eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders
Hyperuricemia: Treatment & Medication
Updated: Sep 29, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Asymptomatic hyperuricemia
Most patients with asymptomatic hyperuricemia never develop gout or stones. Treatment for asymptomatic hyperuricemia carries some risk. It is not considered beneficial or cost-effective and, generally, is not recommended. The exception to this is in an oncologic setting in which patients receiving cytolytic treatment may be treated prophylactically to prevent acute uric acid nephropathy.
Symptomatic hyperuricemia
The clinical scenarios under which hyperuricemia can be symptomatic are gout, uric acid stones, or uric acid nephropathy.
- Acute gouty arthritis
- The initial goal in acute gouty arthritis is to provide symptomatic relief from pain.
- Indomethacin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are the drugs of choice for acute gouty arthritis. NSAIDs are prescribed for approximately a 7- to 10-day course or until 3-4 days after all signs of inflammation have resolved. Use NSAIDs with caution or avoid them in patients in edematous states, such as heart failure, and in patients with peptic ulcer disease or renal insufficiency.
- Colchicine, which inhibits neutrophil activation, is effective but is currently used less frequently because of its adverse effects. Traditionally, colchicine is administered as a 0.6-mg dose every hour until improvement occurs, adverse gastrointestinal effects occur, or a total of 10 doses is reached and no relief is noted. The adverse gastrointestinal effects include abdominal pain, diarrhea, and nausea, which occur in most patients started on colchicine. Although colchicine can be administered intravenously, this is usually avoided because of its potential for serious toxicity.
- Use intra-articular glucocorticoids in patients with contraindications to NSAID or colchicine use. Occasionally, intra-articular glucocorticoids may be used in patients with gouty arthritis refractory to NSAIDs or colchicine.
- Chronic gout therapy
- After the symptoms of acute gout subside, patients enter the intercritical period during which a decision must be made regarding the need for treating the patient with a urate-lowering medication. One important point to consider during treatment is that abrupt lowering of urate levels can precipitate an attack of acute gout during the intercritical period. Thus, these patients receive prophylactic colchicine coverage irrespective of which urate-lowering medication is used.
- The choice of urate-lowering medications is uricosuric drugs (which promote uric acid excretion) or xanthine oxidase inhibitors (which inhibit uric acid production).
- Probenecid, which is a uricosuric drug, inhibits the tubular reabsorption of filtered and secreted urate, thereby increasing urate excretion. The ideal candidates for probenecid therapy are those with a 24-hour urine uric acid excretion of less than 800 mg in 24 hours, no history of nephrolithiasis, and good renal function (creatinine clearance >80 mL/min). The starting dose for probenecid is 250 mg twice a day, which can be increased gradually to a maximum daily dose of 3 g/d. Some degree of gastrointestinal irritation is experienced by approximately 2% of patients.
- Allopurinol is the most widely used antihyperuricemic agent. The major metabolite of allopurinol is oxypurinol, and both allopurinol and oxypurinol are competitive inhibitors of the enzyme xanthine oxidase.
- The ideal candidates for allopurinol treatment are uric acid overproducers (24-h urinary uric acid excretion >800 mg on general diet or >600 mg on a purine-restricted diet); patients with renal insufficiency, nephrolithiasis, or tophaceous gout; or patients at risk for developing uric acid nephropathy. Although allopurinol can be used in almost any hyperuricemic state, the above-mentioned conditions are more specific indications for allopurinol use. The usual maintenance dose for adults is 200-300 mg/d. The long half-life of oxypurinol makes once-daily dosing possible. Very importantly, adjust the dose in persons with chronic renal insufficiency because a higher incidence of adverse effects is observed if the dose is not adjusted.
- Allopurinol is well tolerated by most patients, but hypersensitivity reactions may develop, which can be severe or fatal. Because a skin rash may progress to a severe hypersensitivity reaction, patients who develop a skin rash should discontinue allopurinol. Hepatotoxicity, bone marrow depression, and interstitial nephritis are rare but serious adverse effects of allopurinol.
- Uric acid nephrolithiasis
- Allopurinol is the mainstay of drug therapy in patients with hyperuricemia who develop uric acid stones. Patients with calcium stones who are hyperuricosuric may also benefit from allopurinol because urate crystals in the urine may act as a nidus for other stones to form.
- Potassium citrate and occasionally sodium bicarbonate or acetazolamide may be required to alkalinize the urine and to decrease the solubility of uric acid.
- Adequate hydration is recommended to maintain a high urine output of at least 2 L unless otherwise contraindicated for other medical conditions where volume overload may be a concern.
- Uric acid nephropathy
- Over the years, efforts to prevent uric acid nephropathy, especially in the oncological setting, have resulted in a decrease in mortality from uric acid nephropathy.
- Intravenous hydration with saline and the administration of furosemide or mannitol (to dilute the urine) are necessary to prevent further precipitation of uric acid. Alkalinizing the urine with sodium bicarbonate or acetazolamide may be necessary to further enhance uric acid elimination.
- Rasburicase, a recombinant urate oxidase, is now approved for use in preventing complications of hyperuricemia during the tumor lysis syndrome. It facilitates the conversion of urate to a more soluble product, allantoin.
- Higher doses than usual (600-900 mg/d) are administered to decrease uric acid production prior to chemotherapy in patients with leukemias and lymphomas; allopurinol and hydration are continued for several days.
- If acute renal failure develops despite these measures, then early hemodialysis is indicated to reduce the total body burden of uric acid, thereby facilitating recovery of renal function.
Consultations
- Consultation with a rheumatologist may be indicated for patients with acute or chronic gouty arthritis.
- Consultation with a renal medicine specialist may be indicated for patients with acute urate nephropathy or chronic renal failure.
- Consultation with a urologist is indicated for patients who present with symptomatic uric acid nephrolithiasis.
Diet
- The use of a low-purine diet may significantly lower serum uric acid levels.
- This diet principally consists of sugars, starches, and fats, with protein supplied by eggs and cheese.
- Meats, poultry, fish, seafood, organ meats, alcohol, beans, and peas should be avoided.
Activity
- No limitation exists on activity for patients with hyperuricemia, although strenuous exercise may raise serum uric acid levels.
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Pharmacotherapy for hyperuricemia is based on whether patients are overproducers or undersecretors. Allopurinol continues to be the mainstay for the treatment of patients who are overproducers, although the drug febuxostat is being investigated as a possible replacement for allopurinol. Febuxostat is a nonpurine selective xanthine oxidase inhibitor for the treatment of gout.6
A 52-week randomized study published in 2005 evaluated over 700 patients with gout and serum uric acid levels of at least 8 mg/dL. More than 50% of patients taking 80 mg/d of febuxostat achieved a serum uric acid level of less than 6 mg/dL at the last 3 monthly measurements, according to the study. This was in comparison to 62% of patients who reached this primary endpoint with 120 mg/d of febuxostat and 21% of patients who achieved this target with 300 mg/d of allopurinol.
However, follow-up comments by the author acknowledged that discontinuation of the drug occurred 2 times as often in the low-dose febuxostat group and 3 times as often in the high-dose febuxostat group, as it did in the allopurinol group. Moreover, the occurrence of 4 deaths in the febuxostat groups, as compared with none in the allopurinol group, is a concern, and therefore, febuxostat needs further study.6,7,8 Febuxostat was approved by the US Food and Drug Administration (FDA) in February 2009 for long-term treatment of hyperuricemia in gout.
Rasburicase is another medication that was introduced to control hyperuricemia. It is a recombinant urate oxidase that is indicated for preventing complications of hyperuricemia during the tumor lysis syndrome. Since losartan has been found to have an uricosuric property, it may be worthwhile to use it in hypertensive patients with hyperuricemia that lack any contraindication to angiotensin receptor blockers. Other uricosuric drugs used in underexcretors are mentioned below.
Nonsteroidal anti-inflammatory drugs
Management of pain and inflammation in gout. Have analgesic, anti-inflammatory, and antipyretic properties. Inhibit the enzyme cyclooxygenase, thus inhibiting biosynthesis of prostaglandins and thromboxanes from arachidonic acid.
Indomethacin (Indochron E-R, Indocin)
Rapidly absorbed. Metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.
Discontinue 3-4 d following symptom resolution.
Adult
25-50 mg IR bid/tid
75 mg SR bid; not to exceed 200 mg/d
Pediatric
1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, ACE inhibitors, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants or antiplatelet agents (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity
Documented hypersensitivity; GI bleeding; renal insufficiency
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Category D in third trimester of pregnancy; caution in acute renal insufficiency and chronic renal impairment; hyperkalemia; hyponatremia; cardiac dysfunction; hypertension; liver disease; epilepsy; history of GI bleeding; patients with coagulation defects or receiving anticoagulant/antiplatelet agents
Xanthine oxidase inhibitors
Prevent gouty arthritis attacks and nephropathy. Used to treat hyperuricemia secondary to diuretics or antineoplastics. Prevent recurrent uric acid nephrolithiasis.
Allopurinol (Zyloprim)
Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. Reduces synthesis of uric acid without disrupting biosynthesis of vital purines.
Adult
CrCl 100-140 mL/min: 200-600 mg/d PO qd, divided bid when >300 mg/d
Dose adjustment in renal impairment (based on CrCl)
80 mL/min: 250 mg PO qd
60 mL/min: 200 mg PO qd
40 mL/min: 150 mg PO qd
20 mL/min: 100 mg PO qd
10 mL/min: 100 mg PO qod
0 mL/min: 100 mg PO q3d
Pediatric
<10 years: 10 mg/kg/d PO divided bid/tid; not to exceed 600 mg/d
>10 years: 200-600 mg/d PO
Alcohol decreases effects; increases incidence of skin rash when used concurrently with ampicillin, amoxicillin, and, possibly, ACE inhibitors; large amounts of vitamin C acidify urine and may cause kidney stone formation; inhibits metabolism of azathioprine, cyclophosphamide, and mercaptopurine
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Not for use in asymptomatic hyperuricemia; reduce dose in renal insufficiency; monitor liver function and perform CBC count before initiating therapy and periodically thereafter
Febuxostat (Uloric)
Xanthine oxidase inhibitor. Prevents uric acid production and lowers elevated serum uric acid levels. Indicated for long-term management of hyperuricemia associated with gout.
Adult
40 mg PO qd initially; after 2 wk, if serum uric acid levels are not <6 mg/dL, increase to 80 mg/d
Pediatric
Not established
Coadministration with xanthine oxidase substrate drugs (eg, azathioprine, mercaptopurine, theophylline) may increase plasma concentration of these substrates, resulting in toxicity
Documented hypersensitivity; coadministration with azathioprine, mercaptopurine, or theophylline
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increased gout flares frequently observed during initiation of therapy (use prophylactic therapies, such as NSAIDs or colchicine); higher rate of thromboembolic events observed in patients treated with febuxostat compared with allopurinol in clinical trials (monitor for signs and symptoms of MI and stroke); may increase liver transaminase levels; common adverse effects include nausea, arthralgia, and rash
Uricosuric agents
Competitively inhibit reabsorption of uric acid in proximal renal tubule. This promotes excretion of uric acid and lowers serum uric acid levels.
Probenecid (Benemid)
Used to treat and prevent hyperuricemia associated with gout and gouty arthritis.
Adult
250 mg PO bid for 1 wk; increase to 500 mg bid, may increase q4wk; not to exceed 2-3g/d
Pediatric
<2 years: Not recommended
>2 years: 40 mg/kg/d PO divided qid
Salicylates at high dosages and nitrofurantoin may decrease effects; increases levels/toxicity of methotrexate, beta-lactam antibiotics, gatifloxacin, acyclovir, thiopental, clofibrate, dyphylline, pantothenic acid, ketorolac, benzodiazepines, rifampin, sulfonamide, dapsone, zidovudine, and sulfonylureas
Documented hypersensitivity; known blood dyscrasia; uric acid kidney stones; ketorolac levels/toxicity significantly increased when coadministered
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Initiate treatment after acute gout attack subsides; crosses placental barrier; use of any drug in women with childbearing potential requires that anticipated benefits be weighed against possible hazards; caution in history of peptic ulcer; may not be effective in patients with CrCl <30 mL/min; exacerbates acute gouty attack
Antigout agents
Treatment of gouty arthritis attacks and prevention of their recurrence. Used in management of familial Mediterranean fever.
Colchicine
Reduces formation of uric acid crystals in affected joint, thereby reducing amount of acute inflammation and pain; also decreases uric acid levels in blood. Can be used in combination with probenecid on long-term to prevent gout or can be used alone to treat pain and inflammation of acute gout attacks. Discontinue when pain of gout attack begins to subside, when maximum dose is reached, or when GI symptoms (eg, nausea, vomiting, diarrhea) indicate cellular poisoning. Decreases leukocyte motility and phagocytosis in inflammatory responses.
Adult
Acute gout attack: 0.5-1.2 mg PO initially, followed by 0.5-0.6 q1-2h or 1-1.2 mg q2h until a satisfactory response is attained; not to exceed 4 mg/attack
1-3 mg IV initially, followed by 0.5 mg q6h until a satisfactory response is attained; not to exceed 4 mg/d
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Sympathomimetic agent toxicity and effect of CNS depressants significantly increased
Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Not to exceed cumulative doses >4 mg/attack; minimum 3-d colchicine-free interval between dosage regimens; use IV with extreme caution; patients who become pregnant while receiving colchicine therapy may be at greater risk of producing trisomic offspring; most common adverse reactions are GI-related (eg, nausea, vomiting, diarrhea, abdominal pain); may cause agranulocytosis, aplastic anemia, or bone marrow suppression
Carbonic anhydrase inhibitors
Decrease solubility of uric acid. Adequate hydration recommended to maintain high urine output.
Acetazolamide (Diamox, Diamox sequels)
Used to further enhance uric acid elimination.
Adult
250 mg PO q8-12h, alternatively 500-mg ER cap PO q12-24h
Pediatric
5-10 mg/kg/dose IV/IM q6h
10-15 mg/kg/d PO divided q6-8h
Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine
Documented hypersensitivity; hepatic disease, severe renal disease, adrenocortical insufficiency, or severe pulmonary obstruction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some diabetic patients
Glucocorticoids
Have both anti-inflammatory (glucocorticoid) and salt retaining (mineralocorticoid) properties. Glucocorticoids have profound and varied metabolic effects and modify the body's immune response to diverse stimuli.
Prednisone (Deltasone, Orasone, Meticorten)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Adult
5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve
Pediatric
4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve
Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Dexamethasone (Decadron, AK-Dex, Alba-Dex)
Decreases inflammation by suppressing migration of PMN leukocytes and reducing capillary permeability.
Adult
0.75-9 mg/d PO/IV/IM in divided doses q6-12h
Pediatric
0.08-0.3 mg/kg/d or 2.5-10 mg/m2/d PO/IV/IM divided q6-12h
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering; abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Urate oxidase enzyme (recombinant)
Tumor lysis syndrome.
Rasburicase (Elitek)
A recombinant form (derived from Saccharomyces cerevisiae -synthesized, Aspergillus flavus) of the enzyme urate oxidase, which oxidizes uric acid to allantoin. Indicated for treatment and prophylaxis of severe hyperuricemia associated with the treatment of malignancy. Hyperuricemia causes a precipitant in the kidneys, which leads to acute renal failure. Unlike uric acid, allantoin is soluble and easily excreted by the kidneys. Elimination half-life is 18 h.
Adult
0.15-0.2 mg/kg/d IV infused over 30 min for 5 d; dilute in 50 mL 0.9% NaCl
Pediatric
Administer as in adults
None reported
Documented hypersensitivity; G-6-PD deficiency
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hemolytic anemia secondary to hydrogen peroxide produced during uric acid oxidation; may cause methemoglobinemia; other adverse effects include fever, nausea, or vomiting; children <2 y may experience more vomiting, diarrhea, fever, and rash; avoid shaking or vortexing during product reconstitution; highly antigenic, multiple administration may produce allergic reaction, anaphylaxis, or death; produces false low uric acid levels, accurate levels obtained by collecting blood into prechilled heparin-containing tubes kept at 4°C and centrifuged at that temperature, maintain resultant plasma at 4°C and analyze within 4 h of collection
Alkalinizing Agent, Oral
These agents are used to raise the pH in the urine.
Potassium citrate (Citra K, Polycitra K)
Pleasant-tasting oral systemic alkalizer containing potassium citrate and citric acid in a sugar-free base.
Each unit dose packet contains potassium citrate monohydrate 3300 mg and citric acid monohydrate 1002 mg. Each unit dose packet, when reconstituted, supplies the same amount of active ingredients as is contained in 15 mL (1 tablespoonful) Polycitra-K oral solution and provides 30 mEq potassium ion and is equivalent to 30 mEq bicarbonate.
Absorbed and metabolized to potassium bicarbonate, thus acting as a systemic alkalizer. Effects are essentially those of chlorides before absorption and those of bicarbonates subsequently. Oxidation is virtually complete so that <5% of the potassium citrate is excreted in the urine unchanged.
Highly concentrated and, when administered after meals and before bedtime, allows one to maintain an alkaline urinary pH at all times, usually without necessity of 2 am dose. Alkalinizes urine without producing systemic alkalosis in recommended dosage.
Adult
30-60 mEq/d PO in divided doses tid/qid with food only if no other medical problems that may impair potassium excretion exist (see Contraindications); serum chemistries need to be monitored carefully
Pediatric
10-40 mEq/d PO in divided doses tid/qid with food only if no other medical problems that may impair potassium excretion exist (see Contraindications); serum chemistries need to be monitored carefully
Increased drug effect with potassium-containing medications, potassium-sparing diuretics, ACE inhibitors, or cardiac glycosides (could lead to toxicity); drugs that slow GI transit time (ie, anticholinergics) are expected to increase GI adverse effects
Documented hypersensitivity; severe renal impairment with oliguria/azotemia; hyperkalemia; untreated Addison disease; acute dehydration
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Frequent monitoring of serum potassium concentration is recommended; caution in CHF, hypertension, edema, or any condition sensitive to sodium or potassium intake; conversion of citrate to bicarbonate in the liver may be blocked in severe illness, shock, or hepatic failure associated with GI distress; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest
More on Hyperuricemia |
| Overview: Hyperuricemia |
| Differential Diagnoses & Workup: Hyperuricemia |
 Treatment & Medication: Hyperuricemia |
| Follow-up: Hyperuricemia |
| References |
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Further Reading
Keywords
gout, nephrolithiasis, uric acid, uric acid overproduction, uric acid underexcretion, uric acid under-excretion, renal insufficiency, renal failure, diuretic therapy, diabetes insipidus, diabetic ketoacidosis, ethanol intoxication, salicylate intoxication, starvation ketosis, Lesch-Nyhan syndrome, Kelley-Seegmiller syndrome, leukemia blast crisis, rhabdomyolysis, cytotoxic therapy, ethanol consumption, familial juvenile gouty nephropathy, FJGN, medullary cystic disease, chronic lead nephropathy, syndrome X, hypertension, preeclampsia, eclampsia, hyperparathyroidism, sarcoidosis, lead intoxication, lead poisoning, lead toxicity, lead exposure, occupational lead exposure, moonshine consumption, trisomy 21, purine-rich diet, tumor lysis syndrome, deficiency of aldolase B, aldolase B deficiency, glucose-6-phosphatase deficiency, G-6-P deficiency, glycogen storage disease, GSD, glycogenosis type I, von Gierke disease
