Meier P B, Levitt M D
J Lab Clin Med. 1986 Dec;108(6):628-34.
The mechanism of the increased renal clearance of amylase and the amylase to creatinine clearance ratio (CAM/CCR) in acute pancreatitis remains controversial with both renal tubular dysfunction and altered glomerular permeability being invoked as explanations. To differentiate between these mechanisms, we investigated the quantity and character of protein excretion in 10 patients with pancreatitis. For a short period of time, seven of 10 patients had mild proteinuria with a mean protein excretion rate of 230 +/- 154 mg/24 hr. Proteinuria decreased in 9/9 survivors to 17 +/- 18 mg/24 hr. Albumin excretion rate initially was minimally increased in 10/10 patients with a mean of 61 +/- 40 mg/24 hr, decreasing during recovery in 8/9 survivors to 10.9 +/- 10.4 mg/24 hr (P less than 0.01). Electrophoresis of urine obtained during the acute phase consistently showed a low molecular weight proteinuria pattern that cleared with recovery. Twenty-one of 22 urinary samples with an elevated CAM/CCR had a low molecular weight protein pattern. All the above findings can be explained by alterations in renal tubular reabsorption of proteins without changes in glomerular permeability. In 2/4 patients a low molecular weight protein was present in urine specimens from the acute phase that was not present in highly concentrated urine specimens from the recovery period. This raises the possibility that an abnormal low molecular weight protein enters the serum in acute pancreatitis, which, after glomerular filtration, produces the renal tubular malfunction found in acute pancreatitis.
急性胰腺炎时淀粉酶肾清除率增加以及淀粉酶与肌酐清除率比值(CAM/CCR)升高的机制仍存在争议,肾小管功能障碍和肾小球通透性改变均被用作解释。为了区分这些机制,我们研究了10例胰腺炎患者的蛋白质排泄量和特征。在短时间内,10例患者中有7例出现轻度蛋白尿,平均蛋白质排泄率为230±154mg/24小时。9例存活患者中,蛋白尿降至17±18mg/24小时。10例患者的白蛋白排泄率最初均略有升高,平均为61±40mg/24小时,9例存活患者在恢复过程中降至10.9±10.4mg/24小时(P<0.01)。急性期采集的尿液进行电泳,始终显示出低分子量蛋白尿模式,恢复时消失。22份CAM/CCR升高的尿液样本中有21份呈现低分子量蛋白质模式。上述所有发现均可通过肾小管蛋白质重吸收改变来解释,而肾小球通透性未发生变化。4例患者中有2例急性期尿液标本中存在低分子量蛋白质,恢复期高度浓缩尿液标本中则不存在。这增加了一种可能性,即急性胰腺炎时一种异常的低分子量蛋白质进入血清,经肾小球滤过后,导致急性胰腺炎时出现的肾小管功能障碍。