There are few studies regarding the evaluation of the
kinin system in patients with
systemic lupus erythematosus (SLE). In this study, we evaluated the plasma levels of
high-molecular weight kininogen (HKg),
low-molecular weight kininogen (LKg) and
plasma kallikrein; the plasma activity of
tissue kallikrein and
kininase II, and
urinary kallikrein and
kininase II activities in patients presenting with active
lupus nephritis. A total of 30 patients (29 women) aged 21-62 years (median = 39) and 30 controls matched to the patients for sex and age were studied. Patients presenting with other underlying diseases or using drugs, which could interfere with the
kinin system, were excluded. HKg and LKg levels were indirectly evaluated by ELISA.
Plasma kallikrein,
tissue kallikrein, and
kininase II were evaluated by their enzymatic activity on selective substrates. The Mann-Whitney test was used for statistical analysis. HKg, LKg and
plasma kallikrein levels were significantly increased in patients (p < 0.001, for each comparison). Similarly,
tissue kallikrein and
kininase II activities were significantly increased in plasma and urine of patients (p <0.001, for each comparison). In urine, the activities of
tissue kallikrein and
kininase II were at least seven times higher than those seen in the plasma of patients. These results indicate that the
kinin system is involved in the acute manifestations of
lupus nephritis.
Kinins may facilitate immunecomplex deposition and may induce the release of other pro-inflammatory mediators, including
cytokines actively involved in the pathogenesis of
lupus nephritis.