AHTN use was associated with an increased risk of KC compared to no use, even after accounting for hypertension, with the highest risk observed for CCB. Our findings highlight the potential KC risks associated with different AHTN classes, with optimal cardiovascular care remaining an important consideration.
When not adjusting for hypertension variables: all classes of antihypertensive medications (AHTN) showed a statistically significant association with increased kidney cancer risk, with relative risks (RR) ranging from 1.48 to 1.75. After adjusting for hypertension variables: the risk for ACE inhibitors was no longer statistically significant (RR 1.19, 95% CI 0.93–1.52), while the risks for ARBs, beta-blockers (BB), and diuretics (DU) remained statistically significant, with RRs ranging from 1.09 to 1.36.
JCR Quartile: Consistently stable in Q2 (ranking between the top 25% and 50%) in the “Oncology” category.
Before I continue sharing multiple papers, let me mention something interesting. In the first two papers (from Sweden and China), I found that ACEi drugs are truly unique regarding cancer risk. While other antihypertensive drugs all show an increased cancer risk, ACEi not only does not increase the risk but also exhibits a slightly decreasing trend. This is indeed very interesting.
Wrong. The kidney cancer paper does not show a decreased risk with ACEI, it’s actually higher than for ARBs: “RR 1.19, 95% confidence interval (CI) 0.93-1.52 for angiotensin-converting enzyme inhibitor; RR 1.15, 95% CI 1.00-1.31 for angiotensin receptor blocker; RR 1.09, 95% CI 1.03-1.16 for beta-blocker, RR 1.40, 95% CI 1.12-1.75 for calcium channel blocker (CCB); RR 1.36, 95% CI 1.20-1.55 for diuretic”
I thought my words wouldn’t be misunderstood in context. An RR of 1.19 is obviously greater than 1, but its confidence interval indicates no statistical significance. Clearly, I was referring to the basal cell carcinoma study, which showed an OR of 0.98 (95% CI 0.96–1.00) — that clearly represents a slight but significant decrease.
I think it is very interesting that while other blood pressure-lowering drugs show an increase in cancer, ACEi remain unchanged, especially from two studies of different cancers in different countries.
Telmisartan may indeed be the optimal choice among ARBs.
In this large real-world matched cohort of over 83,000 patients, telmisartan was associated with superior cardiovascular and cerebrovascular outcomes compared to other ARBs, supporting its potential as a preferred antihypertensive agent in high-risk populations.
But that’s not the case. One study finds ACEi risk to be higher than ARB. Yes the BCC one finds a minimal decrease with ACEi. But that’s a single paper. Compared to dozens that found no differences between ACEi and other drug classes:
Yes, so I said that before continuing to share the papers, I found an interesting phenomenon based on these two papers from 2025. Of course I know that the cancer risk is controversial. Statements should be analyzed in context, right?
You wrote: “I think it is very interesting that while other blood pressure-lowering drugs show an increase in cancer, ACEi remain unchanged, especially from two studies of different cancers in different countries”
That’s bullshit, as among the two papers you shared, one (KC) finds a higher risk with ACEi vs ARB.
So this is the point of confidence intervals—are you only looking at the risk without considering the confidence interval? That’s a factor in determining statistical significance.
The risks of other antihypertensive drugs are statistically significant, while ACEi are not. Moreover, the Swedish study even showed a decrease. Never mind — you’re just looking for an argument. I can’t be bothered to discuss whether 1+1 equals 2.
It’s unpleasant to feel like I’m talking to an AI.
But anyway you wrote: “In the first two papers (from Sweden and China), I found that ACEi drugs are truly unique regarding cancer risk. While other antihypertensive drugs all show an increased cancer risk, ACEi not only does not increase the risk but also exhibits a slightly decreasing trend.”
I just say that the above statement is CORRECT for the Swedish BCC study but INCORRECT for the Chinese KC one. Do you agree or not?
Kidney cancer meta-analysis (actually not Chinese btw but Stanford + UCSD):
ACEI: 1.19 (0.93-1.52)
ARB: 1.15 (1.00-1.31)
BB: 1.09 (1.03-1.16)
CCB: 1.40 (1.12-1.75)
Diuretic (thiazide, loop, K): 1.36 (1.20-1.55)
Other: 1.40 (1.13-1.75)
So yes, I now get your point: non-ACEI are associated with a higher risk of BCC and KC in those studies (although ARB is borderline in the KC one as 1.00 is within CI) while ACEI is not: minimal protective effect in BCC (but 1.00 within CI) and on the wrong side of null for KC with large CI that includes 1.00.
Is that relevant though? I don’t think so vs the other papers we have on the topic.
Increased risks were seen for basal cell carcinoma with calcium channel blockers (relative risk [RR] = 1.17, 95% confidence interval [CI] = 1.11–1.22), diuretics (RR = 1.06, 95% CI = 1.03–1.10), and thiazides (RR = 1.10, 95% CI = 1.04–1.16); for squamous cell carcinoma with calcium channel blockers (RR = 1.08, 95% CI = 1.01–1.14), diuretics (RR = 1.29, 95% CI = 1.17–1.43), and thiazides (RR = 1.36, 95% CI = 1.15–1.61); and for melanoma in angiotensin-converting enzyme inhibitors (RR = 1.09, 95% CI = 1.03–1.14), calcium channel blockers (RR = 1.08, 95% CI = 1.03–1.12), and thiazides (RR = 1.09, 95% CI = 1.02–1.17)
This one did not find an increased risk with ARBs, nor did it find a reduced risk with ACEIs. Worse, it found an INCREASED risk with ACEI for melanoma.
That’s why we cannot reach a conclusion based on a single study with a null hypothesis; we have to look at the whole body of evidence, which indicates that ARBs and ACEIs seem to carry a similar cancer risk.
It is an abstract so not yet peer-reviewed but high-quality journal (Cancer Research, published by the American Association for Cancer Research), good research team (University of Utah, University of Colorado, UPenn), massive cohort (2,658,758 veterans) and long follow-up (10 years).
Conclusion:
ARB initiation was associated with a lower 10-year risk of any cancer (RR, 0.79; 95% CI, 0.75-0.83) and a similar 10-year risk of non-cancer mortality (RR, 1.03; 95% CI, 0.88-1.07) compared with ACEI initiation. Associations were consistent across most cancer types, except for inconclusive findings for breast and renal cancers. ARB initiators had a lower risk of developing any cancer compared with initiation of ACEIs, with no observed difference in non-cancer or all-cause mortality. We also reported stronger inverse association for ARBs in older adults in subgroup analyses. Further research should clarify underlying biological mechanisms, confirm causality in randomized trials, and evaluate personalized antihypertensive strategies that incorporate cancer risk considerations.
I am planning to categorize and share based on year and whether the evidence points to increased or decreased cancer risk, so the first two posts are both from 2025 and both show negative findings. Of course I know that drawing a firm conclusion requires synthesizing multiple studies, but others have already covered the older evidence. I’m simply aggregating research from the last two years — updating the “Bayesian priors” in people’s minds.
You previously said: “The kidney cancer paper does not show a decreased risk with ACEI, it’s actually higher than for ARBs.” Anyone with a college education would conclude from the RR and CI that ACEI shows no statistically significant association with increased cancer risk — not “it’s actually higher than for ARBs.” In fact, ARBs’ RR might show a statistically significant association with increased cancer risk, whereas ACEI absolutely does not.
There’s no “debating game” here. We’re just random people trying to improve our common knowledge and our health. Your attitude does not seem compatible with this goal. Either change your behavior or go away.
MR analyses demonstrated causal protective effects of genetically proxied ACEI/ARB use on gastric [odds ratio (OR) =0.834, P<0.001], colorectal (OR =0.900, P=0.006), lung (OR =0.928, P=0.02), breast (OR =0.942, P=0.03), and endometrial cancer (OR =0.900, P=0.006). These causal associations remained consistent in validation and sensitivity analyses. Mediation analyses indicated the causal, protective effects were partially mediated by vascular endothelial growth factor A (VEGF-A), total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C).