Hyperuricemia is largely genetically mediated, but factors including high intake of purine rich foods, renal dysfunction, and diuretic use can impair urate clearance or increase the serum urate level.
Standard treatment of hyperuricemia consists of allopurinol, urinary alkalinization, hydration and osmotic diuresis.
Defined as a serum uric acid level of more than 7 mg/dL in men or more than 6 mg/dL in women.
Hyperuricemia may cause gout and is linked by observational studies to adverse health outcomes from hypertension and cardiovascular disease to metabolic syndrome and chronic kidney disease.
Increases with age.
Most patients are asymptomatic and never develop gout.
80-90% of gout patients are undersecreters.
10-15% of patients overproduce uric acid.
X-linked enzyme disorders increase in uric acid production: hypoxanthine-guanine phosphoribosyltransferase deficiency and phosphoribosylpyrophosphate synthetase overactivity.
The risk of gout increases with increasing serum uric acid level.
Rising uric acid levels, even within the normal range, are associated with increased risk for developing renal complications or tumor lysis syndrome.
In hematologic malignancies patients receiving their first chemotherapy, everyone milligram per deciliter increase in serum uric acid was associated with a 2.2 fold increase in the odds of developing renal complications.
Patients with serum uric acid level more than 10 mg/dL have a 5-year prevalence of gout of 30%.
The 5-year prevalence of gout is 0.6% in patients with serum uric acid levels less than 7 mg/dL.
Current recommendations do not support urate-lowering therapy for asymptomatic hyperuricemia.
Allopurinol use associated with decreased cardiovascular risk among hyperuricemic patients.
Associated with cancer chemotherapy treatment when the cancer cells luxe and release their cellular contents including potassium, phosphorus, and nucleic acids.
The nucleic acids are metabolized into uric acid and should be eliminated in the urine because they cannot be further broken down.
Patients with hyperuricemia and hyperphosphatemia are at risk for tumor lysis syndrome and can die from hyperkalemic arrest the first few days of therapy.
Renal excretion is the primary method of eliminating uric acid and phosphate from the body.
When the uric acid accumulation occurs more quickly than can be excreted and can lead to inflammatory renal damage.
Renal damage leads to decreased urine output and reduced GFR or acute kidney injury which can further accumulate more uric acid and phosphorus and worsening acute kidney injury can occur leading to end stage renal disease.
Uric acid make cause kidney injury by a crystal-dependent pathway, that calcium phosphate and urate crystals precipitate in the renal tubules, causing mechanical extraction and localized information that leads to acute kidney injury.
A crystal-independent pathway can also cause acute kidney injury by the release of inflammatory mediators and vasoconstriction by uric acid accumulation.
If serum uric acid reach hyperuricemic range and is left untreated, nephropathy can result and can contribute to tumor lysis syndrome.
Drug treatment trials of irate lowering drugs, with different mechanisms of action, have been associated with a higher mortality or trends to higher mortality in gout patients, with the largest decreases in serum urate.
Urate accounts for most of the antioxidant capacity of plasma.eq