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CHRONICLES IN CHOLESTEROLAn Insiders Guide to State of The Art Cardiovascular

Prevention Laboratory Testing Available From

Everest Clinical Laboratories

High uric acid level (hyperuricemia) is an excessiveconcentration of uric acid in your blood. Uric acid iswaste produced during the breakdown of purine, asubstance found in many foods. Uric acid normallypasses through the kidneys and is eliminated in urine.

A high uric acid level may not cause problems.However, some people develop gout, kidney stones orkidney failure due to high uric acid levels. A high uricacid level may appear prior to the development of high

blood pressure, heart disease or chronic kidneydisease. But it's often unclear whether a high uric acidlevel is a direct cause or merely an early warning signof these conditions.

Causes of High Uric Acid

Diuretics such as thiazides

Alcohol consumption especially beer

Excessive caffeine consumption

Genetic predisposition

Hodgkin's lymphoma

Hypothyroidism

Leukemia

Niacin, or vitamin B-3 Non-Hodgkin's lymphoma

Obesity

Psoriasis

Purine-rich diet organ meat, game meat,anchovies, herring, gravy, dried beans, driedpeas and other foods

Some immunosuppressants

Fructose?

Uric acid is the relatively water-insoluble end product of

purine nucleotide metabolism. It poses a special problem

for humans because of its limited solubility, particularly in

the acidic environment of the distal nephron of thekidney. It is problematic because humans do not possess the

enzyme uricase, which converts uric acid into the more

soluble compound allantoin. Three forms of kidney disease

have been attributed to excess uric acid: acute uric acid

nephropathy, chronic urate nephropathy, and uric acid

nephrolithiasis. These disorders share the common element

of excess uric acid or urate deposition, although the clinical

features vary.

August, 2012 VOL 2 ISSUE 6

In This Issue: Uric Acid

Gout risk was 74% higher among women who

drank a serving of sweetened soft drinks each day

than those who drank less than one serving per

month, a 2010 analysis of the 79,000-participant

Nurses Health Study found. Diet soda didnt

cause gout to rise.

Men who ate the most seafood were 50% more

likely to develop gout than those who ate the

least.

Anchovies, herring, redfish (ocean perch),

sardines and tuna are among proteins that cause

gout pain and should be limited to 4-6 ounces per

day

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Uric acid stones, which represent 5-10% of all renal calculi

in the United States, also result from uric acid precipitation

in the collecting system. Uric acid stones are related to uric

acid exceeding its solubility in the urine; thus, patients

with hyperuricosuria have an increased risk of uric acidnephrolithiasis. Urine oversaturation with uric acid and

subsequent crystal formation is determined largely by

urinary pH. Individuals who form uric acid stones tend to

excrete less ammonium, which contributes directly to low

urinary pH. In addition, persons with gout and those who

form stones, in particular, have a reduced postprandial

alkaline tide (alkaline urinary pH).

Lead exposure may affect urate excretion by the kidney,

leading to chronic hyperuricemia and kidney disease.Renal excretion of uric acid involves 4 pathways:

filtration, reabsorption, secretion, and postsecretory

reabsorption. Urate is freely filtered at the glomerulus. An

active anion-exchange process in the early proximal

convoluted tubule reabsorbs most of it. Most urinary uric

acid appears to be derived from tubular secretion, possibly

from the S2 segment of the proximal tubule. Overall, 98-

100% of filtered urate is reabsorbed; 6-10% is secreted,

ultimately appearing in the final urine.

The major factors that affect urate excretion are the tubular

fluid pH, the tubular fluid flow rate, and renal blood flow.

The first 2 factors primarily diminish uric acid and urate

precipitation in the collecting ducts, while the third is

important in urate secretion. In disorders such as sickle cell

disease, hypertension, and eclampsia, hyperuricemia out of

proportion with decreases in glomerular filtration resultfrom decreased renal blood flow. Organic acids, such as

lactic acid and ketoacids, also can impair the proximal

secretion of uric acid.

By Spencer Kroll MD PhD

National Lipid Association Board Certified

Board of Directors, Northeast Lipid Association

August, 2012 VOL 2 ISSUE 6

An increased serum LDH level is suggestive of alarge tumor burden and correlates with risk.

Uric acid and sodium monourate crystals may beobserved.

Uric acid levels in the urine may be as high as 150-200 mg/dL.

A random ratio of urinary uric acid to creatininehigher than 1 is also suggestive of acute uric acidnephropathy.

A disproportionate elevation in serum uric acid levelsalso can be a diagnostic clue.

Elevated serum and urinary uric acid levels correlate

with the frequency of nephrolithiasis, and 50% ofpatients with serum uric acid levels greater than 13mg/dL or urinary uric acid secretion higher than 1100mg/d will form stones.