Kidney haemodynamics appear to change after the early phases of diabet
ic nephropathy: increases in glomerular filtration rate and in renal p
lasma flow have been widely reported, while kidney size is increased.
As the renal kallikrein-kinin system has been demonstrated to regulate
kidney blood circulation, we have evaluated the excretion of urinary
kallikrein in 87 Type 1 (insulin-dependent) diabetic patients with and
without hyperfiltration. Urinary kallikrein excretion was measured in
24-h urine collections. The esterolytic activity was determined by fl
uorimetric assay. The excretion of urinary kallikreins was significant
ly higher in hyperfiltering patients (472 +/- 125 esterase units/24 h)
than in normofiltering (168 +/- 77 esterase units/24 h) and control s
ubjects (151 +/- 39 esterase units/24 h), p < 0.001. Furthermore, we o
bserved a positive correlation between urinary kallikrein excretion an
d glomerular filtration rate (r = 6.785). These data suggest that vari
ations of kallikrein and kinin concentrations may play a role in the a
lteration of renal haemodynamics in Type 1 diabetes. It is possible th
at the kinin-kallikrein system. the renin-angiotensin system and the p
rostaglandins may interact to determine the haemodynamic alterations w
hich arc present in the diabetic discase.