Paricalcitol

Also sold as Zemplar.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Paricalcitol is a synthetic, already-bioactive vitamin D2 analog (19-nor ring, modified side chain) that selectively activates the vitamin D receptor (VDR) to suppress parathyroid hormone synthesis and secretion in chronic kidney disease. Per its FDA label, it is extensively protein bound (≥99.8%), metabolized by mitochondrial CYP24 together with CYP3A4 and UGT1A4, and eliminated mainly by the hepatobiliary/fecal route (about 70% of a radiolabeled dose in feces, 18% in urine, only about 2% unchanged). That gives it real, labeled hepatic and mitochondrial metabolic machinery of its own, unlike a drug cleared unchanged. It does not meaningfully induce or inhibit host CYP enzymes, so it carries no classical absorption-interference, catabolism-acceleration, or renal-wasting mechanism aimed at an unrelated nutrient. Its entire pharmacology is aimed at the calcium/phosphorus/PTH axis itself.

ATC H05BX02 · also sold as Zemplar (capsule and injection); generic paricalcitol · reviewed 2026-09-26. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Paricalcitol in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe: severe: ≥2 independent Tier A sources, this drug in the studied cohort, the nutrient/category directly measured, consistent direction, clinically meaningful magnitude, a named plausible mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate: moderate: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or a functional rather than confirmed circulating measure.
Yellow — Low: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for reverse-direction/protective findings and context flags.
Not graded — disclosed evidence gap: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: evidence gap: no Tier B/C evidence exists to support even a yellow grade, and no circulating consumer claim exists to rebut as white. A disclosed gap in the literature (or in what could be accessed this session), never reworded as reassurance.

What the research found

Calcium

Red — Severe

See study details

Paricalcitol's own labeled mechanism produces calcium retention; excess dosing causes hypercalcemia and hypercalciuria. This is a retention/excess finding, not a calcium deficiency, and must not be read as one.

Full detail and limits

What the grade means here: severe: ≥2 independent Tier A sources, this drug in the studied cohort, the nutrient/category directly measured, consistent direction, clinically meaningful magnitude, a named plausible mechanism, no substantial contradicting Tier A evidence. RED

Limits on what this shows

Key null/negative: None identified — this is an established, expected, and actively monitored effect, not a disputed one.
At-risk subgroups: Patients also taking calcium-containing phosphate binders or calcium/vitamin D supplements; peritoneal dialysis patients (12.4% predicted incidence vs 0.8% on hemodialysis); baseline serum calcium must be ≤9.5 mg/dL before starting the CKD stage 5 dosing algorithm.
Counter-evidence: None on record; direction is not contested in the literature searched.

Regulatory status

Labeled warning: "excessive administration of vitamin D compounds, including Zemplar Capsules, can cause over suppression of PTH, hypercalcemia, hypercalciuria, hyperphosphatemia, and adynamic bone disease." Contraindicated in patients with evidence of vitamin D toxicity or hypercalcemia.

Population evidence

CKD stage 3-4 pivotal RCT, n=107 treated, 24 weeks: dose reduced whenever serum calcium reached 10.4-11.0 mg/dL and withheld above 11.0 mg/dL, irrespective of iPTH. CKD stage 5 dosing-simulation (label): predicted hypercalcemia incidence 0.8% (hemodialysis) and 12.4% (peritoneal dialysis) over 12 weeks using the label's iPTH/80 titration algorithm.

Mechanism

Genomic VDR activation upregulates intestinal and renal calcium transport machinery, the same class mechanism as native vitamin D, though paricalcitol's side-chain/ring modifications are designed to reduce (not eliminate) calcemic activity relative to calcitriol.

Counter-evidence held on record

This is an excess/retention risk, not a deficiency. Never use this entry to justify calcium or vitamin D supplementation. The labeled response to rising calcium is dose reduction or withholding paricalcitol under prescriber guidance, monitored on the schedule in the Monitoring panel below.

Phosphorus

Red — Severe

See study details

Paricalcitol's VDR-mediated increase in intestinal phosphate absorption compounds chronic kidney disease's own phosphate retention, producing labeled hyperphosphatemia risk. This is a retention/excess finding, not a phosphorus deficiency.

Full detail and limits

Limits on what this shows

Confounding by indication: Hyperphosphatemia is near-universal in CKD from the underlying disease itself. Paricalcitol's genomic effect on intestinal absorption is an addition to, not the root cause of, disease-driven phosphate retention; this is stated explicitly to avoid overstating attribution.
Key null/negative: None identified specific to paricalcitol; direction is not contested.
At-risk subgroups: Patients on calcium/phosphate-containing binders or with poor dietary phosphate restriction adherence.

Regulatory status

Hyperphosphatemia is named alongside hypercalcemia and adynamic bone disease in the label's over-suppression warning; serum phosphorus is monitored on the identical schedule as calcium and iPTH.

Population evidence

Same pivotal trials as the Calcium entry (CKD 3-4, n=107 treated, 24 weeks; CKD 5 dosing simulations); phosphorus tracked as a co-primary safety parameter throughout.

Mechanism

VDR-mediated increase in intestinal phosphate absorption, paired with the calcium-absorption pathway; additive to, not the primary cause of, CKD's own renal phosphate excretion failure.

Counter-evidence held on record

Excess/retention risk. Never a rationale for phosphate supplementation. Managed by dose titration and dietary/binder strategy under a prescriber, per the label's monitoring schedule.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Yellow — Low

See study details

In two independent paricalcitol-specific animal studies in unrelated organ systems (heart, brain), paricalcitol increased markers of mitochondrial fusion/biogenesis and reduced markers of pathological fission. No human mitochondrial data exist for paricalcitol.

Full detail and limits

What the grade means here: low/theoretical: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where at least one class member has real data but this drug does not; also used for reverse-direction/protective findings and context flags. YELLOW

Limits on what this shows

Key null/negative: None identified.

Population evidence

(a) Nizami S et al. Oxid Med Cell Longev. 2022;2022:5554290. Male Sprague-Dawley rats, 20-week high-fat/high-fructose diet to induce metabolic-syndrome-associated cardiac dysfunction; paricalcitol 0.08 µg/kg/day IP during weeks 12-20. Increased cardiac Mfn2 (fusion protein) and PGC-1α (biogenesis regulator) expression; VDR silencing in cardiomyoblasts abolished the Mfn2 increase, confirming VDR-dependence; improved ejection fraction. (b) Tian M et al. Neurotherapeutics. 2025;23(1):e00767. C57BL/6 mice with intracerebral hemorrhage plus hemin-exposed primary cortical neurons; paricalcitol 0.5 µg/kg IP. Enhanced inhibitory phosphorylation of DRP1 (fission driver, Ser637) via cAMP-PKA signaling, reducing pathological mitochondrial fission and neuronal death.

Mechanism

VDR-dependent transcriptional/signaling effects on mitochondrial dynamics proteins (Mfn2, DRP1) and biogenesis (PGC-1α), demonstrated in both studies to require VDR activation specifically.

Tier and bound

Tier B, animal/primary-neuron only, drug-specific in both. Cardiac and neuronal disease-injury models only; no renal, hepatic, or general human mitochondrial data exist for paricalcitol. Both findings are protective/reverse-direction (paricalcitol improving mitochondrial dynamics under a disease insult), not paricalcitol itself burdening mitochondria.

Overlap

Shares its underlying source with the ATP production entry (study a) and the Iron entry (study b) — see Overlap map.

Counter-evidence held on record

Mechanistic and preclinical only. Not evidence of a human mitochondrial deficiency and not a rationale for any supplement.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress

Orange — Moderate

See study details

In hemodialysis patients, those receiving paricalcitol or calcitriol showed significantly higher total antioxidant status and lower total oxidant status/oxidative stress index than non-users, with no difference between the two drugs. This is a protective association, bounded by a single cross-sectional design.

Full detail and limits

What the grade means here: moderate: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or a functional rather than confirmed circulating measure. ORANGE

Limits on what this shows

Key null/negative: None identified specific to paricalcitol beyond the study's own null comparison between paricalcitol and calcitriol (i.e., no evidence paricalcitol differs from calcitriol on this marker).

Regulatory status

Not a labeled effect; identified through independent literature search.

Population evidence

Yeter HH et al., Int J Vitam Nutr Res. 2021;91(3-4):335-342. Cross-sectional study, N=83 hemodialysis patients, minimum one year dialysis vintage, excluding active infection, malignancy or chronic inflammatory disease. Total antioxidant status higher in vitamin-D-compound users (p=0.006); total oxidant status and oxidative stress index both higher in non-users (p=0.005 and p=0.004); paricalcitol vs calcitriol comparison non-significant across all three markers (p=0.6, 0.4, 0.7).

Mechanism

Proposed antioxidant/anti-inflammatory genomic VDR signaling. Consistent in direction with Tier B animal data cited in a narrative cardiorenal review (paricalcitol reduced serum malondialdehyde and renal thiobarbituric-acid-reactive substances in a contrast-induced nephropathy model, and reduced cardiac oxidative stress in uremic rats when combined with enalapril) — these primary animal studies were not independently opened this session and are not used to raise this entry's tier; they are cited only as directionally consistent context, disclosed in Sources.

Why not RED

Single cross-sectional observational study (N=83, one center); confounding by indication is plausible (healthier or more treatment-adherent patients may be preferentially prescribed active vitamin D) and was not excluded by the study design.

Counter-evidence held on record

This is a protective association observed in existing users, not a deficiency, and does not imply or support an antioxidant supplement.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron

Yellow — Low

See study details

In a mouse intracerebral hemorrhage model, paricalcitol reduced markers of iron-dependent lipid peroxidation (ferroptosis) via VDR-cAMP-PKA-DRP1 signaling. This is a distinct, mechanistic iron-pathway finding, not the same as the hematologic hemoglobin effect graded separately under Oxygen delivery/utilization.

Full detail and limits

Limits on what this shows

Key null/negative: No drug-specific human iron-panel study was found despite searching PubMed listings, Crossref, and OpenAlex for paricalcitol combined with iron, hepcidin, and ferritin terms across multiple phrasings.

Population evidence

Tian M et al. Neurotherapeutics. 2025;23(1):e00767 — the same study cited in the Mitochondrial burden entry; see Overlap map. Paricalcitol (0.5 µg/kg IP, optimal dose, daily for 7 days post-injury) reduced 4-hydroxynonenal (4-HNE) accumulation and normalized malondialdehyde (MDA) and glutathione (GSH) levels in both the in vivo ICH model and hemin-exposed primary cortical neurons.

Mechanism

VDR activation → cAMP-PKA signaling → inhibitory DRP1 phosphorylation, reducing pathological mitochondrial fission that otherwise potentiates iron-driven lipid peroxidation and ferroptotic neuronal death.

Tier and bound

Tier B, animal and primary-neuron-culture only, drug-specific. Neuronal/CNS injury model only; no renal, hepatic, or systemic human iron-status data (ferritin, transferrin saturation, hepcidin) exist for paricalcitol.

Overlap

Shares its underlying source entirely with the Mitochondrial burden entry — see Overlap map. Do not read these as two independent confirmations.

Counter-evidence held on record

Preclinical, organ-specific, protective-direction signal. Not a human iron-deficiency or iron-overload finding, and carries no dosing implication in either direction.

Copper

Not graded — disclosed evidence gap

See study details

No evidence at any tier connects paricalcitol to copper status, and no circulating consumer claim exists to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. UNGRADED

Limits on what this shows

Why no grade: Both conditions for UNGRADED are met: (1) no Tier B or Tier C evidence exists linking paricalcitol, or the vitamin-D-analog/VDR-activator class generally, to copper or ceruloplasmin status; (2) no circulating consumer nutrient-depletion claim naming paricalcitol and copper was found in the sources checked. This reflects a genuine literature gap as of this review, not a finding of safety, and is never to be reworded as "no known effect."

Search channels tried

PubMed search-listing pages (multiple phrasings, one attempt blocked by bot-verification), Crossref API bibliographic query ("paricalcitol copper trace element" — zero relevant results among five returned works, all on unrelated copper topics), and general web search (zero relevant results). Attempted across more than one host and phrasing before settling on ungraded, per protocol.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk

Yellow — Low

See study details

No paricalcitol-specific gut microbiome study was found. VDR-knockout mice and calcitriol (not paricalcitol) show that vitamin D receptor signaling regulates Paneth cell defensin expression and gut microbiota composition. Because paricalcitol activates the same receptor, the mechanism is plausible, but the direction of effect for this specific molecule has not been tested.

Full detail and limits

Limits on what this shows

Key null/negative: None identified for paricalcitol specifically; drug-specific PubMed and Crossref searches for paricalcitol plus gut microbiome/microbiota terms returned no relevant results after multiple phrasings.

Population evidence

Frontiers in Physiology, 2016 (Paneth cell defensins/gut microbiota study). BALB/c mice on vitamin-D-replete vs vitamin-D-depleted, standard vs high-fat diets, plus VDR-knockout (B6.129S4-Vdr tm1Mbd /J) vs wild-type mice on a high-phosphorus/high-calcium diet. Calcitriol (not paricalcitol) 5 ng/g IP was used to test ileal responsiveness. Combined vitamin-D-deficiency plus high-fat feeding produced large shifts ( Helicobacter hepaticus up 1,000- to 7,000-fold; Akkermansia muciniphila down 8- to 626-fold across conditions), with synthetic α-defensin-5 supplementation partially reversing both the dysbiosis and downstream insulin resistance/hepatic steatosis.

Tier and class-extrapolation label

Tier C. The tested compound (calcitriol) is chemically distinct from paricalcitol, though both are VDR ligands; paricalcitol itself is absent from this cohort. Labeled here explicitly as class extrapolation, not drug-specific evidence.

Additional context

Paricalcitol's own label documents dose-related GI adverse effects (diarrhea 7-11% vs placebo 4-11%; nausea/vomiting 5-6% vs placebo 0-5% across the pivotal trials), which could independently alter gut transit or the luminal environment (mechanism screen category H, changed intake/transit), though no trial measured this as a microbiome outcome.

Counter-evidence held on record

This is a mechanistic extrapolation from a different molecule and from genetic knockout models, not paricalcitol-specific data in either direction. No probiotic or microbiome-support recommendation follows from it.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Orange — Moderate

See study details

In a randomized trial of anemic CKD stage 3b-5 patients, paricalcitol raised hemoglobin by 0.89 g/dL over six months while calcitriol lowered it by 0.61 g/dL, an effect the trial found independent of inflammation, PTH, and iron balance. This is an incidental hematologic effect, not a deficiency.

Full detail and limits

Limits on what this shows

Key null/negative: None identified specific to paricalcitol; the calcitriol comparator arm declined, which is informative but does not test paricalcitol against no-vitamin-D-analog use.

Regulatory status

Not a labeled indication or effect; identified through independent literature search. Paricalcitol is not indicated for anemia management.

Population evidence

Riccio E, Sabbatini M, Bruzzese D, Capuano I, Migliaccio S, Andreucci M, Pisani A. PLOS ONE 2015;10(3):e0118174. Randomized trial, N=60 (30 per arm), CKD stage 3b-5 with anemia, 6 months. Paricalcitol 1 mcg/day vs calcitriol 0.5 mcg every other day. Hemoglobin trajectory: paricalcitol +0.16 g/dL/month (95% CI 0.10 to 0.22, p<0.001), cumulative +0.89 g/dL at 6 months; calcitriol -0.10 g/dL/month (95% CI -0.17 to -0.04, p<0.001), cumulative -0.61 g/dL. Group×time interaction F(1,172)=31.4, p<0.001. ESA dosing essentially stable in both arms (one paricalcitol patient reduced ESA dose 25%; one patient per arm discontinued ESA), so the hemoglobin divergence was not simply an ESA-sparing artifact.

Mechanism

Authors propose a direct effect on erythroid progenitor cells; inflammation, PTH change, and iron balance were explicitly tested and excluded as confounders by the trial design.

Why not RED

A single RCT (N=60), specific to pre-dialysis CKD 3b-5 with anemia, not a dialysis-general population. A second, drug-specific corroborating study identified in search (erythropoietin resistance across calcitriol, cinacalcet and paricalcitol in hemodialysis patients) could not be opened this session after repeated attempts across PubMed, the publishing journal, and three literature APIs (all blocked or rate-limited); it is disclosed in Sources and excluded from this grade rather than counted toward a second independent Tier A source.

Counter-evidence held on record

This is an incidental hematologic effect of the drug, explicitly shown independent of iron status in the source trial — it is not an iron-deficiency finding and carries no supplement implication. Any ESA dose change should be made by the prescribing nephrology team, not in response to this entry.

ATP production

Yellow — Low

See study details

In the same rat metabolic-syndrome heart-failure model cited under Mitochondrial burden, paricalcitol increased cardiac citrate synthase activity (a marker of oxidative/ATP-generating capacity) without increasing raw mitochondrial content, alongside PGC-1α upregulation.

Full detail and limits

Limits on what this shows

Key null/negative: None identified; drug-specific PubMed, Crossref, and OpenAlex searches for "paricalcitol" plus ATP/energy metabolism terms returned zero additional results.

Population evidence

Nizami S et al. Oxid Med Cell Longev. 2022;2022:5554290 — the same study cited in the Mitochondrial burden entry; see Overlap map. No Drp1, mitochondrial membrane potential, or direct ATP-level measurements were reported in this study.

Mechanism

PGC-1α-driven mitochondrial biogenesis signaling proposed as the route to increased oxidative capacity (citrate synthase activity), VDR-dependent per the same silencing experiment.

Tier and bound

Tier B, single animal study, cardiac tissue only, disease (metabolic syndrome) model only. No human ATP-production data exist for paricalcitol.

Overlap

Shares its underlying source entirely with the Mitochondrial burden entry — see Overlap map. Do not read these as two independent confirmations.

Counter-evidence held on record

Preclinical, protective-direction signal from a single animal study. Not a human ATP-deficiency finding and not a rationale for any supplement.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

"Paricalcitol depletes vitamin D"
Where it comes from: General pattern in consumer drug-nutrient-depletion sources of listing broad "vitamin-D-affecting drug" categories. No source checked (US Pharmacist drug-nutrient-depletion review, a general drug-nutrient-depletion practice guide, a chiropractic drug-nutrient depletion chart) named paricalcitol or vitamin D analogs specifically — the claim as applied to this drug appears to be an assumed extension of the vitamin D deficiency concept rather than a documented one.
Why it fails: Paricalcitol is itself a synthetic, already-bioactive VDR ligand that does not require host 1α- or 25-hydroxylation (per its labeled mechanism of action), is not measured by or metabolically dependent on serum 25(OH)D assays, and is not documented in its label or in the pharmacokinetic literature searched to suppress endogenous vitamin D synthesis or serum 25(OH)D.
"Paricalcitol (or vitamin D analogs generally) causes magnesium wasting"
Where it comes from: Plausible-sounding extrapolation tested as a candidate mechanism (renal tubular calcium and magnesium share some overlapping handling pathways), rather than a documented consumer claim traced to a specific handbook entry.
Why it fails: A Tier A human study directly measured this and found no effect: "urinary creatinine, magnesium and phosphate excretion also remained unchanged over the study periods irrespective of the treatment" during calcitriol and paricalcitol administration in healthy volunteers (PMID 18397683). Accessed via a PubMed search-results abstract snippet; the direct article page was blocked by bot-verification this session, disclosed in Sources.

All references used above

ZEMPLAR (paricalcitol) Capsules, full prescribing information. — FDA label, accessdata.fda.gov, 2009 (021606s004lbl.pdf). Opened in full; source for pharmacokinetic basis, calcium/phosphorus grading, drug interactions, pregnancy/pediatric/hepatic-impairment data, and adverse-event rates.
ZEMPLAR (paricalcitol capsule, liquid filled) label. — DailyMed, National Library of Medicine. Opened; cross-checked mechanism of action, metabolism, and warning language against the FDA PDF label.
Paricalcitol, ATC code H05BX02. — WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index. Opened; confirmed classification path H → H05 (calcium homeostasis) → H05B (anti-parathyroid agents) → H05BX (other anti-parathyroid agents) → H05BX02, and DDD of 2 mcg.
Yeter HH et al. Association between calcitriol and paricalcitol with oxidative stress in patients with hemodialysis. — Int J Vitam Nutr Res. 2021;91(3-4):335-342. Cross-sectional, N=83. Opened via Europe PMC REST API (direct PubMed article page was blocked by bot-verification). Source for the Oxidative stress entry.
Riccio E, Sabbatini M, Bruzzese D, Capuano I, Migliaccio S, Andreucci M, Pisani A. Effect of Paricalcitol vs Calcitriol on Hemoglobin Levels in Chronic Kidney Disease Patients: A Randomized Trial. — PLOS ONE. 2015;10(3):e0118174. RCT, N=60, 6 months. Opened in full; source for the Oxygen delivery/utilization entry.
Nizami S et al. Paricalcitol Attenuates Metabolic Syndrome-Associated Heart Failure through Enhanced Mitochondrial Fusion. — Oxid Med Cell Longev. 2022;2022:5554290. Animal study (rat), Tier B. Opened in full; source for the Mitochondrial burden and ATP production entries.
Tian M et al. Paricalcitol-mediated vitamin D receptor activation attenuates neuronal ferroptosis via cAMP-PKA-DRP1 signaling pathway after intracerebral hemorrhage. — Neurotherapeutics. 2025;23(1):e00767. Animal + primary neuron culture, Tier B. Opened in full; source for the Mitochondrial burden and Iron entries.
Calcium balance during calcitriol and paricalcitol administration in healthy humans. — PMID 18397683. Human study, Tier A. Accessed only via a PubMed search-results abstract snippet quoting the magnesium/phosphate-excretion null finding; the direct article page returned a bot-verification challenge on repeated attempts this session. Used only for the magnesium Fails-verification entry, not for any tier-raising claim beyond the quoted snippet.Direct article page blocked by bot-verification; accessed via PubMed search-listing snippet only.
The influence of selective vitamin D receptor activator paricalcitol on cardiovascular system and cardiorenal protection. — Clin Interv Aging. 2013;8:433-441 (narrative review). Opened via Dovepress PDF. Tier C for its own synthesis; cited here only for its description of two animal studies (contrast-induced nephropathy malondialdehyde reduction; enalapril+paricalcitol cardiac oxidative stress in uremic rats) that were not independently opened this session. Used only as directionally consistent context in the Oxidative stress entry, not as tier-defining evidence.
Vitamin D Signaling through Induction of Paneth Cell Defensins Maintains Gut Microbiota and Improves Metabolic Disorders and Hepatic Steatosis in Animal Models. — Front Physiol. 2016;7:498. Animal study, calcitriol and VDR-knockout mice (paricalcitol not tested). Opened in full; source for the Gut microbiome risk entry, labeled explicitly as Tier C class extrapolation.
Drug-Induced Nutrient Depletions: What Pharmacists Need to Know. — US Pharmacist (consumer/professional circulating-claims source). Opened and searched; no mention of paricalcitol, Zemplar, vitamin D analogs, or vitamin D receptor activators found. Used as negative evidence in the circulating-claim audit.
Drug-Nutrient Depletion and Interaction Charts. — Chiro.org compilation (consumer/practitioner circulating-claims source). Opened and searched; no mention of paricalcitol or vitamin D analogs found. Used as negative evidence in the circulating-claim audit.
Managing drug-nutrient depletions in clinical practice. — Practice guide PDF (consumer/practitioner circulating-claims source). Opened and searched; no mention of paricalcitol, Zemplar, or vitamin D analogs/receptor activators found. Used as negative evidence in the circulating-claim audit.
Crossref API bibliographic searches. — Three separate queries opened directly against api.crossref.org: "paricalcitol copper trace element" (5 results, none relevant), "paricalcitol gut microbiome microbiota" (5 results, none relevant), "paricalcitol ATP mitochondrial energy metabolism" (3 results, none relevant). Used as thoroughness evidence supporting the Copper ungraded entry and the absence of drug-specific ATP/microbiome data beyond the animal studies already cited.
Afsar B et al. Comparison of erythropoietin resistance in hemodialysis patients using calcitriol, cinacalcet, or paricalcitol. — J Clin Pharmacol. 2015. PMID 26032009.Could not be opened this session: PubMed direct page returned bot-verification; publisher (Wiley) page returned HTTP 403; Europe PMC website disallowed by robots.txt; Europe PMC REST API and Semantic Scholar API both returned persistent 429/rate-limit responses across repeated attempts. Not used as evidence for any grade in this dossier; listed for disclosure only.
Fang Y et al. Role of mitochondria in paricalcitol-mediated cytoprotection during obstructive nephropathy. — Am J Physiol Renal Physiol. 2012. PMID 22492946.Could not be opened this session: PubMed direct page returned bot-verification; journal site (journals.physiology.org) returned HTTP 403; Europe PMC website disallowed by robots.txt; Europe PMC REST API and Semantic Scholar API both returned persistent 429/rate-limit responses; NCBI E-utilities blocked at the network egress layer. Not used as evidence for any grade in this dossier; listed for disclosure only.
Paricalcitol protects against hydrogen peroxide-induced injury in endothelial cells through suppression of apoptosis. — In vitro study (endothelial cell line).Could not be opened this session: repeated bot-verification challenge on the PMC article page. Not used as evidence for any grade in this dossier; listed for disclosure only.

Paricalcitol

Findings for this medication

What the research found

Calcium

Phosphorus

The five body-system areas

⚡Mitochondrial Burden

Mitochondrial burden

💥Oxidative Stress

Oxidative stress

⚖️Copper and Iron Balance

Iron

Copper

🌿Gut Microbiome Risk

Gut microbiome risk

💨Oxygen and ATP Output

Oxygen delivery/utilization

ATP production

Claims checked and not supported

"Paricalcitol depletes vitamin D"

"Paricalcitol (or vitamin D analogs generally) causes magnesium wasting"

Mitochondrial Burden

Oxidative Stress

Copper and Iron Balance

Gut Microbiome Risk

Oxygen and ATP Output