NSAIDs in long races: why the “just in case” pill hits your kidneys

Half an hour before the gun goes off, you can watch the same ritual play out in every start village: someone pulls out a blister pack, pops an ibuprofen tablet and washes it down with sports drink. Not because anything hurts right now — but "just in case", so the knee does not start complaining at kilometre thirty. This is probably the most widespread and most underestimated mistake in amateur endurance sport.

How common is it, and does it help

The scale of the phenomenon is striking. According to the review by Pannone and Abbott (2024), published in BMJ Open Sport & Exercise Medicine, 84% of triathletes and 88% of recreational runners had taken NSAIDs within the previous 12 months. In one separate survey of triathletes, 196 out of 327 reported using them — almost two thirds. The authors specifically note that routine use at doses above those recommended occurs among elite and amateur athletes alike.

Now for the key point. What is it all for? Studies do record biochemical shifts — markers of inflammation and oxidative stress — but they find no difference in athletic performance between the NSAID and placebo groups. In other words, you get the full set of side effects in exchange for zero seconds at the finish line.

The quality of the evidence deserves a separate mention: the review covered 30 studies, of which only 4 were randomised controlled trials, and just 7 out of 30 included more than a hundred participants. The authors honestly state that evidence of harm to the health of ultramarathon runners is still very limited. But "little data" is not the same as "proven safe". And one signal stands out in particular.

What happens to the kidneys

The strongest study on the subject is the randomised, double-blind, placebo-controlled trial by Lipman and colleagues (Emergency Medicine Journal, 2017). It involved 89 participants, desert races in the Gobi, the Atacama, Ecuador and Sri Lanka, a distance of 80 km (50 miles), and ibuprofen at 400 mg every 4 hours versus placebo.

The result: acute kidney injury (AKI) developed in 52% of the ibuprofen group versus 34% of the placebo group. The difference of 18 percentage points (95% CI −4% to 41%) formally fell short of the threshold for statistical significance. But the number worth remembering is NNH 5.5: for roughly every five and a half people who take ibuprofen instead of placebo, there is one additional case of kidney injury. The authors' conclusion, in essence, is that taking NSAIDs on a long-distance event deserves careful thought, since it may worsen kidney injury.

The physiology explains why. During prolonged exertion, three factors hit the kidneys at once:

Sympathetic activation constricts the renal vessels — blood is redistributed to the working muscles and the skin.
Dehydration triggers the renin-angiotensin-aldosterone system, which constricts the vessels even further.
NSAIDs block prostaglandins — and prostaglandins are precisely what drive the protective dilation of the renal arterioles, the last mechanism keeping blood flow afloat.

The first two factors are the unavoidable price of a long race. The pill knocks out the third, compensatory support. That is exactly why the combination of heat + dehydration + NSAIDs is more dangerous than any of those components on its own, and exactly why taking a pill "preventively, before the start" is the worst possible scenario: you are switching off your protection before the load has even begun.

Gut, sodium and recovery

Sodium. In a British study of marathon runners who took ibuprofen, serum sodium concentration fell by an average of 2.1 mmol/L, whereas in the control group it rose by 2.3 mmol/L (p=0.0039). In one observational study at an Ironman, every athlete who developed hyponatraemia had been taking NSAIDs. The data on this question are contradictory overall — several large studies found no association — but the direction of the signal matches the mechanism: NSAIDs affect free water excretion. If you drink a lot of plain water and chase it with a painkiller, you are stacking two risk factors on top of each other.

The gut. Intestinal barrier function already suffers from ischaemia during prolonged exertion. The targeted evidence here is thinner: in the review, four studies on the gastrointestinal tract found no clear correlation, while an older prospective study from 1987 recorded increased faecal blood loss during a marathon, amplified by analgesics, although the authors considered it clinically insignificant.

Recovery. Christensen and colleagues (2012) showed that NSAIDs significantly blunt the exercise-induced increase in collagen synthesis in the patellar tendon. Post-training inflammation is not a breakdown — it is the signal to remodel the tissue. Suppress it, and you also suppress the adaptation you trained for in the first place.

What to do instead

Pain during a race is information, not an obstacle. Silencing it does not remove the cause; it deprives you of the only sensor that will tell you when it is time to change your form or to drop out.

Pacing strategy. Most "sudden" pain in the second half is the consequence of starting too fast. Plan your pace in advance and hold it through the first third.
Cooling. Ice under the cap, a sponge, water on the neck and wrists at every aid station. Less heat load means less strain on the kidneys.
Hydration with sodium, not just water. Base it on your own sweat losses, not on "drink plenty". Estimate the volume in advance with a fluid loss calculator.
Treat the cause before the start. Taping, work with a physiotherapist, adjusting your shoes and your training volume — weeks in advance, not 30 minutes before the gun.
About paracetamol. It works differently and does not block renal prostaglandins, but that does not make it a "safe substitute" or grounds for self-prescription — discuss its use and dosing with a doctor.

Key takeaways

A great many athletes take NSAIDs during races (up to 84–88% among triathletes and runners), but they deliver no performance gain — only biochemical shifts.
In an RCT over 80 km, ibuprofen at 400 mg every 4 hours produced AKI in 52% versus 34% on placebo, NNH 5.5.
The mechanism: renal vasoconstriction + dehydration with RAAS activation + blockade of protective prostaglandins = three hits at once.
Taking a pill "just in case" before the start is the worst option: protection is switched off before the load begins, and in the heat the risks compound.
The signals on hyponatraemia and collagen synthesis point the same way: fluid-electrolyte balance and adaptation both suffer.
What works is not a pill, but pacing, cooling, sodium and a cause of pain treated in advance.

This material is educational and does not replace consultation with a doctor. Do not start or stop taking medication on your own. If pain recurs, intensifies or interferes with your training, see a specialist.

Sources: Pannone L., Abbott A. Effects of NSAIDs on the health of marathon and ultramarathon runners: a scoping review. BMJ Open Sport & Exercise Medicine, 2024;10(1):e001846. https://doi.org/10.1136/bmjsem-2023-001846 · Lipman G.S. et al. Ibuprofen versus placebo effect on acute kidney injury in ultramarathons: a randomised controlled trial. Emergency Medicine Journal, 2017;34(10):637–642. https://doi.org/10.1136/emermed-2016-206353