Purkerson M L, Hoffsten P E, Klahr S
Kidney Int. 1976 May;9(5):407-17. doi: 10.1038/ki.1976.50.
The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
本研究旨在描述大鼠部分肾梗死后肾脏存活部分发生的肾小球病变的程度及发病机制。具有两个正常肾脏的对照大鼠平均血压为112 mmHg，蛋白尿极少，光镜（LM）、电镜（EM）或免疫荧光显微镜（IFM）检查均无肾小球病变。一侧肾脏三分之二梗死的大鼠（II期）出现高血压，尽管两侧肾脏中不到4%的肾小球异常。一侧肾脏三分之二梗死且对侧肾切除的大鼠（III期），无论给予正常、低钠或高钠饮食，都会出现蛋白尿和高血压。光镜检查显示，部分梗死和对侧肾切除28天后，37%的肾小球异常，此后异常肾小球的比例增加。在II期或III期大鼠的肾脏中可检测到免疫球蛋白和补体（C3），但总是伴有更广泛的白蛋白和纤维蛋白沉积。电镜下未见免疫复合物特征性的基底膜沉积物。给III期大鼠服用抗高血压药物可显著降低血压，并减少光镜下异常肾小球的数量；然而，免疫荧光显微镜检查异常仍然很突出。电镜下可见血小板血栓，免疫荧光显微镜检查可见大量肾小球纤维蛋白沉积，提示凝血机制可能在肾病变的发病机制中起重要作用。肝素治疗的III期大鼠血尿素氮浓度、血压和异常肾小球比例显著降低，尽管免疫荧光显微镜检查仍可见血清蛋白在肾小球沉积。这些观察结果表明，这种肾小球病是由一种未知因素引发的，该因素增加了毛细血管通透性。这种病变通过血栓形成机制进展，肝素给药可预防该机制。
