Peritoneal Dialysis removes protein, Vitamin D, magnesium, etc.

Peritoneal dialysis filters out Vitamin D. Claude AI - March 2026

Evidence of Vitamin D Loss During Peritoneal Dialysis

A study of 14 patients on continuous ambulatory peritoneal dialysis (CAPD) measured both serum and dialysate levels of 25-hydroxyvitamin D (25-OHD3), 1,25-dihydroxyvitamin D, and vitamin D-binding protein. Measurable quantities of all three were found in the dialysate effluent. Peritoneal clearance of 25-OHD3 was approximately 0.40 mL/min, and DBP clearance was 0.18 mL/min. The mass transfer of 25-OHD3 was approximately −10.4 nmol per 24 hours. The researchers concluded that CAPD leads to ongoing losses of both 25-OHD3 and DBP [1].

PD Patients Have Lower Vitamin D Levels Than Hemodialysis Patients

An observational study of 115 prevalent dialysis patients found that hypovitaminosis D occurred in 100% of patients, with 51% frankly deficient and 42% insufficient. Only 7% had normal levels. Notably, PD patients had the lowest 25(OH)D levels of all dialysis modalities. The authors noted that documented loss of vitamin D through the peritoneal effluent likely explains the especially high prevalence of deficiency in PD patients compared to hemodialysis (HD) patients [2].

A comparative study further quantified this difference: 33% of PD patients were vitamin D deficient (below 25 nmol/L) compared to only 4% of HD patients [3].

A separate study of 169 dialysis and CKD patients confirmed that vitamin D levels are lower in both HD and PD patients compared to renal transplant recipients, supporting the recommendation for routine vitamin D supplementation in all CKD patients regardless of GFR [4].

Therapeutic Use: PD to Treat Vitamin D Toxicity

The ability of PD to remove vitamin D has even been exploited therapeutically. A case report described a 75-year-old man with severe vitamin D toxicity (25-OHD levels above 200 ng/mL) causing hypercalcemia, acute kidney injury, and pancreatitis. After conventional treatments failed to durably control his calcium levels, 10 sessions of peritoneal dialysis were performed. Each cycle was estimated to extract approximately 75,000–90,000 ng of vitamin D, and the treatment resulted in resolution of both the hypercalcemia and the elevated vitamin D levels [5]. This approach was first described in a 1966 case report [6].

Contributing Factors to Vitamin D Deficiency in Dialysis Patients

Beyond peritoneal losses, multiple factors contribute to low vitamin D in CKD and dialysis patients: reduced cutaneous synthesis of vitamin D3 as GFR declines and with aging, decreased sunlight exposure due to fatigue and dialysis schedules, higher melanin content in at-risk populations, and dietary restrictions on vitamin D-fortified foods (such as dairy) due to phosphorus concerns [7].

Vitamin D Supplementation May Have Pleiotropic Benefits in PD

A review of 29 observational and 11 interventional studies (1,036 subjects) found that vitamin D administration in PD patients was associated with decreased PTH levels in most studies, reduced peritonitis risk in two studies, and decreased proteinuria in four studies. The authors suggested that vitamin D could help preserve residual renal function and maintain effective peritoneal membrane dialysance [3].

Additionally, vitamin D deficiency in PD patients has been correlated with anemia, microinflammation, oxidative stress, and cognitive impairment [3].

A pilot randomized controlled trial is investigating whether oral vitamin D supplementation (2,000 IU/day of cholecalciferol) can prevent PD-related peritonitis in patients who have already experienced an episode [8].

Clinical Implications

PD patients require vitamin D replacement to counteract the continuous drain of vitamin D metabolites and binding protein through the peritoneal membrane. This is especially important for underserved populations already at elevated risk for vitamin D deficiency, including Native American communities served by Indian Health Service clinics.

References

Vitamin D and vitamin-D-binding protein kinetics in patients treated with continuous ambulatory peritoneal dialysis (CAPD). PubMed (PMID: 2488382). https://pubmed.ncbi.nlm.nih.gov/2488382/
Gracia-Iguacel C, et al. Vitamin D Deficiency in Dialysis Patients: Effect of Dialysis Modality and Implications on Outcome. Journal of Renal Nutrition, 2010. https://www.sciencedirect.com/science/article/abs/pii/S1051227610000762
VitaminDWiki. Peritoneal dialysis probably consumes a lot more vitamin D than haemodialysis
Comparison of Serum Vitamin D Levels Among Patients With Chronic Kidney Disease, Patients in Dialysis, and Renal Transplant Patients. PubMed (PMID: 26093729). https://pubmed.ncbi.nlm.nih.gov/26093729/
Vitamin D Toxicity Managed with Peritoneal Dialysis. PMC, 2021. https://pmc.ncbi.nlm.nih.gov/articles/PMC8261186/
Peritoneal Dialysis Removes Vitamin D. JAMA, 1966. https://jamanetwork.com/journals/jama/article-abstract/661786
How Vitamin D May Help CKD Patients. Renal and Urology News, 2024. https://www.renalandurologynews.com/features/how-vitamin-d-may-help-ckd-patients/
The effects of oral vitamin D supplementation on the prevention of peritoneal dialysis-related peritonitis: study protocol for a randomized controlled clinical trial. PMC, 2019. https://pmc.ncbi.nlm.nih.gov/articles/PMC6883549/

Chat-GPT AI

Yes — peritoneal dialysis (PD) can remove some forms of vitamin D from the body, but the effect depends on which form of vitamin D you're talking about.

1️⃣ 25-hydroxyvitamin D (25-OH D, calcidiol)

This is the main circulating storage form measured on blood tests.

It is tightly bound to vitamin D binding protein (VDBP).
Because it is protein-bound, it is not efficiently filtered across dialysis membranes.
However, small amounts of VDBP can be lost in dialysate, especially in PD (which causes more protein loss than hemodialysis).
Over time, this can contribute to lower 25-OH D levels.

👉 So PD does not directly “filter out” free vitamin D, but it can cause protein losses that secondarily reduce vitamin D levels.

2️⃣ 1,25-dihydroxyvitamin D (calcitriol)

This is the active hormonal form.

It is present in very low concentrations
Also mostly protein-bound
Dialysis removal is minimal

However:

In kidney failure, the main issue is reduced production, not dialysis loss.
The kidneys normally convert 25-OH D into active 1,25-OH₂ D.
In advanced CKD or dialysis, this conversion is impaired.

So deficiency of active vitamin D in dialysis patients is primarily due to:

Loss of kidney 1-alpha hydroxylase activity
Elevated FGF-23
Secondary hyperparathyroidism

—not dialysis filtering it out.

3️⃣ Why dialysis patients often have low vitamin D

Patients on PD frequently show low 25-OH D because of:

Reduced sun exposure
Dietary restriction
Chronic inflammation
Protein losses in dialysate (more significant in PD than hemodialysis)
Reduced binding protein levels

PD patients lose 5–15 grams of protein per day in dialysate, which includes some VDBP.

4️⃣ Clinical implications

Because of this:

Most nephrology guidelines recommend checking 25-OH D levels
Supplementing cholecalciferol (D3) or ergocalciferol (D2) if low
Often also prescribing active vitamin D analogs (calcitriol, alfacalcidol, paricalcitol) to manage secondary hyperparathyroidism

Bottom line

Peritoneal dialysis does not significantly filter out vitamin D directly, but:

✔ It can contribute to lower vitamin D levels through protein loss ✔ The bigger issue is impaired kidney activation of vitamin D ✔ Supplementation is usually required in dialysis patients

Peritoneal Dialysis also reduces muscle Claude AI - March 2026

Peritoneal Dialysis removes magnesium Claude AI - March 2026

Dialysis also removes: water-soluble vitamins, Glutathione, Zinc, etc.

Claude AI March 2026

Water-soluble vitamins — B1 (thiamine), B2 (riboflavin), B6 (pyridoxine), B12, folic acid, and vitamin C are all lost during dialysis
Vitamin D — already depleted in kidney disease due to impaired conversion to active form (1,25-dihydroxy), and further affected by the dialysis process
Protein/amino acids — albumin and amino acids are lost, especially with peritoneal dialysis (which loses more protein than hemodialysis)
Magnesium — removed depending on dialysate magnesium concentration
Zinc and other trace elements (selenium, copper)
Carnitine (L-carnitine) — commonly depleted in dialysis patients
Glutathione — given your interest in this, worth noting that oxidative stress is markedly increased in dialysis patients, partly due to glutathione depletion
Iron — lost through blood left in the dialyzer and tubing Calcium — can be lost or gained depending on the dialysate calcium level

A few dialysis clinics replace Vitamin D (100,000 IU monthly)

Claude AI

Unfortunately, about half the vitamin D used by the body requires a healthy kidney, the other half is processed outside of the kidney

Serum 25-Hydroxyvitamin D Levels and Longitudinal Changes in Muscle Mass and Function in Peritoneal Dialysis Patients: A Prospective Cohort Study

J Nutr Sci Vitaminol (Tokyo) . 2026;72(1):1-8. doi: 10.3177/jnsv.72.1.

Lailiang Wang 1, Congping Xue 1, Beixia Zhu 1, Fangfang Zhou 1, Qun Luo 1

Data regarding to how serum 25 hydroxyvitamin D (25(OH)D) levels affect muscle mass and function in end-stage renal disease (ESRD) patients have led to inconclusive results. The main goal of this research was to examine the relationship between 25(OH)D levels and the risk of deterioration in muscle mass and function among ESRD patients on continuous ambulatory peritoneal dialysis (CAPD). Eligible ESRD patients on CAPD were prospectively included, and followed up at 3-mo intervals in Ningbo No. 2 Hospital, the tertiary care center in the Ningbo region, Zhejiang Province, China for 12 mo.

The mean 25(OH)D level <20 ng/mL of all visits during the 12-mo follow-up period was the exposure of interest. Primary outcome was defined as the deterioration of muscle mass and function at the end of the 12-mo follow-up. The absolute difference with 95% confidence interval (CI) of the incidence of deterioration of muscle mass and function between the groups with mean 25(OH)D<20 ng/mL and ≥20 ng/mL were estimated. The relationship between 25(OH)D levels and the risk of deterioration in muscle mass and function was examined by employing multivariate logistic regression models. Participants with 25(OH)D<20 ng/mL or 25(OH)D≥20 ng/mL in each visit were included as a sensitivity analysis. Subgroup analysis was conducted based on the age (<60 y and ≥60 y). Two hundred twenty-one eligible participants were included for the final statistical analysis. Among these 221 participants, patients with the mean 25(OH)D<20 ng/mL was 64.7% (143/221).

During the 12-mo follow-up period, the incidence of deterioration in muscle mass and function was 37.6% (83/221). Compared to paticipants with mean 25(OH)D≥20 ng/mL, the incidence in paticipants with mean 25(OH)D<20 ng/mL was significantly higher (46.2% vs 21.8%, p<0.001), with an absolute difference of 24% (95%CI 12-37%). After adjustment for potential confounding factors, mean 25(OH)D<20 ng/mL was still associated with increased risk of the deterioration in muscle mass and function (OR=3.18, 95%CI 1.51-6.70, p=0.002). The association was consistent in the sensitivity analysis (OR=3.22, 95%CI 1.49-6.97, p=0.003). In subgroup analysis, the relationship between mean 25(OH)D<20 ng/mL and the deterioration in muscle mass and function remained consistent (OR=5.59, 95%CI 1.82-17.15, p=0.003) in paticipants with age ≥60 y; however, no significant relationship was identified in patients with age <60 y (OR=2.05, 95%CI 0.72-5.84, p=0.18).

Our study demonstrated that lower serum 25(OH)D levels were significantly associated with an increased risk of the deterioration in muscle mass and function in ESRD patients on CAPD, especially in elderly individuals, implicating that vitamin D supplementation might represent an effective way to prevent and treat sarcopenia, frailty and their clinical complications. However, due to inherent limitations in the study, further research is necessary to establish a definitive causal relationship.

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