Key result
Chronic glomerulonephritis is linked to protracted ANP increases after albumin and blunted frusemide-induced volume reduction.
Why the study?
The regulation of blood volume and related hormonal responses in patients with chronic glomerulonephritis during albumin and frusemide administration was unclear.
How do blood volume and neurohormonal responses to albumin and frusemide differ between patients with chronic glomerulonephritis and healthy controls?
How do blood volume and neurohormonal responses to albumin and frusemide differ between patients with chronic glomerulonephritis and healthy controls?
Patients with chronic glomerulonephritis exhibit abnormal blood volume regulation characterized by protracted ANP elevation after volume expansion and blunted volume reduction after diuresis.
Answers are grounded in this paper and cite their sources.
May reflect impaired volume regulation in chronic glomerulonephritis; leaves open effects on diuretic efficacy and outcomes.
Blood volume, blood pressure, plasma concentrations of atrial natriuretic peptide (ANP), cyclic 3',5'-guanosine monophosphate (cGMP), angiotensin II, aldosterone, and arginine vasopressin (AVP), and urinary excretion rates of cGMP, sodium, and water were determined before and after infusion of human albumin 20%, 3.5 ml/kg body-weight to 12 patients with chronic glomerulonephritis and 19 healthy control subjects (Study 1); and before and after frusemide injection, 0.75 mg/kg to 15 patients with chronic glomerulonephritis and 19 healthy control subjects (Study 2). In Study 1 blood volume was expanded to the same degree in patients (8.8 and 7.5%, medians, after 90 and 180 min) and controls (8.6 and 6.1%). ANP was enhanced in the patients (5.9 to 11.0 pmol/l, P less than 0.01) and the controls (4.9 to 7.1 pmol/l, P less than 0.01), but the elevated level was protracted in the patients simultaneously with a delayed sodium excretion. Plasma cGMP increased, aldosterone decreased and AVP was unchanged in both groups, whereas angiotensin II decreased in the patients (P less than 0.01), but not in the controls. In Study 2 blood volume was reduced to a smaller extent in the patients than in the controls (8.9% versus 9.9%, P less than 0.05). ANP an cGMP decreased, and angiotensin II, aldosterone and AVP increased in both patients and controls. In conclusion, patients with glomerulonephritis respond to albumin- and frusemide induced changes in blood volume with essentially the same counter-regulatory changes in ANP, angiotensin II, aldosterone and AVP as do healthy subjects. The more protracted increase in ANP and the decrease in angiotensin II after albumin, and the smaller blood volume reduction after frusemide suggest an abnormal regulation of blood volume in glomerulonephritis.
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Jespersen et al. (1990) studied Chronic glomerulonephritis. Human albumin and frusemide vs. Healthy control subjects was evaluated on Changes in blood volume and plasma concentrations of ANP, cGMP, angiotensin II, aldosterone, and AVP. Patients with chronic glomerulonephritis exhibited a more protracted increase in ANP after albumin infusion and a smaller blood volume reduction after frusemide (8.9% vs 9.9%, P<0.05) than healthy controls.
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