Erdafitinib
Severe
Database
Clinical effect not specified
Source: DDInter
Drug reference
Iron Sucrose
Iron Supplement · Iron supplement; Agent for iron deficiency anemia
Also known as Saccharated Iron Oxide, Ferric Hydroxide Sucrose Complex, Venofer
START
Confirm iron deficiency (ferritin <100 ng/mL + TSAT <20% in CKD; ferritin <30 ng/mL in general). Baseline CBC, ferritin, TSAT, creatinine. Ensure epinephrine and resuscitation equipment available for first dose.
TYPICAL MAX
200-300 mg per infusion (product-dependent). Cumulative 1000 mg per course. Do not exceed TSAT >50% or ferritin >800 ng/mL.
STOP IF
Anaphylaxis, severe hypersensitivity, iron overload (ferritin >800 or TSAT >50%), severe hypophosphatemia
WATCH
Ferritin and TSAT at baseline and every 1-2 months, hemoglobin (weekly during EPO therapy), hypersensitivity reactions (especially first 5 minutes of infusion), blood pressure during infusion
CDSCO approvedJan AushadhiNPPA price-controlledATC B03AC02
KDIGO 2024 + manufacturer label
- ONSET
- 8min · absorption onset
- PEAK
- 30min · Immediate (IV)
- t½
- 6h · ~6 h (distribution to RES)
- DURATION
- 12w · Months (iron stores)
EXCRETION
Minimal renal iron excretion; body tightly conserves iron
route + CYP
INTERACTIONS
1 major
SEVERE in our sources
PREGNANCY
FDA PLLR: Animal studies showed no teratogenicity. Limited human data. Use only if benefit clearly outweighs risk, especially in first trimester. Iron deficiency anemia is common in pregnancy; oral iron preferred.
FDA category + note
Top interactionssee all 8 →
- ErdafitinibSevereDatabaseDDInter
Available in India
391 branded formulations. Look up specific brands in the Drugs workspace.
Jan Aushadhi — generic available at GoI pharmacies
Mechanism
Iron sucrose is a parenteral iron preparation consisting of a polynuclear iron(III)-hydroxide core stabilized within a sucrose carbohydrate shell. After intravenous administration, the iron-sucrose complex is taken up by reticuloendothelial system (RES) macrophages via endocytosis. Within macrophages, the iron is released from the sucrose carrier and either: (1) incorporated into ferritin for storage; (2) exported via ferroportin and bound to transferrin for transport to erythroid precursor cells in the bone marrow; or (3) incorporated into hemoglobin for red blood cell production. The sucrose component is metabolized and excreted. This bypasses the gastrointestinal absorption pathway, making it effective in patients with malabsorption, intolerance to oral iron, or insufficient response to oral iron.
Indications
Iron deficiency anemia in patients with chronic kidney disease (CKD) on hemodialysisIron deficiency anemia in CKD patients not on dialysisIron deficiency anemia in patients receiving erythropoietin (EPO) therapyIron deficiency anemia where oral iron is ineffective or poorly toleratedFunctional iron deficiency (inflammation blocks iron mobilization)Preoperative iron deficiency anemia (off-label)
Dosing
- Adult
- CKD on hemodialysis: 100 mg IV during each dialysis session for 10 doses (total 1000 mg). OR 125 mg IV twice weekly x 4 weeks (total 1000 mg). Non-dialysis CKD: 200 mg IV over 2-5 minutes, repeated 5 times over 14 days (total 1000 mg). Max single dose: 200-300 mg (varies by product).
- Pediatric
- Not recommended <2 years. ≥2 years: weight-based dosing; follow product-specific labeling.
- Renal adjustment
- No adjustment required. Primarily indicated for CKD patients.
- Hepatic adjustment
- Use caution; no specific adjustment. Monitor iron stores.
- Geriatric
- No specific adjustment. Monitor for hypersensitivity reactions.
- Max dose
- 200-300 mg per infusion (product-dependent); cumulative 1000 mg per course
Pharmacokinetics
Onset
Rise in hemoglobin within 2-4 weeks; peak at 8-12 weeks.
Peak effect
IV: immediate distribution to RES. Iron available for erythropoiesis within days.
Duration
Iron stores replenished for months. Repeat dosing based on iron parameters.
Half-life
~6 hours (distribution from plasma to RES). Sucrose component eliminated more rapidly than iron.
Bioavailability
100% (IV).
Protein binding
Iron is bound to transferrin in plasma (normal saturation ~30%).
Metabolism
Iron is not metabolized in the traditional sense. It is incorporated into hemoglobin, myoglobin, and enzymes or stored as ferritin/hemosiderin. Sucrose is metabolized by normal carbohydrate pathways.
Excretion
Iron: minimal renal excretion (body tightly conserves iron). Sucrose: renal excretion.
Contraindications
- Hypersensitivity to iron sucrose or any component
- Anemia not caused by iron deficiency (must confirm iron deficiency before treatment)
- Iron overload (hemochromatosis, hemosiderosis)
- History of anaphylactic reaction to parenteral iron preparations
Side effects
Common
Hypotension (during infusion)Nausea, vomitingDiarrhea or constipationHeadacheMuscle crampsInjection site reactions (pain, discoloration)Dizziness
Serious
- Anaphylaxis and severe hypersensitivity reactions (rare but potentially fatal; more common with high-molecular-weight iron dextran than iron sucrose)
- Iron overload (hemosiderosis) with excessive dosing — monitor ferritin and TSAT
- Hypophosphatemia (can be severe and prolonged with some IV iron formulations)
- Hypertension (during infusion)
- Bronchospasm, dyspnea
- Chest pain
- Seizures (rare)
Pregnancy & lactation
Pregnancy
FDA PLLR: Animal studies showed no teratogenicity. Limited human data. Use only if benefit clearly outweighs risk, especially in first trimester. Iron deficiency anemia is common in pregnancy; oral iron preferred.
Lactation
Iron is a normal component of breast milk. Parenteral iron supplementation increases milk iron concentration. Compatible with breastfeeding.
Drug interactions
Chloramphenicol
Moderate
Database
Delayed response to iron therapy due to chloramphenicol-induced bone marrow suppression
Monitor hematological parameters closely. Consider alternative antibiotics if possible, or delay iron therapy until chloramphenicol course is complete.
Source: DDInter
Dimercaprol
Moderate
Database
Dimercaprol forms a toxic complex with iron. Concurrent use can cause severe toxicity.
Avoid concurrent use. If both needed for different indications, separate timing and monitor closely.
Source: Kimi deep-research + Cla
Erythropoietin
Moderate
Database
Standard combination in CKD. EPO stimulates erythropoiesis, increasing iron demand. Iron supplementation prevents functional iron deficiency. No direct pharmacokinetic interaction.
Standard of care in CKD anemia. Monitor hemoglobin (target 10-11.5 g/dL per KDIGO), ferritin, and TSAT monthly. Adjust EPO and iron doses accordingly.
Source: Kimi deep-research + Cla
Gastric Acid Suppressants
Moderate
Database
PPIs/H2-blockers reduce gastric acid, impairing absorption of oral iron. This is NOT a concern with IV iron sucrose, but patients may be on both.
No interaction with IV iron. If patient transitions to oral iron, consider PPI timing or switch to IV iron if ongoing acid suppression needed.
Source: Kimi deep-research + Cla
Levothyroxine
Moderate
Database
Iron binds levothyroxine in the GI tract, reducing thyroid hormone absorption. This interaction applies if patient takes oral iron and levothyroxine concurrently.
Separate administration by at least 4 hours. Monitor TSH when starting or stopping iron therapy.
Source: Kimi deep-research + Cla
Mycophenolate Mofetil
Moderate
Database
Reduced systemic exposure and efficacy of mycophenolate mofetil
Separate administration by at least 2 hours. Monitor mycophenolate levels and clinical response.
Oral Iron Supplements
Moderate
Database
Excessive combined iron dosing increases risk of iron overload (hemosiderosis, organ damage). Serum ferritin and TSAT must guide dosing.
Do not give oral iron concurrently with IV iron unless specifically indicated. Monitor ferritin and TSAT. Stop oral iron during IV iron course.
Source: Kimi deep-research + Cla
4 additional low-confidence interactions hidden — those rows lack a documented mechanism or management plan in our sources.
Related guidelines
Chronic kidney disease — assessment and management
KDIGO · Nephrology · 2024
Iron deficiency anaemia in pregnancy
ICMR · Obstetrics & Gynaecology · 2022
Iron deficiency anaemia in adults
ICMR · Hematology · 2023
Acute kidney injury
KDIGO · Nephrology · 2012
Chronic kidney disease — assessment and management
NICE · Nephrology · 2021
Other Iron Supplement drugs
Ask House about Iron Sucrose
Continue into a citation-backed clinical answer with the drug context already attached.
Sources: Goodman & Gilman 14e, Katzung, BNF, Harriet Lane·Verified: 2026-05-18 · House clinical team·Cockpit curated: 2026-05-18