Levison M E, Pitsakis P G
J Infect Dis. 1984 Oct;150(4):554-60. doi: 10.1093/infdis/150.4.554.
Escherichia coli-induced pyelonephritis was studied in untreated alloxan-diabetic rats, insulin-treated diabetic rats, glucose water-drinking (diuresing) nondiabetic rats, and tap water-drinking (nondiuresing) nondiabetic rats following injection of E. coli either into the emptied urinary bladder, into the left kidney, or intravenously. For prevention of an ascending infection in the right kidney, the right ureter was ligated and transected immediately prior to bladder or intrarenal inoculation. These experiments established that in normal rats ascending renal infection alone occurred following introduction of small inocula into the bladder--and then only when facilitated by diuresis. In diabetic rats both ascending and hematogenous renal infection occurred following introduction of small inocula into the bladder. Insulin treatment that reduced hyperglycemia also reduced glycosuria and restored urinary antibacterial activity against small inocula of E. coli but only partially reduced polyuria and prevented hematogenous but not ascending infection. Thus, hyperglycemia was probably the major factor promoting hematogenous renal infection, whereas polyuria--and therefore vesicoureteral reflux--was the major factor promoting ascending infection.
在未治疗的四氧嘧啶糖尿病大鼠、胰岛素治疗的糖尿病大鼠、饮用葡萄糖水(利尿)的非糖尿病大鼠以及饮用自来水(非利尿)的非糖尿病大鼠中,研究了大肠杆菌诱导的肾盂肾炎。在将大肠杆菌注入排空的膀胱、左肾或静脉后,为防止右肾发生上行感染,在膀胱或肾内接种前立即结扎并切断右输尿管。这些实验表明,在正常大鼠中,向膀胱内引入少量接种物后仅发生上行性肾脏感染——而且只有在利尿的促进下才会发生。在糖尿病大鼠中,向膀胱内引入少量接种物后会发生上行性和血源性肾脏感染。降低高血糖的胰岛素治疗也减少了糖尿,并恢复了对少量大肠杆菌接种物的尿液抗菌活性,但仅部分减少了多尿,并预防了血源性感染而非上行性感染。因此,高血糖可能是促进血源性肾脏感染的主要因素,而多尿——以及由此导致的膀胱输尿管反流——是促进上行性感染的主要因素。