Microplastics and Kidney Disease: The Evidence So Far

Microplastics have rapidly moved from being primarily an environmental issue to an emerging area of human health research. These small plastic particles are now widespread in air, water and food and have subsequently been detected in human blood and a growing number of tissues and organs, including the kidneys.

The kidneys are of particular interest because they continuously filter the circulation and play an important role in eliminating waste products and environmental compounds from the body. Microplastics have now been detected directly within human kidney tissue and urine, while experimental research suggests that exposure can contribute to oxidative stress, inflammation, cellular injury and renal fibrosis (Massardo et al. 2024; Lee et al. 2025).

For people living with chronic kidney disease (CKD), this raises several important questions. Could microplastics contribute to kidney damage? Does declining kidney function alter their clearance? And could a kidney that is already compromised be more susceptible to their effects?

Research is developing rapidly, but it is important to distinguish biological plausibility from demonstrated clinical harm. There is increasingly convincing experimental evidence that micro- and nanoplastics can adversely affect renal cells and tissues. However, we do not yet have good prospective human evidence demonstrating that everyday microplastic exposure causes CKD or accelerates its progression (Augey et al. 2026).

What Are Microplastics?

Microplastics are generally defined as plastic particles smaller than 5 millimetres, while nanoplastics are much smaller, generally below 1 micrometre. They arise either as intentionally manufactured small particles or through the gradual breakdown of larger plastic materials.

Human exposure occurs principally through ingestion and inhalation. Micro- and nanoplastics have been identified in drinking water, food and indoor and outdoor air. Their size is important because smaller particles appear more capable of crossing biological barriers, entering the circulation and potentially reaching internal organs (de Oliveira et al. 2024; Lee et al. 2025).

One difficulty when interpreting the research is that ‘microplastics’ describes a very diverse group of particles. Different polymers vary in size, shape and surface chemistry, and environmental particles may also contain chemical additives or have other pollutants attached to their surfaces. Experimental studies commonly investigate a single polymer, particularly polystyrene, under controlled conditions that do not necessarily reproduce normal human exposure.

Microplastics Have Been Found in Human Kidneys

One of the more important developments in this field has been the direct detection of microplastics within human renal tissue.

Massardo and colleagues examined healthy portions of kidney tissue obtained during nephrectomy, together with urine samples from healthy donors, using micro-Raman spectroscopy. Microplastic particles were identified in both. The particles detected in kidney tissue ranged from approximately 1 to 29 μm, with polyethylene and polystyrene among the most frequently identified polymers (Massardo et al. 2024).

This study provides evidence that at least some plastic particles can reach the human kidneys and that particles can also be eliminated through urine.

However, finding a particle within an organ does not establish that it has caused disease. The study was small, analysing kidney tissue from ten nephrectomies and ten urine samples from healthy donors, and methods for detecting and quantifying microplastics in biological tissues remain technically challenging.

At present, we therefore know considerably more about the presence of microplastics in the human kidney than we know about the clinical consequences of that exposure.

How Might Microplastics Damage the Kidneys?

Although human outcome data remain limited, experimental research has identified several plausible mechanisms through which microplastics could contribute to kidney injury.

Oxidative stress and mitochondrial dysfunction

Oxidative stress is one of the most consistent findings.

Wang and colleagues investigated polystyrene microplastic exposure in human proximal tubular kidney cells and mice. Exposure increased mitochondrial reactive oxygen species and was associated with endoplasmic reticulum stress, inflammatory signalling and altered autophagy — the process through which cells recycle damaged cellular components. Kidney abnormalities were also identified in exposed mice (Wang et al. 2021).

This is potentially important in CKD because mitochondrial dysfunction and oxidative stress are already involved in many pathways contributing to progressive renal damage. Excess reactive oxygen species can damage cellular membranes, proteins, DNA and mitochondria while simultaneously amplifying inflammatory signalling.

Inflammation and cellular injury

Microplastic exposure also appears capable of activating inflammatory pathways within renal tissue.

Experimental studies have identified effects involving NF-κB and MAPK signalling, inflammatory cytokines, endoplasmic reticulum stress and several forms of regulated cell death. These include apoptosis, pyroptosis and ferroptosis, together with disturbances in normal autophagy (Tan et al. 2025).

The importance of these findings is not that any individual molecular pathway proves that microplastics cause kidney disease in humans. Rather, different experimental models are increasingly pointing towards a similar pattern: plastic particles can create cellular stress, increase inflammatory signalling and interfere with normal renal cell function.

Renal fibrosis

Perhaps the most relevant finding for CKD is the potential relationship with renal fibrosis.

Fibrosis is the progressive accumulation of extracellular matrix and scar-like tissue within the kidneys. Regardless of the original cause of kidney injury, fibrosis is one of the principal pathways through which ongoing damage eventually results in permanent loss of functioning renal tissue.

Animal studies have demonstrated increased interstitial fibrosis following microplastic exposure. Kuang and colleagues also found that microplastic exposure aggravated kidney injury and fibrosis following experimentally induced renal ischaemia-reperfusion injury in mice (Kuang et al. 2024).

Again, these findings cannot be directly translated into normal human environmental exposure. They do, however, provide a plausible mechanism through which microplastics could potentially add to existing renal injury.

What About People Who Already Have Chronic Kidney Disease?

This is perhaps the most clinically relevant emerging question.

Many of the pathways affected by microplastics — oxidative stress, inflammation, mitochondrial dysfunction and fibrosis — are already involved in the progression of CKD. It is therefore reasonable to ask whether microplastic exposure might have a greater effect on an already compromised kidney.

A 2026 study specifically investigated this using mice with experimentally induced CKD. Polystyrene microplastic exposure reduced creatinine clearance and increased markers of renal dysfunction even in otherwise healthy animals. In animals with CKD, exposure further increased tubular injury, inflammation, oxidative stress, DNA damage and interstitial fibrosis (Beegam et al. 2026).

This is interesting because it raises the possibility that microplastics may act less as a single cause of kidney disease and more as an additional environmental stressor capable of amplifying pathological processes that are already present.

However, this remains an animal study. The doses, particle sizes and polymers used experimentally cannot simply be equated with the complex mixture and generally lower concentrations encountered through normal human exposure.

At present, these findings are therefore best considered an important signal requiring further investigation rather than evidence that microplastic exposure accelerates CKD in people.

Could Reduced Kidney Function Affect Microplastic Clearance?

The relationship between the kidneys and microplastics may potentially work in both directions.

Finding microplastics in human urine suggests that the kidneys participate in the elimination of at least some particles. Current models propose that sufficiently small particles may interact with the glomerular filtration barrier and renal tubules before being excreted in urine (Tan et al. 2025).

This raises the possibility that declining kidney function could reduce the elimination of certain particles and contribute to greater systemic retention. Recent nephrology reviews have proposed this type of bidirectional relationship: microplastics may contribute to renal stress, while impaired renal function may simultaneously alter their distribution and clearance (de Oliveira et al. 2024; Augey et al. 2026).

However, this remains poorly understood. Particle size, shape and surface properties are likely to influence clearance, and renal elimination is only one possible route through which plastic particles may leave the body.

Microplastics, Environmental Chemicals and Dialysis

Dialysis adds another level of complexity.

People receiving haemodialysis have substantially reduced or absent native kidney clearance, which could potentially increase retention of substances normally eliminated through urine. At the same time, dialysis exposes blood to an extracorporeal circuit containing synthetic membranes, tubing and other plastic components.

A small 2026 clinical study examined blood immediately before and after haemodialysis in nine patients and also investigated water passing through dialysis equipment. Microplastics were detected after passage through components of the dialysis system, while measured circulating microplastic concentrations were significantly higher after dialysis. However, the study was very small and does not establish the effect of dialysis on long-term microplastic accumulation (Deng et al. 2026).

Importantly, dialysis should not simply be viewed as an additional source of environmental exposure.

Dialysis can simultaneously provide an alternative route of removal for some circulating environmental compounds. Research involving phthalates illustrates this complexity. In an earlier haemodialysis study, serum concentrations of the plasticiser DEHP and some of its metabolites increased during dialysis, consistent with exposure from dialysis tubing. In contrast, concentrations of phthalic acid, a downstream metabolite, fell significantly during treatment, suggesting dialytic removal (Mettang et al. 1996).

A more recent review of endocrine-disrupting chemicals in dialysis similarly found that kidney failure can impair elimination of these compounds while dialysis equipment itself may introduce additional exposure (Cambien et al. 2023).

It is important not to equate phthalates with microplastics. Phthalates are soluble chemical compounds associated with plastics, whereas microplastics are physical particles. They may behave very differently during dialysis.

The most useful way to think about dialysis is therefore as a dynamic exchange. Some environmental compounds may be introduced through the treatment system while others are removed from the circulation. For micro- and nanoplastics themselves, we do not yet know whether repeated haemodialysis produces a net increase or reduction in long-term body burden.

Microplastics May Carry Other Environmental Pollutants

Microplastics are also not necessarily biologically inert fragments of plastic.

Their surfaces can adsorb metals and organic environmental contaminants, while plastics themselves may contain chemical additives including bisphenols and phthalates. This has led to the proposed ‘Trojan horse’ effect, whereby plastic particles may transport other environmental contaminants into tissues.

Experimental studies suggest that co-exposure to microplastics and other contaminants can sometimes produce greater toxicity than either exposure alone (Lee et al. 2025; Augey et al. 2026).

This may ultimately prove important for kidney health because real-world environmental exposures rarely occur independently. Microplastics may represent one component of a broader cumulative environmental burden rather than functioning as an isolated renal toxin.

Practical Ways to Reduce Microplastic Exposure

Completely avoiding microplastics is unrealistic. They are now widespread throughout our environment, and attempting to eliminate every possible exposure is neither practical nor necessary.

There are, however, reasonable ways to reduce avoidable exposure.

Avoid heating food in plastic where possible. Experimental research has shown substantially greater release of micro- and nanoplastics from some plastic food containers during microwave heating compared with refrigerated or room-temperature storage (Hussain et al. 2023). Glass or ceramic containers are a simple alternative for reheating food.

Using glass or stainless steel for frequently used food and drink containers may also reduce repeated exposure, particularly where plastic containers are heated, scratched or degraded.

Bottled water should not automatically be assumed to provide a lower microplastic exposure than tap water. Plastic particles have been detected in both, while appropriate water filtration technologies may reduce particulate exposure to varying degrees (Lee et al. 2025).

Reducing unnecessary single-use plastics is another practical strategy. It may reduce some direct sources of exposure while also addressing the wider environmental plastic burden from which secondary microplastics originate.

Indoor air and dust are also relevant. Synthetic textiles, furnishings, carpets and other materials can release plastic fibres into the indoor environment, making inhalation another potential route of exposure.

The aim does not need to be creating a completely plastic-free life. Reducing the most obvious and repeated sources of exposure is a more realistic approach.

Putting the Evidence Into Perspective

The evidence surrounding microplastics and kidney health has developed considerably over the past few years.

We now know that microplastics can reach human kidneys and that particles can be detected within both kidney tissue and urine. Experimental studies consistently identify mechanisms relevant to kidney disease, including oxidative stress, mitochondrial dysfunction, inflammation, cellular injury and fibrosis. Emerging experimental evidence also suggests that pre-existing CKD may increase susceptibility to these effects.

What we do not yet know is equally important.

There is currently no established human toxic threshold for microplastics, and prospective human evidence has not demonstrated that normal environmental exposure causes CKD or accelerates its progression. Accurately measuring human exposure also remains difficult, while experimental studies frequently use particle types and concentrations that differ substantially from real-world exposure (Augey et al. 2026).

For someone living with kidney disease, microplastics are therefore best considered a possible additional environmental contributor to cumulative renal stress rather than an established primary cause of CKD.

Reducing avoidable exposure is reasonable, particularly where this involves simple measures such as avoiding heating food in plastic and reducing unnecessary plastic use. However, this sits alongside the factors we already know are important for protecting remaining kidney function, including appropriate blood pressure and metabolic management, individualised nutrition, medication and supplement safety, and ongoing monitoring of kidney function.

As the research develops, environmental exposures such as microplastics are likely to become an increasingly important part of our understanding of kidney health. At present, the most appropriate approach is to take the emerging evidence seriously while remaining clear about what it can — and cannot — yet tell us.

References

Augey L, Berdougo-Tritz J, Mbarek A, Jadoul M, Massy Z, Deray G and Liabeuf S (2026) ‘Effects of microplastics and nanoplastics on the kidneys’, Nephrology Dialysis Transplantation, 41(8):1412–1420, https://doi.org/10.1093/ndt/gfag034

Beegam S, Al-Salam S, Zaaba NE, Elzaki O, Greish YE, Ali BH and Nemmar A (2026) ‘Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1’, Life Sciences, 385:124142, https://doi.org/10.1016/j.lfs.2025.124142

Cambien G, Dupuis A, Guihenneuc J, Bauwens M, Belmouaz M and Ayraud-Thevenot S (2023) ‘Endocrine disruptors in dialysis therapies: a literature review’, Environment International, 178:108100, https://doi.org/10.1016/j.envint.2023.108100

de Oliveira RB, Pelepenko LE, Masaro DA, Lustosa GMMM, de Oliveira MC, Roza NAV, Marciano MA, dos Reis LM, Kamel S, Louvet L and Mazon T (2024) ‘Effects of microplastics on the kidneys: a narrative review’, Kidney International, 106(3):400–407, https://doi.org/10.1016/j.kint.2024.05.023

Deng Y, Sun T, Long Z, Luo X, Geng X, Lin Z, Chen C and Li X (2026) ‘Microplastic entry into bloodstream via hemodialysis: a dual-simulation clinical study’, Environmental Pollution, 398:128085, https://doi.org/10.1016/j.envpol.2026.128085

Hussain KA, Romanova S, Okur I, Zhang D, Kuebler J, Huang X, Wang B, Fernandez-Ballester L, Lu Y, Schubert M and Li Y (2023) ‘Assessing the release of microplastics and nanoplastics from plastic containers and reusable food pouches: implications for human health’, Environmental Science & Technology, 57(26):9782–9792, https://doi.org/10.1021/acs.est.3c01942

Kuang Q, Gao L, Feng L, Xiong X, Yang J, Zhang W, Huang L, Li L and Luo P (2024) ‘Toxicological effects of microplastics in renal ischemia-reperfusion injury’, Environmental Toxicology, 39(4):2350–2362, https://doi.org/10.1002/tox.24115

Lee YH, Zheng CM, Wang YJ, Wang YL and Chiu HW (2025) ‘Effects of microplastics and nanoplastics on the kidney and cardiovascular system’, Nature Reviews Nephrology, 21(9):585–596, https://doi.org/10.1038/s41581-025-00971-0

Massardo S, Verzola D, Alberti S, Caboni C, Santostefano M, Verrina EE, Angeletti A, Lugani F, Ghiggeri GM, Bruschi M, Candiano G, Rumeo N, Gentile M, Cravedi P, La Maestra S, Zaza G, Stallone G, Esposito P, Viazzi F, Mancianti N, La Porta E and Artini C (2024) ‘MicroRaman spectroscopy detects the presence of microplastics in human urine and kidney tissue’, Environment International, 184:108444, https://doi.org/10.1016/j.envint.2024.108444

Mettang T, Thomas S, Kiefer T, Fischer FP, Kuhlmann U, Wodarz R and Rettenmeier AW (1996) ‘Uraemic pruritus and exposure to di(2-ethylhexyl) phthalate (DEHP) in haemodialysis patients’, Nephrology Dialysis Transplantation, 11(12):2439–2443, https://doi.org/10.1093/ndt/11.12.2439

Tan RY, She QY, Ma YC, Liu MH, Li LJ, Huang LL, Zhong YW and Bi HX (2025) ‘The threat of microplastics to human kidney health: mechanisms of nephrotoxicity and future research directions’, Environmental Research, 283:122124, https://doi.org/10.1016/j.envres.2025.122124

Wang YL, Lee YH, Hsu YH, Chiu IJ, Huang CCY, Huang CC, Chia ZC, Lee CP, Lin YF and Chiu HW (2021) ‘The kidney-related effects of polystyrene microplastics on human kidney proximal tubular epithelial cells HK-2 and male C57BL/6 mice’, Environmental Health Perspectives, 129(5):057003, https://doi.org/10.1289/EHP7612