Effect Of Raised Blood Pressure (Hypertension) On Gout And Hyperuricemia

Hypertension is another name for high blood pressure (hyper increased; tension pressure in the arteries). Some hypertension is due to kidney disease and, in such cases, the kidney disease can cause hyperuricemia. In the more common variety of hypertension, referred to as essential hypertension, the high blood pressure itself is the primary problem and is not the result of disease in the kidneys or elsewhere. However, essential hypertension may reduce the kidney’s ability to eliminate urate. Thus, hyperuricemia due to renal under-excretion of urate may be a consequence of primary essential hypertension.
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In addition, thiazide diuretics, such as chlorothiazide (Chlotride) or frusemide (Lasix), are often used to treat hypertension and these drugs always lead to the development of hyperuricemia as a side-effect. In this case following a healthy low purine gout diet can help reduce the symptoms somewhat.

A number of body metabolites which act on the kidney can reduce its ability to eliminate urate. Important among these is the hormone angiotensin, which is involved in causing hypertension. The newly developed ACE (angiotensin converting enzyme) inhibitors (such as Captopril and Enalapril), which reduce the production of angiotensin, are often very valuable in the treatment of hypertension, and control of hypertension will often cause a reduction in serum urate concentrations.
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The Effect Of Drugs On Serum Urate Concentration

The production of urate can be increased by drugs used in cancer chemotherapy. Such drugs cause destruction of cells and breakdown of nucleoprotein from the cell nuclei, thereby promoting hyperuricemia.

Other drugs affect the renal handling of urate directly. Some drugs act only on the excretion of urate by the kidney. Those which increase the excretion of urate by the kidney are referred to as uricosuric drugs. Other drugs act on the kidney transport of urate to reduce its urate excretion. These drugs include aspirin in low dosage (4-6 tablets/day), the antituberculous agents pyrazinamide and ethambutol, and nicotinic acid.

Something of a paradox exists in that some drugs may reduce the renal elimination of urate in low doses but be uricosuric (increase elimination) in high doses. An example is aspirin. The extent of the effect is modified by the acidity of the urine.

Almost all diuretics, such as the thiazide diuretics used to treat hypertension (see above), except spironolactone, will tend to cause hyperuricemia by reducing renal elimination of urate.

Other Diseases

Insulin-dependent diabetes is not usually associated with hyperuricemia, except when diabetic control is extremely poor and body fats are metabolised, resulting in diabetic ketosis. These ketones will cause a transient severe hyperuricemia by reducing renal excretion of urate. However, with correction of the ketosis, the hyperuricemia will revert to normal. The main problem is the associated insulin resistance in the diabetic which, if sustained and associated with obesity, may promote both hypertriglyceridaemia and hyperuricemia.

Untreated hypothyroidism (reduced thyroid function) is often associated with hyperuricemia, as are disorders of the parathyroid glands. In each case, restoration of normal hormonal function or replacement hormone therapy will correct the hyperuricemia.

Hyperuricemia is found in a wide range of acute medical conditions. Increased turnover of the bone marrow, such as occurs in marrow malignancies, leukaemias, marrow proliferative disorders and infectious mononucleosis (glandular fever), can lead to an increase in urate production. Greater body acidity in the form of a respiratory acidosis or inadequate oxygenation of tissues, as occurs in respiratory failure, can again promote hyperuricaemia. Psoriasis, by increasing the turnover of skin cells, can also cause hyperuricemia.

All of these generalized diseases cause hyperuricemia by an effect on either purine degradation and/or urate production or on the elimination of urate by the kidney.

A brief summary of impacts and causes of hyperuricemia and kidney disease
Genetic over-production is a rare but important cause of hyperuricemia.
Rates of urate excretion vary widely, and under-excretion can exist independently of other kidney problems.
Kidney disease can cause under-excretion; if the kidney disease can be treated the excretion rate can improve.
High body weight is closely associated with high serum urate concentration and a reduction in body weight with a reduction in urate concentration.
Although the purine content of the diet contributes to the urate load, a diet that complies with Heart Foundation recommendations is unlikely to cause problems for most gout sufferers.
High alcohol consumption increases urate production through increased breakdown of ATP, and decreases urate excretion.
High blood fat (triglycerides) found with hyperuricemia may be an early warning of cardiovascular disease.
Diuretics prescribed for high blood pressure lead to the development of hyperuricemia.
Some other medications and acute diseases can contribute to hyperuricemia.

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