Mechanism and significance of kinin formation in nephrotic syndrome

There were few reports demonstrating behavior of kinin and kininogen in the nephrotic syndrome. In this paper, coagulation factors related to contact activation, such as factor XII (FXII), factor XI (FXI), prekallikrein (PK), high molecular weight kininogen (HMWKG), and kinins were measured in 15 cases of nephrotic syndrome, and clinical significance of these results were discussed. Plasma FXII activity was markedly decreased in the onset and florid stages of nephrotic syndrome, and this decrease was not correlated with plasma albumin level, which suggested marked activation of this factor in these stages. However, the decrease of PK was slight at the above stages. Activations of contact factors were not parallely occurred with the marked consumption of FXII. Plasma kinin activity was not increased in the onset and critical stages of the nephrotic syndrome but increased in the convalescent and chronic stages, while HMWK level was maintained higher than normal throughout the course. Plasma angiotensin-converting enzyme (kininase II) activity was increased in the early stage and decreased lower than normal during the course of the disease. It was concluded that kinin formation in the nephrotic syndrome was not due to the activation of intrinsic coagulation system but due to release of kinin from low molecular weight kininogen. This increased level of kinin activity in convalescent and chronic stage may be related to the healing process during the course of this syndrome. Low kinin activity in the early stage of this disease might be also explained by increased kininase II activity.