Urinary kallikrein excretion in renal transplant patients

Urinary kallikrein, as a reflection of the intrarenal kallikrein, is distinct from plasma kallikrein. The kallikrein-kinin system, activated via antigen-antibody complexes, has been implicated in the pathophysiology of acute transplant rejection. We studied urinary excretion of sodium, potassium, protein, and kallikrein following renal transplantation in nine patients, In four patients who took steroids daily and were followed from the time of transplantation (without rejection episodes), urinary kallikrein remained stable (3.7 +/- 0.5 EU/24 hr, x +/- SEM). Since sodium-retaining steroids influence urinary kallikrein excretion, two patients were studied 2 and 3 months post-transplantation while receiving alternate-day prednisone. Values from urinary kallikrein in these patients did not differ from those in patients taking steroids daily (3.7 +/- 0.5 versus 2.7 +/- 0.3 EU/24 hr). In three patients experiencing acute rejection episodes, urinary kallikrein excretion rose markedly (24 to 260 EU/24 hr) and remained elevated until the patients became oliguric. Furthermore, this rise occurred 1-3 days before the clinical diagnosis of rejection was made. For the group as a whole there was no significant correlation between urinary kallikrein excretion, the excretion of sodium or potassium, or urine volume. Although the number of patients studied is small, the increases observed in urinary kallikrein suggest that activation of the intrarenal kallikrein-kinin system is associated with acute transplant rejection.