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Silent Killer: Chronic Urate Nephropathy
Jun 24, 2016

High uric acid nephropathy is the most common and most damaging chronic urate nephropathy, amorphous crystallization of micro calculi of uric acid deposition in the renal interstitial, chronic inflammation, fibrosis and chronic renal failure. The disease onset is difficult to detect is often called "the silent killer".
Diagnosis of chronic urate nephropathy:
1. high uric acid (HUA) definition: under normal diet, not 2 times on the same day of fasting serum uric acid levels: male >416 μ mol/l (7.0mg/DL), female >360 μ mol/l (6.0mg/DL) for hyperuricemia. This is the international standard, but is suitable also to be confirmed.
2. kidney damage: urine concentraton declines, advanced renal insufficiency;
3. renal pathology: double refraction in the renal Medulla of urate crystals;
4. the need to exclude other kidney disease.
Laboratory tests:
1. urine: low specific gravity of urine, low molecular weight proteinuria, white blood cells, mild hematuria and urine tubes;
2. high uric acid: elevated serum uric acid levels often exceed the degree of renal impairment;
3. renal: renal insufficiency, increased BUN and SCr.
High uric acid nephropathy: a clinical diagnosis and treatment of:
National guidelines recommend, keeping uric acid level<357umol/l (6mg/DL) is the key to treating gout.
Treatment principle: to respond quickly and effectively to control uric acid in acute kidney injury; corrected hyperuricemia; stop of new MSU Crystal deposition has deposited crystals dissolved; reverse joint damage, prevention and protection of renal function, ameliorates renal vascular injury
Treatment time:
(1) serum uric acid >540umol/L (9mg/DL);
(2) >480umol/L of serum uric acid (8mg/DL) with cardiovascular risk factors: high blood pressure, impaired glucose tolerance and diabetes, high cholesterol, kidney dysfunction, stroke, coronary heart disease;
(3) other hyperuricemia and life coaching 3-6 months ' treatment is invalid.