Uric acid

Hypoxanthine is converted to xanthine in the liver and it is converted to uric acid by xanthine oxidase.

End product of purine metabolism.

An important bellwether for cardiometabolic health.

Uric acid is an antioxidant oxypurine produced from xanthine by the enzyme xanthine oxidase, and is an intermediate product of purine metabolism.

Uric acid is the highest concentration antioxidant in human blood.

Uric acid acts as an antioxidant by mitigating the oxidative stress caused by high-altitude hypoxia.

Uric acid has the highest concentration of any blood antioxidant and provides over half of the total antioxidant capacity of human serum.

Normal levels less than 6 mg per dL in women and less than 7 mg per dL in men.

Normally is completely ionized and highly soluble at the natural pH of the body.

In the acidic renal tubules and collecting ducts it becomes less soluble.

Solubility at pH of 5 is one twentieth the solubility at a ph of 7.

Primarily excreted by the kidney.

The serum uric acid level increases linearly with decreasing glomerular filtration rate as a result of reduced excretion.

Urinary concentration mechanisms increase the risk of crystallization.

Elevated serum irate levels are associated with increased risk of onset and progression of chronic kidney disease and end-stage kidney disease.

There is a correlation between high uric acid and obesity, hypertension, and diabetes. 

Uric acid is generated when the body metabolizes purines. 

There is a linear association between serum urate levels and albuminuria, onset of chronic kidney disease, progression to end-stage disease kidney disease, cardiovascular events and death.

Uric acid can raise blood pressure by constricting blood vessels, and over time, the kidneys ­develop a low-grade injury in response to reduced blood flow, driving high blood pressure even if uric-acid levels come down.

Uric acid can harm mitochondria.

high uric acid increases your risk of heart disease, type 2 diabetes, hyper­tension, and kidney disease. 

Reduced excretion associated with thiazide diuretics, loop diuretics, low-dose salicylates, cyclosporine, niacin, ethambutal, pyrazinamide, and didanosine.

Consumption of alcohol, obesity and dietary excess can to lead to increased uric acid production.

These organic purine compounds are abundant in an array of food and drink, with the highest concentration found in red meat, beer and spirits, and in certain seafoods. 

Is an antioxidant, and accounts for most of the anti-oxident capacity of plasma.

Uric acid metabolism is linked to oxidative stress and is the end product of purine metabolism.

The body creates their purines and subsequently uric acid, when fructose and alcohol are metabolized.

Uric acid cannot be broken down and needs to excreted: a third of it goes through the gut, and the other two-thirds go through the kidneys.

Reducing fructose consumption, reduces uric acid.

Uric acid levels tend to fluctuate in response to food, alcohol, purines, heat stress, and intense exercise.

Limiting high-purine foods and alcohol, and drinking tart cherry juice can lower serum levels of uric acid.

Vitamin C has been shown in multiple studies to lower uric acid and protect against gout. 

Both too little and too much exercise can increase uric-acid production.

The breakdown of muscle tissues increases the supply of purines for the body to metabolize, leading to spikes in uric acid.

Being sedentary for more than 10 hours a day is more likely to have high uric acid than those who were inactive for fewer than five hours per day. 

Low – and moderate-intensity physical activity reduce the risk of elevated uric-acid levels by 12 percent, and a routine including some vigorous physical activity reduced the risk by 29 percent.

Data suggest limiting food intake to an eight-to-12-hour window can improve insulin sensitivity, blood pressure, fat metabolism, gut function, and immune function. 

It can also lower inflammation and help regulate uric acid.

Some medications, like diuretics, proton pump inhibitors, beta-blockers, and blood pressure medicines, are associated with elevated uric acid. 

Whole fruits contain nutrients — such as vitamin C, flavonoids, potassium, and fiber tend to block the harmful effects of fructose. 

Most fruit juices, though, lack many of these beneficial substances and concentrate fructose at much higher levels. 

Likewise, dried fruit is higher in fructose than its fresh counterparts.

Dehydration concentrates the blood and can lead to elevated uric acid.

 Uric acid does not penetrate the blood–brain barrier well. 


Oxidative stress due to uric acid is now thought to figure in metabolic syndrome, atherosclerosis, and stroke, all syndromes associated with high uric acid levels. 

Reduced renal clearance related to decreased GFR, hyperinsulinism, renal vasoconstriction or diuretic usage.

Alcohol intake, tissue ischemia, and oxidative stress can increase the generation of uric acid.

Prior to the use of hypouricemic agents studies revealed more than 50% of patients with gout had some amount of clinical renal disease and 100% had pathologic disease at autopsy.

Gouty nephropathy characterized by arteriosclerosis, glomerulosclerosis, interstitial fibrosis and the presence of urate crystals in the outer medulla (Talbot).

A strict purine-free diet will reduce serum urate by about 15-20%.

Epidemiologic studies indicate relation of serum uric acid levels with hypertension metabolic syndrome, coronary artery disease, cerebrovascular disease, vascular dementia, kidney disease and preeclampsia.

Allopurinol decreases production by inhibiting xanthine oxidase.

Decreases serum levels of uric acid by approximately 10-15%.

In patients with chronic kidney disease, urate lowering treatment with allopurinol does not slow the  decline in GFR as compared with placebo.

Elevation not accepted as a risk factor for cardiovascular disease, but is associated with many established risk factors.

When excess uric acid overwhelms the ability to excrete it, it forms  crystals in the kidneys that can develop into kidney stones, and accumulate in joints, leading to the painful swelling and inflammation known as gout.

About 80 percent of people with gout have crystals in their aorta or in their coronary arteries, with the potential to damage the heart. 

Gout and kidney stones become more likely when uric-acid levels ­exceed 7 milligrams/deciliter.

It is suspected cardiovascular risks occur at lower levels, even in the absence of ­other symptoms.

Uric acid can act as a potent oxidant, causing oxidative stress and damaging the lining of the blood vessels, and levels should be below 5.5 mg/dL.

Cardiometabolic risk from Uric acid begins at 5.5 mg/dL level in men, women, and children.

Uric acid has been linked with heart attacks, heart disease, and systemic inflammation.

Levels higher in postmenopausal women, blacks, hypertensives, patients with metabolic syndrome and those with renal disease.

As populations move to Western diets and from rural to urban areas uric acid levels rise.

Increased rates in the U.S. of diabetes, hypertension, obesity, and kidney disease also associated with increases in serum uric acid in the population.

Uric acid levels ≥7 mg/dL in men are associated with higher risk of hip fractures compared with uric acid levels of <7 mg/dL.

Women have a lower level of uric acid by 0.5-1 mg /dL probably as a result of the uricosuric effect of estrogens.

It is suspected cardiovascular risks occur at lower levels, even in the absence of ­other symptoms.

Uric acid can act as a potent oxidant, causing oxidative stress and damaging the lining of the blood vessels, and levels should be below 5.5 mg/dL.

Cardiometabolic risk from Uric acid begins at 5.5 mg/dL level in men, women, and children.

Rasburicase, a recombinant urate oxidase that converts existing uric acid into allantoin which is soluble, even at acidic pH, and easily excreted by the kidney.

Its accumulation is avoided by the use of rasburicase.

While hyperuricemia is linked to adverse health outcomes from hypertension and cardiovascular disease, metabolic syndrome, and chronic kidney disease, it is controversial with the hyperuricemia has a causal role.

Randomized trials of urate lowering drugs have suggested safety concerns about mortality: mortality rates or trends to higher mortality was seen with the largest decreases in serum uric acid.

Studies suggest that there is a U curve relationship between serum urate and cardiovascular mortality.

The safety of long-term lowering of serum urate below 5 mg/dL has not been established and there are suggestions that it may be unsafe.

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