PDF(Pubmed)
Abstract：
Serum uric acid levels are altered by kidney disorders because the kidneys play a dominant role in uric acid excretion. Here, major kidney disorders which accompany hyperuricemia or hypouricemia, including their pathophysiology, are discussed. Chronic kidney disease (CKD) and hyperuricemia are frequently associated, but recent clinical trials have not supported the pathogenic roles of hyperuricemia in CKD incidence and progression. Diabetes mellitus (DM) is often associated with hyperuricemia, and hyperuricemia may be associated with an increased risk of diabetic kidney disease in patients with type 2 DM. Sodium-glucose cotransporter 2 inhibitors have a uricosuric effect and can relieve hyperuricemia in DM. Autosomal dominant tubulointerstitial kidney disease (ADTKD) is an important hereditary kidney disease, mainly caused by mutations of uromodulin (UMOD) or mucin-1 (MUC-1). Hyperuricemia and gout are the major clinical manifestations of ADTKD-UMOD and ADTKD-MUC1. Renal hypouricemia is caused by URAT1 or GLUT9 loss-of-function mutations and renders patients susceptible to exercise-induced acute kidney injury, probably because of excessive urinary uric acid excretion. Hypouricemia derived from renal uric acid wasting is a component of Fanconi syndrome, which can be hereditary or acquired. During treatment for human immunodeficiency virus, hepatitis B or cytomegalovirus, tenofovir, adefovir, and cidofovir may cause drug-induced renal Fanconi syndrome. In coronavirus disease 2019, hypouricemia due to proximal tubular injury is related to disease severity, including respiratory failure. Finally, serum uric acid and the fractional excretion of uric acid are indicative of plasma volume status; hyperuricemia caused by the enhanced uric acid reabsorption can be induced by volume depletion, and hypouricemia caused by an increased fractional excretion of uric acid is the characteristic finding in syndromes of inappropriate anti-diuresis, cerebral/renal salt wasting, and thiazide-induced hyponatremia. Molecular mechanisms by which uric acid transport is dysregulated in volume or water balance disorders need to be investigated.
摘要：
血清尿酸水平因肾脏疾病而改变，因为肾脏在尿酸排泄中起主导作用。这里,伴随高尿酸血症或低尿酸血症的主要肾脏疾病，包括他们的病理生理学，正在讨论。慢性肾脏病（CKD）和高尿酸血症经常相关，但最近的临床试验并未支持高尿酸血症在CKD发病和进展中的致病作用.糖尿病（DM）通常与高尿酸血症有关，高尿酸血症可能与2型糖尿病患者的糖尿病肾病风险增加有关。钠-葡萄糖协同转运蛋白2抑制剂具有排尿作用，可以缓解DM患者的高尿酸血症。常染色体显性遗传性肾小管间质肾病(ADTKD)是一种重要的遗传性肾脏病，主要由尿调蛋白（UMOD）或粘蛋白-1（MUC-1）突变引起。高尿酸血症和痛风是ADTKD-UMOD和ADTKD-MUC1的主要临床表现。肾性低尿酸血症是由URAT1或GLUT9功能丧失突变引起的，使患者容易受到运动诱发的急性肾损伤，可能是因为尿尿酸排泄过多。肾性尿酸消耗引起的低尿酸血症是范可尼综合征的一个组成部分，可以是遗传的或后天获得的。在治疗人类免疫缺陷病毒期间，乙型肝炎或巨细胞病毒，替诺福韦,阿德福韦,和西多福韦可引起药物诱导的肾Fanconi综合征。在2019年冠状病毒疾病中，近端肾小管损伤引起的低尿酸血症与疾病严重程度有关，包括呼吸衰竭.最后,血尿酸和尿酸排泄分数是血浆容量状态的指示;尿酸重吸收增强引起的高尿酸血症可由容量消耗引起,尿酸排泄分数增加引起的低尿酸血症是不适当利尿综合征的特征性发现，脑/肾盐消耗，和噻嗪引起的低钠血症。需要研究尿酸转运在体积或水平衡紊乱中失调的分子机制。
