- Disorder characterised by ↑levels of Uric acid
- Hypoxanthine → xanthine → UA (final product of degradation of purines)
Causes
- 1o – increased production and consumption
- 2o – decreased GFR in CKD
Kidney function decreases by
- Chronic interstitial nephritis – crystals of urate in tubule, interstitium and joints
- Nephrolithiasis of uric acid stone – obstructive uropathy
- Chronic PN – triggered by stone
Clinical features
- Decreased urine, ↑creatinine
- Acute UA nephropathy – in pts with malignant tumours. Hyperuricemia due cellular debris, UA deposits cause tubular damage and obstruction
- Chronic UA nephropathy – in obese pts with hyperlipidemia. HTN, polydypsia, microhematuria
- Urate nephrolithiasis – can occur independently without joint disease
Diagnosis
- Uric acid and creatinine in blood
- Urine analysis – if urine uric acid >8.8 mg/dL = risk of stone formation
- Joint fluid test
- USS/XR
Treatment
- Diet
- Diuretics – ↑urine output so prevent deposition of UA
- Allopurinol – xanthine oxidase inhibitor – not given in acute exacerbations, may also cause bone marrow suppression
- Colchicine
- NSAIDS