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A multivariate factor analysis of the high plasma concentration of cyclic AMP in patients with chronic renal failure
Insights
Elevated cyclic AMP in chronic renal failure (CRF) patients is linked to kidney dysfunction. This study suggests cyclic AMP retention, not overproduction, causes higher plasma levels in CRF due to impaired renal function.
Area of Science:
- Nephrology
- Endocrinology
- Biochemistry
Background:
- Cyclic adenosine monophosphate (cAMP) acts as an intracellular mediator for hormone action.
- Elevated plasma cAMP concentrations are observed in patients with chronic renal failure (CRF).
Purpose of the Study:
- To investigate the relationship between plasma cAMP levels and clinical parameters in CRF patients.
- To determine the underlying causes of increased plasma cAMP in CRF.
Main Methods:
- Correlation analyses were performed on clinical data from CRF patients and healthy subjects.
- Multivariate analyses, including factor analysis and cluster analysis, were employed.
Main Results:
- Plasma cAMP concentrations significantly correlated with serum creatinine, urea, parathyroid hormone (PTH), and glucagon levels in CRF patients.
- Factor analysis revealed cAMP, creatinine, and blood urea nitrogen (BUN) as a primary factor, while PTH was associated with a secondary factor.
- Cluster analysis grouped cAMP, creatinine, and BUN together, and PTH and glucagon in a separate cluster.
Conclusions:
- The elevated plasma cAMP in CRF patients is primarily due to impaired renal excretion (retention) rather than increased production.
- Decreased renal function in CRF leads to the accumulation of cAMP in the plasma.
Abstract:
The concentration of cyclic AMP which is known as an intracellular mediator of hormone action increased in the plasma of patients with chronic renal failure (CRF). In the present study, the plasma concentration of cyclic AMP significantly correlated not only with serum, creatinine, and urea levels, but also with plasma PTH and glucagon in patients with CRF. Furthermore, plasma concentrations of PTH and glucagon correlated with the serum creatinine concentration to a significant extent. To discuss the cause of the increased cyclic AMP concentration in plasma of patients with CRF, multivariate analyses were carried out on the obtained clinical data from patients and normal subjects. In the factor analysis on the clinical data from 61 subjects, cyclic AMP, creatinine and BUN correlated with the first factor and PTH correlated with the second factor. The cumulative contribution ratio by the second factor was 76%. The results of the cluster analysis indicated that cyclic AMP, creatinine, and BUN formed a cluster and PTH glucagon made another cluster. These results suggest that the elevated plasma concentration of cyclic AMP in patients with CRF was mainly introduced not by overproduction but by the retention of cyclic AMP due to the decreased renal function.