This study was carried on 60 subjects classtfied into 4 groups. Group 1
consisted of 10 healthy control subjects. Group 11 consisted of 20 normotensive
non-nephropathic well controlled 1DDM patients Group 1.11 consisted
of 20 hypertensive non-nephropathic well-controlled 1DDM patients
and Group IV consisted of 10 hypertensive non-nephropathic non-diabetic
patients. All members of the study were subjected to the following investigations:
assay of microalbuminuria, serum creatinine. biochemical liver
functions. plasma glucose (fasting & 2 hours postprandial). serum Na+
level. 24 hours urinary Na+and base line plasma ANP level. All subjects
received saline infusion (2 mato( / Kg / 90 min) & diabetic patients received
l.V. insulin infusion (15 rn.uglh). then 24 hours urinary Na+ & plasma
ANP level were remeasured. Tests of autonomic nervous system were
performed to diabetic patients.
Base line plasma ANP level was significantly higher in both diabetic
and hypertensive patients when compared to controL Elevated ANP level
in diabetic patients was explained by hyperinsulinemia. which causes
Na+ & H20 retention whereas ANP elevation in hypertensive patients
was attributed to positive Na+ balance, increased cardiac filling pressure
as well as elevated renin & aldosterone. We found that ANP was signficandy
elevated after saline challenge in control & hypertensive patients
whereas it was unchanged in diabetic patients. This could be explained
by exhaustion of cardiac stores of ANP & impaired responsiveness, of
atrial stretch receptors in diabetes. Our work showed that the kidneys
had impaired responsiveness to ANP in diabetes. This was inferred from
the following: non significant change in urinary No.+ in IDDM either the
base line or after saline challenge & significant negative correlation between
plasma ANP & urinary Na+ . Our study showed that autonomic
neuropathy had no significant impact on ANP in IDDM whereas disease
duration, age ez, blood pressure significantly altered ANP level. |
