Bernard D B, Alexander E A, Couser W G, Levinsky N G
Kidney Int. 1978 Nov;14(5):478-85. doi: 10.1038/ki.1978.152.
We have studied sodium retention during volume expansion in rats with autologous immune complex nephropathy (AICN), a model of nephrotic syndrome (NS) in which GFR after volume expansion was not different from that in adjuvant-injected controls (C). AICN rats developed heavy proteinuria (298 +/- 27 vs. less than 10 mg/day), hypoalbuminemia (2.14 +/- 0.15 vs. 3.08 +/- 0.12 g/100 ml) and hypercholesterolemia (181 +/- 22 vs. 58 +/- 4 mg/100 ml). After saline, there were no significant differences in blood pressure (119 +/- 2 vs. 114 +/- 2 mm Hg), renal plasma flow (4.9 +/- 0.41 vs. 4.1 +/- 0.28 ml/min), inulin clearance (1.37 +/- 0.06 vs. 1.55 +/- 0.10 ml/min), or SNGFR (47 +/- 2 vs. 53 +/- 4 nl/min). Sodium excretion, however, was significantly lower in NS rats (4.7 +/- 1.1 vs. 9.2 +/- 1.2 muEq/min). Proximal sodium reabsorption was decreased in NS rats (35 +/- 2 vs. 41 +/- 2%, 2.5 +/- 0.2 vs. 3.3 +/- 0.2 nEq/min). Sodium delivery into the loop, however, was equal in NS and C, since the slightly lower filtered load in NS rats offset the depression in proximal reabsorption. Sodium reabsorption by the loop and by the distal convoluted tubules were equal in NS and C. Thus, sodium delivered into the cortical collecting ducts was the same in both groups (0.33 +/- 0.17 vs. 0.34 +/- 0.07 nEq/min; 4.5 +/- 0.6% of filtered sodium vs. 4.4 +/- 0.3%). The percent of filtered sodium excreted in the urine, however, was significantly lower in the NS rats, 2.18 +/- 0.48% vs. 4.0 +/- 0.58%. We conclude that antinatriuresis in this model of NS is determined beyond the superficial late distal convoluted tubule. The inability to excrete the sodium load during volume expansion is due to either enhanced reabsorption by the collecting duct or to abnormal function in deep nephrons.
我们研究了患有自身免疫复合物肾病（AICN）的大鼠在容量扩张期间的钠潴留情况。AICN是一种肾病综合征（NS）模型，在该模型中，容量扩张后的肾小球滤过率（GFR）与注射佐剂的对照组（C）并无差异。AICN大鼠出现大量蛋白尿（298±27 vs. 小于10mg/天）、低白蛋白血症（2.14±0.15 vs. 3.08±0.12g/100ml）和高胆固醇血症（181±22 vs. 58±4mg/100ml）。给予生理盐水后，两组在血压（119±2 vs. 114±2mmHg）、肾血浆流量（4.9±0.41 vs. 4.1±0.28ml/min）、菊粉清除率（1.37±0.06 vs. 1.55±0.10ml/min）或单个肾单位肾小球滤过率（SNGFR）（47±2 vs. 53±4nl/min）方面均无显著差异。然而，NS大鼠的钠排泄显著降低（4.7±1.1 vs. 9.2±1.2μEq/min）。NS大鼠近端钠重吸收减少（35±2 vs. 41±2%，2.5±0.2 vs. 3.3±0.2nEq/min）。然而，由于NS大鼠滤过负荷略低抵消了近端重吸收的降低，因此进入髓袢的钠输送在NS组和C组中是相等的。NS组和C组中髓袢和远曲小管的钠重吸收相等。因此，两组进入皮质集合管的钠是相同的（0.33±0.17 vs. 0.34±0.07nEq/min；占滤过钠的4.5±0.6% vs. 4.4±0.3%）。然而，NS大鼠尿液中排泄的滤过钠百分比显著降低，为2.18±0.48% vs. 4.0±0.58%。我们得出结论，在这种NS模型中，钠排泄减少是在浅表晚期远曲小管之后确定的。容量扩张期间无法排泄钠负荷是由于集合管重吸收增强或深部肾单位功能异常所致。
