Wilson D R, Honrath U
Department of Physiology, University of Toronto, Ontario, Canada.
Clin Invest Med. 1988 Jun;11(3):157-66.
Inner medullary collecting duct function in ischemic acute renal failure: The purpose of this study was to determine the role of the medullary collecting duct in the increased urine sodium concentration, decreased urine osmolality, and altered potassium excretion with hyperkalemia which are characteristic of ischemic acute renal failure. Microcatheterization of the inner medullary collecting duct (0.1 to 5 mm from papillary tip) was carried out in rats 24 h after bilateral renal artery clamping for 45 min (n = 8) or sham-operated (n = 8). In ischemic acute renal failure (ARF), tubular fluid osmolality did not increase significantly along the inner medullary collecting duct (IMCD). Tubular fluid sodium concentration was similar to controls at the beginning of the IMCD but was significantly higher at the papillary tip. Tubular fluid to plasma potassium concentration ratio (TF/PK) increased to a greater extent along the IMCD in ischemic ARF than in controls. During acute KCl loading in two additional groups, tubular fluid potassium concentration and TF/PK were much lower at the beginning of the IMCD in ischemic ARF than in controls but increased similarly along the IMCD. In ischemic ARF, with or without KCl loading, renal tissue electrolytes showed reduced potassium concentration in the outer medullary region. The results indicate that impaired IMCD function contributes significantly to the increase in urine sodium concentration and the decrease in urine osmolality which are characteristic of ischemic acute renal failure. In ischemic ARF with mild hyperkalemia, an adaptive increase in K secretion occurred in the IMCD. Severe hyperkalemia and decreased potassium excretion during acute potassium loading in ischemic ARF were determined in more proximal nephron segments and were associated with decreased outer medullary tissue potassium, presumably due to tubular necrosis. Decreased outer medullary tissue potassium could contribute to hyperkalemia by diminishing K secretion in the pars rectae and descending limbs or in the cortical and outer medullary collecting ducts.
本研究旨在确定髓质集合管在缺血性急性肾衰竭所特有的尿钠浓度升高、尿渗透压降低以及高钾血症时钾排泄改变中所起的作用。在大鼠双侧肾动脉夹闭45分钟后24小时(n = 8)或假手术(n = 8)后,对距乳头尖端0.1至5毫米的髓质集合管进行微导管插入。在缺血性急性肾衰竭(ARF)中,沿髓质集合管(IMCD)的肾小管液渗透压没有显著增加。肾小管液钠浓度在IMCD起始处与对照组相似,但在乳头尖端显著更高。与对照组相比,缺血性ARF中沿IMCD的肾小管液与血浆钾浓度比(TF/PK)升高幅度更大。在另外两组急性氯化钾负荷期间,缺血性ARF中IMCD起始处的肾小管液钾浓度和TF/PK比对照组低得多,但沿IMCD的升高情况相似。在缺血性ARF中,无论有无氯化钾负荷,肾组织电解质在外髓质区域显示钾浓度降低。结果表明,IMCD功能受损显著导致了缺血性急性肾衰竭所特有的尿钠浓度升高和尿渗透压降低。在轻度高钾血症的缺血性ARF中,IMCD中钾分泌出现适应性增加。缺血性ARF中急性钾负荷期间的严重高钾血症和钾排泄减少是在更近端的肾单位节段确定的,并且与外髓质组织钾减少有关,推测是由于肾小管坏死。外髓质组织钾减少可能通过减少直部和降支或皮质和外髓质集合管中的钾分泌而导致高钾血症。