Prevalence of Primary Aldosteronism among Unselected Hypertensive Patients: A Prospective Study Based on the Use of an Aldosterone/Renin Ratio above 25 as a Screening Test

Fogari, Roberto; Preti, Paola; Zoppi, Annalisa; Rinaldi, Andrea; Fogari, Elena; Mugellini, Amedeo

doi:10.1291/hypres.30.111

Cited by 107 publications

(60 citation statements)

References 45 publications

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“…However, we did not see any significant correlation within these parameters (correlation coefficient: 0.140, 0.028 and 0.010, respectively; NS). The ratio of plasma aldosterone to renin activity, 34 a useful screening test for the diagnosis of primary aldosteronism, was not correlated with urinary prostasin (correlation coefficient: 0.022; NS). Furthermore, renal function that is estimated by the eGFR formula had no effect on either urinary prostasin or urinary aldosterone levels (correlation coefficient: 0.044 and 0.040, respectively; NS).…”

Section: Urinary Prostasin In Humansmentioning

confidence: 93%

Urinary prostasin in humans: relationships among prostasin, aldosterone and epithelial sodium channel activity

et al. 2009

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Prostasin, a membrane-bound serine protease, is known to increase the activity of the epithelial sodium channel (ENaC). Gene expression of prostasin was shown to be regulated by aldosterone, which increases the rate of sodium reabsorption through ENaC. To clarify the physiological relationships among prostasin, aldosterone and ENaC, we developed a specific radioimmunoassay (RIA) for human prostasin. Prostasin levels in urine were determined in 26 normotensive and 121 hypertensive subjects. Aldosterone content in urine and plasma, urinary Na/K ratio and other clinical parameters were also measured. We observed a highly significant correlation between prostasin and aldosterone concentration in urine (correlation coefficient: 0.673, Po0.0001). A significant correlation was also found between urinary prostasin and plasma aldosterone concentration (correlation coefficient: 0.229, Po0.05). In addition, urinary prostasin excretion was inversely correlated with urinary Na/K ratio (correlation coefficient: À0.425, Po0.0001). In conclusion, we developed a prostasin-specific RIA and applied it to the clinical study. Our findings suggest that urinary prostasin level is strongly correlated with urinary or plasma aldosterone level and may serve as a surrogate marker for ENaC activation in hypertensive patients. However, it is not clear, at the present time, whether endogenous aldosterone regulates prostasin expression or vice versa.

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Section: Urinary Prostasin In Humansmentioning

confidence: 93%

Urinary prostasin in humans: relationships among prostasin, aldosterone and epithelial sodium channel activity

et al. 2009

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“…1 An aldosterone-renin ratio greater than 25 suggests the possibility of PAL, 2 which is confirmed by demonstrating that aldosterone is not suppressible despite suppression of renin by salt loading. Elevated levels of aldosterone, associated with adrenocortical hyperplasia or aldosterone-producing adenoma, usually result in suppressed renin levels in all cases and hypertension in most cases.…”

Section: Introductionmentioning

confidence: 94%

Further study of chromosome 7p22 to identify the molecular basis of familial hyperaldosteronism type II

et al. 2010

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Familial hyperaldosteronism type II (FH-II) is an inherited form of hyperaldosteronism associated with hypertension in most patients. The mutations that cause FH-II are unknown, but linkage analysis has mapped them to chromosome 7p22. As FH-II is clinically indistinguishable from sporadic primary aldosteronism, a common and treatable condition, unravelling the cause of FH-II has important implications for these sporadic cases. To investigate whether FH-II is caused by large deletions or insertions, we examined the virtual karyotype of four pairs of affected and unaffected individuals using highdensity bead chips. We also sequenced the coding regions of five 7p22 candidate genes that were prioritized because of their putative role in cell growth. We found no evidence of single-nucleotide polymorphism (SNP) copy number variation between pairs, and from the widest gap on the chip, chromosome 7p22 deletions or insertions exceeding B50 kb in these pedigrees can be excluded. We found 15 SNPs (two of which were novel), but none of them were non-synonymous and segregated with the disease in the FH-II pedigrees. We have been able to exclude large genomic deletions or insertions at 7p22 and refine the candidate gene list for this locus, but the mutations causing FH-II remain elusive.

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“…Recently, the wide use of aldosterone-renin ratio (ARR) as a screening test in hypertensive patients has led to a 5-to 15-fold increase in the detection of PA (Mulatero et al 2004). The reported prevalence of PA ranges from 2% to 11.2% in hypertensive population (Lund et al 1981;Young 1999;Rossi et al 2006a;Fogari et al 2007), while the prevalence in normotensive subjects is about 1% (Gordon 1994;Brown et al 1996;Mosso et al 2003). The two most common etiologies of primary aldosteronism are aldosterone-producing adrenal adenoma (APA) and bilateral adrenal hyperplasia.…”

Section: Factors Determining Cardiovascular and Renal Outcomes After mentioning

confidence: 99%

Factors Determining Cardiovascular and Renal Outcomes after Adrenalectomy in Patients with Aldosterone-Producing Adrenal Adenoma

Chiou

Chiang

Fuh

et al. 2009

Tohoku J. Exp. Med.

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Prevalence of Primary Aldosteronism among Unselected Hypertensive Patients: A Prospective Study Based on the Use of an Aldosterone/Renin Ratio above 25 as a Screening Test

Cited by 107 publications

References 45 publications

Urinary prostasin in humans: relationships among prostasin, aldosterone and epithelial sodium channel activity

Urinary prostasin in humans: relationships among prostasin, aldosterone and epithelial sodium channel activity

Further study of chromosome 7p22 to identify the molecular basis of familial hyperaldosteronism type II

Factors Determining Cardiovascular and Renal Outcomes after Adrenalectomy in Patients with Aldosterone-Producing Adrenal Adenoma

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