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一、概述尿酸乃嘌呤代谢终末产物,嘌岭可来自食物,但主要由核酸分解代谢产生。溶解的尿酸对人体无害,尿酸钠在血中的溶解点约为6～7mg/dl,超过此值即为高尿酸血症。由于超饱和而发生沉淀,在关节可引起痛风性关节炎,在肾脏则引起尿酸性肾病。高尿酸血症可分为原发性和继发性两类,原发性多为遗传代谢性缺陷;继发性系由骨髓增生性疾病,肿瘤经化疗或放疗致尿酸产生过多,以及药物和肾功能衰竭引起尿酸排泄减少所致。原发性高尿酸血症性肾病主要见于40岁以上中老年男性患者,人群普查发现仅20％的原发性高尿酸血症有临床表现,痛风患者亦仅10～20％有临床肾脏表现。但在病理检查中,几乎所有痛风患者都有不同程度的肾病变。关节病变一般出现在肾病之前,亦可在肾病之后。
First, an overview of uric acid is the end product of purine metabolism purine can come from food, but mainly produced by nucleic acid catabolism. Dissolved uric acid harmless to the human body, uric acid in the blood of the dissolution point of about 6 ~ 7mg / dl, more than this value is hyperuricemia. Precipitation due to supersaturation can cause gouty arthritis in the joints and uric acid nephropathy in the kidney. Hyperuricaemia can be divided into two types of primary and secondary, the primary mostly genetic metabolic defects; secondary by myeloproliferative diseases, tumor chemotherapy or radiotherapy caused by excessive uric acid, and drugs And renal failure caused by decreased uric acid excretion. Primary hyperuricemia nephropathy is mainly seen in older men over the age of 40, the population census found only 20% of the primary hyperuricemia clinical manifestations, gout patients only 10 to 20% of the clinical kidney performance. However, in pathological examination, almost all gout patients have varying degrees of nephropathy. Joint lesions generally appear before the kidney disease, but also after kidney disease.