Rieselbach R E, Steele T H
Nephron. 1975;14(1):81-7. doi: 10.1159/000180437.
Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.
由于正常情况下每日尿酸生成量的约三分之二是通过肾脏排泄的，导致尿酸排泄异常的内在肾脏疾病可能会对尿酸稳态产生深远影响。本文深入回顾了慢性肾衰竭时尿酸排泄模式的改变，并描述了残余肾单位中出现的尿酸排泄适应性机制，以移植供体剩余的正常肾脏为例。此外，还描述了在肾单位数量正常情况下尿酸排泄的异常情况。部分痛风患者的高尿酸血症似乎是由于每个肾单位的尿酸排泄减少所致，而导致肾脏尿酸排泄过多的各种肾小管缺陷已被证明是一些低尿酸血症病例的基础。
