Urinary kallikrein excretion in glomerulonephritis and nephrotic syndrome.

To assess the possible role of the renal kallikrein-kinin system in the pathogenesis of glomerulonephritis (GN), 24 h urinary kallikrein excretion (Uka) was measured in normal controls and in 32 patients with GN, 16 of whom had nephrotic syndrome. Compared with controls, Uka was decreased in GN without nephrotic syndrome (4.6 +/- 2.8 nkat day-1, controls 11.5 +/- 3.5 nkat day-1) but was markedly increased in patients with nephrotic syndrome (26.7 +/- 9.9 nkat day-1). The increased kallikrein excretion in nephrotic syndrome was not explained by leakage from plasma, protein binding of active kallikrein, passive 'washout' due to changes in sodium and water excretion, or by increased activity of the renin-angiotensin-aldosterone system, but may relate to changes in extracellular volume, plasma oncotic pressure and volume, or other intrarenal haemodynamic or hormonal factors. Increased activity of the renal kallikrein-kinin system is not a uniform finding in glomerulonephritis, but may be an important aspect of nephrotic syndrome.