tophi of sodium urate affecting the elbow, knuckles, and finger joints. The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of<unk> . This can occur because of diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop<unk>  at some point in their lifetimes. The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/l (9 mg/dL), the risk is 4.5% per year. Lifestyle Dietary causes account for about 12% of<unk> , and include a strong association with the consumption of alcohol, sugar-sweetened beverages, meat, and seafood. Among foods richest in purines yielding high amounts of uric acid are dried anchovies, shrimp, organ meat, dried mushrooms, seaweed, and beer yeast. Chicken and potatoes also appear related. Other triggers include physical trauma and surgery. Studies in the early 2000s found that other dietary factors are not relevant. Specifically, a diet with moderate purine-rich vegetables (e.g., beans, peas, lentils, and spinach) is not associated with<unk> . Neither is total dietary protein. Alcohol consumption is strongly associated with increased risk, with wine presenting somewhat less of a risk than beer or spirits. Eating skim milk powder enriched with glycomacropeptide (GMP) and G600 milk fat extract may reduce pain but may result in diarrhea and nausea. Physical fitness, healthy weight, low-fat dairy products, and to a lesser extent, coffee and taking vitamin C, appear to decrease the risk of<unk> ; however, taking vitamin C supplements does not appear to have a significant effect in people who already have established<unk> . Peanuts, brown bread, and fruit also appear protective. This is believed to be partly due to their effect in reducing insulin resistance. Genetics<unk>  is partly genetic, contributing to about 60% of variability in uric acid level. The SLC2A9, SLC22A12, and ABCG2 genes have been found to be commonly associated with<unk>  and variations in them can approximately double the risk. Loss-of-function mutations in SLC2A9 and SLC22A12 causes low blood uric acid levels by reducing urate absorption and unopposed urate secretion. The rare genetic disorders familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch–Nyhan syndrome, are complicated by<unk> . Medical conditions<unk>  frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases. Other conditions commonly complicated by<unk>  include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants, and myeloproliferative disorders such as polycythemia. A body mass index greater than or equal to 35 increases male risk of<unk>  threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for<unk>  due to the harmful effect of lead on kidney function. Medication Diuretics have been associated with attacks of<unk> , but a low dose of hydrochlorothiazide does not seem to increase risk. Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers, beta blockers, ritonavir, and pyrazinamide. The immunosuppressive drugs ciclosporin and tacrolimus are also associated with<unk> , the former more so when used in combination with hydrochlorothiazide. Hyperuricemia may be induced by excessive use of Vitamin D supplements. Levels of serum uric acid have been positively associated with 25(OH) D. The incidence of hyperuricemia increased 9.4% for every 10 nmol/L increase in 25(OH) D (P < 0.001).
Gout
Septic arthritis
Greyout
Rheumatoid arthritis
Blackout 
Calcium pyrophosphate dihydrate crystal deposition disease
Barefoot
Alkaptonuria