Kuroda S, Aynedjian H S, Bank N
Kidney Int. 1979 Nov;16(5):561-71. doi: 10.1038/ki.1979.166.
Micropuncture studies were carried out in surface nephrons of rats with nephrotoxic-serum (NTS)-induced nephrotic syndrome during a period of active sodium and water retention. It was found that hydrostatic pressure and tubular diameter were increased in the proximal tubules (13.4 +/- 0.2 vs. 10.4 +/- 0.2 mm Hg; 31.3 +/- 0.9 vs. 18.4 +/- 0.7 mu), whereas pressure and tubular diameter were normal in the distal tubules. Single nephron glomerular filtration rate (SNGFR) was decreased and fractional reabsorption of fluid was markedly increased in the proximal tubules (74.1 vs. 61.7%). The increased pressure gradient between the proximal and distal tubules suggests a condition of increased resistance to flow between the proximal and distal tubules. Microinfusion of proximal tubules with an isotonic "equilibrium" solution led to little or no rise in intratubular pressure in normal rats but it led to a significant rise in nephrotic rats. When proximal tubules of normal rats were infused with a solution containing 100 mg/100 ml albumin, pressure rose to levels observed in nephrotic rats. The mechanism of the increased resistance to flow appeared to be related, therfore, to the presence of protein in the tubular fluid. Sodium retention in the nephrotic animals might be attributed to the reduction in GFR. In other types of renal disease in animals and man with comparable or greater reductions in GFR, sodium retention does not occur, however, and fractional excretion of sodium in the urine is increased in proportion to the reduction in GFR. Thus, the rise in proximal fractional reabsorption secondary to impaired fluid flow could be an important factor in the sodium retention of this disease.
在肾毒性血清（NTS）诱导的肾病综合征大鼠处于钠和水潴留活跃期时，对其表层肾单位进行了微穿刺研究。结果发现，近端小管的静水压和管径均增加（分别为13.4±0.2 vs. 10.4±0.2 mmHg；31.3±0.9 vs. 18.4±0.7μm），而远端小管的压力和管径正常。近端小管的单肾单位肾小球滤过率（SNGFR）降低，液体重吸收率显著增加（74.1% vs. 61.7%）。近端和远端小管之间压力梯度的增加提示近端和远端小管之间的流动阻力增加。向正常大鼠的近端小管微灌注等渗“平衡”溶液，管内压力几乎没有升高或根本没有升高，但在肾病大鼠中却导致显著升高。当向正常大鼠的近端小管灌注含100mg/100ml白蛋白的溶液时，压力升高至在肾病大鼠中观察到的水平。因此，流动阻力增加的机制似乎与管腔内液体中蛋白质的存在有关。肾病动物的钠潴留可能归因于肾小球滤过率（GFR）的降低。然而，在动物和人类的其他类型的肾脏疾病中，尽管GFR有类似程度或更大程度的降低，但并未出现钠潴留，而且尿钠排泄分数与GFR的降低成比例增加。因此，继发于液体流动受损的近端重吸收分数升高可能是该疾病钠潴留的一个重要因素。
