Urinary kallikrein excretion after renal transplantation: Relationship to hypertension,graft source,and renal function

The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation has been assessed by measurement of urinary kallikrein activity in 41 renal transplant recipients. The urinary tosyl arginine methyl esterase assay was used. The urinary kallikrein in these patients appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertension (mean blood pressure 156 ± 3/98 ± 2 mm Hg) and excreted less kallikrein (4.0 ± 1.2 versus 12.5 ± 4.0 esterase units [EU] per 24 hours, p < 0.05) than their 18 normotensive counterparts (mean blood pressure 132 ± 2/77 ± 1 mm Hg, both p < 0.01). Subjects with renal complications of transplantation (acute tubular necrosis [ATN], nine patients, or acute rejection [AR], eight patients) also excreted less kallikrein than the 28 subjects without such complications (3.4 ± 0.9 versus 10.3 ± 2.7 EU/24 hours, p < 0.02). Among those with acute renal complications, subjects with ATN excreted less kallikrein than those with AR (1.3 ± 0.3 versus 5.7 ± 1.7 EU/24 hours, p < 0.02). Cadaver graft recipients excreted less kallikrein than living related donor graft recipients (2.1 ± 0.4 versus 13.0 ± 3.5 EU/24 hours, p < 0.01), perhaps reflecting their higher blood pressures (mean systolic pressure 151 ± 3 versus 140 ± 3 mm Hg, p < 0.04), relatively impaired renal function (creatinine clearance values 42 ± 8 versus 62 ± 5 ml/min, p < 0.04), and higher incidence of ATN (nine cases versus none). The kallikrein-kinin system may be involved in the pathogenesis of hypertension and some forms of renal dysfunction after renal transplantation.