Ormrod D, Miller T, Stewart E
Invest Urol. 1978 Jul;16(1):23-6.
Renal uptake of 99mTechnetium sulphur colloid (99mTcSC) was investigated in 99 animals with experimentally induced unilateral pyelonephritis and in 60 animals with a thermally induced renal injury. The degree of localization of 99mTcSC in the kidney was determined by direct counting of retained isotope after bilateral nephrectomy at autopsy. Phagocytosis of 99mTcSC by inflammatory tissue has been reported and it was anticipated that renal infection would lead to an increase in 99mTcSC uptake by the kidney. In fact it was found that renal infection with pathologic changes resulted in a significant decrease in the localization of 99mTcSC in the pyelonephritic kidney. A similar decrease was found in the thermally injured kidney but renal infection without pathologic changes did not give rise to any changes in radionuclide uptake. These findings suggested that phagocytosis by the proximal convoluted tubular cells is the normal mechanism for 99mTcSC accumulation in the kidney and that renal infection reduced the phagocytic capability of these cells.
在99只实验性诱导单侧肾盂肾炎的动物和60只热诱导肾损伤的动物中,研究了99m锝硫胶体(99mTcSC)的肾脏摄取情况。通过尸检时双侧肾切除后对保留同位素的直接计数,确定了99mTcSC在肾脏中的定位程度。已有报道称炎症组织可吞噬99mTcSC,预计肾脏感染会导致肾脏对99mTcSC的摄取增加。事实上,发现伴有病理改变的肾脏感染导致99mTcSC在肾盂肾炎肾脏中的定位显著减少。在热损伤的肾脏中也发现了类似的减少,但无病理改变的肾脏感染并未引起放射性核素摄取的任何变化。这些发现表明,近端肾小管细胞的吞噬作用是99mTcSC在肾脏中积累的正常机制,而肾脏感染降低了这些细胞的吞噬能力。