Primary Renal Calculi: Anderson-Carr-Randall Progression?

Primary Renal Calculi: Anderson-Carr-Randall Progression?
Afthough numerous reports deal with the histology of renal
medullary calcification, there has been only limited application
of radiographic methods for its description. From routine
autopsy material, findings on 61 kidneys studied by high
resolution radiography are presented and related to those of
Randall (1937), Anderson (1945), Carr (1954), and others.
Histologically Anderson found microscopic plaques formed
from coalesced calcific “droplets” in the pyramids of practically
all of 168 kidneys, including some very young infants.
Carr, using microradiographic techniques, also found calcific
deposits in nearly all of 209 kidneys from patients over 9 years
of age. Anderson and Carr separately concluded that the
calcific deposits they demonstrated could, by migration, form
the subepithelial plaques that Randall observed earlier. The
present work illustrates some radlologic aspects of renal
calcification which seem to support a hypothesis that primary
renal calculi result, under certain circumstances, from the
migration of calcific deposits from the substance to the surface
of renal papillae. In order to emphasize the pathogenetic
sequence of the work of the previously mentioned authors, it
is proposed that the sequence of events be referred to as the
Anderson-Carr-Randall morphologic progression of primary
renal calculus formation. Proposals are made for additional
experimental work.
Although much literature relates to the role of the kidney
in the physiology and pathophysiology of calcium me-
tablism [1 , 2], the site of the formation of primary renal
calculi is still uncertain. This is illustrated, for example,
by some of the questions and answers given during
discussions of the subject at a recent National Research
Council Conference on the physical aspects of urolithia-
sis [3]. To the question whether a stone is formed in the
renal substance or at the outlet of the tubules, the
answer was that this is not known and that there are
several points of view [3]. To a similar question another
speaker replied that there was no certainty whether a
stone formed in the renal papilla or in the calyces
or perhaps even at a higher level than the papilla
‘ ‘ . . . where stones actually originate constitutes a
problem [3].
Whereas some of the pieces of the puzzle of primary
renal stone-formation seem to have been uncovered, a
definitive study putting them together into a recognizable
whole is still to be done. These include the observations
of Randall [4, 5] suggesting an “ initiating lesion”
arising from a subepithelial calcium-containing plaque
(Randall’s plaque); the finding by Anderson and Mc-
Donald [6, 7] that microscopic calcareous deposits in the
renal papilla are very common and may be normal; the
work of Carr [8, 9] who showed that calcium could
frequently be radiographically demonstrated in the kidney,
and who theorized that the function of the renal
Received July 6. 1978; accepted after revision January 29, 1979.
Radiology, Ltd., no. 59. 601 North Wilmot, Tucson, Arizona 85711.
AJR 132:751-758, May 1979
© 1979 American Roentgen Ray Society
ANDR#{201}BRUWER1
lymphatic system plays a critical role in renal stone
formation.
Building on an earlier proposal by Carr [8] and on
more recent work by Haggitt and Pitcock [10] on the
electron microscopic demonstration of renal parenchymal
calcification, the following hypothesis is stated:
1 . Histologically demonstrable calcium-containing
structures are normally present in the human kidney.
2. Under abnormal conditions the normally present
calcium accumulates in larger concretions which may
either remain within the renal parenchyma or may migrate
centrally, to the surface of one or more renal
papillae and may then become clinically significant.
Under these circumstances the calcium may be radiologically
detectable, either by clinical or experimental radiographic
methods, depending on the size of the accumulation.
Such abnormal conditions would include one or
more of many factors (e.g., biochemical, dietary, geographic,
hormonal, immunologic, etc). The extent of the
abnormal renal calcium deposition would depend on
whether the entire environment of the kidney (renal
macroenvironment) or only a small segment of the environment
of the kidney (renal microenvironment) had
been affected by such factors.
In the hope that an eponymous title will maintain a
focus on the pathogenetic unity of the contributions of
the original workers, the term Anderson-Carr-Randall
progression of renal calculus formation is proposed.
There is a remarkable lack of radiographic literature
dealing with the demonstration of renal calcific patterns
in autopsy material. I present relatively limited radio-
graphic findings from routine autopsy material, as they
seem to lend support to the findings of those observers
previously mentioned and to the hypothesis presented.
Certain observations suggest further work that might
define more clearly the pathogenesis of renal calculus
formation.
Materials and Methods
The material presented in this report was derived from 61
grossly normal (except for postmortem congestion) kidneys
removed at an equal number of autopsies. The 61 kidneys were
from 27 female and 34 male patients aged 14-83 years. Most of
the patients had died of conditions common to most busy
community hospitals: chronic pulmonary diseases, diseases
associated with arteriosclerosis, leukemia, and also following
various types of surgery and subsequent complications. The
state of hydration and nutrition and the biochemical composition
of each patient’s blood and urine prior to death unfortunately
were not recorded and cannot be determined in retrospect.
They might have provided interesting correlations with
the radiographic studies of the autopsy tissue. Although many
interrelated factors in the nutritional aspects of metabolic problems
are associated with urolithiasis, the patient’s fluid intake is
by far the most important factor relating to the actual formation
751 0361 -803Xl79ll325-0751 $0.00

752 BRUWER AJR:132, May 1979
Fig. 1.-A and B, 51-year-old woman who died of multiple sclerosis. A, Radiograph of slice of kidney. Papilla (arrow) shows fan-shaped calcific
pattern. B. Detail of A. C and D. 57-year-old woman who died of reticulum cell sarcoma. C, Radiograph of slice of tip of complex renal papilla
demonstrating fan-shaped calcific pattern. D. Detail of C. E, Alizarin red-stained full-thickness section of histopathologic preparation of renal papilla
(reprinted with permission from [11]).
or lack of formation of renal calculi according to Smith et al.
[2].
The kidneys we examined were part of a larger group (160
kidneys) removed for the purpose of vascular anatomic injections.
For various reasons the 61 cases used for this paper were
found to be unsuitable for injection studies.
Radiography was first performed on the intact kidneys. Subsequently
the kidneys were immersed in formalin for 2-3 days.
Longitudinal coronal slices about 4 mm thick were then made,
and the slices were radiographed.
All radiography was performed with Faxitron (Hewlett-Packard)
equipment and Eastman Kodak industrial type film, either
Type M or Type R, or both. The whole kidneys were exposed at
28 kVp and the slices at 16-18 kVp. Using a x7 calibrated hand
lens, we were able to see calcific particles of about 100 .tm and
perhaps even somewhat smaller.
In only 10% of these cases were radiographs that included
the renal areas taken prior to death. In none of these could renal
calcification be detected with any certainty.
Observations
Excluding calcification seen in arteriosclerotic vessels
and in one tumor, we found evidence of varying degrees
of parenchymal calcification in 39 of the 61 kidneys
examined. This seemed to confirm radiologically a num-

AJR:132, May 1979 PRIMARY RENAL CALCULI 753
A B C
Fig. 2.-A, 59-year-old woman who died ofemphysema and cor pulmonale. Radiograph of slice of kidney, considerably enlarged. Cortical margin on
right and pyramids at left. Numerous rounded 0.2 mm calcific densities throughout renal substance. B, 73-year-old woman who died with severe
arteriosclerosis, active pyelonephritis, and arteriolar nephrosclerosis. Radiograph of slice near renal surface, considerably enlarged. Much of the
calcification evident only under hand lens magnification. C, 66-year-old man who died with generalized arteriosclerosis. Radiograph of renal papilla.
Note many tiny globular and streaky calcifications extending throughout pyramid. Several large calcifications near tip. Because of the thickness of the
slice, some calcifications appear to lie outside contour of papilla. They are converging from bases of complex pyramid.
ber of calcific patterns previously described by others in
histologic material. Thus, we demonstrated the following
predominant patterns:
1 . A fan-shaped pattern of calcific streaks, focusing on
the tip of the renal papilla (figs. lA-iD). This pattern
conforms to the calcific pattern shown, for instance, in
the full-thickness photomicrograph of a renal papilla
illustrated by Cooke (fig . 1 E) [1 1]. This pattern was found
in 25 of the 61 kidneys, occurring in patients 28-83 years
old.
2. A second pattern, composed of spherical stipples of
calcification varying in size from being barely perceptible
through a x7 hand lens to about 0.2 mm, occurred in 23
kidneys of patients 14-77 years old . These calcific deposits
varied widely in number, from a few scattered or
clustered deposits to, in one case, a veritable cloud of
particles. Such particles could be seen in any part of a
kidney, but appeared to be more frequent in the medulla
(fig. 2).
In 10 patients calcifications conforming to both patterns
A and B were seen.
3. Another pattern, with the impression of calcific
spherules clustered in a mulberry pattern, was seen in
three middle-aged patients. One (fig. 3A) had an appearance
similar to a case described by Randall in 1 937 [4] . It
was triangular, about 4 x 1 .5 mm, and seemed plastered
against the side of a complex papilla in the region of the
fornix. An almost identical calcific density, identified as
a “Randall’s plaque,” was illustrated in figure 4 of the
article by Stewart [12], from a previously unpublished
radiograph attributed to Carr.
Photographic magnification of the “plaque” in my
case unexpectedly revealed that it was apparently com-
posed of multiple tiny spherules (fig. 3B). It is obvious
that this finding is identical to that of Carr in 1954 [8]. He
found that ‘ ‘radiographs of thick sections through papillae
with adherent stones confirm the view that in
reality the ‘plaque’ is composed of multiple concretions
aggregated together
A kidney from another patient showed a semispherical
calcific mass located along the lateral aspect of a papilla.
This 4.5 x 3 mm density also had a mulberry appearance.
A kidney of a third patient showed a 4-mm-diam
calcific deposit at the tip of a papilla (fig. 4A). Of interest
is the fact that the main calcific mass appears to be
“followed” by several smaller globular densities of the
type described by Carr [8]. Of additional interest in the
latter kidneys was the appearance of a striated calcific
pattern in another papilla, which also contained a few
tiny calcific spherules (fig. 4B). One can only speculate
that the renal papilla of figure 4A at one time might have
had the appearance seen in figure 4B.
Discussion
In 1937 Randall [4] first described his findings of a
“milk patch” at or near the tip of one renal papilla in 12
kidneys from 104 routine autopsies. These plaques were
visible by a hand lens and microscopically were seen to

754 BRUWER AJR:132, May 1979
A B
be subepithelial. In one kidney such plaques had eroded
through the papillary epithelium and had become the
‘ ‘initiating lesion” for the formation of a triangular mulberry
calyceal calculus plastered against the side of its
papilla.
Subsequently, Randall [5] reported such plaques as
occurring in 19.6% of kidneys examined in 1 154 autopsies.
He proposed that they developed in a small area of
degenerated papillary tissue.
In a recent microscopic study of renal med uliary calcifications
involving 200 kidneys from 100 randomly selected
autopsies, Haggitt and Pitcock [10] noted that the
renal papillae of 23 of the patients contained grossly
“l.
Fig. 3-58-year-old man who died
of bronchogenic carcinoma. A, Radiograph
of slice of kidney. Calcification
(arrow) near fornix of complex papilla.
B, Detail of calcification. Actual size
of calculus about 1.5 x 3 mm. Note
mulberry contour.
Fig. 4.-A, Radiograph of papillary
tip and calyx. Calculus at tip of papilla.
Note small, separate globular calcifications
migrating (?) toward tip. Also
fine calcific streaks in body of pyramid.
B, Another papilla from same
patient. Note striated pattern of calcific
stipples and streaks in pyramid
and calyceal wall.
recognizable Randall’s plaques. Figure 5 is reproduced
from their article, a beautiful illustration of the entity
known as a Randall’s plaque.
The work of Anderson and McDonald [6, 7] gave a
reasonable clue to the nature and origin of Randall’s
“initiating lesion.” In studying 148 surgically removed,
diseased kidneys and 20 apparently normal autopsy
kidneys, Anderson found microscopic evidence of calcareous
plaques or tiny stones in the parenchyma of
renal pyramids in almost all specimens [6]. In only three
grossly diseased kidneys, all from patients under age 2,
he did not find such calcific deposits. Anderson pointed
out that his determinations were made from an average

AJR:132, May 1979 PRIMARY RENAL CALCULI 755
Fig. 5.-Subepithelial calcium deposit (Randall’s plaque) at lateral
margin of renal papilla reduced from x35 (reprinted with permission
from [10]).
of only three microscopic sections per kidney. He estimated
that it would take 10,000 microscopic sections to
completely examine a kidney with 10 pyramids.
Anderson [6] cited two “generally accepted postulates
regarding kidney physiology’ ‘ and correlated them with
his microscopic findings, proposing as a result ‘ ‘a somewhat
different interpretation of the etiology of kidney
stones” from the one proposed by Randall. The postulates
to which Anderson referred were: (1 ) the concentra-
tion of calcium and related ions is high in the tissue
fluids about the renal tubules, and (2) phagocytic cells,
probably macrophages, are abundant about renal tu-
bules, and macrophages have an affinity for calcium.
The interstitial calcareous plaques (microplaques)
demonstrated by Anderson seemed to be the result of
coalescence of innumerable microspherules of calcareous
material. Anderson referred to the microspherules
as ‘ ‘droplets.” These “droplets” were apparently formed
as a result of calcareous material being absorbed by
phagocytic cells, these cells subsequently dying and
leaving calcareous “droplets” in the interstitial tissues
(fig. 6).
Location of these ‘ ‘droplets’ ‘ beneath the epithelial
covering of the renal papilla might be followed by erosion
of the epithelium. Anderson proposed that Randall’s
plaques were probably the result of aggregation of microcalculi
which he had described and not due to primary
degenerative changes in the papilla.
Carr’s work [8] offers the best radiographic studies to
date. Unfortunately Randall, Anderson, and Haggitt and
Pitcock [10] did not use radiography in conjunction with
histologic methods. Carr examined , by extremely sophisticated
radiographic techniques, 98 partial nephrectomy
specimens and 1 1 1 kidneys obtained at autopsies from
patients dying of nonrenal causes. Intact kidneys and
slices of kidneys were radiographed. Extremely thin
slices were examined at voltages so low that a vacuum
had to be used between the tube and the specimen,
some exposures lasting 24 hr. Fine-grain film allowing
4
v’-. ...‘
r
i:
Fig. 6.-Photomicrograph from section of pyramid of pyelonephritic
kidney (x700). Clearly apparent coalescence of microscopic “droplets”
and of such droplets into calcific plaques. (Reprinted with permission
from [7].)
magnification of 200-300 diameters was used. He found
that, in practically all kidneys from patients over age 9,
small concretions just visible to the naked eye could be
demonstrated. Usually one or two could be seen, but
some kidneys contained a dozen or more. The majority
of these concretions, when they reached a diameter of
about 0.2 mm, were spherical. Some were as large as 1-2
mm in diameter.
Carr’s concretions were primarily located in three
regions: (1) just outside the calyceal fornices or at the
sides of the renal pyramids in line with the interlobar
vessels; (2) in the corticomedullary junction zone; and
(3) immediately beneath the renal capsule.
An aggregation of these concretions could in some
kidneys be seen in the region of the fornix or adherent to
the side of a papilla, and such ‘ ‘plaques” could be seen
to be composed of numerous macroscopic round con-
cretions, much as Anderson’s microliths were composed
of numerous microscopic “droplets.” Even when a large
stone formed at the tip of a papilla, smaller ones were
seen behind its base. This would seem to match our
figure 4A.
So consistently did Carr, radiologist, and Stewart, his
surgical colleague, find small concretions in the region
of the fornix (just extrinsic of the forniceal lumen) that
they have used, respectively, the terms Stewart’s nest [9]
and Carr’s pouch [12] in their publications.
Carr suggested that because the microliths demonstrated
by Anderson are apparently a normal phenomenon,
one must account for the way in which the body
disposes of them. He proposed that this function is
performed by the lymphatic system. Carr cites the work
of Goodwin and Kaufman (cited [9]) and of Rawson [13]
on the lymphatic system, and indicates that the renal
lymphatic system undoubtedly plays an enormously vital
“cleansing” role in the kidney. To quote Carr [9]:
We know that in the lungs particulate matter
inhaled gets into the alveoli, and then it is
taken up in the lymphatics and transported to
‘
‘.

756 BRUWER AJR:132, May 1979
where it can do no more harm, as long as the
mechanism is working properly. I believe that
the kidney functions in the same way. I think
that effete cells, debris of all sorts, calcium
which has been re-absorbed and come out of
solution in the interstitial fluid where there is
always debris available to act as a nucleus to
precipitation all get removed with the protein
and interstitial fluid into the lymphatics.
Carr postulated that any abnormality that can result in
overload of calcium in the kidney, or interference with
lymphatic drainage, could result in overproduction of
microliths and the development and accumulation of
larger concretions. The rounded shape of the latter, he
postulated, can be attributed to their being molded in
lymphatic channels. Any of these concretions (macro-
liths formed from microliths) could eventually erode into
the calyceal lumen. They may be washed out or, by being
adherent, grow in size in a calyx. Because of microregional
pathologic changes in the kidney, calculi would
tend to re-form in the same region after having passed or
having been removed without resection of the involved
area.
Epstein [1] pointed out that the glomeruli of a healthy
adult filter about 9-1 0 g of calcium per day and that 98%
of this is reabsorbed by the renal tubules. Ullrich and
Jarausch (cited in [1]) believed that the calcium content
of the kidney manifests a gradient, the concentration
being progressively higher toward the papillary tip. Such
a chemical gradient was confirmed by the work of Cooke
and Rosenzweig [14]. They found, by chemical analysis
of calcium content in samples of kidney tissue, evidence
of a calcium gradient in the human renal medulla, the
highest values being in the region of the papilla.
Cooke [11], in a careful histologic examination of 62
apparently normal kidneys, found calcification in 43
cases (69 %). Calcium was seen in the papilla in all these
cases, usually in substantial amounts, and occasional
deposits were seen in the outer medulla in 20 cases. In
nine cases calcification was seen in the cortex. Cooke’s
study showed that the location of papillary calcification
was invariably in the basement membrane of the long
loops of Henle, which descend for variable distances
into the medulla, sometimes as far as the papilla. Although
some showed evidence of calcium in all parts of
the kidney, all showed calcium in the papilla. Cooke did
not find calcium to lie free in the tubular lumens. Figure
1E, reproduced from Cooke’s article, shows the fanshaped
calcific pattern, similar to that which we frequently
encountered in our radiographs.
Anderson [6], too, concluded that the microscopic
collections of calcium ‘ ‘seemed to occur anywhere ex-
cept within the lumen of the tubule. A few specimens
were found with the deposits within the tubules, but it
seemed to me that they had eroded into the tubules from
the surrounding parenchyma.”
We should make reference to the work of Vermeulen
et al. [15] on experimental calculogenesis. For example,
by mixing oxamide in the diet of rats, they could rapidly
produce spectacular oxamide deposits that extruded
from the papillary tip. Streaks of oxamide crystals could
be shown to involve the renal papillary substance exten-
sively and these deposits were described as being ‘ ‘ in
the collecting ducts” [15], that is, quite unlike the find-
ings of Anderson and Cooke in humans. Vermeulen et
al. speculated that such accumulations usually “abort
into the pelvis” and, being small enough, presumably
usually wash out. But occasionally a small piece might
be caught at the ostium of a duct of Bellini, thus
providing an “embryo” upon which, under the right
circumstances, crystallization would result in the devel-
opment of a calculus.
Carr [9] does not believe that the work of Vermeulen et
al. is relevant to the process of so-called primary renal
calculus formation. He believes that their experimental
results relate to nephrocalcinosis (i.e. , “a totally different
disease process to that of calculus formation”).
Spheroidal morphology may have special significance.
I was struck by the fact that many of the calculi demon-
strated in the study material conformed to the spheroidal
pattern described by Carr [8]. I also noted, as did Carr,
that concretions might lie in a line or a chain. Another
appearance that I noted was that spherules tend to
cluster in the region of the papillary tip, sometimes
seeming to follow a large calculus which appeared to be
composed of multiple macrospherules in a mulberry or
botryoidal pattern (figs. 3 and 4). Spheroidal geometry
seems to play a basic role in the life cycle of primary
renal calculi, from the microspheroidal stage to macro-
spheroidal agglomerations.
Haggitt and Pitcock [10] performed light and electron
microscopic studies of renal medullary tissue obtained
at necropsy from 100 patients aged 18-91 years. In
all 100 pairs of kidneys examined, they were able to
demonstrate minute laminated spherules which stained
for calcium in the medullary interstitium and in the
basement membranes of collecting ducts (fig. 7A). One
of their illustrations of a typical spherule, enlarged
x54,000, demonstrates the lamination of these bodies
beautifully (fig. 7B).
Doyle et al. [16] recently demonstrated concentric
layering in concretions smaller than 50 m obtained
from mollusk kidneys (fig. 8).
Boyce [17] observed calcium and phosphate-contain-
ing microspherules and macrospherules by light, elec-
tron, and scanning electron microscopic analysis of
calculi recovered from 28 patients classified as “idio-
pathic oxalate or phosphate stoneformers.” Lamination
was a common finding in their material.
Anderson and McDonald [6, 7] and Haggitt and Pitcock
[10] found a strong tendency for aggregations of the
concretions which they had described to migrate into a
subepithelial location in the renal papillae, that is, for the
formation of Randall’s plaques, with a consequential
proclivity to erode through the epithelium and initiate
the development of a free calculus.
Conclusions
Hypothesis of Anderson-Carr-Randall progression of
primary renal calculus pathogenesis. Anderson’s histo-
logic studies demonstrated the ‘ ‘normal” presence of

AJR:132, May 1979 PRIMARY RENAL CALCULI 757
Fig. 7.-A, Reproduction of laminated
electron-dense bodies in basement
membrane of collecting duct.
Duct epithelium shows postmortem
degeneration. Reduced from x21 .000.
(Reprinted with permission from [10].)
B, Laminated electron-dense body in
interstitium, surrounded by collagen
fibrils. Reduced from x54,000. (Reprinted
with permission from [10].)
A B
Fig. 8.-A, Tissue section (6 Mm thick) of Argopecten irradians kidney choked with phosphorite concretions. Note concentric layering of
concretion (A). H and E stain. (Reprinted with permission from [16]. B, Close-up of concretion from kidney of mollusk Mercenaria mercenaria,
showing microbotryoidal texture (compare human “mulberry” texture). (Reprinted with permission from (16].)
calcium in the tissues of the renal papilla, work that has
been confirmed by others [10, 11]. Carr’s radiologic
studies have substantiated, at the microradiographic
level, Anderson’s original work. Only the impossible-
moving pictures of the drift of Anderson’s and Carr’s
calcific deposits from a locus within the substance of a
papilla to a subepithelial location near or at the surface
ofthe papilla-could “prove” that Randall’s subepithelial
plaques and “initiating lesions” originate from deeper
calcific deposits. I believe that the circumstantial evi-
dence is overwhelming and there is useful logic in
thinking of the formation of primary renal calculi as
being initiated by a pathogenetic progression that I
propose to call the Anderson-Carr-Randall progression
of primary renal calculus formation.
Much more correlated information is needed concerning
histopathologic and radiographic findings on much
larger ‘ ‘normal” populations, under known conditions of
hydration and nutrition. Investigations such as those
being performed on the renal lymphatic system by Clark
and Cuttino [18] are also of interest. For example, can
methods of “sifting” the main renal lymphatics for calcareous
microspherules under varying conditions of diet
and hydration be developed? Or can the main renal
lymphatics be obstructed with a view to subsequent
radiologic and microscopic evaluations of the renal papillae
for evidence of Carr’s concretions and Randall’s
plaques?
Because of the common finding of calcific microspherules
in the tissues of the renal papilla histologically and

758 BRUWER AJR:132, May 1979
radiographically, might one speculate, for example, that
some or many cases of microhematuria might be due to
erosion of these tiny plaques into the lumen of the
urinary tract, and might electron microscopy of the
urinary sediment from such patients be worthwhile?
Furthermore, because the degree of physioloic hydration
apparently affects the extent of the presence of
calcium within the renal papilla and presumably, therefore,
the chance of calculus formation [2] , might electron
microscopy of urinary sediment under various conditions
of hydration perhaps be expected to yield, or not to
yield, microcalculi?
We know that calcific “droplets” and microcalculi
commonly exist in the renal pyramids. We also know that
small , subepithelial calcific plaques composed of calcific
microspherules are not uncommonly found in renal papillae,
and that the epithelial cover of these plaques can
erode to allow them to become ‘ ‘initiating lesions’ ‘ for
free primary calculi. Short of proving a central-to-surface
drift of microcalculi by serial imaging, it is possible that
additional pieces of circumstantial evidence in the form
of investigation of the lymphatic system and urinary
sediment under various conditions of controlled hydration
and nutrition and other variables, might “ prove” the
Anderson-Carr-Randall progression hypothesis.
ACKNOWLEDGMENTS
I thank Dr. Mary-Ellen Shields for assistance with this project;
and Richard Durbin, Dr. Richard Armstrong, and Dr. Gerd
Schloss, Tucson Medical Center.
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