Why the study?
How do plasma ANP concentrations and circulating forms differ between normal individuals and patients with chronic renal failure, and how do they respond to physiological changes?
How do plasma ANP concentrations and circulating forms differ between normal individuals and patients with chronic renal failure, and how do they respond to physiological changes?
Plasma ANP levels are elevated in chronic renal failure in proportion to volume status and respond to physiological stimuli like exercise and head-down tilt, suggesting release is mediated by atrial stretch.
ANP tracks volume in chronic renal failure but should not change practice; hypothesis-generating for biomarker validation in CKD.
A specific and sensitive radioimmunoassay has been developed and used to measure circulating atrial natriuretic peptide (ANP) in normal man and in patients with chronic renal failure. Circulating ANP levels rose with head-down tilt and exercise, and were raised in patients with chronic renal failure in proportion to volume status. This suggests that ANP release is mediated via increased atrial stretch, although other release mechanisms cannot be excluded. Extracts of normal human plasma subjected to reverse phase HPLC showed one major peak of immunoreactivity co-migrating with alpha-human ANP. However, when plasma extracts from patients with renal failure were chromatographed on a similar system, a second later eluting peak of ANP immunoreactivity was observed. This may represent circulating ANP precursors or degradation molecules. Significant arteriovenous differences in plasma ANP concentration were observed in patients with chronic renal failure. Arterial and venous plasma ANP levels decreased slightly after haemodialysis. Plasma ANP concentrations were inversely correlated with haematocrit in these patients.
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Ogawa et al. (1987) studied this question.
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