Dosage guidance:
Dosing: Dose is expressed in mg of elemental iron. A test dose typically is not required.
Clinical considerations : IV iron replacement is preferred over oral replacement in several clinical situations (eg, poor GI absorption, lack of response to or poor tolerability of oral iron, need for rapid repletion, chronic kidney disease, active inflammatory bowel disease, cancer, chronic or extensive blood loss) (Ref).
Chemotherapy-associated anemia (off-label use): IV: 200 mg once every 3 weeks for 5 doses (Ref) or 100 mg once weekly during weeks 0 to 6, followed by 100 mg every other week from weeks 8 to 14 (Ref) or 200 mg once a week after each platinum-based chemotherapy cycle for up to 6 doses (Ref) or 200 mg after each platinum-based chemotherapy cycle for 6 cycles (Ref).
Iron-deficiency anemia in chronic kidney disease: IV:
Hemodialysis-dependent chronic kidney disease: 100 mg administered during consecutive dialysis sessions; the usual cumulative total dose is 1,000 mg (10 doses); may repeat treatment if clinically indicated.
Peritoneal dialysis-dependent chronic kidney disease: Two infusions of 300 mg administered 14 days apart, followed by a single 400 mg infusion 14 days later (total cumulative dose of 1,000 mg in 3 divided doses); may repeat treatment if clinically indicated.
Non-dialysis-dependent chronic kidney disease: 200 mg administered on 5 different occasions within a 14-day period (total cumulative dose: 1,000 mg in 14-day period); may repeat treatment if clinically indicated. Note: Dosage has also been administered as 2 infusions of 500 mg on day 1 and day 14 (limited experience).
Iron-deficiency anemia, treatment, patients without chronic kidney disease (off-label use): IV: 100 to 300 mg per dose; repeat doses may be given until total iron requirements are met (Ref). Dosing schedule depends on iron deficit and ease of scheduling. Cumulative doses >1 g generally are not required during a single treatment course unless there is ongoing blood loss (Ref).
The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS.
Altered kidney function: No dosage adjustment necessary for any degree of kidney dysfunction (Ref); limited amounts of iron (~5%) eliminated in urine (Ref).
Hemodialysis, intermittent (thrice weekly): Not significantly dialyzed (Ref): No supplemental dose or dosage adjustment necessary (Ref).
Peritoneal dialysis: Unlikely to be significantly dialyzed (large molecular weight): No dosage adjustment necessary (Ref).
CRRT: No dosage adjustment necessary (Ref).
PIRRT (eg, sustained, low-efficiency diafiltration): No dosage adjustment necessary (Ref).
There are no dosage adjustments provided in the manufacturer's labeling.
Refer to adult dosing.
(For additional information see "Iron sucrose: Pediatric drug information")
Dosage guidance:
Safety: Multiple forms of parenteral iron exist; close attention must be paid to the specific product when ordering and administering; incorrect selection or substitution of one form for another without proper dosage adjustment may result in serious over- or underdosing.
Dosing: Doses are expressed as mg of elemental iron.
Iron-deficiency anemia in chronic kidney disease (CKD):
Repletion treatment: Limited data available: Children ≥2 years and Adolescents ≤15 years: IV: 1 mg/kg/dose per dialysis session; repeat dose with each dialysis session until patient-specific lab goals are met, then follow with maintenance dosing. Dosing based on a dose-finding trial in 14 pediatric patients (ages 2 to 15 years) receiving iron sucrose in combination with epoetin for absolute or functional iron deficiency. Due to a rapid increase in ferritin levels (from 59 mcg/L to 496 mcg/L) observed in the first 6 weeks of the trial, the dosing protocol for iron sucrose was changed from 3 mg/kg/dose per dialysis session to 1 mg/kg/dose per dialysis session; the dose of 1 mg/kg/dose per dialysis session was continued until a patient was considered replete based on study criteria, at which point the patient was transitioned to the maintenance group within the study (Ref).
Maintenance therapy: Children ≥2 years and Adolescents:
Hemodialysis-dependent CKD: IV: 0.5 mg/kg/dose every 2 weeks for 12 weeks (6 doses); maximum dose: 100 mg/dose; may repeat if clinically indicated.
Peritoneal dialysis-dependent CKD (in combination with erythropoietin therapy): IV: 0.5 mg/kg/dose every 4 weeks for 12 weeks (3 doses); maximum dose: 100 mg/dose; may repeat if clinically indicated.
Nondialysis-dependent CKD (in combination with erythropoietin therapy): IV: 0.5 mg/kg/dose every 4 weeks for 12 weeks (3 doses); maximum dose: 100 mg/dose; may repeat if clinically indicated.
Iron-deficiency anemia, treatment, patients without chronic kidney disease: Limited data available:
Infants, Children, and Adolescents: IV: 2.5 to 7 mg/kg/dose; repeat every 3 to 7 days until patient-specific goals are met or total calculated deficit replaced; maximum dose: 300 mg/dose; less frequent administration has been reported and some experts recommend maximum initial dose of 100 mg/dose (Ref).
Nondialyzable. There are no dosage adjustments provided in the manufacturer's labeling.
There are no dosage adjustments provided in the manufacturer's labeling.
Rates of infusion reactions associated with IV iron preparations vary across studies (Ref); higher rates of infusion reactions with iron sucrose compared to other formulations (Ref). Immediate hypersensitivity reactions to IV iron preparations, including iron sucrose, range in severity from mild self-limited reactions (eg, pruritus, urticaria, asymptomatic hypotension) to severe anaphylaxis and anaphylactic shock (Ref). Transient flushing and truncal myalgias, known as Fishbane reactions, occur in ~30% of all infusion reactions, quickly resolve after discontinuing the infusion, and do not recur when the infusion is restarted at a slower rate (Ref). Delayed hypersensitivity reactions, most often exanthematous cutaneous reactions, have also been reported (Ref). There is a lack of cross-reactivity between iron sucrose and iron dextran (Ref).
Mechanism: Non–dose-related; may be immunologic or nonimmunologic (more common) (Ref). Immediate hypersensitivity reactions (eg, anaphylaxis): mechanism unknown (Ref). Nonimmunologic reactions (eg, Fishbane reactions) may be due to activation of complement, referred to as complement activation-related pseudo-allergy (CARPA) (Ref). Delayed hypersensitivity reactions are commonly T-cell mediated (Ref).
Onset: Rapid; occur most frequently within the first 10 minutes of the infusion but may occur more than 30 minutes after completion of the infusion (Ref).
Risk factors:
• Higher dose and faster infusion rates (Ref)
• Previous reaction to IV iron (Ref)
IV iron, including iron sucrose, may be associated with an increased risk of infection (Ref).
Mechanism: Non–dose-related; IV iron can increase levels of non–transferrin-bound iron, which can lead to impaired T-cell and neutrophil function (Ref).
Onset: Varied; can occur after single- or multiple-dose administrations (Ref).
Risk factors:
• Patients with inflammatory bowel disease (Ref)
Excessive iron therapy may lead to iron overload (with the possibility of iatrogenic hemosiderosis) in patients with kidney failure (Ref).
Mechanism: Dose-related; occurs when administered iron exceeds the carrying capacity of transferrin, leading to the release of labile, non–transferrin-bound iron (Ref).
Onset: Delayed; following chronic exposure (Ref).
Risk factors:
• High IV iron doses (Ref)
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported adverse reactions are for adults with hemodialysis dependent (HDD), non-dialysis dependent (NDD), and/or peritoneal dialysis dependent (PDD) chronic kidney disease (CKD), unless otherwise noted.
>10%:
Cardiovascular: Hypotension (children and adolescents: 2%; adults: HDD-CKD: 39%, NDD/PDD-CKD: 2% to 3%) (table 1)
Drug (Iron Sucrose) |
Comparator |
Population |
Dosage Form |
Indication |
Number of Patients (Iron Sucrose) |
Number of Patients (Comparator) |
Comments |
---|---|---|---|---|---|---|---|
2% |
N/A |
Children and adolescents |
IV injection |
CKD |
141 |
N/A |
N/A |
39% |
N/A |
Adults |
IV injection |
HDD-CKD |
231 |
N/A |
N/A |
2% |
0.7% |
Adults |
IV injection |
NDD-CKD |
139 |
139 |
Comparator: Oral iron |
3% |
2% |
Adults |
IV injection |
PDD-CKD |
75 |
46 |
Comparator: Erythropoietin |
Gastrointestinal: Nausea (children and adolescents: 3%; adults: 5% to 15%)
Nervous system: Headache (children and adolescents: 6%; adults: HDD-CKD: 13%, NDD/PDD-CKD: 3% to 4%)
Neuromuscular & skeletal: Muscle cramps (HDD-CKD: 29%, NDD/PDD-CKD: ≤3%)
Respiratory: Nasopharyngitis (≤16%) pharyngitis (≤16%), sinusitis (≤16%), upper respiratory tract infection (≤16%)
1% to 10%:
Cardiovascular: Arteriovenous fistula site complication (thrombosis: children: 2%), chest pain (1% to 6%), heart failure (>1%), hypertension (children and adolescents: 2%; adults: 7% to 8%), peripheral edema (3% to 7%)
Dermatologic: Pruritus (2% to 4%) (table 2)
Drug (Iron Sucrose) |
Comparator |
Population |
Dosage Form |
Indication |
Number of Patients (Iron Sucrose) |
Number of Patients (Comparator) |
Comments |
---|---|---|---|---|---|---|---|
4% |
N/A |
Adults |
IV injection |
HDD-CKD |
231 |
N/A |
N/A |
2% |
4% |
Adults |
IV injection |
NDD-CKD |
139 |
139 |
Comparator: Oral iron |
3% |
0% |
Adults |
IV injection |
PDD-CKD |
75 |
46 |
Comparator: Erythropoietin |
Endocrine & metabolic: Hyperglycemia (3%), hypervolemia (1% to 3%), hypoglycemia (HDD/NDD-CKD: <1%, PDD-CKD: 4%)
Gastrointestinal: Abdominal pain (1% to 4%), diarrhea (5% to 8%), dysgeusia (≤8%), peritonitis (children: 4%), vomiting (children and adolescents: 4%; adults: 5% to 9%)
Infection: Sepsis (>1%)
Local: Infusion-site reaction (≤6%; including burning and infusion-site pain)
Nervous system: Asthenia (≤3%), dizziness (children and adolescents: 4%; adults: HDD/NDD-CKD: 7%, PDD-CKD: 1%)
Neuromuscular & skeletal: Arthralgia (1% to 4%), back pain (1% to 2%), gout (3%), limb pain (3% to 6%), myalgia (1% to 4%)
Ophthalmic: Conjunctivitis (≤3%)
Otic: Otalgia (2%)
Respiratory: Cough (children and adolescents: 4%; adults: 1% to 3%), dyspnea (1% to 6%), nasal congestion (1%), viral respiratory tract infection (children: 4%)
Miscellaneous: Fever (children and adolescents: 4%; adults: ≤3%)
Postmarketing (any population):
Cardiovascular: Bradycardia, collapse, ischemic heart disease, shock
Dermatologic: Hyperhidrosis
Genitourinary: Urine discoloration
Hypersensitivity: Hypersensitivity reaction (including anaphylactic shock, anaphylaxis, and angioedema) (Behera 2015, Mishra 2013)
Nervous system: Confusion, loss of consciousness, paresthesia, seizure
Neuromuscular & skeletal: Joint swelling
Respiratory: Bronchospasm
Known hypersensitivity to iron sucrose or any component of the formulation
Canadian labeling: Additional contraindications (not in the US labeling): Iron overload; anemia not caused by iron deficiency
Concerns related to adverse effects:
• Hypotension: Clinically significant hypotension has been reported; monitor for signs/symptoms of hypotension. Hypotension may be related to total dose or rate of administration (avoid rapid IV injection).
Use parenteral iron products with caution in premature neonates; necrotizing enterocolitis has been reported; however, no causal relationship established.
Strength of iron sucrose is expressed as elemental iron.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous [preservative free]:
Venofer: 20 mg/mL (2.5 mL, 5 mL, 10 mL)
No
Solution (Venofer Intravenous)
20 mg/mL (per mL): $8.83
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Venofer: 20 mg/mL (5 mL)
Generic: 20 mg/mL (5 mL)
IV: Administer intravenously as a slow IV injection (not for rapid IV injection) or as an IV infusion. Equipment for resuscitation and trained personnel experienced in handling medical emergencies should always be immediately available. Can be administered through dialysis line.
Slow IV injection: May administer doses ≤200 mg undiluted by slow IV injection over 2 to 5 minutes. When administering to hemodialysis-dependent patients, give iron sucrose early during the dialysis session (generally within the first hour).
Infusion: Infuse diluted doses ≤200 mg over at least 15 minutes; infuse diluted 300 mg dose over 1.5 hours; infuse diluted 400 mg dose over 2.5 hours; infuse diluted 500 mg dose over 3.5 to 4 hours (limited experience). When administering to hemodialysis-dependent patients, give iron sucrose early during the dialysis session.
Parenteral: May administer IV; not for IM use.
Premature Neonates: Infusion: Infuse over at least 1 to 2 hours (Ref).
Infants, Children, and Adolescents:
Treatment of iron deficiency anemia in patients with chronic kidney disease (CKD):
Slow IV injection: Administer undiluted over 5 minutes.
Infusion: Dilute and infuse over 5 to 60 minutes.
Iron deficiency anemia in patients without CKD: Infuse diluted doses over 30 to 90 minutes (reported range: 15 minutes to 3.5 hours) (Ref). Some experts recommend to dilute to 1 mg/mL and infuse at 1 to 1.3 mL/minute (Ref). Undiluted doses (≤200 mg) may be infused as slow IV push (eg, over 5 minutes) (Ref).
Others recommend the following infusion times based on dose (Ref):
For doses ≤100 mg, infuse over at least 30 minutes.
For doses >100 mg and ≤200 mg, infuse over at least 60 minutes.
For doses >200 mg and ≤300 mg, infuse over at least 90 minutes.
Iron-deficiency anemia: Treatment of iron-deficiency anemia in chronic kidney disease (CKD)
KDIGO guideline recommendations: For CKD patients with anemia and receiving dialysis, IV iron may be indicated if an increase in the hemoglobin concentration (without initiating or increasing the dose of an erythropoiesis stimulating agent) is desired and the transferrin saturation (TSAT) is ≤30% and ferritin is ≤500 ng/mL; for CKD patients not on dialysis, a trial of oral iron is suggested, although the route of administration is selected based on the severity of iron deficiency, venous access, response to prior oral iron therapy, patient adherence, and cost. There is insufficient evidence to recommend IV iron if ferritin level is >500 ng/mL or TSAT is >30% (KDIGO 2012).
Iron deficiency anemia, treatment, patients without chronic kidney disease
Iron sucrose may be confused with ferric carboxymaltose, ferric gluconate, ferumoxytol, iron dextran complex
Venofer may be confused with Vfend, Vimpat
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider therapy modification
Amisulpride (Oral): May enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy
Arginine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Blood Pressure Lowering Agents: May enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination
Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Dimercaprol: May enhance the nephrotoxic effect of Iron Preparations. Risk X: Avoid combination
DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy
Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy
Iloperidone: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Levodopa-Foslevodopa: Blood Pressure Lowering Agents may enhance the hypotensive effect of Levodopa-Foslevodopa. Risk C: Monitor therapy
Levonadifloxacin: Iron Preparations may decrease the serum concentration of Levonadifloxacin. Risk X: Avoid combination
Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy
Obinutuzumab: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider therapy modification
Pentoxifylline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy
Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Silodosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy
Iron transfer to the fetus is regulated by the placenta (BSH [Pavord 2020]; NAS 2020).
There is a risk of adverse maternal reactions (eg, anaphylaxis, hypotension, shock) following use of parenteral iron that may result in fetal bradycardia, especially during the second and third trimesters. Although the risk is rare, immediate treatment for anaphylactoid and/or hypersensitivity reactions should be available (BSH [Pavord 2020]).
Maternal iron requirements increase during pregnancy. Untreated iron deficiency and iron deficiency anemia (IDA) in pregnant patients are associated with adverse pregnancy outcomes, including low birth weight, preterm birth, and increased perinatal mortality (ACOG 2021; BSH [Pavord 2020]). Maternal iron deficiency is also associated with fatigue, increased risk of postpartum depression, and possibly postpartum hemorrhage (BSH [Pavord 2020]).
Oral and parenteral iron are effective at replacing iron stores in pregnant patients (ACOG 2021), Most studies note iron therapy improves maternal hematologic parameters; however, data related to clinical outcomes in the mother and neonate are limited (FIGO 2019; NAS 2020; USPSTF [Siu 2015]). Parenteral iron therapy may be used in pregnant patients who cannot tolerate or respond to oral iron, when iron deficiency occurs later in pregnancy, or when malabsorption is present (ACOG 2021; BSH [Pavord 2020]).
Iron sucrose has been evaluated in multiple studies for the treatment of IDA during pregnancy (Govindappagari 2019; Hamm 2021; Lewkowitz 2019; Qassim 2018; Qassim 2019; Radhika 2019; Rogozińska 2021; Shin 2021). However, due to limited safety data in early pregnancy, use of IV iron is generally not started until the second or third trimester (ACOG 2021; BSH [Pavord 2020]; FIGO 2019).
Iron is present in breast milk.
Endogenous iron concentrations in breast milk vary by postpartum age and are lower than concentrations in the maternal plasma (Dorea 2000; Emmett 1997). Breast milk concentrations of iron are maintained in lactating patients with mild to moderate iron deficiency anemia (IDA), but concentrations decrease if IDA is moderate to severe (El-Farrash 2012) or severe (Kumar 2008).
Iron concentrations in breast milk were not increased following a single infusion of iron sucrose 100 mg IV to 10 women (2 to 3 days postpartum) with iron-deficiency anemia; milk concentrations were evaluated for 4 days after the injection (Breymann 2007).
Iron sucrose has been evaluated in multiple studies for the treatment of postpartum IDA (Sultan 2019).
Iron deficiency and IDA are associated with adverse effects in postpartum patients (eg, altered cognition, depression, fatigue), which may influence interactions with the infant. Iron supplementation in the postpartum patient should be initiated as soon as possible following delivery when gestational anemia is a concern (WHO 2016). Parenteral iron therapy may be used in postpartum patients with uncorrected anemia at delivery who cannot tolerate, do not respond to, or are noncompliant with oral iron therapy, or the severity of anemia requires prompt management (BSH [Pavord 2020]).
According to the manufacturer, the decision to breastfeed during therapy should consider the risk of infant exposure, the benefits of breastfeeding to the infant, and the benefits of treatment to the mother; monitor the breastfed infant for GI toxicity (eg, constipation, diarrhea).
Hematocrit, hemoglobin, serum ferritin, serum iron, transferrin, percent transferrin saturation (TSAT), total iron-binding capacity (TIBC) (takes ~4 weeks of treatment to see increased serum iron and ferritin, and decreased TIBC); iron status should be assessed ≥48 hours after last dose (due to rapid increase in values following administration); signs/symptoms of hypersensitivity reactions (during and ≥30 minutes following infusion); hypotension (during and following infusion); signs and/or symptoms of active systemic infection.
Evaluate iron status (TSAT and ferritin) when deciding to start or continue iron therapy, and at least every 3 months in patients also receiving erythropoietin-stimulating agent (ESA) therapy. Monitor ferritin and TSAT more frequently when monitoring response to IV iron therapy, when initiating or increasing ESA dose, when there is blood loss, and in any other situations where iron stores may become depleted (KDIGO 2012).
Chemotherapy-associated anemia (off-label use): Iron, total iron-binding capacity, transferrin saturation, or ferritin levels at baseline and periodically (ASCO/ASH [Bohlius 2019])
Anemia:
Hemoglobin, whole blood:
Female: 12 to 16 g/dL (SI: 120 to 160 g/L) (ABIM 2023).
Male: 13 to 18 g/dL (SI: 130 to 180 g/L) (ABIM 2023; WHO 2011).
Iron deficiency:
Ferritin, serum: Note: Ferritin is an acute phase reactant; levels may be elevated in the presence of inflammation or infection which is independent of iron status (WHO 2020).
Female: 24 to 307 ng/mL (SI: 53.9 to 689.8 picomole/L).
Male: 24 to 336 ng/mL (SI: 53.9 to 755 picomole/L).
Iron, serum: 50 to 150 mcg/dL (SI: 9 to 26.9 micromole/L).
Total iron binding capacity, serum: 250 to 310 mcg/dL (SI: 44.8 to 55.5 micromole/L).
Transferrin saturation: 20% to 50%.
Transferrin, serum: 200 to 400 mg/dL (SI: 24.6 to 49.2 micromole/L).
Chronic kidney disease-associated anemia: To achieve and maintain target hemoglobin for patients with nondialysis-dependent chronic kidney disease, patients with a transferrin saturation (TSAT) ≤30% and a serum ferritin level ≤500 ng/mL (SI: ≤1,123.5 picomole/L) will often respond to iron supplementation (Gutiérrez 2021; KDIGO 2012).
Iron sucrose is dissociated by the reticuloendothelial system into iron and sucrose. The released iron increases serum iron concentrations and is incorporated into hemoglobin.
Onset of action: Hematologic response to either oral or parenteral iron salts is essentially the same; red blood cell form and color changes within 3 to 10 days
Maximum effect: Peak reticulocytosis occurs in 5 to 10 days, and hemoglobin values increase within 2 to 4 weeks
Distribution: Vdss: Healthy adults: 7.9 L
Metabolism: Dissociated into iron and sucrose by the reticuloendothelial system
Half-life elimination: Healthy adults: 6 hours; Non-dialysis-dependent adolescents: 8 hours
Excretion: Healthy adults: Urine (5%) within 24 hours
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