Supplements and Herbal Medicines in Kidney Disease: Are They Safe?
One of the most common questions I am asked by people with kidney disease is whether a particular supplement is safe. It sounds like a straightforward question, but in practice it rarely has a simple yes or no answer. Kidney disease alters the way the body handles minerals, vitamins, amino acids, medications and their metabolites, and these changes become more important as kidney function declines. Dialysis then changes the picture again by increasing losses of some nutrients and amino acids, while kidney transplantation introduces a different set of considerations related to immunosuppressant medications.
This means that a supplement can be appropriate at one stage of kidney disease and less appropriate at another. It also means that avoiding supplements altogether is not necessarily the best approach. Nutrient deficiencies occur in chronic kidney disease (CKD), dialysis can increase nutritional requirements, and selected supplements and herbal medicines may have useful therapeutic roles.
The more useful question is therefore not whether a supplement is simply ‘kidney safe’, but whether it is appropriate for the individual person, at a particular dose, at their current stage of kidney disease.
Why the stage of kidney disease matters
The kidneys have an important role in electrolyte balance, acid–base regulation, mineral metabolism and the excretion of metabolic waste. As renal function declines, potassium, magnesium and other substances may become more difficult to regulate, while protein and amino-acid metabolism also changes.
Current KDIGO guidelines recommend a protein intake of around 0.8 g/kg/day for most adults with CKD stages G3–G5 and suggest avoiding sustained high protein intake above 1.3 g/kg/day in people at risk of progression (KDIGO, 2024). However, once a person commences dialysis, protein requirements generally increase because amino acids and small peptides are lost during dialysis.
This illustrates why supplement advice needs to change with the clinical situation. Someone with stage 2 CKD and normal potassium is in a very different position to someone with stage 5 CKD and recurrent hyperkalaemia, while a person receiving haemodialysis has different nutritional requirements again.
Common supplements that require some consideration
Potassium is one of the clearest examples. People with CKD do not automatically have high potassium, and there is no reason to universally restrict potassium in earlier kidney disease where blood levels remain normal. However, as renal potassium excretion becomes impaired, supplements containing potassium can make an important contribution to total intake.
Potassium may be obvious on the label as potassium chloride, potassium citrate or potassium gluconate, but it can also occur in electrolyte powders, hydration products, salt substitutes, greens powders and multi-mineral formulas (National Kidney Foundation, 2025).
The issue is therefore not that potassium itself is harmful. Potassium is an essential nutrient. The question is whether supplemental potassium is required and whether it remains appropriate in the context of kidney function, blood results, diet and medications.
Vitamin A
Vitamin A is another nutrient where the form and stage of kidney disease matter. Preformed vitamin A, including retinol, retinyl palmitate and retinyl acetate, can accumulate in advanced kidney disease. Elevated vitamin A concentrations have been described in haemodialysis patients, and clinically significant hypervitaminosis A has occurred with excessive supplementation (Fishbane et al., 1995).
This does not mean vitamin-A-containing foods should be avoided, nor are carotenoids such as beta-carotene metabolically equivalent to high-dose supplemental retinol. However, routine supplementation with preformed vitamin A becomes increasingly difficult to justify without a clear indication as kidney function declines.
Calcium and magnesium
Calcium and magnesium are similarly difficult to assess without context. CKD alters the relationship between calcium, phosphate, parathyroid hormone and vitamin D, particularly as CKD-mineral and bone disorder develops.
A European consensus statement suggests a total elemental calcium intake of around 800–1,000 mg/day in adults with CKD, including calcium from diet and medications, and generally recommends not exceeding 1,500 mg/day unless there is a specific indication (Evenepoel et al., 2024). This is quite different from simply adding a 1,000 mg calcium supplement because calcium is considered beneficial for bone health.
Magnesium presents an interesting contrast. Low magnesium may occur and there is increasing interest in the potential therapeutic benefits of magnesium in CKD. However, renal magnesium regulation changes as GFR declines, while in dialysis patients magnesium balance is substantially influenced by the dialysis prescription (van de Wal-Visscher, Kooman and van der Sande, 2018).
Neither calcium nor magnesium therefore needs to be universally avoided. Their use needs to be considered alongside the individual's diet, kidney function and mineral metabolism.
Vitamin B6
Vitamin B6 is a particularly good example of why the answer is not simply to avoid supplements in kidney disease.
Biochemical B6 deficiency has been reported in haemodialysis patients. A systematic review found deficiency in approximately 24–56% of patients studied, while dialysis reduced circulating B6 concentrations by 28–48% depending on the dialyser used (Corken and Porter, 2011). This suggests B6 supplementation may have a useful role in some renal patients.
However, excessive supplemental B6 can cause peripheral neuropathy. The Therapeutic Goods Administration (TGA) has reported neuropathy at supplemental intakes below 50 mg/day, particularly where people are unknowingly taking B6 across several products, and products providing more than 10 mg/day now require a neuropathy warning in Australia (TGA, 2026).
B6 may appear as pyridoxine hydrochloride or pyridoxal-5-phosphate (P5P). P5P is the biologically active coenzyme form and may be considered where B6 supplementation is indicated, rather than relying on large doses of pyridoxine. However, this distinction should not be overstated. P5P should not be regarded as completely free of toxicity risk and the total dose, duration and reason for supplementation remain important.
Creatine
Creatine is frequently described as harmful to the kidneys, although the evidence is considerably more nuanced.
Creatine is converted to creatinine and can therefore increase serum creatinine, which may make a creatinine-based eGFR appear lower. This can create the impression that kidney function has deteriorated even where true filtration has not changed.
A 2026 systematic review and meta-analysis of 26 studies, which included people with CKD, found that creatine supplementation increased serum creatinine and reduced creatinine-based estimates of GFR. However, there was no significant deterioration when GFR was assessed using Cr-EDTA, nor significant changes in albuminuria or proteinuria (de Souza Almeida et al., 2026).
This suggests that an increase in creatinine during creatine supplementation does not necessarily represent kidney injury.
It does not establish that creatine is appropriate in every person with CKD, particularly as evidence in more advanced kidney disease remains limited. However, it does mean that simply describing creatine as nephrotoxic is inaccurate. If creatine has a clear therapeutic or nutritional purpose, its effect on creatinine-based monitoring needs to be understood and, in some circumstances, cystatin C or measured GFR may provide useful additional information.
Glutamine and individual amino acids
Glutamine, tyrosine, phenylalanine and tryptophan are commonly used individually for gut health, exercise recovery, mood, sleep or neurotransmitter support. However, long-term supplemental use has been poorly studied in people with significant kidney disease.
A recent case report described tubular acute kidney injury in a patient consuming 18 g/day of L-glutamine (Bhoelan et al., 2026). A single case does not demonstrate that glutamine routinely damages the kidneys, but it does suggest that large supplemental doses should not be treated as metabolically insignificant in someone with impaired renal function.
Tyrosine and phenylalanine demonstrate how amino-acid metabolism itself changes in kidney failure. The kidney contributes to the conversion of phenylalanine to tyrosine, and this process becomes impaired in chronic kidney failure. As a result, tyrosine concentrations may fall while phenylalanine concentrations remain normal or increase (Kopple, 2007).
Tryptophan metabolism is also altered in uraemia. Indoxyl sulphate, a gut-derived metabolite of tryptophan, accumulates as kidney function declines and forms part of the group of protein-bound uraemic retention solutes associated with CKD (Ellis et al., 2016).
None of this demonstrates that normal supplemental doses of tyrosine, phenylalanine or tryptophan directly damage the kidneys. Rather, it highlights that amino-acid metabolism in advanced CKD differs from normal physiology. Therefore, the reason for supplementation, dose and overall protein and nitrogen intake need to be considered.
Vitamin C
Vitamin C provides another example of a useful nutrient where the dose matters.
Vitamin C may be beneficial where dietary intake is inadequate, and dialysis can contribute to losses of water-soluble vitamins. However, vitamin C is partly metabolised to oxalate, which relies heavily on renal excretion.
In haemodialysis patients, increasing oral vitamin C supplementation from 100 mg to 500 mg/day significantly increased plasma oxalate concentrations (Rolton et al., 1991).
The implication is not that vitamin C should be avoided. Rather, the common assumption that large amounts of a water-soluble vitamin are harmless because the excess will simply be excreted becomes less reliable when renal excretion is severely impaired.
Herbal medicine and kidney disease
Herbal medicine can have a useful role in people with kidney disease, but it should be prescribed with the same consideration given to other pharmacologically active interventions.
The relevant questions include the plant species, extraction method, dose, duration, electrolyte content, product quality and potential interactions with medications.
There are genuine herbal nephrotoxins, with aristolochic acid being the clearest example. However, many of the practical considerations are more subtle. A herb may influence blood pressure, potassium, blood glucose, coagulation or medication metabolism without being directly toxic to the kidneys.
The preparation also matters. A defined dose of a professionally formulated liquid herbal extract is a very different intervention to an unidentified or poorly regulated powdered herbal product purchased online.
For this reason, I prefer to assess the actual herbal formulation rather than make broad statements that an individual herb is always either ‘good’ or ‘bad’ for kidney disease.
Kidney transplantation requires another level of consideration
Following kidney transplantation, supplement use becomes particularly important because of potential interactions with immunosuppressant medications.
Tacrolimus is one of the most commonly prescribed immunosuppressants following kidney transplantation and has a relatively narrow therapeutic range. Underexposure increases the risk of rejection, while excessive exposure increases adverse effects, including nephrotoxicity to the transplanted kidney (Bentata, 2020).
St John's wort provides a good example. In ten stable kidney transplant recipients, two weeks of St John's wort reduced dose-adjusted tacrolimus exposure substantially, with the median tacrolimus dose needing to increase from 4.5 mg/day to 8 mg/day to maintain therapeutic concentrations (Mai et al., 2003).
An interaction can also move in the opposite direction. Schisandra sphenanthera extract has been studied as a means of increasing tacrolimus exposure. In kidney transplant recipients, it increased dose-adjusted tacrolimus trough concentrations by approximately 199% and overall tacrolimus exposure by approximately 126% (Li et al., 2017).
This does not mean Schisandra is directly toxic to the transplanted kidney. In the study it was deliberately being used as a tacrolimus-sparing intervention. However, it demonstrates that a herbal medicine can alter exposure to a critical medication to a clinically significant degree.
This is why I think supplementation after kidney transplantation requires a different approach. A supplement or herbal medicine may still be useful, but anything capable of altering immunosuppressant concentrations should be discussed with the transplant team before it is commenced, stopped or substantially changed.
Why a kidney-focused supplement review is useful
The difficulty with generic supplement advice is that it rarely accounts for why the supplement is being taken or the clinical context in which it is being used.
When I review supplements in someone with kidney disease, I consider the cause and stage of their kidney disease, the trajectory of kidney function, albuminuria or proteinuria, potassium, phosphate, calcium, magnesium and bicarbonate, dialysis where relevant, prescription medications, diet, and the actual dose of each supplement being taken.
It is also important to look for duplication. Vitamin B6, magnesium, potassium and vitamin A, for example, may occur across several different products, making the total daily intake considerably greater than the person realises.
Sometimes a review identifies something that is no longer appropriate. At other times it identifies a supplement that has been unnecessarily avoided, a nutritional deficiency that has not been addressed, or a potentially useful intervention that can be introduced with appropriate monitoring.
This is why I do not think the aim should be to take supplements away from people with kidney disease. The aim is to make their use more specific.
A naturopath with a particular clinical focus in kidney disease can be well placed to undertake this type of review because nutritional supplements and herbal medicines can be assessed alongside renal pathology, diet, medications and current blood results rather than being considered as a separate layer of treatment. For people receiving dialysis or living with a kidney transplant, this also provides an opportunity to integrate complementary care appropriately with their renal team.
The question is therefore not simply:
‘Is this supplement safe for kidneys?’
A more useful question is:
‘Is this supplement appropriate for my kidneys, at this dose, at this stage of kidney disease, and alongside everything else I am taking?’
The answer to that question may change as kidney function, treatment and nutritional requirements change.
References
Bentata, Y. (2020) ‘Tacrolimus: 20 years of use in adult kidney transplantation. What we should know about its nephrotoxicity’, Artificial Organs, 44(2), pp. 140–152. doi:10.1111/aor.13551. View article
Bhoelan, S., Kürül, S., Krol, C.G., van Midden, D. and Bakker, R. (2026) ‘L-Glutamine-Induced Acute Kidney Injury: A Clinical Observation’, Nephron, 150(1), pp. 47–51. doi:10.1159/000548247. View article
Corken, M. and Porter, J. (2011) ‘Is vitamin B6 deficiency an under-recognized risk in patients receiving haemodialysis? A systematic review: 2000–2010’, Nephrology, 16(7), pp. 619–625. doi:10.1111/j.1440-1797.2011.01479.x. View article
de Souza Almeida, A. et al. (2026) ‘Impact of creatine supplementation on kidney health: a systematic review and meta-analysis’, International Urology and Nephrology. doi:10.1007/s11255-026-05287-x. View article
Ellis, R.J., Small, D.M., Vesey, D.A., Johnson, D.W., Francis, R., Vitetta, L., Gobe, G.C. and Morais, C. (2016) ‘Indoxyl sulphate and kidney disease: causes, consequences and interventions’, Nephrology, 21(3), pp. 170–177. doi:10.1111/nep.12580. View article
Evenepoel, P. et al. (2024) ‘Recommended calcium intake in adults and children with chronic kidney disease—a European consensus statement’, Nephrology Dialysis Transplantation, 39(2), pp. 341–366. doi:10.1093/ndt/gfad185. View article
Fishbane, S., Frei, G.L., Finger, M., Dressler, R. and Silbiger, S. (1995) ‘Hypervitaminosis A in two hemodialysis patients’, American Journal of Kidney Diseases, 25(2), pp. 346–349. doi:10.1016/0272-6386(95)90020-9. View article
KDIGO CKD Work Group (2024) ‘KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease’, Kidney International, 105(Suppl. 4S), pp. S117–S314. View guideline
Kopple, J.D. (2007) ‘Phenylalanine and tyrosine metabolism in chronic kidney failure’, Journal of Nutrition, 137(6 Suppl. 1), pp. 1586S–1590S. doi:10.1093/jn/137.6.1586S. View article
Li, J. et al. (2017) ‘Wuzhi Tablet (Schisandra sphenanthera extract) is a promising tacrolimus-sparing agent for renal transplant recipients who are CYP3A5 expressers: a two-phase prospective study’, Drug Metabolism and Disposition, 45(11), pp. 1114–1119. doi:10.1124/dmd.117.076737. View article
Mai, I., Störmer, E., Bauer, S., Krüger, H., Budde, K. and Roots, I. (2003) ‘Impact of St John's wort treatment on the pharmacokinetics of tacrolimus and mycophenolic acid in renal transplant patients’, Nephrology Dialysis Transplantation, 18(4), pp. 819–822. doi:10.1093/ndt/gfg002. View article
National Kidney Foundation (2025) ‘Herbal supplements and kidney disease’. View resource
Rolton, H.A., McConnell, K.M., Modi, K.S. and Macdougall, A.I. (1991) ‘The effect of vitamin C intake on plasma oxalate in patients on regular haemodialysis’, Nephrology Dialysis Transplantation, 6(6), pp. 440–443. View article
Therapeutic Goods Administration (TGA) (2026) ‘Peripheral neuropathy with supplementary vitamin B6 (pyridoxine)’, Australian Government, updated 25 February 2026. View TGA advice
van de Wal-Visscher, E.R., Kooman, J.P. and van der Sande, F.M. (2018) ‘Magnesium in Chronic Kidney Disease: Should We Care?’, Blood Purification, 45(1–3), pp. 173–178. doi:10.1159/000485212. View article