The renal kallikrein-kinin system is involved in sodium and water homeostas
is, blood pressure regulation and inflammation. Tissue kallikrein and kinin
levels were measured in the urine of patients with renal disease and in th
e urine of Living related kidney donors prior to uninephrectomy who served
as controls. Tissue kallikrein and kinin B1 and B2 receptors were immunoloc
alised by confocal microscopy in renal biopsy material from patients with r
enal disease and controls (fresh autopsy material and normal kidney tissue
from nephrectomies for malignancy). Urinary tissue kallikrein excretion was
significantly decreased in patients with mild renal disease (16.6 +/- 6.7
ng tissue kallikrein (TK)/ng protein; p < 0.05) and more markedly so (1.8 /- 0.7 ng TK/mu g protein; p < 0.01) in patients with severe renal failure
requiring dialysis compared to normal controls (78.9 +/- 31.7 ng TK/mu g pr
otein). Basal kinin values were unchanged in patients with renal disease (1
4 +/- 0.8 ng/ml) compared to controls (13.3 +/- 0.56 ng/ml). In control kid
ney tissue kallikrein was immunolocalised in the distal connecting tubules
and collecting ducts whereas decreased immunolabelling was observed with re
nal disease. Kinin B2 receptor labelling was present in the entire nephron
in the normal control kidney but was reduced with renal disease. While kini
n B1 receptor immunolabelling was not observed in the control kidneys, labe
lling of distal tubules and collecting ducts was noted in renal disease, su
ggesting an upregulation of B1 receptors in renal parenchymal disease, (C)
1999 Elsevier Science B.V. All rights reserved.