Lower Blood Pressure Is Better for the Heart...Even in CKD
Andrew Kowalski, MD, FASN
Why This Question Matters
The world of medicine and medical care is changing at a rapid pace. Recommendations and "hard rules," when I was in training, are no longer considered "standard of care."
This is great in many ways, especially when it comes to offering the patient the best advice, guidance and care that we can offer. The struggle is keeping up with the newest research, findings and suggestions.
At one time, "Guidelines" from major societies would come out every decade or so. Now it seems like what was recommended 2 years ago is obsolete and new recommendations have replaced the old ones. Fortunately, the field of medicine has evolved outside of patient care, where information can quickly be pulled, digested and implemented in "record speeds."
I was excited to see a new research article in JAMA Cardiology concludes that lowering systolic blood pressure more aggressively protects the heart just as well in people with CKD as in people without it. For every 10 mm Hg lower systolic pressure (otherwise can be understood as a 10 point drop in the top blood pressure number), major cardiovascular events fell by 15%, and kidney failure did not increase.
This matters because people with CKD are far more likely to die of heart disease than to ever need dialysis. Yet the best blood pressure target for them has been genuinely unsettled. The 2021 KDIGO guideline (major kidney organization) recommended a systolic target below 120 mm Hg when tolerated, but a 2024 Cochrane review limited to CKD patients found no clear cardiovascular benefit from lower targets. Observational studies showing a "J-curve," where very low pressures track with worse outcomes, have added to the hesitation.
The new analysis, led by Fotini Iatridi and colleagues from Oxford, set out to break that stalemate by adding three large trials published since the last reviews: ESPRIT, BPROAD, and STEP.
What the Researchers Did
The team searched many medical databases through January 16, 2026, for randomized trials that assigned adults to an intensive versus a standard blood pressure target and followed them for at least one year. Dialysis, pregnancy, hospitalized, and acute-care populations were excluded.
They found 27 trials covering 88,830 participants. Fourteen trials reported results for people with CKD (11,103 participants), and 19 reported results for people without CKD (76,785 participants). Five trials also contributed long-term post-trial follow-up for kidney outcomes, extending observation to as long as 10.6 years.
The key methodological move was standardization. Trials achieved very different blood pressure gaps between their arms, from 1.3 to 15.4 mm Hg. Rather than lumping them together, the authors scaled each trial's result to what would be expected per 10 mm Hg of systolic separation (or a 10 point drop). This lets a modest trial like HOMED-BP and an aggressive trial like ESPRIT be compared on equal footing. The average achieved separation was nearly identical in CKD and non-CKD groups (11.1 vs 11.2 mm Hg), which makes the head-to-head comparison fair.
Key Findings
1. The heart benefit is real, and CKD does not change it. Across 5,640 cardiovascular events in 24 trials, each 10 mm Hg lower systolic pressure cut major cardiovascular events by 15% (relative risk [RR] 0.85; 95% CI, 0.81-0.89). In CKD the reduction was 11% (RR 0.89; 95% CI, 0.81-0.99), and in people without CKD it was 16% (RR 0.84). The difference between groups was not statistically meaningful (P = .26), meaning that they were not very different and very similar.
2. People with CKD may gain the most in absolute terms. Because heart attacks, strokes, and heart failure are more common in CKD, the same relative benefit prevents more real events. The authors estimate about 4.2 events avoided per 1,000 person-years of treatment in CKD versus 2.7 without CKD. Put plainly, the people we have been most cautious about treating may be the people who benefit most.
3. Kidney failure did not increase. Among 580 kidney failure events in 11 trials, intensive lowering had no effect (RR 0.97; 95% CI, 0.84-1.11). When post-trial follow-up was added, giving 1,331 kidney failure events, the result was similar and leaned slightly favorable (RR 0.93; 95% CI, 0.84-1.02).
4. But eGFR does drop. Intensive lowering increased the risk of a sustained 30% or greater eGFR decline by 42% (RR 1.42) and a 40% or greater decline by 47% (RR 1.47). Larger declines of 50% or a doubling of creatinine were not significantly increased within trials. The authors attribute much of this to hemodynamics (changes in blood flow due to changes in blood pressure). The intensive groups of recent trials used far more diuretics (43% vs 15% in ESPRIT; 67% vs 43% in SPRINT), which produce an expected, functional dip in filtration rather than structural kidney injury.
What is also worth mentioning, and needs to be understood, is that a change in eGFR DOES NOT automatically suggest kidney injury or damage. Changes in eGFR have many reasons that are addressed in another article. What is important to know is that a change in eGFR can be like they way you feel in the morning; some days you do not want to get out of bed...others you are ready to hit the ground running. Both of these scenarios do not suggest that you are sick or well.
Furthermore, I'm sure each of you reading this can come up with multiple reasons why you would have a sluggish morning or an energetic morning. The same goes with eGFR. Remember the "e" in eGFR stands for "estimated" not 100% for sure.
5. Death rates fell. In an exploratory analysis of 2,737 deaths, all-cause mortality was 11% lower per 10 mm Hg (RR 0.89; 95% CI, 0.83-0.95), again with no difference by CKD status.
So, by decreasing blood pressure by 10 points, you can decrease your chance of dying from almost any cause by 11%. Add this to other changes that can be made and this percentage can add up quickly in your favor!
6. Albuminuria improved. In BPROAD and SPRINT, new albuminuria (type of protein spilling in the urine that suggests 'TRUE' kidney damage) among people without CKD fell by 13% and 29% with intensive treatment, a signal that the lower pressure was PROTECTING the glomerulus (main filter) even as eGFR changed.
Pros and Cons of the Study
Strengths | Weaknesses |
Largest intensive-vs-standard dataset to date: 27 trials, 88,830 people, about 5,600 cardiovascular events | Uses trial-level summary data, not individual patient data, so subgroups by diabetes, eGFR stage, or albuminuria could not be tested or commented on |
Includes three major recent trials (ESPRIT, BPROAD, STEP) that earlier CKD reviews lacked | The CKD group is heavily weighted toward four trials (SPRINT, ACCORD, HOT, AASK), which contribute 72% of CKD cardiovascular events |
Standardizes every trial to a 10 mm Hg difference, enabling fair comparison of CKD vs non-CKD | Standardization assumes a straight-line (log-linear) relationship between BP and risk, which J-curve skeptics dispute |
Long-term post-trial follow-up, up to 10 years, captures late kidney failure events | Most new trial data come from China, which may limit generalizability to US patients (not the same population, culture or exposure). |
Data supplied directly by MDRD, AASK, and ESPRIT investigators for CKD subgroups | BP measurement methods varied (unattended automated, attended office, home), and some trials targeted diastolic or mean pressure (therefore different perameters of focus) |
16 of 27 trials rated low risk of bias; sensitivity analyses (unstandardized, trials over 500 people) gave the same answers | Funnel plots showed some asymmetry for cardiovascular outcomes, raising the possibility of small-study effects |
Verified: Every figure in this table comes directly from the published article.
Limitations to Keep in Mind
The authors acknowledge three main limitations, and a careful reader should add a few more.
First, advanced CKD remains a blind spot. Only one small trial, PERFORMANCE (108 people), enrolled patients with eGFR below 30 mL/min. The conclusions apply most confidently to stage 3 CKD, and the authors themselves call for more trials below an eGFR of 30.
Second, the "non-CKD" groups almost certainly contain people with unrecognized kidney disease, since many trials defined CKD only by eGFR and did not test for albuminuria. This blurs the comparison between groups, although it does not change the overall estimate.
Third, measurement technique matters. SPRINT used largely unattended automated office readings, which run several points lower than routine clinic readings, due to the strict way it is outlined to be taken. A "120" in SPRINT is NOT the same as a "120" taken quickly in a busy office.
Fourth, the analysis did not systematically look at potential harms that the patients faced. Syncope (passing out), falls, hypotension (low BP), electrolyte disturbances, and acute kidney injury are mentioned, but not quantified. In SPRINT, acute kidney injury occurred in 4.4% of intensive versus 2.6% of standard participants, and in ESPRIT, syncope was about 3x more common with intensive treatment.
Finally, the trial populations were selected. People with heart failure, dialysis, recent hospitalization, frailty severe enough to exclude them from trials, or short life expectancy were largely absent.
Caution: These results should not be read as a mandate to drive every patient to 120 regardless of age, frailty, or tolerance.
How This Fits With Other Research
Evidence that supports the findings
The landmark trials point the same way. SPRINT, which enrolled 9,361 high-risk adults without diabetes, stopped early because a systolic target below 120 mm Hg reduced cardiovascular events and death! Its pre-specified CKD subgroup of 2,646 people showed a similar pattern, with no significant difference in the main kidney outcome of a 50% eGFR decline or kidney failure (15 vs 16 events).
ESPRIT and BPROAD, the two large Chinese trials added in this analysis, independently confirmed cardiovascular benefit at a target below 120 mm Hg, including in people with diabetes or prior stroke. STEP showed a 26% reduction in cardiovascular events in adults aged 60 to 80 treated to 110 to 129 mm Hg.
Other meta-analyses agree that CKD does not blunt the heart benefit. The Blood Pressure Lowering Treatment Trialists' Collaboration (BPLTTC) reported in 2013 that each 5 mm Hg reduction lowered major cardiovascular events by a similar proportion regardless of eGFR (it doesn't matter, lower appears to be better). A much larger 2026 individual-participant analysis from the same group, pooling 285,124 people from 46 trials, found nearly identical benefit with and without CKD (hazard ratio per 5 mm Hg 0.91 vs 0.90), with no attenuation in stages 4 and 5 and benefit preserved down to pressures below 120/70 mm Hg. A 2017 JAMA Internal Medicine meta-analysis of 15,924 people with stage 3 to 5 CKD found 14% lower all-cause mortality with more intensive control.
The eGFR dip appears hemodynamic, not structural. In a SPRINT substudy of 978 people with CKD, intensive treatment lowered eGFR by about 3 mL/min, but did not raise any of 8 urine biomarkers of tubular injury. This is very importent to understand and also shows the weakness of using eGFR. These patients hade a drop in their eGFR, but the 8 urine proteins that specifically point to direct damage were not there...This drop in eGFR CAUSED NO DAMAGE to the kidneys!
Long-term SPRINT follow-up using electronic health records for a median of 8.3 years found that excess eGFR decline occurred only during active treatment and did not continue after the trial ended. This is the same functional "creatinine bump" familiar from starting an ACE inhibitor, ARB, or SGLT2 inhibitor. Simply put, the patients experienced a change in blood flow that the balanced out in the end...no permanent damage.
Evidence that questions or qualifies the findings
The 2024 Cochrane review reached a different conclusion. specifically looked into six trials and 7,348 people with CKD, it found that lower targets probably do not reduce death, serious adverse events, or cardiovascular events. Two caveats explain much of the gap. Only half of those trials actually achieved the lower target, and the review did not standardize for the size of the BP difference. The new analysis also adds roughly 65% more CKD cardiovascular events (1,142 vs 693).
Diabetes may be the exception within CKD. ACCORD, which tested the same 120 vs 140 targets in type 2 diabetes, missed its primary cardiovascular endpoint, though it was underpowered. Meaning that though it found this benefit, it was not designed to look at this and the statistics would be garunteed to not be entirely trustworthy). More notably, the 2026 BPLTTC analysis found the relative benefit was blunted in people with both CKD and diabetes (hazard ratio 0.96; 95% CI, 0.90-1.02) compared with CKD without diabetes (0.88).
So what does this suggest?
BPROAD offsets some of this concern, but the diabetic CKD patient remains the least certain group that may benefit from this blood pressure target.
A small kidney harm has not been excluded. With post-trial data, doubling of serum creatinine rose by 15% (RR 1.15; 95% CI, 1.04-1.27), even though kidney failure did not. The authors acknowledge that a modest harm to the kidenys, throughtchanges in blood flow, cannot be ruled out, and the specific J-cure was likely the result of having sicker patients with already lower pressures. Additionally, this has not been tested in the frail, the very old, or advanced CKD.
Where guidelines stand
KDIGO has recommended a systolic target below 120 mm Hg in CKD, when tolerated, since 2021.
The 2025 AHA/ACC guideline recommends a target of at least below 130 mm Hg for most adults, with encouragement toward below 120 mm Hg. This meta-analysis provides the strongest pooled evidence to date supporting the KDIGO position for stage 3 CKD.
Basically, aim for a blood pressure with the top number loweer that 130, and if possible, aim for 120 or slightly lower.
What This Means for You
If you live with CKD, your heart is the organ most at risk, and blood pressure is one of the most powerful levers you have to protect it. This study says that aiming lower, toward a systolic reading in the 120s or below when you tolerate it, protects your heart at least as much as it protects someone without kidney disease.
Expect your creatinine to rise a little, and your eGFR to dip, when your blood pressure comes down, remember this is likely not a problem for various reasons. In most people this is a sign that pressure inside the kidneys’ filters has eased, NOT a sign of damage. Do not stop your medicines on your own because a lab number moved. Instead, ask your care team whether the change is within the expected range.
Three practical habits make intensive control safer:
Measure correctly at home whike seated, back supported, feet flat, arm at heart level, after five quiet minutes
Report dizziness, lightheadedness, or falls promptly, since these are signals that your target may need adjusting
Keep your lab follow-up, particularly checks of creatinine and potassium in the weeks after any medicine change.
For clinicians, the message is to treat toward lower targets in stage 3 CKD with deliberate monitoring: standardized BP measurement, labs within 2 to 4 weeks of intensification, attention to volume status when diuretics are added, and individualized targets for frail, very elderly, or advanced CKD patients.
In my CRIMS framework, this is a clear win for the cardio-renal axis --> protecting the heart is part of protecting the kidney patient.
Key Points
• Intensive blood pressure lowering reduced major cardiovascular events by 15% for every 10 mm Hg lower systolic pressure, with no meaningful difference between people with and without CKD.
• Because cardiovascular risk is higher in CKD, the absolute benefit was at least as large in CKD: about 4 events prevented per 1,000 person-years versus about 3 without CKD.
• Intensive lowering DID NOT increase kidney failure, even with up to 10 years of follow-up.
• It did increase the risk of 30% to 40% eGFR declines, which appear largely hemodynamic, driven partly by greater diuretic use, and not progressive after treatment ends.
• All-cause mortality was 11% lower per 10 mm Hg in an exploratory analysis.
• The findings align with SPRINT, ESPRIT, BPROAD, STEP, and the 2026 BPLTTC individual-patient analysis, and contrast with the narrower 2024 Cochrane CKD review.
• Evidence is thinnest for eGFR below 30, for people with both CKD and diabetes, and for frail or very elderly patients, where targets should be individualized.
Bottom line --> Aim lower for heart protection in CKD, measure BP carefully, and monitor kidney function and electrolytes after each step up in therapy.
References
1. Iatridi F, Roddick AJ, Staplin N, et al. Intensive vs standard blood pressure lowering in people with and without chronic kidney disease: a systematic review and meta-analysis. JAMA Cardiol. Published online October 7, 2026. doi:10.1001/jamacardio.2026.4445
2. Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int. 2021;99(3S):S1-S87.
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