Magaldi A J, Yasuda P N, Kudo L H, Seguro A C, Rocha A S
Laboratório de Pesquisa Básica da Unidade de Doenças Renais, Faculdade de Medicina, Universidade de São Paulo, Brasil.
Nephron. 1992;62(3):332-9. doi: 10.1159/000187069.
The kidney involvement in leptospirosis appears to be a special form of acute renal failure due to a higher frequency of polyuric forms and the presence of hypokalemia with an elevated urinary fractional excretion of potassium. Using a clearance technique, we detected higher fractional urinary potassium excretion in leptospirotic guinea pigs (26.5 +/- 4.7%) than in normal animals (14.1 +/- 2.8%, p < 0.05). After blocking distal NaCl reabsorption with furosemide, it was observed that in leptospirotic animals both fractional sodium excretion (40.0 +/- 7.4%) and fractional potassium excretion (136.3 +/- 32.7%) were higher than in normal animals (20.4 +/- 3.8%, p < 0.05, and 43.6 +/- 9.0%, p < 0.05, respectively). Microperfusion studies showed that the normal and leptospirotic medullary thick ascending limb had both identical transepithelial potential difference (+3.7 +/- 0.4 vs. 3.9 +/- 0.2 mV) and relative sodium-to-chloride permeability. The same technique showed that the osmotic water permeability (Posm; 0.9 +/- 0.4 x 10(-5) cm/s.atm) and diffusional permeability (34.7 +/- 6.6 x 10(-5) cm/s) observed in the leptospirotic inner medullary collecting duct (IMCD) in the presence of vasopressin were unchanged, as was also the case for urea permeability (3.74 +/- 0.7 x 10(-5) cm/s). These data show that acute renal failure in leptospirosis is characterized by tubular changes leading to potassium secretion probably due to a decrease in proximal sodium reabsorption. Furthermore, the inability to concentrate urine evidenced by the low P(o)sm present in leptospirotic animals is due, at least in part, to IMCD resistance to vasopressin.
钩端螺旋体病中的肾脏受累似乎是急性肾衰竭的一种特殊形式，这是因为多尿型更为常见，且存在低钾血症以及尿钾排泄分数升高。运用清除技术，我们检测到钩端螺旋体病豚鼠的尿钾排泄分数（26.5±4.7%）高于正常动物（14.1±2.8%，p<0.05）。在用呋塞米阻断远端氯化钠重吸收后，观察到钩端螺旋体病动物的钠排泄分数（40.0±7.4%）和钾排泄分数（136.3±32.7%）均高于正常动物（分别为20.4±3.8%，p<0.05；43.6±9.0%，p<0.05）。微灌注研究表明，正常和感染钩端螺旋体的髓袢升支粗段的跨上皮电位差相同（+3.7±0.4对3.9±0.2 mV），且钠与氯的相对通透性相同。同样的技术显示，在血管加压素存在的情况下，感染钩端螺旋体的内髓集合管（IMCD）的渗透水通透性（Posm；0.9±0.4×10⁻⁵ cm/s·atm）和扩散通透性（34.7±6.6×10⁻⁵ cm/s）未发生变化，尿素通透性（3.74±0.7×10⁻⁵ cm/s）也是如此。这些数据表明，钩端螺旋体病中的急性肾衰竭的特征是肾小管改变导致钾分泌，这可能是由于近端钠重吸收减少所致。此外，钩端螺旋体病动物中低渗尿所证明的尿液浓缩能力下降至少部分是由于内髓集合管对血管加压素的抵抗。
