INCREASED NOREPINEPHRINE SECRETION IN PATIENTS WITH THE NEPHROTIC SYNDROME AND NORMAL GLOMERULAR-FILTRATION RATES - EVIDENCE FOR PRIMARY SYMPATHETIC ACTIVATION
Sn. Rahman et al., INCREASED NOREPINEPHRINE SECRETION IN PATIENTS WITH THE NEPHROTIC SYNDROME AND NORMAL GLOMERULAR-FILTRATION RATES - EVIDENCE FOR PRIMARY SYMPATHETIC ACTIVATION, American journal of nephrology, 13(4), 1993, pp. 266-270
Considerable controversy exists in regard to the state of arterial cir
culatory integrity in patients with the nephrotic syndrome. Increased
sympathetic nervous system activity, along with activation of the reni
n-angiotensin-aldosterone system and the nonosmotic release of vasopre
ssin, is seen in other states of arterial underfilling. Thus, in the p
resent study, sympathetic nervous system activity was assessed by dete
rmining plasma norepinephrine secretion and clearance rates using a wh
ole-body steady-state radionuclide tracer method in 6 edematous patien
ts with the nephrotic syndrome of various parenchymal etiologies and 6
normal control subjects in the supine position. Patients were withdra
wn from all medications 7 days prior to study. Mean creatinine clearan
ces and serum creatinine concentrations were normal in both the nephro
tic syndrome patients and controls (99 +/- 1 3 vs. 112 +/- 15 ml/min,
p = NS, 1.1 +/- 0.1 vs. 0.8 +/- 0.0 mg/dl, p = 0.03, respectively). Ho
wever, the nephrotic syndrome patients exhibited significant hypoalbum
inemia (2.0 +/- 0.4 vs. 3.8 +/- 0.1 g/dl, p < 0.01). The supine plasma
norepinephrine level was elevated in the patients with the nephrotic
syndrome as compared with controls (240 +/- 5 8 vs. 119 +/- 22 pg/ml,
p = 0.07). More significantly, the secretion rate of norepinephrine wa
s markedly increased in nephrotic patients (0.30 +/- 0.07 vs. 0.13 +/-
0.02 mug/m2/min, p < 0.05), whereas the clearance rate of norepinephr
ine was similar in the two groups (2.60 +/- 0.29 vs. 2.26 +/- 0.27 l/m
in, p = NS). Plasma renin activity and plasma aldosterone, arginine va
sopressin and atrial natriuretic peptide concentrations were not diffe
rent in nephrotic syndrome patients compared with controls. We conclud
e that the sympathetic nervous system is activated in patients with th
e nephrotic syndrome, as assessed by the increased whole-body norepine
phrine secretion rate, prior to a significant fall in glomerular filtr
ation rate or a marked activation of either the renin-angiotensin-aldo
sterone system or the nonosmotic release of vasopressin. These data su
pport the presence of arterial underfilling in the nephrotic syndrome.