Constipation and Kidney Disease: Why Bowel Motility Matters

17 May

Constipation is often treated as little more than an uncomfortable gastrointestinal symptom. However, in chronic kidney disease (CKD), bowel motility may have wider implications. The colon is an important site of microbial metabolism, including the production of compounds that are normally excreted through the kidneys. When intestinal transit slows, these compounds may remain in contact with the gut for longer, potentially increasing their production and absorption.

At the same time, the relationship appears to work in the opposite direction. As kidney function declines, constipation becomes increasingly common. Fluid restrictions, dietary restrictions, medications, reduced physical activity, changes in the gut microbiome and altered gastrointestinal motility can all contribute.

For people with advanced CKD and particularly those receiving dialysis, bowel regularity may therefore be more important than it initially appears.

What Does Bowel Movement Frequency Tell Us?

Bowel frequency varies considerably between individuals, and constipation cannot be defined by frequency alone. Stool consistency, straining, incomplete evacuation and difficulty passing a bowel movement are also important.

Nevertheless, bowel movement frequency provides a simple indication of intestinal transit and has recently attracted greater research interest.

A 2024 study by Johnson-Martínez and colleagues examined clinical, dietary, microbiome and blood metabolite data from more than 1,400 generally healthy adults. Participants were divided into constipation, low-normal, high-normal and diarrhoea groups according to their bowel movement frequency. The high-normal group, having approximately one to three bowel movements per day, tended to demonstrate greater abundance of fibre-fermenting gut bacteria and more favourable microbial metabolism (Johnson-Martínez et al., 2024).

In contrast, constipation was associated with a shift towards microbial protein fermentation and higher circulating concentrations of several microbiota-derived metabolites. Of particular interest for kidney health was indoxyl sulphate, sometimes reported as 3-indoxyl sulphate or 3-IS, which was elevated with lower bowel movement frequency and associated with poorer kidney function.

This does not establish that constipation causes kidney disease. The study was observational and conducted predominantly in people without established chronic disease. However, it provides an important biological link between intestinal transit, gut microbial metabolism and kidney function.

Constipation, Protein Fermentation and Uraemic Toxins

Much of the interest in bowel motility in CKD relates to gut-derived uraemic toxins.

When dietary carbohydrate and fermentable fibre reach the colon, certain gut bacteria ferment them to produce short-chain fatty acids such as butyrate, acetate and propionate. These compounds have important roles in maintaining the intestinal environment and epithelial barrier.

When fermentable carbohydrate becomes less available, bacterial metabolism can shift towards greater fermentation of amino acids. Tryptophan metabolism can produce indole, which is subsequently converted to indoxyl sulphate, while tyrosine and phenylalanine fermentation can contribute to the production of p-cresol and ultimately p-cresyl sulphate.

Normally, the kidneys contribute substantially to clearing these compounds from the circulation. As kidney function falls, however, their concentrations increase.

Slower intestinal transit may add another layer to this problem by increasing the time available for colonic protein fermentation.

Evidence for this has also been demonstrated directly in people with CKD. Ramos and colleagues studied 43 people with non-dialysis-dependent CKD with an average eGFR of approximately 21 mL/min/1.73 m². Around one-third had constipation. Participants with harder stools and less regular bowel habits had significantly higher concentrations of p-cresyl sulphate, even after accounting for kidney function and the dietary protein-to-fibre ratio (Ramos et al., 2020). Interestingly, the same relationship was not demonstrated for indoxyl sulphate, highlighting that different microbial toxins do not necessarily behave in the same way.

The evidence therefore suggests that intestinal transit can influence microbial toxin production, although we do not yet have clinical trials demonstrating that simply increasing bowel movement frequency reduces CKD progression.

Is Constipation Associated With Kidney Disease Progression?

Large population studies have also identified an association between constipation and subsequent kidney disease.

One of the largest involved more than 3.5 million US veterans who did not have CKD at baseline. Over approximately seven years, people with constipation had a higher risk of subsequently developing CKD, progressing to kidney failure and experiencing a more rapid decline in eGFR. The associations became progressively stronger as constipation severity increased (Sumida et al., 2017).

These findings are significant because of the enormous sample size, but they still do not prove causation. Constipation may partly represent other factors associated with poorer health, medication use, diet, physical inactivity or metabolic disease.

Nevertheless, when considered alongside the emerging research on the gut microbiome and gut-derived uraemic toxins, constipation is increasingly difficult to dismiss as an entirely unrelated gastrointestinal complaint in CKD.

Kidney Disease Can Also Slow the Bowel

Importantly, the relationship between constipation and kidney disease appears to go in both directions.

A large Japanese study published in 2026 examined more than 900,000 person-year observations from 217,734 people. Constipation became progressively more common as kidney function declined. It was identified in approximately 9.4% of observations with an eGFR of 60 or above, increasing to 13.1% with an eGFR of 45–59, 20.3% with an eGFR of 30–44, 25.3% with an eGFR of 15–29 and 45.2% when eGFR was below 15 mL/min/1.73 m² (Hirano, Sumida & Fukuma, 2026). Even after adjustment for multiple confounding factors, lower eGFR remained independently associated with constipation.

Several factors may contribute.

People with CKD may consume less fibre, particularly when they have been given broad advice to restrict potassium-rich fruits, vegetables, legumes and wholegrains. Fluid intake may need to be reduced as kidney disease advances. Physical activity may decline, particularly in people with fatigue, anaemia, cardiovascular disease or other comorbidities.

Medications can add to the problem. Oral iron, some phosphate binders, potassium-binding medications, calcium-channel blockers, opioids and some antidepressants can all contribute to constipation. The uraemic environment itself may also alter intestinal microbial composition and gastrointestinal motility (Cha, Park & Camilleri, 2023).

This makes constipation in advanced kidney disease a genuinely multifactorial problem rather than simply a consequence of inadequate fibre or water.

Why Bowel Motility Matters in Haemodialysis

Constipation becomes particularly common once people reach haemodialysis.

A 2025 systematic review and meta-analysis including 22 studies and 4,963 haemodialysis patients estimated that approximately 42% of people receiving haemodialysis experience constipation. Diabetes and lower levels of physical activity were among the significant risk factors identified (Nguyen, Hertanti & Chuang, 2025).

Earlier physiological research also suggests that this is not simply a matter of perception. Wu and colleagues measured colonic transit using radiopaque markers and found that average total colonic transit time was approximately 43 hours in haemodialysis patients, compared with 33 hours in people receiving continuous ambulatory peritoneal dialysis and 24 hours in healthy controls (Wu et al., 2004).

Several characteristics of haemodialysis may contribute. These include fluid restriction, dietary restrictions, medications such as phosphate binders and iron, several hours of physical inactivity during treatment and rapid changes in body fluid associated with ultrafiltration.

Bowel regularity may be particularly relevant because some gut-derived uraemic toxins are difficult to remove effectively with conventional haemodialysis. Indoxyl sulphate and p-cresyl sulphate are highly protein-bound, meaning only the small unbound fraction can readily cross the dialysis membrane. Consequently, conventional dialysis removes these compounds much less efficiently than small water-soluble molecules such as urea (Maheshwari et al., 2021).

This makes their intestinal production potentially important. Dialysis can replace many filtration functions of the kidney, but it does not completely compensate for the kidney's handling of all gut-derived metabolites.

It would be premature to suggest that treating constipation has been proven to lower uraemic toxin concentrations sufficiently to improve survival or other major dialysis outcomes. However, the relationship provides a good rationale for not ignoring persistent constipation in someone receiving haemodialysis.

Peritoneal Dialysis and Constipation

Constipation is also relevant in peritoneal dialysis (PD), although its implications are somewhat different.

A 2023 analysis of 729 participants in the Thailand Peritoneal Dialysis Outcomes and Practice Patterns Study found that self-reported constipation was associated with a shorter time to first episode of peritonitis, higher peritonitis rates and increased all-cause mortality (Halue et al., 2023). These findings are observational and do not establish constipation as the direct cause of these outcomes, but they reinforce the clinical importance of bowel function in PD.

Other research has also linked slower bowel habits in automated PD with higher concentrations of some gut-derived uraemic toxins, particularly p-cresyl sulphate (Ramos et al., 2020).

For someone receiving any form of dialysis, bowel habits therefore deserve to be considered alongside diet, medications, fluid management and other aspects of gastrointestinal health rather than being regarded as an unrelated problem.

What Happens After Kidney Transplantation?

Restoring kidney function through transplantation does not necessarily mean gastrointestinal symptoms disappear.

Immunosuppressive medications can themselves substantially affect the gastrointestinal tract.

In a large study of 4,232 kidney transplant recipients, gastrointestinal symptoms were extremely common. Fifty-eight per cent reported troublesome constipation, 53% diarrhoea and 92% at least one gastrointestinal symptom. Tacrolimus use was independently associated with both diarrhoea and constipation (Ekberg et al., 2007).

Mycophenolate is particularly well recognised for gastrointestinal adverse effects, especially diarrhoea.

A more recent randomised study investigated kidney transplant recipients receiving tacrolimus with or without mycophenolate mofetil. Six months after transplantation, 75% reported troublesome gastrointestinal symptoms. Diarrhoea was the most troublesome symptom and improved significantly when mycophenolate was discontinued according to the study protocol. Constipation, however, remained troublesome over time (Al Fatly et al., 2022).

This is important because gastrointestinal problems after transplantation are not simply issues of comfort. Vomiting, diarrhoea, delayed gastric emptying and other gastrointestinal disturbances can alter the absorption and exposure of immunosuppressive medications, including tacrolimus and mycophenolate (Tielemans et al., 2019).

Persistent diarrhoea in a transplant recipient therefore needs proper investigation rather than simply being treated as an inconvenient medication side effect. Infection, medication toxicity and other gastrointestinal pathology may all need to be considered, and changes to immunosuppressive medication should only occur with the transplant team.

What Is a Healthy Bowel Movement Frequency?

The 2024 research has led to considerable discussion of one or two bowel movements per day as a potential "Goldilocks zone". This is useful conceptually, but it should not become another rigid health rule.

Not everybody needs to open their bowels twice daily.

Someone having one comfortable, well-formed bowel movement each day without straining or incomplete evacuation is unlikely to benefit simply from trying to increase this number. Similarly, an individual who naturally opens their bowels every second day without other features of constipation may not necessarily have clinically significant dysfunction.

Supporting Bowel Regularity in CKD

Managing constipation in kidney disease also requires more care than simply recommending additional water, magnesium or large amounts of high-potassium fruit.

Fluid intake needs to be appropriate to the stage of kidney disease and, for people receiving dialysis, their individual fluid allowance. Fibre intake can often be improved, but the foods chosen may need to take serum potassium, phosphate, diabetes and overall dietary requirements into account.

This is another reason blanket "renal diet" advice can sometimes be counterproductive. Unnecessarily restricting plant foods in earlier-stage CKD may reduce fibre intake and dietary diversity without providing any benefit when blood potassium is normal.

Medications and supplements should also be reviewed. Some commonly used laxatives are not equally appropriate across all stages of kidney disease; for example, magnesium-containing laxatives require particular caution as kidney function becomes severely impaired.

Persistent or new constipation should also not automatically be attributed to CKD. Significant abdominal pain, vomiting, gastrointestinal bleeding, unexplained weight loss, inability to pass stool or wind, or a substantial new change in bowel habit requires medical assessment.

Conclusion

The relationship between bowel motility and kidney health appears increasingly to be a two-way process.

Slower intestinal transit may alter microbial metabolism and increase production or absorption of some gut-derived uraemic toxins. At the same time, declining kidney function creates an environment in which constipation becomes progressively more likely through changes in diet, fluid intake, medications, physical activity, intestinal motility and the gut microbiome.

This becomes particularly relevant in advanced CKD and dialysis, where constipation is extremely common and several gut-derived protein-bound toxins are poorly removed by conventional haemodialysis.

Kidney transplantation changes the picture again. Kidney function may improve dramatically, but gastrointestinal symptoms can remain common because immunosuppressive medications themselves can affect bowel function.

Bowel regularity is therefore more than a question of gastrointestinal comfort in someone with kidney disease. It is one component of the wider gut–kidney relationship and deserves to be considered as part of comprehensive CKD, dialysis and post-transplant care.

References

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Adrian Harper https://www.adrianharper.com.au