University of Colorado School of Medicine, Division of Renal Diseases and Hypertension, Department of Medicine, Aurora, CO, USA.
University of Bologna, Department of Medical and Surgical Sciences, Bologna, Italy.
J Bras Nefrol. 2021 Oct-Dec;43(4):572-579. doi: 10.1590/2175-8239-JBN-2020-U002.
Hyperuricemia is common in chronic kidney disease (CKD) and may be present in 50% of patients presenting for dialysis. Hyperuricemia can be secondary to impaired glomerular filtration rate (GFR) that occurs in CKD. However, hyperuricemia can also precede the development of kidney disease and predict incident CKD. Experimental studies of hyperuricemic models have found that both soluble and crystalline uric acid can cause significant kidney damage, characterized by ischemia, tubulointerstitial fibrosis, and inflammation. However, most Mendelian randomization studies failed to demonstrate a causal relationship between uric acid and CKD, and clinical trials have had variable results. Here we suggest potential explanations for the negative clinical and genetic findings, including the role of crystalline uric acid, intracellular uric acid, and xanthine oxidase activity in uric acid-mediated kidney injury. We propose future clinical trials as well as an algorithm for treatment of hyperuricemia in patients with CKD.
高尿酸血症在慢性肾脏病（CKD）中很常见，在 50%接受透析的患者中可能存在。高尿酸血症可能继发于 CKD 中发生的肾小球滤过率（GFR）受损。然而，高尿酸血症也可能先于肾脏病的发生，并预测 CKD 的发生。高尿酸血症模型的实验研究发现，可溶性和结晶尿酸均可导致明显的肾脏损伤，表现为缺血、肾小管间质纤维化和炎症。然而，大多数孟德尔随机化研究未能证明尿酸与 CKD 之间存在因果关系，临床试验的结果也各不相同。在这里，我们提出了一些潜在的解释，包括结晶尿酸、细胞内尿酸和黄嘌呤氧化酶活性在尿酸介导的肾脏损伤中的作用，以解释这些阴性的临床和遗传发现。我们提出了未来的临床试验以及 CKD 患者高尿酸血症的治疗方案。
