Letteri J M, Asad S N, Caselnova R, Ellis K J, Cohn S H
Clin Nephrol. 1975 Aug;4(2):58-61.
Total body potassium (TB K) and daily urinary creatinine excretion were measured in 12 patients with mild chronic renal disease (CCr/1.73 m2 BSA greater than 40 ml/min, Group I) and 12 patients with severe renal disease (CCr/1.73 m2 BSA less than 19 ml/min, Group II). Creatinine excretion as a function of total body potassium was significantly lower in the males and females of Group II as compared to males and females in Group I. TB K was linearly related to creatinine excretion in both groups of patients. Mean TB K was not significantly different from mean predicted normal values (TB Kp) in both groups. The decreased creatinine excretion observed in severe renal failure cannot be due to a significant loss of lean body mass because TB K was not significantly decreased below predicted normal values. Decreased creatinine biosynthesis, alternate routes of excretion, metabolic reutilization, or conversion of creatinine to other metabolites may have contributed to the decreased creatinine excretion noted in this group of patients with renal failure.
对12例轻度慢性肾病患者（肌酐清除率/1.73 m²体表面积大于40 ml/min，I组）和12例重度肾病患者（肌酐清除率/1.73 m²体表面积小于19 ml/min，II组）测量了全身钾含量（TB K）和每日尿肌酐排泄量。与I组的男性和女性相比，II组的男性和女性中，肌酐排泄量与全身钾含量的函数关系显著更低。两组患者的TB K与肌酐排泄量均呈线性相关。两组的平均TB K与平均预测正常值（TB Kp）无显著差异。在严重肾衰竭中观察到的肌酐排泄减少并非由于瘦体重的显著减少，因为TB K并未显著低于预测正常值。肌酐生物合成减少、排泄的替代途径、代谢再利用或肌酐向其他代谢产物的转化可能导致了该组肾衰竭患者肌酐排泄减少。
