Does Dialysis Remove Uric Acid From the Body?

Dialysis removes uric acid from the blood, and it does so with surprising efficiency in a single session. Studies consistently show that one round of hemodialysis can cut circulating uric acid levels by roughly half to two-thirds. But that per-session drop tells only part of the story, because uric acid doesn’t stay low between treatments, the type of dialysis matters, and stripping too much uric acid too quickly can create problems of its own.

How Much Uric Acid a Single Hemodialysis Session Clears

Uric acid is a small molecule, light enough to pass freely through the pores of a dialysis membrane. That physical property makes it one of the substances hemodialysis handles well. In a study of patients with gout on hemodialysis, average pre-session uric acid was 8.4 mg/dL and dropped to about 4.0 mg/dL afterward, a reduction of roughly 4.5 mg/dL per session.¹ A separate study in sub-Saharan Africa measured a mean uric acid clearance of about 66% per session, with most patients achieving moderate clearance.² And a scoping review of patients taking allopurinol on hemodialysis found that sessions decreased urate concentrations by 56 to 71%.³

Those numbers converge on a consistent picture: a single hemodialysis session typically removes somewhere between half and two-thirds of the uric acid in your blood. For context, healthy kidneys filter uric acid constantly and maintain a steady-state level, usually between about 3.5 and 7.0 mg/dL. A hemodialysis session accomplishes in a few hours what the kidneys would normally manage around the clock, but then the machine gets unplugged.

Peritoneal Dialysis and Continuous Therapies

Hemodialysis isn’t the only form of dialysis, and the alternatives handle uric acid differently. Peritoneal dialysis, which uses the lining of your abdomen as the filter, is gentler and slower. Among peritoneal dialysis methods, continuous cycling peritoneal dialysis showed the highest uric acid clearance and the best achievement of target uric acid levels.⁴ Even so, a review of allopurinol use found that peritoneal dialysis patients achieved target uric acid levels less often than hemodialysis patients (around 47% versus 61%), and required lower medication doses because peritoneal dialysis clears the drug’s active metabolite more slowly.³

For critically ill patients with acute kidney injury, continuous renal replacement therapy (CRRT) runs around the clock at lower flow rates. A multicenter study found that CRRT clears uric acid at least as effectively as it clears other small waste molecules like urea and creatinine, and in some time windows the uric acid reduction rate was actually higher.⁵ In children with tumor lysis syndrome, where cancer cells break down and flood the bloodstream with purines, continuous therapies are generally preferred over peritoneal dialysis because they produce better uric acid and phosphate clearance and faster clinical improvement.⁶

A more advanced technique called hemodiafiltration combines the diffusion of standard hemodialysis with additional filtration under pressure. It strips middle-molecular-weight toxins more aggressively, and it also clears small molecules like uric acid. One study noted that this effective clearance of uric acid, which actually functions as a natural antioxidant in the blood, may contribute to a temporary spike in oxidative stress during sessions.⁷ That observation hints at a tension that runs through the entire topic: uric acid is a waste product you want to keep in check, but it also does something useful in the body.

Why Uric Acid Comes Back Between Sessions

If hemodialysis can cut uric acid by more than half in one sitting, you might wonder why high uric acid remains a chronic problem for dialysis patients. The answer is timing. Standard hemodialysis runs three times a week, usually for about four hours each session. Between sessions, the body keeps producing uric acid from the normal breakdown of purines in food and from cell turnover. In people with end-stage kidney disease, this production continues unchecked because the kidneys are no longer excreting uric acid on their own.

Research has shown that the pattern of purine breakdown shifts in dialysis patients, with more of the intermediate compounds being pushed toward their final degradation product: uric acid.⁸ So each session starts with uric acid levels that have climbed back up since the last treatment. The result is a sawtooth pattern: a sharp drop during dialysis, a gradual rise over the next day or two, and then another drop at the next session. Pre-session levels often remain above the normal range even though post-session levels look reassuringly low.

How Gout Behaves Differently on Dialysis

You would expect that people with persistently elevated uric acid would be plagued by gout attacks. But one of the counterintuitive findings in kidney disease is that gouty flares actually become less common as kidney function worsens, even as uric acid levels rise. Researchers have noted that while hyperuricemia is increasingly linked with cardiovascular problems in patients with advanced kidney disease, the frequency of acute gout attacks drops as the kidneys fail.⁹ The reasons aren’t entirely settled, but several explanations have been proposed: the chronic inflammatory state of kidney failure may desensitize the immune response to urate crystals, and uremia itself may blunt the acute immune reaction that causes a gout flare.

That doesn’t mean gout disappears entirely. Some dialysis patients still experience attacks, and the condition can be tricky to manage because several standard gout medications are cleared by the kidneys and accumulate in people on dialysis. Colchicine, for instance, requires careful dose reduction, and non-steroidal anti-inflammatory drugs are generally avoided because of the bleeding and cardiovascular risks they carry in kidney patients.

When Dropping Uric Acid Too Fast Triggers a Flare

Here’s a frustrating wrinkle: even though high uric acid contributes to gout over time, bringing it down rapidly can trigger an acute attack. When blood uric acid drops quickly, existing urate crystal deposits in joints can become unstable and shed into the joint space. This is called a mobilization flare, and it’s a recognized complication of starting urate-lowering therapy in anyone, not just dialysis patients.

In a case report involving a patient who received hemodialysis along with a uric acid-dissolving enzyme called rasburicase, kidney function improved rapidly but the sharp decline in uric acid provoked a classic mobilization gout attack.¹⁰ The practical takeaway: if you’re starting dialysis or beginning a new medication to lower uric acid, your medical team may also prescribe anti-inflammatory prophylaxis for the first weeks or months to prevent exactly this kind of paradoxical flare.

Managing Uric Acid Medications Around Dialysis Sessions

Many dialysis patients take medications to reduce uric acid production between sessions. Allopurinol is the most common, and its dosing on dialysis is more complicated than in people with normal kidneys. The drug’s active metabolite, oxypurinol, is normally cleared by the kidneys. When the kidneys aren’t working, hemodialysis becomes the main route for removing oxypurinol, and sessions reduce its concentration by roughly 39 to 57%.³ That means the drug is being stripped from your system during the very treatment it’s supposed to complement.

To compensate, researchers have suggested giving allopurinol after dialysis sessions rather than before. This way the drug has a full inter-dialytic period to work before the next session washes it away. Hemodialysis patients in the review used doses ranging from 100 to 600 mg per day, substantially higher than the 110 to 125 mg typical for peritoneal dialysis, because hemodialysis strips both the drug and uric acid more aggressively. Over time, allopurinol treatment brought uric acid levels down by about 14 to 41% and cut gout flares from an average of two per year down to about 0.1 per year.³

Febuxostat, the other major uric acid-lowering drug, works through the same enzyme pathway but is processed primarily by the liver rather than the kidneys. That makes it an attractive option for kidney patients. A study comparing the two drugs in people with chronic kidney disease and gout found that allopurinol and febuxostat were similarly effective and well-tolerated when doses were adjusted to hit a target uric acid level, though allopurinol was associated with fewer gout flares during treatment.¹¹

When Low Uric Acid Becomes the Problem

This is where things get philosophically uncomfortable. Uric acid is the reason people get gout. It’s linked to cardiovascular disease. Dialysis strips it out. You’d think lower is always better. But several studies have found the opposite in hemodialysis patients: people with the lowest uric acid levels actually have higher mortality.

One study of patients starting hemodialysis divided them into groups based on uric acid levels and tracked survival. The group with the lowest uric acid had more than double the risk of death compared to the middle group, even after accounting for other health factors.¹² This association held specifically in patients who also had poor nutrition and high levels of other illnesses. The likely explanation is that very low uric acid in a dialysis patient is often a marker of malnutrition and wasting rather than a cause of death in itself. People who are eating poorly and losing muscle mass produce less uric acid simply because they’re breaking down fewer purines.

But there may be a direct biological cost as well. Uric acid is one of the most important antioxidants in human blood, responsible for scavenging reactive oxygen species that damage cells. When hemodiafiltration aggressively strips uric acid along with other solutes, researchers have observed a temporary surge in oxidative stress and markers of red blood cell damage during the session.⁷ The clinical significance of that transient dip in antioxidant defense is still debated, but it illustrates that uric acid removal isn’t purely beneficial. The sweet spot for dialysis patients likely falls somewhere between “high enough to cause gout and cardiovascular damage” and “low enough to signal malnutrition or strip away antioxidant protection.”

Uric Acid and Remaining Kidney Function

Many people on peritoneal dialysis still have some residual kidney function, meaning their kidneys produce a small but meaningful amount of urine and still clear some waste. Preserving this residual function matters because it improves quality of life and survival. Uric acid may play a role in how quickly that residual function fades.

A study of peritoneal dialysis patients found that those with hyperuricemia experienced a significantly faster decline in residual kidney function than those with normal uric acid levels, even after adjusting for age, diabetes, and other factors.¹³ But a later study complicated the picture by showing a U-shaped relationship: both very low and very high uric acid levels were linked to faster residual function loss.¹⁴ In other words, there seems to be a middle range where the remaining kidneys fare best, and straying too far in either direction accelerates their decline.

Research into peritoneal uric acid clearance has also uncovered links between how much uric acid crosses the peritoneal membrane and local inflammation. Higher uric acid clearance across the peritoneum was associated with elevated inflammatory markers both in the dialysis fluid and in the blood.¹⁵ Whether that inflammation is driving the uric acid clearance, responding to it, or just traveling alongside it remains an open question.

How the Gut Steps In When the Kidneys Fail

In healthy people, the kidneys handle about two-thirds of uric acid disposal, with the remaining third eliminated through the gut. When kidney function collapses, the intestines appear to compensate by ramping up their share of the work. Animal studies in rats with most of their kidney tissue removed have shown increased uric acid excretion into the intestinal lumen. The mechanism involves upregulation of a high-capacity uric acid transporter called ABCG2 in the gut lining.¹⁶

This gut compensation is a reminder that the body doesn’t rely on a single exit route for uric acid, and dialysis is really a third pathway layered on top of whatever the failing kidneys and the gut can still manage. For dialysis patients, this has practical implications. Diet still matters, because the purines you eat influence how much uric acid your body produces. And medications that affect gut bacteria or intestinal transit could, in theory, alter how much uric acid your gut can eliminate between dialysis sessions. This area of research is still young, but it may eventually change how clinicians think about managing uric acid in kidney failure, shifting some attention from the dialysis membrane and the bloodstream to what happens in the digestive tract.

There’s also a genetic dimension worth noting. Variants in the ABCG2 transporter gene are among the strongest genetic risk factors for gout in the general population. In dialysis patients who carry less-functional versions of this transporter, the gut’s compensatory ability may be impaired, leaving them more reliant on dialysis sessions and medications to control uric acid. Genetic testing for these variants isn’t routine in dialysis care, but as the research develops, it could help explain why some patients struggle with uric acid control despite adequate dialysis prescriptions while others manage just fine.

1
PubMed Central. Urate-lowering therapy for patients with gout on hemodialysis
2
PubMed Central. Assessment of the efficacy of hemodialysis on uric acid clearance in a sub-Saharan African population at the end stage kidney disease
3
PubMed Central. Dosing practices, pharmacokinetics, and effectiveness of allopurinol in gout patients receiving dialysis: a scoping review
4
PubMed. Urate levels and clearance in renal patients under peritoneal dialysis
5
PubMed Central. Reduction Rate of Uric Acid in Blood during Continuous Renal Replacement Therapy for Acute Kidney Injury: A Multicenter Retrospective Observational Study
6
PubMed Central. Tumor lysis syndrome in childhood malignancies
7
PubMed. Short-term effects of hemodiafiltration versus conventional hemodialysis on erythrocyte performance
8
Renal Failure. Circulating purine compounds, uric acid, and xanthine oxidase/dehydrogenase relationship in essential hypertension and end stage renal disease
9
PubMed. Advanced kidney failure and hyperuricemia
10
BMC Nephrology. Dialysis-requiring acute urate nephropathy and mobilization gout flare in a patient with alcoholic ketoacidosis: a case report
11
American Journal of Kidney Diseases. Efficacy and Safety of Allopurinol and Febuxostat in Participants With Gout and Chronic Kidney Disease
12
PubMed Central. Low serum uric acid level is a risk factor for death in incident hemodialysis patients
13
PubMed. Uric acid is associated with the rate of residual renal function decline in peritoneal dialysis patients
14
PubMed. U-shaped relationship between uric acid and residual renal function decline in continuous ambulatory peritoneal dialysis patients
15
Nephrology Dialysis Transplantation. #626 Association between peritoneal uric acid clearance, inflammation, and peritoneal membrane function in normouricemic patients undergoing peritoneal dialysis
16
PubMed Central. Electrochemical analysis of uric acid excretion to the intestinal lumen: Effect of serum uric acid-lowering drugs and 5/6 nephrectomy on intestinal uric acid levels