Opinion TRENDS in Endocrinology and Metabolism Vol.16 No.

3 April 2005

Plasma renin and aldosterone

measurements in low renin
hypertensive states
Jean E. Sealey1, Richard D. Gordon2 and Franco Mantero3
1
Cardiovascular Center, Weill Medical College of Cornell University, 1300 York Ave, New York, NY, 10021, USA
2
University of Queensland Endocrine Hypertension Research Unit, Greenslopes Hospital, Greenslopes, Queensland, 4120, Australia
3
Unita Operativa di Endocrinologia Dip.to di Scienze Mediche e Chirurgiche Univ.ta di Padova Via Ospedale 105, 35100, Padova, Italy

Plasma renin concentrations are extremely low, requir- Problems with plasma renin measurements
ing high sensitivity methods to detect low renin Identification of low plasma renin levels is complicated by
hypertensive states. Moreover, plasma prorenin must plasma prorenin, which can be inadvertently measured as
not cryoactivate to renin to avoid falsely high values. renin. Moreover, because renin circulates at 10K12 M,
The enzyme kinetic plasma renin activity (PRA) test has compared with 10K10 M for aldosterone and insulin, and
the required sensitivity, whereas direct renin assays and 10K7 M for cortisol, low renin levels are at or below the
PRA tests with short incubation times are usually not limits of sensitivity of even the most sensitive immunoas-
accurate enough. Test specificity is essential for plasma says. Fortunately, these are not insurmountable problems.
aldosterone. The Nichols Advantage aldosterone assay
is fast and automated but requires great attention to
quality control. Here, the impact of renin on the Plasma prorenin and its cryoactivation
aldosterone:renin ratio as a screening test for primary Approximately tenfold more prorenin than renin normally
aldosteronism is reviewed. A sensitive plasma renin test circulates in human plasma, with almost 100 times more
is essential for the diagnosis of low renin hypertensive being seen in some low renin patients. At temperatures
states and, currently, can be consistently achieved only below 258C, prorenin develops intrinsic renin activity, and
with the PRA radioimmunoassay. the prosequence becomes vulnerable to cleavage by
plasma enzymes, resulting in irreversible formation of
renin in vitro. The lower the temperature (short of
freezing) the more likely these processes are to occur,
Introduction albeit slowly [6,7].
Hypertension itself, through baroreceptor activity,
reduces renin secretion. Reciprocally, lack of suppression
of renin in the hypertensive patient indicates the presence Box 1. The spectrum of low renin hypertension
of renin-dependent hypertension [1]. Low renin hyperten- Low renin, low aldosterone
sion (Box 1) is usually caused by excess sodium retention Liddle’s syndrome
resulting from (i) intrinsic renal abnormalities or (ii) 11b-Hydroxysteroid dehydrogenase deficiency
inappropriate mineralocorticoid activity. Primary aldos- Licorice abuse
Ectopic adrenocorticotropin syndrome
teronism is the most common currently recognized form of
11-Desoxycorticosterone-secreting tumor
inappropriate mineralocorticoid activity, and the aldoster- 11b-Hydroxylase deficiency
one:renin ratio (ARR) is widely used to screen for this 17a-Hydroxylase deficiency
condition in hypertensive populations [2,3]. Because assay Activating mineralocorticoid receptor mutations
problems associated with commercially available methods Glucocorticoid resistance syndrome
Diabetic renal disease
were identified by participants of the First International
Cyclooxygenase inhibitors
Workshop on Endocrine Hypertension in Ancona, Italy, Non-steroidal anti-inflammatory drugs
4–6 April 2004, the authors were delegated the task of Gordon’s syndrome
exploring these issues [4,5]. Some elderly patients (O70 years)
Therefore, the present paper addresses technical
problems in the measurement of renin and aldosterone Low renin, normal aldosterone
Primary aldosteronism
that might prevent meaningful interpretation of plasma Gordon’s syndrome
levels. For renin, sensitivity is of paramount importance. Some elderly patients (O70 years)
For aldosterone, specificity and accuracy are essential,
particularly if an ARR is determined. Low renin, raised aldosterone
Primary aldosteronism
Corresponding author: Sealey, J.E. (jsealey@med.cornell.edu). Gordon’s syndrome

www.sciencedirect.com 1043-2760/$ - see front matter Q 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.tem.2005.02.006
 Opinion TRENDS in Endocrinology and Metabolism
Table 1. Effect of blank subtraction to the accuracy of PRA measurements in relation to Ang I generation time
Incubation Ang Ia PRA
time (h) (pg 10 mlK1) (ng mlK1 hK1)
1.5 10 0.65
3 10 0.33
18 10 0.06
a
Lowest point on standard curveZ10 pg; 10 ml plasma assayed in RIA.
Because renin is remarkably stable in plasma at
room temperature, to avoid cryoactivation of prorenin,
blood samples for renin should be processed for plasma
at room temperature. Prorenin does not cryoactivate in
frozen plasma, or during rapid freezing and thawing.
Thus, frozen plasma can be thawed in front of a fan
but never in a refrigerator. Plasma can be shipped on
dry ice, but samples must not thaw during shipment.
Bloods collected for renin measurement can be safely
kept in an unopened EDTA Vacutainer for up to 24 h
at ambient temperature. We recommend centrifuging
blood at room temperature and then freezing the
plasma, if necessary.
Renin assay sensitivity
Most commercial and hospital laboratories do not invest
the time or the technical skill required to perform the most
sensitive plasma renin test – the plasma renin activity
(PRA) enzyme kinetic radioimmunoassay (RIA). In this
approach, sensitivity is achieved by allowing renin to
generate Ang I in plasma at 378C until enough angiotensin
I (Ang I) is produced to be measured accurately by RIA.
PRA is expressed as ng mlK1 hK1 of Ang I [8,9]. The PRA
enzyme kinetic RIA assay is unpopular because it is labor
intensive, not subject to automation and takes two days to
perform in low renin patients. Both plasma renin and
angiotensinogen levels influence the test. Therefore, it
reflects the capacity of blood to generate angiotensin – the
active hormone of the renin–angiotensin system – which is
usually the required information. Some investigators
measure plasma renin concentration (PRC) instead of
PRA using an enzyme kinetic radioimmunoassay similar
to that of PRA, in which excess angiotensinogen is added
to plasma to eliminate the impact of changes in plasma
angiotensinogen [9–11].
Reluctance to use the PRA or PRC assays has been
heightened by the development of simpler, direct renin
sandwich radioimmunoassays [12–15] and a commercially
available (Nichols Institute Diagnostics, San Clemente,
CA, USA) automated sandwich chemiluminescent immu-
noassay (irR). We have reported [16,17] that these
methods do not approach the sensitivity of the enzyme
kinetic assays, although others have a more favorable
point of view [18]. The key question is whether they are
sensitive enough to detect low renin with sufficient
accuracy to be useful to the practicing physician. The
answer is ‘maybe’, but not yet, without safeguards and
improvements [16–18].
PRA measured by enzyme kinetic RIA
This method is the most sensitive as long as the Ang I
generation step is prolonged to 18 h for samples with PRA
!1.0 ng mlK1 hK1. In the Sealey–Laragh laboratory [1,6],
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Vol.16 No.3 April 2005 87
PRA minus blank (ng mlK1 hK1)
BlankZ0 pg BlankZ5 pg BlankZ10 pg
0.65 0.33 0
0.33 0.16 0
0.06 0.03 0
the PRA cut-off point for low plasma renin is 0.65 ng
mlK1 hK1. Table 1 shows that 0.65 ng mlK1 hK1 is the
limit of sensitivity if Ang I is generated for only 1.5 h.
However, if Ang I generation is extended to 3 or 18 h
the limits of sensitivity are lowered to 0.33 and
0.06 ng mlK1 hK1, respectively. Thus, by incubating
for 18 h it is possible to explore a tenfold range of
renin in the low renin range.
Table 1 illustrates that plasma per se can interfere with
the renin test, causing falsely high or low values. All
commercially available PRA enzyme kinetic kits advocate
measuring Ang I in native plasma (from here on called the
‘blank’) and subtracting it from Ang I measured after the
378C incubation. For low renin samples, the blank is not
Ang I but is primarily non-specific assay interference. The
error of estimation of the blank can be as much as 100%.
Table 1 shows that if the blank is measured as 5 pg it could
actually range between 0 and 10 pg. If the Ang I
generation step is carried out for only 1.5 hr, this range
of error might result in PRA levels that ranged between 0
and 0.65 ng mlK1 hK1 – spanning the whole range of low
renin levels – by contrast, if an 18 h incubation is used
instead, the blank has very little impact on the final result.
Thus, the shorter the Ang I generation time, the greater
the impact of the blank on the PRA level. Because the
blank cannot be measured accurately – and might even
disappear during the 378C incubation [8] – the Sealey–
Laragh PRA method does not measure it but instead
generates Ang I long enough to make the blank
irrelevant quantitatively, while at the same time
extending the range of renin levels that can be defined
well into the subnormal range.
Therefore, if a PRA test is used, an 18 h Ang I
generation step should be adopted for samples below
1.0 ng mlK1 hK1. This can be done easily by incubating
overnight the sample that was previously used for the
blank and running the RIA on the second day, if necessary.
Another type of plasma renin activity test, developed by
Paulsen and Jorgenson et al. [19], and used by Nussberger
et al. [20], is referred to as ‘antibody trapping’. Excess
antibodies are added to plasma during a 30 min Ang I
generation step at pH 7.4. The antibodies capture the
formed Ang I and protect it from degradation by
angiotensinases. This method is especially useful for
measuring PRA in the presence of renin inhibitor drugs,
because angiotensinase inhibitors commonly used in
enzyme kinetic assays disrupt the equilibrium of drug
binding to plasma proteins or to renin. The disadvantage
of this technique for the identification of low renin
patients is its lower sensitivity as a result of the use of
pH 7.4 for Ang I generation. With the antibody trapping
method the cut-offfor low renin in the ambulatory patient will
probably be half of that at pH 7.4 (i.e. !0.33 ng mlK1 hK1).
88 Opinion TRENDS in Endocrinology and Metabolism
Direct renin tests
These tests measure the concentration of renin in plasma.
In all direct renin tests, ‘low renin’ falls at or below the
lowest point of the standard curve – the same range as the
blank in the PRA enzyme kinetic RIA. When radioactivity
is used – as in the Bio-Rad Renin II kit (now marketed by
Schering; not available in the USA) – the counts at the cut-
off point for low renin are close to 1% of the total counts,
O20% of which are non-specific binding. With chemilu-
minescence, the relative light units are also very low in
the low renin range.
Direct renin radioimmunoassays. In the best of
research laboratories – the direct renin sandwich radio-
immunoassay can discriminate low from medium plasma
renin levels [13]. Ferrari et al. also seemed to show that a
direct renin radioimmunoassay can identify low renin
levels [21]. Thus, they showed a good correlation between
ARRs comparing the Bio-Rad direct renin radioimmuno-
assay and the Sealey PRA method. The surprising finding
is that in their study only one patient with documented
primary aldosteronism had low PRA according to the
Sealey/Laragh criteria (!0.65 ng mlK1 hK1) [1]. Using the
same PRA assay, Blumenfeld et al. [22] found in 82
patients with primary aldosteronism that 71% with an
adenoma and 41% without adenoma had PRA
!0.2 ng ml K1 h K1 . Mean PRA was 0.17 and
0.50 ng ml K1 hK1 in cured and non-cured patients,
respectively (difference, 0.33 ng mlK1 hK1; confidence
interval, 0.14 to 0.52 ng mlK1 hK1; P!0.001). Thus, the
mean values in the Blumenfeld study were below the
lowest value reported by Ferrari et al. (range 0.6 to
1.23 ng mlK1 hK1). A possible explanation for the virtual
absence of patients with low renin in the Ferrari study,
which included nine patients with documented adrenal
adenoma, is that prorenin cryoactivated before the renin
assay was performed. For whatever reason, this study did
not succeed in exploring the low renin range that occurs in
most patients with primary aldosteronism.
Thus, as with the PRA assay, direct renin assays also
require fastidious laboratory conditions to avoid the
possibility of falsely high values. Unfortunately, at
present, physicians cannot routinely expect a sufficiently
high degree of accuracy from commercial clinical
laboratories.
Direct renin chemiluminescence immunoassay. An
automated chemiluminescence sandwich immunoassay
for renin has recently been developed by Nichols Institute
Diagnostics (NID) and has been marketed worldwide. This
Table 2. Cut-off values for identification of low renin in ambulatory patients and relationships between various renin and
aldosterone units
PRA (ng mlK1 hK1)
Low renina !0.65
Relationship between renin units 1 12.8
0.810
1.2
1.9
PA (ng dlK1)
Relationship between aldosterone units 10
a
Cut-off values for low renin are calculated from a PRA value of 0.65 ng mlK1 hK1 [1]. PRA levels are expressed as the rate of Ang I generation, in which Ang I can be reported
as either mass units (ng mlK1 hK1) or molarity (pmol lK1 minK1). Immunoreactive renin (irR) levels are usually reported as mass units in terms of either mU mlK1 or ng lK1.
Aldosterone levels are reported as either mass units (ng dK1) or molarity (pmol lK1).
www.sciencedirect.com
Vol.16 No.3 April 2005
has the potential for standardizing and increasing the
accuracy of the renin test and eliminating the need for
skilled laboratory technicians. Initially, the test showed
great promise and correlated well with the PRA in the low
renin range. However, more recently, the test has shown
many of the previously described shortcomings that
appear whenever clinically relevant values fall at or
below the lowest portion of the standard curve [i.e.
variation in sensitivity between reagent lots, falsely high
values and the need for highly skilled maintenance of the
automated platform (Advantage machine)]. Physicians
have described patients with primary aldosteronism who
were at first misdiagnosed because the direct renin test
did not detect the low renin level, whereas a subsequent
PRA test did. At the other end of the spectrum,
extraordinarily high direct renin levels have been
found in patients who do not have proportionally
high PRA levels. Thus, to date, the direct renin test
seems to exhibit occasional problems at both the high
and low ends of the standard curve sufficiently often
for this to be a serious concern.
Clinical tests are usually designed to encompass the
clinical range but the direct renin test does not do that.
Thus, w30% of untreated hypertensive patients have low
renin levels (ambulatory PRA ranges from 0.1 to
0.65 ng mlK1 hK1; direct renin from 2 to 5 mU mlK1),.
w60% have medium renin levels (ambulatory PRA from
0.65 to 4.5 ng mlK1 hK1; direct renin 5 to 36 mU mlK1), and
w10% have high renin levels (ambulatory PRA 4.5 to
50 ng mlK1 hK1; direct renin 36 to 400 mU mlK1). Supine
values are usually w50% of those measured in ambulatory
patients. For the direct renin test, the cut-off for low renin
is 5.3 mU mlK1 (Table 2) but the lowest Advantage
machine calibration point is 6 mU mlK1. Thus, more than
30% of all hypertensive patients fall below the lowest point
on the calibration curve, the portion of the standard curve
with the greatest errors. Therefore, it is not surprising
that the test sometimes fails to detect suppressed renin
levels in patients with low renin hypertension.
This leaves clinicians with a dilemma if they do not
have access to an accurate PRA test (such as the one
performed by Quest Diagnostics in the USA under test
# 01537N; Quest uses reagents from the Sealey–Laragh
laboratory and follows their protocol). The question then
remains: is no test better than a potentially inaccurate
test if there are no other options? The answer is to try as
hard as possible to get an accurate PRA test (18 h
incubation) performed. If this is not possible, a direct
PRA (pmol lK1 minK1) IrR (mU mlK1) IrR (ng lK1)
!8.3 !5.3 !3.4
8.2 5.2
6.3 4.3
16 10 6.7
24 16 10
PA (pmol lK1)
280
3.6 100
 Opinion TRENDS in Endocrinology and Metabolism
renin test can be ordered, which is better than a PRA test
that utilizes a short incubation time (less than 3 h) with
blank subtraction. However, direct renin tests can reliably
tell only whether the renin level is high or not, and cannot
accurately measure within the low range because it falls
below the lowest calibration point of the machine.
Plasma aldosterone measurements
Plasma aldosterone levels are orders of magnitude lower
than those of other circulating steroids, making plasma
aldosterone difficult to measure accurately because speci-
ficity is of paramount importance. This can be overcome
only by using antibodies with very high sensitivity and
specificity.
The NID Advantage aldosterone chemiluminescent
immunoassay is gaining popularity because it provides a
result in less than an hour, with minimal input from the
technician, being fully automated and preprogrammed.
The patient’s plasma aldosterone first interacts for 10 min
with an aldosterone antibody, before a second, acridinium
(for chemiluminescence)-labeled aldosterone antibody is
added. Competition for binding occurs for 10 min. The
chemiluminescent activity of the bound complex adherent
to magnetic particles is then measured. Ingenious in
design, the method depends on perfect functioning of
equipment and critical quality control. Because the
system is fully automated, only two ‘calibrators’ (run in
duplicate) are used to correlate the ‘relative light units’ of
the user’s system with those of a ‘Master System’ specific
for each new batch of reagents; but are two enough? The
system depends upon photomultiplier tubes to measure
(in 2 s) the chemiluminescence that develops. Because no
two photomultiplier tubes are alike, this introduces a
potential problem not inherent in RIAs, and makes
regular calibration crucial. One of the authors (RDG)
experienced a photomultiplier tube problem, which was
unrecognized for some months, despite routine quality
control tests. During this time, results were considered
uninterpretable by clinicians. New photomultiplier tubes
solved the problem.
The manufacturers recommend that each laboratory
should establish its own normal range but they also
(i) supply normal ranges for ‘ambulatory’ levels at
08.00–10.00 h (when peak aldosterone levels normally
occur) established after 15 min of ambulation, and ‘supine’
levels that were drawn after 30 min recumbency, and
(ii) provide evidence that levels in EDTA plasma
(1.5–47.4 ng dlK1) are slightly lower than in serum
(3.1–53.9 ng dlK1). Using this test we have seen higher
aldosterone values than with traditional assays, particu-
larly at and above the upper end of the normal range.
Precision at the upper and lower ends of the normal range
might prove to be an ongoing problem.
Table 3. Cut-off values for a positive ARR using various renin and aldosterone unitsa
PRA
Aldosterone ng mlK1 hK1
ng dlK1 27
pmol lK1 750
a
Reformatted from Ferrari et al. [21]. ARR results below these values are thought to rule out primary aldosteronism. PRA results are expressed as a rate of Ang I generation in
which the Ang I is reported as either mass units (ng mlK1 hK1) or molarity (pmol lK1 minK1). Immunoreactive renin (irR) levels are usually reported as mass units in terms of
either mU mlK1 or ng lK1.
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Vol.16 No.3 April 2005 89
Lack of precision will lead to failure to identify patients
with truly suppressed aldosterone levels as a consequence
of sodium-volume excess. For patients with borderline
increases in aldosterone, crossreacting steroids or other
assay-related problems will artificially increase the ARR,
the screening test most often used to identify patients with
primary aldosteronism. In such cases, the clinician will be
faced with the dilemma of whether or not to proceed to an
aldosterone suppression test.
For those who use commercially available aldosterone
RIA kits it is important to ensure (i) that the antibody has
not been changed without notice and (ii) that the antibody
is specific enough to detect low aldosterone levels with
accuracy, even in the presence of high levels of cross-
reacting steroids. For the physician or laboratory with the
appropriate resources, concurrent testing of the aldoster-
one level in a control pool of pregnancy plasma with
known aldosterone content can be a useful control,
because pregnancy plasma has high levels of crossreacting
steroids. It would be even more useful if commercial
laboratories were mandated to report with each aldoster-
one result the aldosterone level in an international
standard created for the assessment of crossreactivity.
For those using the NID Advantage assay, full attention to
all recommended quality control steps is essential, as is
immediate discussion of unexpected or unexplained
results with the manufacturer, as problems are progress-
ively ironed out. For clinicians referring patients to
laboratories using the assay, your recognition and discus-
sion of clinically puzzling results will be essential to its
further improvement.
The aldosterone:renin ratio
The ARR screening test for patients with primary
aldosteronism is based on the premise that plasma renin
is the primary determinant of circulating aldosterone
levels, and that above a particular cut-off point the ratio is
a measure of autonomy of aldosterone secretion. Table 3
gives the approximate cut-off values for a positive ARR
test for various plasma aldosterone and plasma renin
units [2,3,9]. However, given the variations in method-
ology, the best approach would be for each laboratory to
establish its own criteria.
The ARR screening test has proved useful but has its
limitations [23]. It is important to remember that
adrenocorticotropin and body potassium levels increase
aldosterone without affecting renin; changing posture
affects renin faster than aldosterone. Moreover, b-adre-
nergic blockers, a-methyl DOPA and clonidine give false
positive results; converting enzyme inhibitors, angio-
tensin receptor blockers, diuretics and aldosterone recep-
tor blockers give false negative results. Stowasser et al.
recommend drawing blood at midmorning, after patient
IrR
pmol lK1 minK1 mU mlK1 ng lK1
2.1 3.3 5.4
59 90 150
90 Opinion TRENDS in Endocrinology and Metabolism Vol.16 No.3 April 2005

Table 4. Impact of different plasma renin or plasma aldosterone (PA) levels on the ARR
Constant plasma aldosterone of 20 ng lK1 Constant plasma renin of 0.65 ng mlK1 hK1
PRA (ng mlK1 hK1) ARR D ARRa PA (ng dlK1) ARR D ARR
1 20 20 31
0.9 22 2 21 32 1
0.8 25 3 22 34 2
0.7 29 4 23 35 1
0.6 33 4 24 37 2
0.5 40 7 25 38 1
0.4 50 10 26 40 2
0.3 67 17 27 42 2
0.2 100 33 28 43 1
a
Change in ARR caused by a 0.1 ng mlK1 hK1 decrease in PRA or by a 1 ng dlK1 increase in PA.

Table 5. Plasma aldosterone (PA): how low can PA be for a positive ARR?a
PRA Immunoreactive renin Plasma aldosterone
ng mlK1 hK1 pmol lK1 minK1 mU mlK1 ng lK1 ng dlK1 pmol lK1
0.15 1.9 1.2 0.8 3.8 114
0.25 3.3 2 1.3 6.8 188
0.5 6.5 4 2.5 13.5 375
Cut-off for low renin is a PRA of 0.65 ng mlK1 hK1 b
1.0 13 8 5 27 750
2.5 32 20 12.5 63 1875
5.0 64 40 25 125 3750
a
See Table 3 for definitions of positive ARRs. Ferrari et al. [21] do not calculate the ARR below an aldosterone lower limit of 650 pmol lK1.
b
Laragh [1].

ambulation for at least 2 h, then seated for 5–15 min [3],
as discussed elsewhere in this issue of TEM.
Errors in the measurement of aldosterone or renin can
have a devastating effect on ARR and render it unin-
terpretable. Because plasma renin is in the denominator
it can have a large influence on the ratio (Table 4). Thus,
in a patient whose PA is 20 ng dlK1 and whose PRA
is 1 ng mlK1 hK1 a 0.1 ng mlK1 hK1 decrement in PRA
increases ARR by 2 units. Between 0.5 and 0.4 ng mlK1 hK1
the same decrement increases ARR by 10 units. Between
0.3 and 0.2 ng mlK1 hK1 it increases the ARR by 33 units.
Thus, the usual range of error of PRA and irR measure-
ments in this low range of renin that is found in most
patients with primary aldosteronism can lead to large
changes in the ARR ratio. By contrast, because plasma
aldosterone is in the numerator of the ARR, it has much
less impact on the ratio (Table 4).
Most groups who use ARR as a screening test use a
minimum cut-off of plasma aldosterone below which ARR
should not be calculated (e.g. 650 pmol lK1 in Ferrari et al.
[21]) because when plasma renin levels are very low,
plasma aldosterone levels as low as 114 pmol lK1 might
result in a positive ARR (Table 5).
In summary, to obtain an accurate ARR it is essential to
have an accurate estimate of plasma renin levels and to
identify a lower limit for circulating plasma aldosterone
levels. It is also essential to control for, avoid or take into
account all those factors that can influence the ratio and
make it difficult (and occasionally impossible) to interpret.
These are discussed elsewhere [2,3] and in other reports
from the First International Workshop on Endocrine
Hypertension.
Conclusion
A sensitive plasma renin test is essential for the accurate
diagnosis of low renin hypertensive states. At this time,
such sensitivity can be achieved consistently only with the
www.sciencedirect.com
PRA enzyme kinetic assay. Low plasma renin levels can be
detected by automated or manual direct renin tests that
utilize the sandwich radio- or chemi-luminescent immu-
noassay technique but with lesser accuracy and
reproducibility.
Specificity is of greater importance with the plasma
aldosterone test. Commercial laboratories could provide
assurance of specificity if an international standard were
made available for the assessment of crossreactivity.
DISCLOSURE: Quest Diagnostics currently purchases
its reagents for the PRA test from the Cardiovascular
Center Laboratory, Weill Medical College of Cornell
University. Quest Diagnostics performs the PRA test as
described by Sealey et al. [6]. Sealey and Laragh have no
financial arrangement or contract with Quest Diagnostics
but from time to time have served as consultants.
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AGORA initiative provides free agriculture journals to developing countries

The Health Internetwork Access to Research Initiative (HINARI) of the WHO has launched a new community scheme with the UN Food
and Agriculture Organization.

As part of this enterprise, Elsevier has given 185 journals to Access to Global Online Research in Agriculture (AGORA). More than 100
institutions are now registered for the scheme, which aims to provide developing countries with free access to vital research that will
ultimately help increase crop yields and encourage agricultural self-sufficiency.

According to the Africa University in Zimbabwe, AGORA has been welcomed by both students and staff. ‘It has brought a wealth of
information to our fingertips’ says Vimbai Hungwe. ‘The information made available goes a long way in helping the learning, teaching
and research activities within the University. Given the economic hardships we are going through, it couldn’t have come at a better time.’

For more information visit:

http://www.healthinternetwork.net

www.sciencedirect.com