What will happen if the uric acid
level increases.
How to detect the problem
(is there any symptom) and what will be the natural way to reduce or balance uric acid level.
1 Answers
What is uric acid? Uric acid is the final breakdown product of purine (essential components of DNA and RNA) degradation in humans. In plasma extracellular fluid and synovial fluid, uric acid is found in its ionised form called urate. When plasma is saturated with urate, urate crystal can precipitate. Similarly in urine, depending on the pH (acid vs basic), urate can precipitate and form renal stones.
According to the Harrison’s Principles of Internal Medicine,
Mean serum urate values of adult men and premenopausal women are 415 and 360 μmol/L (6.8 and 6 mg/dL), respectively. After menopause, values for women increase to approximate those of men. In adulthood, concentrations rise steadily over time and vary with height, body weight, blood pressure, renal function, and alcohol intake.
Increased production or decreased excretion of uric acid lead to hyperuricemia.
Hyperuricemia is defined as a plasma (or serum) urate concentration > 405 μmol/L (6.8 mg/dL).
A detailed list of causes of hyperuricemia can be found in the table below
The most common complications of hyperuricemia are:
- gouty arthritis (the risk of developing gouty arthritis increases with high serum irate levels)
- nephrolithiasis (= renal stones)
- urate nephropathy (= monosodium urate crystal deposition in the renal interstitium)
- uric acid nephropathy (= uric acid crystals deposition in renal collecting ducts, pelvis and ureters)
Detection of hyperuricemia relies on the patient's symptoms. Hyperuricemia can be asymptomatic and not necesseraly be associated to any disease. As such, evaluation of hyperuricemia will be guided by the clinical presentation and by the clinician's suspicion. Typically uric acid can be measured in the blood. Also, in some cases, quantification of uric acid excretion can help to investigate whether hyperuricemia is due to increased production or reduced excretion.
Finally, while in some cases, antihyperuricemia therapy is indicated, routine treatment of hyperuricemia is not recommended. A systematic review (when authours review all the current scientific literature regarding a specific topic/question) conducted in 2014 regarding risk factors for gouty arthritis found following risk factors:
Alcohol consumption increased the risk of incident gout, especially beer and hard liquor. Several dietary factors increased the risk of incident gout, including meat intake, seafood intake, sugar sweetened soft drinks, and consumption of foods high in fructose. Diary intake, folate intake and coffee consumption were each associated with a lower risk of incident gout and in some cases a lower rate of gout flares. Thiazide and loop diuretics were associated with higher risk of incident gout and higher rate of gout flares. Hypertension, renal insufficiency, hypertriglyceridemia, hypercholesterolemia, hyperuricemia, diabetes, obesity and early menopause were each associated with a higher risk of incident gout and/or gout flares.
So working on these risk factors should reduce the risk of developing hyperuricemia.
Sources:
- Singh JA, Reddy SG, Kundukulam J. Risk Factors for Gout and Prevention: A Systematic Review of the Literature. Current opinion in rheumatology. 2011;23(2):192-202. doi:10.1097/BOR.0b013e3283438e13.
- Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 18e. New York, NY: McGraw-Hill; 2012. p 3181-3185

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