Table 10.3.2
Causes of hyperuricaemia and gout

Impaired uric acid excretion

Idiopathic (primary)

Chronic renal disease

Increased tubular reabsorption (extracellular volume contraction)

 Dehydration, diuretics, diabetes insipidus

Decreased tubular secretion

 Starvation, diabetic ketoacidosis

Increased lactic acid production

 Alcohol, exercise, toxemia of pregnancy

Drug treatment

 Low-dose aspirin, ciclosporin, diuretics (especially thiazides and loop diuretics)

Hypothyroidism

Primary hyperparathyroidism

Glucose-6-phosphatase deficiency (von Gierke’s disease)

Increased uric acid production

Idiopathic (primary)

Increased nucleic acid turnover

 Blood dyscrasias, e.g. leukemia, polycythaemia rubra vera

 Malignancies

 Severe psoriasis

Excessive purine intake

Increased purine synthesis (rare)

 HGPRT deficiency (Lesch–Nyhan)

 PRPP overactivity

 Glucose-6-phosphatase deficiency

Impaired uric acid excretion

Idiopathic (primary)

Chronic renal disease

Increased tubular reabsorption (extracellular volume contraction)

 Dehydration, diuretics, diabetes insipidus

Decreased tubular secretion

 Starvation, diabetic ketoacidosis

Increased lactic acid production

 Alcohol, exercise, toxemia of pregnancy

Drug treatment

 Low-dose aspirin, ciclosporin, diuretics (especially thiazides and loop diuretics)

Hypothyroidism

Primary hyperparathyroidism

Glucose-6-phosphatase deficiency (von Gierke’s disease)

Increased uric acid production

Idiopathic (primary)

Increased nucleic acid turnover

 Blood dyscrasias, e.g. leukemia, polycythaemia rubra vera

 Malignancies

 Severe psoriasis

Excessive purine intake

Increased purine synthesis (rare)

 HGPRT deficiency (Lesch–Nyhan)

 PRPP overactivity

 Glucose-6-phosphatase deficiency

HGPRT, hypoxanthine-guanine phosphoribosyltransferase; PRPP, phosphoribosylpyrophosphate synthetase

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