Straub E
Monatsschr Kinderheilkd (1902). 1975 Nov;123(11):723-33.
8 patients suffering from acute renal failure (shock kidney) with anuria extending over 3 to 5 days, were treated with L-thyroxine for 5 to 9 days (5-6 mug per kg body weight per day orally). Diuresis was restored within 34 to 46 hrs. Plasma levels of urea and creatinine decreased earlier and much more rapidly to normal than was to be expected from the natural history of the disease, indicating the prompt and extensive increase of glomerular filtration rate. Polyuria seemed less pronounced and also shortened as compared with the ordinary course of that form of sudden renal insufficiency. Obviously, the well-known diuretic response in the normal individual to high doses of thyroid hormones in not a factor in the induction of diuresis in acute renal failure. The tendency with L-thyroxine treatment to dilate the preglomerular arterial vessel is considered a consequence of the stimulation of sodium reabsorption in the upper nephron. High values of RPF and GFR, regularly observed in hyperthyroidism or after L-thyroxine administration, do not depend on any augmentation of cardiac output or on arterial hypertension, since such symptoms were missed in our patients and, in our view, such an interpretation is excluded by the very existence of the so-called autoregulation of the kidney which leaves RPF (and therefore GFR) independent of systemic blood pressure. The same intrarenal feed-back mechanism, normally adapting the glomerular blood supply to the resorptive capacity of the proximal-tubular epithelium (mediation via the juxta-glomerular apparatus), is responsible for the GFR- and RPF-raising effect of exogenous L-thyroxine in the intact kidney as well as in acute renal failure: both sodium reabsorption and sodium filtration are accelerated.--The special conditions under which L-thyroxine interferes with the pathogenetic process of acute renal failure, the latter being characterised by the critical insufficiency of tubular sodium reabsorption and therefore by preglomerular arterial constriction, is discussed on the basis of a new hypothesis concerning the thyrogenic nephrotropic effects in general.
8例急性肾衰竭（休克肾）且无尿持续3至5天的患者，接受了左旋甲状腺素治疗5至9天（每天口服5 - 6微克/千克体重）。在34至46小时内恢复了利尿。血浆尿素和肌酐水平比疾病自然病程预期的更早且更快地降至正常，这表明肾小球滤过率迅速且大幅增加。与那种形式的急性肾功能不全的普通病程相比，多尿似乎不那么明显且持续时间也缩短了。显然，正常个体对高剂量甲状腺激素的利尿反应在急性肾衰竭利尿诱导中并非一个因素。左旋甲状腺素治疗使肾小球前动脉血管扩张的倾向被认为是上肾单位钠重吸收受刺激的结果。在甲状腺功能亢进或给予左旋甲状腺素后经常观察到的高肾血浆流量（RPF）和肾小球滤过率（GFR）值，并不依赖于心输出量的任何增加或动脉高血压，因为我们的患者未出现此类症状，并且在我们看来，所谓的肾脏自身调节的存在排除了这种解释，这种自身调节使RPF（进而GFR）独立于全身血压。同样的肾内反馈机制，通常使肾小球血液供应适应近端肾小管上皮的重吸收能力（通过球旁器介导），对外源性左旋甲状腺素在完整肾脏以及急性肾衰竭中提高GFR和RPF的作用负责：钠重吸收和钠滤过均加速。——基于关于甲状腺原性肾亲性作用的一般新假说，讨论了左旋甲状腺素干扰急性肾衰竭发病过程的特殊情况，急性肾衰竭的特征是肾小管钠重吸收严重不足，因此表现为肾小球前动脉收缩。
