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Mechanism of Action
US Drug Names
Efficacy has not been established. Due to a lack of clinical data, the National Institutes of Health (NIH) COVID-19 treatment guidelines do not give recommendations for or against the use of anakinra. 100 mg via intravenous infusion given every 6 hours for 15 days is being evaluated. In SARS-CoV-2 infected patients with macrophage activation syndrome (MAS) or immune dysregulation, 1 study is evaluating 200 mg intravenously every 8 hours for 7 days. For patients with renal impairment, the dose is to be reduced to 100 mg intravenously every 8 hours for 15 days. A retrospective cohort study evaluated the use of 5 mg/kg infused over 1 hour twice daily in 29 COVID-19 patients with moderate-to-severe acute respiratory distress and hyperinflammation. On Day 21, the survival rate for patients receiving anakinra (5 mg/kg twice daily) plus standard therapy was 90% compared to 56% for patients receiving standard therapy alone.  
Efficacy has not been established. Due to a lack of clinical data, the National Institutes of Health (NIH) COVID-19 treatment guidelines do not give recommendations for or against the use of anakinra. 100 mg once daily via subcutaneous injection for 28 days or until hospital discharge, whichever is first, is being evaluated. Another study evaluated the use of 100 mg subcutaneously twice daily for 72 hours, followed by 100 mg daily for 7 days.
100 mg subcutaneously once daily, every 24 hours, at approximately the same time each day. Higher doses do not result in increased response. Anakinra may be given alone or in combination with DMARDs other than tumor necrosis factor (TNF) inhibitors.
1 to 2 mg/kg subcutaneously once daily, initially. If needed, increase by 0.5 to 1 mg/kg increments. In a clinical trial, the average maintenance dose was 3 to 4 mg/kg/day. Usually given as a single daily dose. However, splitting the daily dose into twice daily administrations may result in better symptom control for some patients. Max: 8 mg/kg/day.
1 to 2 mg/kg subcutaneously once daily, initially. If needed, increase by 0.5 to 1 mg/kg increments. In a clinical trial, the average maintenance dose was 3 to 4 mg/kg/day. Usually given as a single daily dose. However, splitting the daily dose into twice daily administrations may result in better symptom control for some patients. Max: 8 mg/kg/day. The NOMID premarket clinical trial included 36 pediatric patients, 13 of which were younger than 2 years; the youngest patient studied was 8 months of age. In a retrospective study of 10 patients (2 months to 20 years of age), the 8 oldest patients (ages 6 to 20 years) required dosages of 1 to 3 mg/kg/day, whereas the 2 youngest patients (3 and 4 months) had severe disease and required 6 and 10 mg/kg/day to control symptoms.
2 to 6 mg/kg/day subcutaneously may be considered in highly refractory patients who have failed to respond to a second IVIG infusion, an extended course of steroids, or infliximab.
5 to 10 mg/kg/day IV (preferred) or subcutaneous in 1 to 4 divided doses in patients with refractory MIS-C who do not improve within 24 hours of initial immunomodulatory therapy. Tapering over 2 to 3 weeks, or even longer, may be necessary to avoid rebound inflammation. 
1 to 2 mg/kg/dose (Max: 100 mg/dose) subcutaneously once daily for several months.  
1 to 2 mg/kg/dose subcutaneously once daily, initially. If needed to control active inflammation, increase by 0.5 to 1 mg/kg increments up to a maximum of 8 mg/kg/day.
1 to 2 mg/kg/dose subcutaneously once daily, initially. If needed to control active inflammation, increase by 0.5 to 1 mg/kg increments up to a maximum of 8 mg/kg/day. The DIRA clinical trial included 9 pediatric patients (aged 1 month to 9 years) treated for up to 10 years. Doses were individually adjusted and the highest dose studied was 7.5 mg/kg/day.
Check the patient's neutrophil count before anakinra initiation, followed by monthly for the first 3 months of therapy, and then quarterly for up to 1 year.
100 mg/day subcutaneously for RA; 8 mg/kg/day subcutaneously for NOMID and DIRA.
100 mg/day subcutaneously for RA.
8 mg/kg/day subcutaneously for NOMID and DIRA.
8 mg/kg/day subcutaneously in NOMID and DIRA. Limited data available in young infants; up to 10 mg/kg/day subcutaneously has been used off-label in an infant with severe NOMID.
Safety and efficacy have not been established.
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
CrCl 30 mL/minute or more: No dosage adjustment needed.
CrCl less than 30 mL/minute: Increased risk of adverse reactions; consider administration of the prescribed dose every other day instead of daily for both RA and NOMID.
Anakinra is a recombinant, non-glycosylated form of the human interleukin-1 receptor antagonist (IL-1Ra). The drug is produced by recombinant DNA technology using an E. coli bacterial expression system. Anakinra is useful for treating rheumatoid arthritis (RA) and some other inflammatory conditions. In adults with moderately to severely active RA, anakinra improves signs and symptoms of the disease and slows the progression of structural damage. Anakinra was considered but not included in the American College of Rheumatology 2015 guidelines due to its infrequent use at that time in RA compared to other available treatments and lack of new data since 2012; however, tumor necrosis factor (TNF) inhibitors are usually first-line choices in the biologic treatment categories due to the long-term safety data and the amount of experience associated with the TNF biologics. For adult RA, anakinra may be used as monotherapy; the drug may also be used with other disease-modifying antirheumatic drugs (DMARDs). The ideal combination of therapy for individual RA patients is determined by treat to target strategies and severity of disease. While anakinra has been studied in pediatric patients 2 years and older with polyarticular juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), the study data were insufficient to establish efficacy for this condition, and use for JRA/JIA is not recommended. Anakinra is helpful for the treatment of Deficiency of Interleukin-1 Receptor Antagonist (DIRA), Cryopyrin-Associated Periodic Syndromes (CAPS) such as Muckle-Wells Syndrome (MWS), Familial Cold Auto-Inflammatory Syndrome (FCAS), and Neonatal-Onset Multisystem Inflammatory Disease (NOMID), which is also called Chronic Infantile Neurological, Cutaneous and Articular Syndrome (CINCA). Of all the forms of CAPS, NOMID/CINCA has the highest severity of chronic inflammation. Among patients with NOMID, disease symptoms and serum markers of inflammation usually worsened within 5 days of anakinra withdrawal and promptly responded to anakinra re-initiation.
Updates for coronavirus disease 2019 (COVID-19):
Due to a lack of clinical data, the National Institutes of Health (NIH) COVID-19 treatment guidelines do not give recommendations for or against the use of anakinra. Based on preliminary data from other anti-interleukin medications, studies have evaluated the use of anakinra for COVID-19.
For storage information, see the specific product information within the How Supplied section.
Hypersensitivity reactions including anaphylactoid reactions, angioedema, urticaria, rash, and pruritus have been reported with the use of anakinra. Patients with deficiency of interleukin-1 receptor antagonist (DIRA) may be at increased of hypersensitivity reactions, particularly during the first weeks of therapy; closely monitor patients during this time period. In a study of patients with DIRA, rash was 1 of the most commonly reported adverse reactions and 1 patient experienced a serious reaction of urticaria on day 10 of therapy. If a severe hypersensitivity reaction occurs, discontinue anakinra and initiate appropriate therapy.
The most common adverse reaction of anakinra subcutaneous administration is injection site reaction, which usually occurs during the first 4 weeks of treatment and is more common in patients with rheumatoid arthritis (RA) than in patients with Neonatal-Onset Multisystem Inflammatory Disease (NOMID). In clinical trials of patients with RA (n= 1,565), 71% of patients developed an injection site reaction; 72.6% were characterized as mild, 24.1% as moderate, and 3.2% as severe. In an open-label trial of NOMID patients (n = 43), 16.3% experienced an injection site reaction; during the 60-month study period, 65% of the injection site reactions occurred during the first month and 76% were reported during the first 6 months; 76% were characterized as mild and 24% as moderate. In a study of 9 patients with Deficiency of Interleukin-1 Receptor Antagonist (DIRA), there was 1 report of injection site pain. These reactions typically last for 14 to 28 days and are characterized by localized erythema, ecchymosis, edema, inflammation, itching, and/or pain. To decrease pain, swelling, and bruising at the injection site, apply a cold compress before and/or after the injection and allow the solution warm to room temperature prior to injection.
Anakinra has been associated with an increased risk of serious infections during clinical trials. Anakinra may increase the risk of tuberculosis (TB) or other atypical opportunistic infections. During postmarketing observation and in clinical studies, opportunistic infections consisting of fungal, mycobacterial, and bacterial pathogens have occurred. Infections have been noted in all organ systems and have been reported in patients receiving anakinra alone or in combination with immunosuppressive agents. Discontinue anakinra in patients with rheumatoid arthritis (RA) who develop a serious infection. In anakinra-treated patients with Neonatal-Onset Multisystem Inflammatory Disease (NOMID) or Deficiency of Interleukin-1 Receptor Antagonist (DIRA), weigh the risk of a disease flare when discontinuing anakinra against the potential risk of continued treatment. During RA clinical trials, the incidence of infection during the first 6 months in anakinra-treated patients was 39% vs. 37% in placebo-treated patients. Reported infections in patients with RA included upper respiratory tract infections (14%), sinusitis (7%), and influenza-like symptoms (6%). Serious infections occurred in 2% of anakinra-treated patients with RA over 6 months of therapy and 3% of treated patients after over 1 year of therapy. The serious infections were primarily bacterial infections such as cellulitis, pneumonia, and bone and joint infections. In open-label extension studies, the overall rate of serious infections was comparable to that observed during controlled trials. The use of TNF blockers with anakinra should be avoided. In patients with RA who received both anakinra and a TNF blocker (etanercept) for up to 24 weeks, the incidence of serious infections was 7%. The most common infections consisted of bacterial pneumonia (4 cases) and cellulitis (4 cases). One patient with pulmonary fibrosis and pneumonia died due to respiratory failure. RA patients with asthma had a higher incidence of serious infections during treatment with anakinra versus placebo-treated patients (4.5% vs 0%). In an open-label study of 43 patients with NOMID, infections were the most common type of serious adverse event; reporting frequency was highest in pediatric patients younger than 12 years of age and those younger than 2 years had the highest incidence of infection and related symptoms. The most common infections were upper respiratory tract infection, sinusitis, ear infections (otitis media), and naso-pharyngitis (11.6%). The most common serious infections in NOMID patients were pneumonia and gastroenteritis. There were no deaths or permanent treatment discontinuation due to infection. Most NOMID patients (73%) have continued anakinra therapy once the infection resolved. In a natural history study of 9 patients (aged 1 months to 9 years) with DIRA treated for up to 10 years, infections were the most common type of serious adverse reaction with 5 events reported in 2 patients. Infections reported in patients with DIRA were upper respiratory tract infections, influenza-like illness, cellulitis, and gastroenteritis.
Anakinra treatment has been associated with hematologic side effects, including neutropenia. Monitoring of the absolute neutrophil count (ANC) is recommended prior to and during the first year of treatment with anakinra (monitor at baseline, each month for 3 months, then quarterly). In clinical trials, 8% of patients with rheumatoid arthritis (RA) receiving anakinra had decreases in neutrophil counts of at least one World Health Organization (WHO) toxicity grade compared with 2% in the control group. Neutropenia (ANC 1,000/mm3 or less) was reported in 9 anakinra-treated patients (0.4%) and in 2% of patients treated with anakinra plus etanercept. Two of 43 (4.7%) patients with Neonatal-Onset Multisystem Inflammatory Disease (NOMID) experienced neutropenia after starting anakinra in a clinical trial; both cases resolved during continued anakinra treatment. In RA trials, a total of 9% of anakinra recipients experienced increases in eosinophil differential percentage (eosinophilia) of at least 1 WHO toxicity grade compared to 3% of placebo-treated patients. WHO toxicity grade 1 decreases in platelet countss occurred in 2% of anakinra treated-patients and 0% of placebo-treated patients. Thrombocytopenia, including severe thrombocytopenia (i.e., platelet count less than 10,000/mm3), has been reported with the postmarket use of anakinra.
Adverse gastrointestinal (GI) events reported in 5% or more of patients treated with anakinra during rheumatoid arthritis clinical trials include nausea (8%), diarrhea (7%), and abdominal pain (5%). In an open-label study in 43 NOMID patients, vomiting (14%) was the most common GI adverse event.
Headache and arthralgia are two of the most common adverse reactions to anakinra treatment. Headache occurred in 12% to 14% of patients during all clinical trials. Arthralgia occurred in 6% of anakinra-treated patients during rheumatoid arthritis (RA) clinical trials over a 6 month period and in 11.6% of 43 patients in a study of anakinra for Neonatal-Onset Multisystem Inflammatory Disease (NOMID). In the RA trials, a total of 19% of anakinra recipients experienced worsening of rheumatoid arthritis, compared to 29% of placebo recipients.
In an open-label study in 43 patients with Neonatal-Onset Multisystem Inflammatory Disease (NOMID), treatment-emergent pyrexia (fever) was reported in 11.6% of patients. In a natural history study of 9 patients with Deficiency of Interleukin-1 Receptor Antagonist (DIRA), pyrexia was 1 of the most commonly reported adverse reactions. Fever was not reported as an adverse reaction in clinical trials of patients with rheumatoid arthritis.
Cholesterol elevations were observed in some patients treated with anakinra therapy (hypercholesterolemia incidence not reported).
Elevated hepatic enzymes and non-infectious hepatitis have been reported postmarketing with the use of anakinra.
As with all therapeutic proteins, the use of anakinra carries the risk for immunogenicity. Antibody formation to anakinra detected by the use of a highly sensitive anakinra-binding biosensor assay was present at least once over 36 months in 49% of patients with rheumatoid arthritis in 2 clinical trials. After at least 12 weeks of anakinra, 30 (2%) of the 1,615 patients with available data were seropositive in a cell-based assay for neutralizing antibodies against anakinra. Thirteen of the 30 patients had follow-up data; 5 remained positive for neutralizing antibodies at week 24. No correlation between antibody development and adverse events was noted. Immunogenicity was not evaluated in trials of patients with Neonatal-Onset Multisystem Inflammatory Disease (NOMID).
The role of interleukin-1 blockers such as anakinra in the development of new primary malignancy is unknown. In clinical trials, the number of lymphoma cases among 5,300 patients with rheumatoid arthritis treated with anakinra was 0.12 per 100 patient-years. The rate is 3.6-fold higher than the expected rate for the general population, based upon the National Cancer Institute's Surveillance Epidemiology and End Results database. In addition to lymphoma, 37 other cancers were observed including breast, melanoma, respiratory system, and digestive system.
Anakinra is contraindicated in patients with E. coli protein hypersensitivity or hypersensitivity to anakinra or any components of the product. Hypersensitivity reactions, including anaphylactic reactions and angioedema, have been reported with the use of anakinra. Due to a potential increased risk of allergic reactions, particularly in the first several weeks of anakinra therapy, monitor patients with deficiency of interleukin-1 receptor antagonist (DIRA) closely during this time period. If a severe hypersensitivity reaction occurs, discontinue administration of anakinra and initiate appropriate therapy.
Patients who receive anakinra are at increased risk for developing serious infections. Do not initate anakinra in patients with an active infection. Discontinue administration of anakinra if a patient with rheumatoid arthritis (RA) develops a serious infection. In patients with neonatal-onset multisystem inflammatory disease (NOMID) or deficiency of interleukin-1 receptor antagonist (DIRA), weigh the risk of a disease flare upon discontinuation of anakinra against the potential risk of continued treatment. The safety and efficacy of anakinra in patients with chronic infections or immunosuppression, such as bone marrow suppression, have not been evaluated. The impact of anakinra therapy on active or chronic infections is not known. Similar to other drugs that affect the immune system, anakinra may increase the risk of tuberculosis or other atypical or opportunistic infections. In clinical studies and postmarketing experience, cases of opportunistic infections have been observed and included fungal infection, mycobacterial infection, and infection with bacterial pathogens. Infections have been noted in all organ systems and have been reported in patients receiving anakinra alone or in combination with immunosuppressive agents. Follow current CDC guidelines both to evaluate for and to treat possible latent tuberculosis infections before anakinra initiation. In RA trials, patients with asthma appeared to be at a higher risk of developing serious infections during anakinra treatment. Also, use anakinra cautiously in geriatric patients, as there is, in general, a higher incidence of infections in the elderly.
Decreases in neutrophil count and neutropenia have been reported with anakinra therapy. Neutrophil counts should be checked before anakinra receipt, every month for 3 months, and quarterly after that for a period up to 1 year.
Anakinra is substantially excreted by the kidney; thus, patients with severe renal impairment or renal failure with a creatinine clearance (CrCL) less than 30 mL/minute may be at increased risk for adverse reactions. Consider administration of the prescribed anakinra dose every other day for these patients.
Anakinra is an immunosuppressant and treatment with immunosuppressants may result in an increased risk of cancer. The impact of anakinra on the development of a new primary malignancy is unknown, but malignancies were observed in clinical studies. Consider the risks and benefits of anakinra before initiation in patients with a history of neoplastic disease. Also, consider the risk and benefits of anakinra continuation in patients who develop a malignancy.
Avoid use of live vaccines concurrently with anakinra. No data are available on either the effects of live vaccination or the secondary transmission of infection by live vaccines in patients receiving anakinra. No data are available on the effectiveness of vaccination with inactivated antigens, other than tetanus/diphtheria toxoids vaccine, in patients receiving anakinra. In one clinical trial, no difference in the anti-tetanus antibody response to tetanus/diphtheria toxoids vaccine was noted between patients receiving anakinra and placebo. Since anakinra interferes with normal immune response mechanisms to new antigens, vaccination may not be effective. The interval between live vaccinations and initiation of anakinra therapy should be in accordance with current vaccination guidelines regarding immunosuppressive agents.
Available data from retrospective studies and case reports on anakinra use during human pregnancy are insufficient to identify a drug-associated risk of major birth defects, miscarriage, or maternal and fetal adverse events. The available data have not identified an increased frequency or pattern of birth defects, miscarriage, or adverse maternal or fetal outcomes. Published data do suggest an increased risk of adverse pregnancy outcomes in women with rheumatoid arthritis (RA) or cryopyrin-associated periodic syndromes (CAPS) who have increased disease activity. An international retrospective study of pregnancy outcomes with interleukin-1 inhibitors reported on 23 anakinra-exposed pregnancies. There were 21 live births of healthy infants, 1 miscarriage, and 1 infant with left renal agenesis. The estimated background rate of detected renal malformations is 0.2% to 2% of all newborns. Data for another retrospective study of 10 anakinra-exposed pregnancies in women with CAPS included 9 live births, 1 miscarriage, and 1 fetal death in a twin pregnancy (the surviving twin was healthy). Overall, these data cannot definitively establish or exclude any anakinra-associated risks during pregnancy. Methodological limitations of these data include small sample size and the inability to control for confounders such as the timing of drug exposure, underlying maternal disease, and concomitant medication use. Reproductive studies in animals (rats, rabbits) revealed no evidence of fetal harm at doses up to 25 times the maximum recommended human dose (MRHD) on an mg/kg basis. Guidelines suggest that until further data are available, anakinra use should be avoided during pregnancy if possible in patients with RA.
There are no data on the presence of anakinra in either human or animal milk or the effects on milk production. Limited data from a small retrospective study and postmarketing case reports do not establish an association between maternal anakinra use during lactation and adverse effects in breastfed infants. These limited data during lactation preclude a clear determination of the risk of anakinra to an infant during lactation. The developmental and health benefits of breast-feeding should be considered along with the clinical need for anakinra in the mother and any potential adverse effects to the nursing infant from anakinra or from the underlying maternal condition. Guidelines suggest that until further data are available, anakinra use in patients with RA should be approached with caution and avoided if possible during breast-feeding.
Very limited data are available describing the use of anakinra in infants; use with caution in young infants. Neonates and infants less than 1 month of age were not included in the trial for the treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID). Anakinra prefilled syringes are unable to deliver an anakinra dosage less than 20 mg. Although anakinra has been studied in pediatric patients 2 to 17 years of age with juvenile rheumatoid arthritis (JRA)/juvenile idiopathic arthritis (JIA), the study data were insufficient to demonstrate efficacy.
Anakinra acts similarly to the native interleukin-1 receptor antagonist (IL-1Ra). IL-1Ra blocks the effects of IL-1 by competitively inhibiting the binding of IL-1, specifically IL-1 alpha and IL-1 beta, to the interleukin-1 type 1 receptor (IL-1R1), which is expressed in a wide variety of tissues. IL-1Ra is part of the feedback loop that is designed to balance the effects of inflammatory cytokines. IL-1 is 1 of the primary pro-inflammatory cytokines associated with rheumatoid arthritis, acting synergistically with tumor necrosis factor-alpha (TNF-alpha). Both IL-1 and TNF-alpha are expressed in the synovium of rheumatoid arthritis patients, although, IL-1, specifically IL-1beta, is secreted to a greater extent than TNF-alpha. IL-1 causes cartilage degradation by inducing the rapid loss of proteoglycans and stimulating the production of neutral proteinases in chondrocytes. Since IL-1 stimulates osteoclasts, bone resorption occurs. Rheumatoid arthritis patients who have bone erosions also have higher synovial fluid concentrations of IL-1 than rheumatoid arthritis patients with no bone erosions. These higher concentrations of IL-1 cannot be overcome by endogenous IL-1Ra. By administering exogenous IL-1Ra (i.e., anakinra), the erosive bone effects and bone resorption associated with IL-1 may be inhibited.
The efficacy of anakinra for the treatment of familial cold autoinflammatory syndrome appears to be related to inhibition of IL-1 beta, IL-6, and IL-8 in affected skin and to inhibition of increased IL-6 serum concentrations after cold exposure. In excess, IL-1 has been shown to be a key driver of inflammation in cryopyrin-associated periodic syndromes (CAPS), which is caused by a range of mutations in the gene CIAS1 that encodes the protein cryopyrin. Cryopyrin binds with an intrinsic inhibitor and controls the activation of caspase-1. Caspase-1 cleaves pro-interleukin-1beta and IL-18 into the biologically active forms. Patients with CAPS have increased caspase activity and thus, increased biologically active IL-1 beta. Enhanced caspase-1 activity with subsequent enhanced IL-1 beta and IL-18 release has been demonstrated in a patient with chronic infantile neurologic, cutaneous, articular (CINCA) syndrome. Anakinra receipt to several patients with different CAPS phenotypes led to the reduction of many CAPS clinical manifestations.
Deficiency of IL-1 receptor antagonist (DIRA) is due to mutations in the IL1RN gene leading to loss of secretion of the IL-1Ra. Loss of IL-1Ra results in unopposed signaling of the proinflammatory cytokines IL-1 alpha and IL-1 beta, causing systemic inflammation with skin and bone involvement. Anakinra is the recombinant form of IL-1Ra that patients with DIRA are lacking.
Anakinra is given subcutaneously. In patients with rheumatoid arthritis (RA), no unexpected accumulation of anakinra was observed after daily subcutaneous doses for up to 24 weeks. The terminal half-life of anakinra ranges from 4 to 6 hours among patients with RA. Among patients with Neonatal Onset Multisystem Inflammatory Disease (NOMID), the median half-life was 5.7 hours (range, 3.1 to 28.2 hours). Anakinra is renally eliminated; the mean clearance of the drug increases with increasing creatinine clearance and body weight.
The absolute bioavailability of anakinra after subcutaneous injection in healthy subjects is 95%. After administration to subjects with RA, the maximum plasma concentration occurs within 3 to 7 hours. In NOMID patients (n = 16) receiving a median dose of 3 mg/kg once daily subcutaneously and a median treatment time of 3.5 years, the steady-state median (range) maximal concentration (Cmax) was 3,628 (655 to 8,511) ng/mL and the median (range) 24-hour concentration was 203 (53 to 1,979) ng/mL.
No formal studies have been performed to examine the pharmacokinetic parameters of anakinra administered subcutaneously in patients with hepatic impairment.
The estimated anakinra clearance increased with increasing creatinine clearance and body weight in a pharmacokinetic study using daily subcutaneous doses of anakinra. Among patients with severe or end-stage renal disease, defined as creatinine clearance (CrCl) less than 30 mL/minute, the mean plasma clearance of anakinra decreased by 70% and 75%, respectively. The mean plasma clearance of anakinra decreased by 50% in patients with a CrCl of 30 to 49 mL/minute and by 16% in patients with a CrCl of 50 to 80 mL/minute. Less than 2.5% of an administered dose is removed by either hemodialysis or continuous ambulatory peritoneal dialysis. Based on these observations, a dose schedule change should be considered for subjects with severe renal insufficiency or end-stage renal disease.
After adjusting for creatinine clearance and body weight, age was not a significant factor for the mean plasma clearance of anakinra during a pharmacokinetic study.
After adjusting for creatinine clearance and body weight, gender was not a significant factor for the mean plasma clearance of anakinra in a pharmacokinetic study. In a study of NOMID patients, there was no obvious gender influence on anakinra pharmacokinetics.
The estimated anakinra clearance increased with increasing creatinine clearance and body weight in a pharmacokinetic study.
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