
What about health is general? Metabolic health?
What was your exercise history for the week prior to the test?
Any other drugs or supplements? Even Tylenol?
What is your creatinine? (Edit: normal 1.02)
Alcohol use?

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  • better than normal BMI
  • good health, not even close to insulin resistance
  • didn’t exercise much (I felt weak, maybe because I had a small surgery to remove a molar, and was taking NSAID’s rarely - not in the day before doing the blood work tho’ - and more Metformin or Acarbose than usual)
  • in the week before I didn’t take much else (except standard stuff like vit. D, zinc at times, magnesium)
  • no alcohol use

What is your AST/ALT normally?




I worry you may be showing signs of mild myopathy induced by Sirolimus. Weakness symptom fits here. How is your BP trend?

Case report:

I would be very careful here. I recommend you stop Sirolimus and have subsequent labs analyzed by your physician.

Either way, I’d recheck after 3 weeks off Sirolimus.

If you want to try Sirolimus again, I’d recommend 5mg with no grapefruit.

The case that you linked seems too far removed from my starting situation.

I did measure BP the night before at 20:27 → 95/44, pulse 62
And two hours before doing the blood draw → 92/48, pulse 64
These kinds of low BP values are normal for me.

Sounds good. Elevated BP would be severe myopathy, so your case seems mild. Hope everything gets back to normal for you.

@Rapasailor Great find and thanks for sharing this paper on possible side effect.

And while I’m not proposing there’s a smoking gun here, this is certainly a case that gives me some hesitation on higher doses, especially with grapefruit.

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And why ANYONE messing with Rapamycin needs to do full and regular blood panels, under the care a doctor!


Was reading a bit more. It seems that the mTOR pathway is suspected in many cases of Drug Induced Myopathy (DIM).

I wonder how common subacute DIM is in Sirolimus takers. Might be worth getting a CK/CMP 48 hours post dose on occasion.

Cardiovascular Risk in Kidney Transplant Recipients Receiving Mammalian Target of Rapamycin Inhibitors

We also observed significantly higher creatinine concentrations, as well as incidence of proteinuria, among patients receiving mTOR inhibitors.

In my case, as can be seen in the PDF I uploaded, I didn’t have proteinuria (increased levels of protein in the urine) or high creatinine.

Damn, all of this is so confusing.

I guess we will have to wait a while for the studies to be completed to actually know the full range of side effects and their frequency.

Meanwhile, when I upped my rapamycin dose from 5 mg/week to 10 plus/week, my creatine levels took a nose dive into the more normal range.

(My dose has varied from 10 to 20mg/week with grapefruit juice to find the max dose I can take without adverse side effects)
I plan to test every two months.

I’ve given up on Creatinine in non-CKD labs. Cystatin C has proven much more stable in determining kidney function. Cystatin C | National Kidney Foundation

In many rapamycin/kidney transplant/cancer studies, all manner of kidney function is measured for efficacy. Any insight if Cystatin C could be an efficacy/mTOR marker?

I certainly think Cystatin C is a more sensitive test for GFR than creatinine, especially in the “blind area” where creatinine has proved unable to accurately correlate to early stage KD. Without other diagnostic criteria being met, creatinine alone is almost meaningless for GFR ~45-85. For someone who is showing very mild renal impairment (perhaps age 70+), tracking improvement in renal function against Cystatin C will probably be a more reliable and stable marker to track.

This graph nicely shows the “creatinine blind” region where GFR isn’t really reliable based on creatinine alone. If you’re in that zone and looking for faint markers of improvement, Cystatin C is your best bet.

Indeed, this paper confirms.

Serum cystatin C as a marker of renal function in detection of early acute kidney injury

“We studied 200 healthy subjects and 130 AKI (acute kidney injury) patients over a period of 2 years at a tertiary care hospital. Serum creatinine and serum cystatin C were studied and analyzed in relevance to early AKI. We found that 56.2% of patients of AKI group had normal levels of serum creatinine in early phase, while all patients had elevated serum cystatin C at same time. Multiple logistic regression analysis revealed cystatin C-based GFR reflecting decline in GFR with worsening AKI in better than creatinine-based GFR”

But what I’m looking for is how to use sensitive kidney (or liver) markers as a MARKER of mTOR inhibition.

Attenuation of mTOR Signaling Is the Major Response Element in the Rescue Pathway of Chronic Kidney Disease in Rats

(They didn’t do a Control + Rapamycin only)

The current investigation was undertaken to study the role of mTOR-mediated signaling in CKD using Wistar male rats and adenine-induced CKD as an experimental model. The results suggest that mTOR inhibition significantly attenuated the induction of fibrosis, with restored serum creatinine and blood urea nitrogen levels. Activation of mTOR is the major responsive element with activation of miRNAs as an elementary role in the progression of kidney disease. Hence, targeting mTOR would be a possible strategy of treatment for CKD. Rats injected 1mg/kg for 5 days. The serum levels of creatinine, BUN, and albumin in CKD were significantly increased compared to the controls (Table 2). Rapamycin pretreatment exhibited reduced levels of these blood analytes in the CKD animals, but they were not equivalent to the control animals"

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