I. Clinical
and
Pathologic
Calcium
Oxalate
Findings
in a
Patient
with
Nephrocalcinosis
Thomas
H. Shepard,
II, M.D.,
S. Allison
Creighton,
M.D.,
Edwin
G. Krebs,
M.D.,
Lou-sein
W. Lee, M.S.,
andHorace
C. Thuline,
M.D.
Departments of Pediatrics (T.H.S.) and Biochemistry (E.G.K., L.W.L), School of Medicine, University of Washington, and Department of Pathology (S.A.C., H.C.T.), Children’s Orthopedic Hospital, Seattle
The I)atiellt was a \Vllite male who developed ilematuria, pvuria and recurrent fever at ii months of age and died of renal failure at the age of 7 ‘ears. The diagnosis was suspected because of the roentgenographic demonstration
of nephrocalcinosis in the absence of any demonstrable abnormality of calcium metabo-lisni and confirmed by the demonstration of in-creased excretion of oxalate in the urine.
(Accepted September 15, 1959; submitted May 18.)
This study was supported in part by the U.S.S. Bremerton Fund, Bremerton, Washington. ADDRESS: (T.H.S.) Seattle 5, Washington.
PEDIATRICS, April 1960
PRIMARY
HYPEROXALURIA
P
RIMAIIY IlvpelOxaluria, a disease fre-quentlv beginning early in childhood,is associated with abnormally high oxalate
excretion in the urine and usually results in
(heath (Itle to renal failure from progressive
calcium oxala te npoa9 Tile
term “ri1nary ilvperoxaluria was
intro-duced by Archer et
al.’
in order todif-ferentiate tile disease from two unrelated
conditions : 1) hlyf)eroXaltlria secondary to
ingestion of oxalate and various poisons,
and 2) recurrent renal stones composed of
calcium oxalate without increased urinary
excretion of oxalate. The apparent rarity of
the disease and the difficulty in chemical identification of oxalate have resulted in relatively few cases being diagnosed and
studied during
life.
. Il. 14. 19The
authors wereable
to
find 24 case reports in themedical literature which were sufficiently
documented to satisfy the criteria for
diag-nosis of primary hyperoxaluria (Table I).
It IS tile purpose of this paper to describe
and discuss tile clinical and pathologic find-ings in another case. Certain additional
genetic and metabolic studies will be
re-porte(I in subsequent papers.
CASE
REPORT
History
The mother’s pregnancy was complicated by
severe nausea. The birth (April 6, 1951), was normal and the infant weighed 3. 19 kg. He gained weight normally and was fed a prepared
milk mixture supplemented by a preparation of
multivitamins which provided 1,000 units of
vitamin D. Although the liquid intake orally
was excessive after about 2 years of age the
patient had neither craving for, nor history of,
ingestion of foods containing excessively high quantities of oxalate. The intake of orange
juice was somewhat more than usual, 6 to 10
oz/day, and meat dishes were preferred to
sweets. His developmental landmarks,
intelli-gence and dentition were within normal limits.
The height progressed between the 25th and 50th percentiles and the weight remained close
to the 75th percentile.2021 The family history
was unremarkable and the parents were
un-related. The presence of excessive output of
oxalate in other healthy members of the family
suggested that the hvperoxaluria might be a dominant characteristic; this point will be
developed in more detail in a subsequent
paper. There was no family history of any type of renal disease.
The patient was elltirely well ulltil the age of ii months when he commenced having
re-current attacks of fever associated with pyuria and microscopic hematuria, which led to
hospi-talization for urologic studies at 22 months of
age. Specific gravities of urine were 1.009 and
1.004 and a trace of albumin was present. There were no cellular elements and no
un-usual crystals. On later occasions calcium
oxa-late crystals were observed but not in excessive
amounts. Subsequently slight pyuria and
oc-casional microscopic hematuria were noted.
l)r. C. Thomas Stewart.
any calculi, but the areas of tile renal pyramids vere radiopaque (Fig. 1). Reported
determina-tions of serum calcium were within normal
range and there was no excessive intake of
vitaniin I). At a later time the excretion of oxalate in the urine was found to i)C markedly
elevated (80 to 4:30 mg 24 hr) as compared to
the normal (less than 50 ng 24 hr).
Physical
Findings
Physical exanlination at the age of 41
rcveale(l a healthy active box’. The ileight
‘as 105 cm and the ‘eight 41 kg. Blood
Iresstlre was 80, 62 mm Hg and remained
within iiornial liniits. His color and muscular
de-velOj)fllellt were normal. \Vhen he was 6% ears of age a slightly enlarged firni spleen was first noted and peisisteci. l)uring the last 6 months of
I ife, sniall nonraised yellow sul)conjunctival areas were noted on the lids. A consultant oph-tiialmologist#{176} stated, “This yellowish waxy look-ing niaterial is ill the tarsal glands of Meibomian dn(I has collected there without the norlnal
amount of extrusion. This picture is seen not
unusually III persons 35 \ears of age or older.”
B’ slit lamp examination, no crystals were
detected in the lens or cornea.
Laboratory Findings
Laboratory results are listed in Table II.
These were niainlv notable for the progressive
chemical l)ictslre of uremia and for the eleva-tion of 1)100(1 uric acid. Serum magnesium was
2.0 mg. 100 IflI. Carbonic anhydrase in whole
1)100(1 was e(luivalent to tile control values.
Clutaniic-oxalacetic transammase was 4:3 units.
The amino acid pattern of urine was normal as determined b high voltage paper
electro-pioresis. There was no increase in urinary excretion of glvcine. During tile years 1955 and 1956 the total 24-hour urine volume ranged from 1,000 to 1,500 1111 and in 1957 alld 1958
l)etween 1,500 and 2,500 ml. In 1956 the urea
clearance was 50 of normal. The enclogenous creatinine clearance was 16.4 ml /inin (normal 50 nil ‘mm), and the phenolsulfonephthalein test was 47% in 2 hours. The highest recorded
specific gravity was 1.015, but during tile last year it was seldom over 1.012. The pH of
freshly voided urine was usually between 4.5
and 6. Oxalate crystals in the bone marrow were
not found in 1956 nor ill the spring of 1957. The
FIG. 1. Abdomen showing opacities in the areas of the renal 1yraniids and the faint outline of the
kidneys.
bone niaturation and structure as examined roentgenographically were normal ill 1956 and 1957.
Treatment
and
Course
A number of dietary and therapeutic trials
were carried out and xviii be reported in a
sub-sequent paper. The effects of dietary oxalate,
protein, carbohydrate, glvcine, cortisone,
vita-mill C, magnesium and riboflavin were
as-sessed. Because the urinary excretion of oxalate was proportional to the urinary excretion of
ni-trogen, the patient was treated during tile last
3 months with a moderately low protein diet.
Aluminium hydroxide was also added to the
diet to reduce absorption of phosphate, and ferrous sulfate was given in an unsuccessful
attempt to increase the concentration of hemo-globin.
In February, 1958, 4 days after a 5-day trial
period with 10 gm of glycine added to the diet
daily, the patient developed frequency and
dysuria and was found to have two calculi in
the bladder. This was the first evidence of
stones in the urinary tract. These stones were
TABLE I
DATA FROM REPORTED Ct.s:.s or PRIMARY HYPEROXALURIA WITH CALCIUM OXALATE NEPIIROCALCINOSIS
Autho, Sex Family
History
Presenting
Symptoms
Age of First
Symptom
(yr) Age
of
Deal/i
(yr) Urinary
Oxalate Ezcrelion
(mg/day)
Blood Uric
Acid
(mg/100 ml)
CaJ.thim
Oxalale
in
Urine
Calcium
Ozalale in Bone
Comments
Lepoutr& M - Renal stones 41 - - - + - No details.
\ischer’ M Neg. I)iphtheria &
uremia
11 11 - - + + No urinary calculi.
1)avis et al. M Neg. Intermittent fever, polyuria,
polydypsia
3 1 - - + +
Carson eLa1. M - Uremia ‘, ,‘, - - + Neg. No urinary calculi.
Ostry5
‘..,.
M - Hematuria l 8 - 4. + Neg. Surgical exploration of
neck; normal parathyroid.
Cliou & I)onohue’ M Po.i’ Painless hematuria
7 - - + +
Von Zollinger & Rosenmund7
M Neg. Dyauria & frequency
3 4 - - + + Klippel.Feil syndrome;
No urinary calculi.
Newna & Black#{176} F Pou Pasaed renal stone
8- 9-18 - +
x-ray
Neg. Bone marrow negative for crystals at the age of 1.
Aponte & Fetter9 M Pou.#{176} Frequency &
nocturia
5 16 OO 8.0 + +
M Pos” Ilematuria 10 13 ISO 8.0 + +
M Pos Costovertebral pain
7 90 - 7. + Neg.
Burke et al.’#{176} M Neg. Hematuria 3 1 1f3 - - + + Crystals in spleen & liver.
Dunn” F Neg. ilematuria 4 l5f - - + + Bleeding and low platelets;
parathyroids explored.
Neustein et al.12 M Pos” Pain with
urination
4 - - + + Bleeding from the
gastro-intestinal tract terminally.
Lund &
Reske-Nielsen13
F
-
-
Neg. Renal stone SS55
36 - - +
-F Neg. Renalotone 40 -
-
- +-Archer et at.” M Neg. Ilematuria &
passing stone
1 alive I6-9O 3.8 +
-F Neg. Renal pain & hematuria
4 alive
10
11O-65 5. +
-I)e Toni t.t al.1 M Neg. Poor appetite,
dwarfinm
6 11 - - + + Ichtheosis.
Edwards” F Pos.1 Renal pain. passed stone
35 38 - I I.8 + - Crystals in myocardium
and testes. Calcium
oxa-late monohydrate by x-ray
diffraction. No urinary calculi.
aFather passed a renal stone.
bBrother died at 8 years of age with renal stones. Maternal great uncle passed five stones. CIdentical twins.
dBrother of twins.
1 An uncle had renal stones.
fPatients were brothers. A sister died of renal disease. Atwin brother of one died of “stomach trouble’ associated with persistent vomiting at 8 months of age.
Author S(Z
M
Family
history
Presenting
Symptoms
.4ge
of First
Symptom
(ye) Age
of
Death
(yr) Urinary
Oxalale
Excretion
(mg/day)
Blood
Uric Acid
(mg/tOO ml)
Calcium
Oxalate
in
U,ine Calcium
Oxalate
in
Bone
Comments
Pos.1 t - - + - Calcium oxalate
monoh-(Irate by x-ray diffraction. No urinary calculi.
l.,inl” M Neg. Passed renal
stone
3 2 - - + +
Siniko’ l Neg. Pyuria Il - - + + I)etailed renal function
studies.
Godwin ci al.” ‘SI p05#{149}e Renal stone 5 10 130-180 - + +
‘liepard et al. ‘SI Pos. Recurrent fever & pyuria
ll/1 7 80-430 7. + +
FIG. 2. Kidneys on cut section showing renal stones and the granularity of the cut surface.
TABLE I-(Continued)
re(luce the weight of the powdered stone, but there as a 1.2% weight loss when it was dried
ill an OVCfl at 1 10#{176}Cfor 2 hours. Following the removal of the stolleS, the patient’s urine
re-mained bloody for several da’s, at the end of which he required transfusion because the con-centration of helnOglol)ifl had decreased to 2.5
gIll, ‘100 ml. He did not have any clinical signs
of a (lefect in coagulation of blood.
During the next 2 months, the patient’s gen-eral condition gradually deteriorated and he died of uremia associated with collvulSions on
May 11, 1958.
Necropsy Findings
Gnoss EXAMINATION: The body was well
developed, moderately nourished, and meas-ured 120.6 cm in length. The lungs showed
rather edematous cut surfaces but no evidence
of pneumonia. The blood in the heart chambers was unclotted. The myocardium was firm and of normal color. The thymus gland weighed 18
gm and was not remarkable on section.
Kidneys. The most significant findings were
in the kidneys (Fig. 2). The right kidney
weighed 30 gm, the left kidney 50 gm (normal
TABLE II
LABORATORY DATA
March-April June-August Dec. 1955
1956 1957
Feb-March 19.8
Blood urea nitrogen (nlg/100 Inl) 4 30 53; 60; 10
Carbon (lioxide content (meq/l) 17 3 16
Chloride (Iueq/l) 103 111
Calcium (mg/tOO ml) 10. 11.3 9.5 9.4
Phosphorus (mg/100 tiil) 4.6 4.7 4.7 8.
Alkaline phosphatase (Bodanskv units) 9.1 10 10 13
Fasting blood sugar (mg/100 ml) 89 103
‘Fetal protein (gm/10() 1111) 7 7.0
;\.IbuIllin/globulin (gin/l0O lab 4. .8
Serum uric acid (mg/100 ml) 7. 6.7; 5.4 6.4; 9.7; 8.4
Creatinine (mg/tOO ml) 1 .96
Hemoglobin (gm/100 ml) 13.1 1.3 7.7
Cholesterol (mg/ 100 ml) l4
Urinary calcium (mg/4 hrs) 107w
* While receiving regular diet. Average of 10 determinations; range 0 to 8.6 mg/4 hr.
stripped with slight difficult, revealing the external surfaces to be grayish-yellow to
brownish-red ill color and exhibiting a rather fine granularity. On section, the cortico-medul-lary ratio appeared to be generally maintained
and there was a filie granularity throughout all areas. In the calyces and pelvis of both kidneys were itinierots calculi, appearing slightly
yel-lowish with a frequent orange tint. Others
pre-Selitedi a gray to brown-red appearance.
See-tion through all areas of the kidney presented a grating seiisation against the cutting edge. The
ureters appeared to be of normal size and were
patent throughout. The urinary bladder showed
some redundancy of mucosa but otherwise was not remarkable except for a thickened wall.
MICROSCOPIC EXAMINATION : Sections from
the various organs were examined after fixation
ill 10% formalin and staining with hematoxylin and eosin. The sections were examined under 1)0th the light microscope and the phase micro-scope.
Kidneys. The kidneys contained large num-bers of anisotropic crystals which were
gen-erall’s faintl’s greenish-yellow or colorless (Fig.
3). The crystals varied in size and shape, hut
gellerall\ were seen to be rhomboidal and
fre-quently arranged in a rosette fashion. In other
nlstances they resembled the “sheaf of wheat”
j)attern. These crystals were mainly located in
the cortex with lesser mllnbers in the medulla,
and within the tubular lumina, whose lining
epitheliurn appeared to be markedly flattened.
Crystals occasioiiall’ were seen in glomeruli, and sometimes in the interstitial tissues. Other
features were scattered areas of round cell infil-tration in the interstitial tissues, some fibrous
tissue proliferation and hvalinization of
glomer-ular tufts and thickening of Bowman’s capsules. In some instances the glomeruli were
com-pletelv fibrosed and hyalinized, while in others
there was a partial replacement of the
glomer-ulus. The total number of glomeruli was re-duced. The arterioles showed some thickening
and hypertrophv. There was no acute
inflam-matorv reaction in the sections.
Other Organs. Microscopic sections revealed the presence of anisotropic crystals in the heart, lungs, spleen, thymus (Fig. 4), thyroid,
squam-ous epithelial layer of the esophagus, cartilage
of the trachea, muscular layer of the digestive
trace, bone marrow and lymph nodes. The
see-tions were not remarkable except for the
pres-ence of the crystals and there was no foreign body giant cell reaction. Sections of the para-thyroid glands were not obtained.
The organ weights, with normal weights in
parenthesis, were as follows: heart, 104 gm (100 gm); lungs, right 260 gm (130 gm), left
200 gm (123 gm); spleen, 120 gm (66 gm);
liver, 926 gm (680 gm); adrenals, combined weight 13 gm (4.3 gm); and thyroid, 10.5 gm.
SPECIAL STUDY OF CLOTTING: To investigate
the possible role of the elevated concentration
587
FIG. 3. Microscopic appearance of the kidney showing the crystals.
(x220.)
FIG. 4. Thymus showing a crystal in a Hassall’s body. (x655.)
in the frozen state for 6 months was found to
contain no prothrombin b the methods of Owren (true prothrombin time) and Quick. No flbrinogen could be detected by the
turbo-metric method of Fowell.23 The addition of
cal-cium chloride did not cause a clot and no humoral anti-coagulant could be detected by
DISCUSSION
Clinical Features
In the medical literature 24 cases of
primary hyperoxaluria, reasonably authenti
cated, were found (Table I). Two of the
cases reported by Zollinger and
Rosen-mund7 and the case reported
by
Laasm4
were excluded because there was reason-able doubt that they represented the
pri-mary form of oxalosis. Burke25 has recently
reviewed the clinical findings. Although six
cases in females have been reported, the
disease occurs predominately in males. The
diagnosis in most of the cases was based
On characteristic pathologic findings and in
only six was tile urinary excretion of oxalate
measured.
The onset was usually before 5 years of
age, and often death occurred in
child-ilOod or early adulthood. In five reported
cases’ 16 the patients were in adult life when the first symptom was noted. One of
the patients reported but unrecognized by
Arons et a!. #{176}also had onset of symptoms late in life. The most common first symptom
was hematuria or dysuria related to passage
of renal calculi, and in some there was
pain-less Ilematuria. Urinary calculi occurred in
all but four cases.2’ 4, I(
In
three
cases,
as
in the present case, the initial findings were suggestive of recurrent renal infection.However, during the observations made
(after age 42 years), the patient had no
clear-cut evidence of recurrent renal
infec-tion, and except for the single episode of
stones in the bladder and chronic polyuria lle had no other symptoms referrable to the
genito-urinary tract. In several reported
in-stances the presence of the disease in
an-other sibling was of aid in making the diag-nosis.
The growth of the children was usually
entirely normal, except in those who
termi-nally developed phosphate retention and
renal rickets. The muscle strength in the
majority of cases could be stated to be
normal. The main exception was the
hypo-tonia observed by Simko.18
The
presence
of
splenomegaly is not a common finding, but
in the present case there was definite clini-cal enlargement. Crystals of calcium oxalate
were
found
in the
spleen
and
at necropsyit was twice the normal weight. Infectious mononucleosis was excluded by a normal blood smear and absence of an appreciable rise in the heterophil titer. The yellow ma-terial in the Meibomian glands of the lids was not studied at necropsy. Similiar ocular findings have not been described in the
other
cases,
nor did other members of thefamily demonstrate similar accumulations.
It
would
be
important
to
examine
specifi-cally the eyes in future cases.
Laboratory Features
Radiopacity of the kidneys has been uni-formly present and is always bilateral. The nephrocalcinosis which resembles the
hy-percalciuric
type
is usually
more
prominent
in the
medullary
areas
and
the
presence
of
radially striated stones27 in the calyces is
often
demonstrable.
Arons
et
al.26 havepointed out that in the nephrocalcinosis seen rarely in chronic glomerulonephritis
the density is most prominent in the cortex.
Early in the course of the present patient’s disease, retrograde pyelograms suggested that no stones were present and that the greatest densities were in the areas of the pyramids.
Early in the disease tile concentrations of calcium in serum and urine have been
nor-mal,
but
later
the
picture
has
been
not
un-like
the
end
stages
of primary or secondaryhyperparathyroidism with increased
con-centrations
of
phosphate
and
decreased
calcium in the serum. As a result explora-tions of the parathyroid have been carried
out in some The best method
for
differentiating
the
two
diseases
at
this
stage is the examination of the urine for total content of oxalate. Albright
et
al.2
have reported the presence of oxalate-con-taming stones in primaryhyperparathyroid-ism.
ARTICLES
case reported by Wohl,28 there was
eleva-tion, but in 3 other the uric acid
in serum was normal. In the present case during the time when the blood urea
nitro-gen was not elevated a high level of uric
acid was present (Table II).
The
daily
urinary
excretion
of oxaiate
is
considered to be abnormal if over 50 mg.
In
primary
hyperoxaluria
the
urine
usually
contains more than 100 mg/day.
Occasion-ally
in samples
from
the
present
patient,
as
well as in others, isolated values within the
normal range have been reported. This may
be
due
to loss
by
precipitation
of calcium
oxalate in a metal container as has been pointed out by Archer et al.14
The
samples
should be collected directly into the glass
container which is finally sent for determi-nation. It is not possible to detect the in-creased amount of oxalate by microscopic examination of crystals in the urinary sedi-ment.
Examination of bone marrow during life has not been of diagnostic help. A common location for deposit of crystals is in the articular cartilage. Slit lamp examination of
the lens and cornea has so far not revealed
crystals.
Pathogenesis and therapy will be
dis-cussed in a separate paper. Although only palliative, the removal of stones from the
kidney and bladder has been the main form
of therapy.hl18
Pathologic Findings
The
pathologic
findings
have
been
dis-cussed in detail by Dunn1’ and Edwards.1#{176}
On gross examination the kidneys are gen-erally moderately reduced in size and the
cortical surfaces frequently granular and
stippled with small yellowish flecks. The
capsules are either adherent or readily
stripped from the kidney. A constant ob-servation is the gritty sensation on section of renal tissue. Calyces, and frequently the
pelves, contain yellow or tan-colored calculi
varying
in size.
Fibrosis
of the
parenchyma
may
be
detected
grossly
but
is not
always
a prominent feature.
The heart may show hypertrophy. Other
organs in general are not remarkable except
in some
cases
in which
parathyroid
hyper-trophy is described.
The main histologic findings occur in the kidney. The oxalate crystals character-istically are seen in rosette or in “sheaf of wheat” formation, not unlike sulfadiazine crystals. They are more concentrated in
the
kidneys
than
in other
organs
and
mainly
are
found
in the
cortical
zones.
The
crystals
are
present
in tubules,
glomeruh,
and
may
impinge on
the
tubular
epithelium,
result-ing in its destruction and extension of the
crystals into the interstitial tissues. In the
latter area, foci of round
cell
infiltration
and
fibrosis are usually seen, giving the picture
of
a chronic
inflammatory
reaction.
Rela-tively little foreign body reaction is found
around
the
crystals.
Glomeruli
show
vary-ing degrees of fibrosis, as
do
Bowman’s
capsules, and the vascular walls may he likewise thickened.
The
crystals
do not
stain
with
hematoxy-lin-eosin
and
the
results
of the
von
Kossa
stain
are
variable.
Analysis
of
the
crystals
by x-ray diffraction has revealed calcium
oxalate
dihydrate
except
for
the
study
by
Edwards.16 Godwin et al.19
have
in
addi-tion found tile anhydride form. The walls of arteries, thymus, and epiphyses are most prone to exhibit crystals. In five of the re-ported necropsies, crystals were seen in the
spleene
10, 12, 13and
in three
of these,
crystals
were
seen
in
the
liver.
One
might
expect
a
higher
concentration
of
crystals
in
tile
liver
if this
organ
were
the
site
of the
meta-bolic
abnormality.
The presence of unclotted blood in the
heart has not been previously reported in
this
condition.
Jaegers
and
Murphy2#{176}have
summarized
the
evidence
that
hyper-oxalemia might cause a prolongation of the clotting time. Because neither fibrinogen
nor
prothrombin
could
be
identified
in the
supematant of
the
unclotted
blood
in the
heart, it is assumed that a clot had been
formed
but
later
became
lysed.
This
post-mortem
lysis
has
been
studied
by
Russian
workers
and
is reviewed
by Biggs
and
SUMMARY
Tile clinical and pathologic findings in
a case of )rimary hyperoxaluria and calcium
oxalate nephrocalcinosis in a 7-year-old boy
are described and discussed in relation to
similar reported cases. The diagnosis was suspected because of nephrocalcinosis in
the absence of an abnormality of calcium
metabolism and proven by the demonstra-tion of increased urinary excretion of oxa-late. Splenomegaly and yellow deposits in
the
Meibomian
glands
are
described.
Acknowledgment
The authors wish to thank Drs. Joseph
Had-den and Ole Jensen for help in management of
the patient. Dr. Dave Fisher gave valuable aid
in regard to coagulation studies and Dr. Ru-dolph Vracko translated the German articles. Dr. Hi-soo Kim assisted in the pathologic study.
REFERENCES
1. Lepoutre, C. : Calculs multiples de voies,
urinaires chez en enfant (oxalate de
chaux): infiltration du parenchyme renal par des d#{233}p#{244}tscristallins.
J.
d’urol.,20:424, 1925.
2. Vischer, W. : Calciumoxalatschrumpfniere
mit Uraemie. Schweiz. Ztschr. f. Path U. Bakt., 10:286, 1947.
3. Davis,
J.
S., Klingberg, W. C., and Stowell,H. E. : Nephrolithiasis and
nephrocal-cinosis with calcium oxalate crystals in
kidneys and bones.
J.
Pediat., 36:323, 1950.4. Carson, s1.
J.,
Mtilloy, M., and Knutti, R.: Los Angeles Childrens Hospital clinicalconference, case 4: an unusual case of calcium oxalate deposits in kidney of
young infant.
J.
Pediat., 39:251, 1951.5. Ostry, H. : Nephrocalcinosis. Canad. M. A.
J.,
65:465, 1951.6. Chou, L. Y., and Donohue, \V. L.:
Oxa-losis: possible inborn error of metabo-lism with nephrolithiasis and nephro-calcinosis due to calcium exalate as pre-dominating features. PEDIATRICS,
10:
660, 1952.
7. Von Zollinger, H. V., and Rosenmund, H.: Ur#{228}miebei endogen bedingter
subaku-ter und chronischer Calciumoxalathiere
(Calciumoxalatnephritis und
Calcium-oxalatschrumpfniere). Schweiz. med.
Wchnschr., 82:1261, 1952.
8. Newns, C. H., and Black,
J.
A.: Case ofcalcium oxalate nephrocalcinosis. Creat
Ormand St.
J.,
June, 1953, p. 40.9. Aponte, C. E., and Fetter, T. R. : Familial
idiopathic oxalate nephrocalcinosis. Alli.
J.
Clin.
Path.,
24:1363, 1954.10. Burke, E. C., Baggenstoss, A. H., Owen,
C. A., Power, M.
H.,
and Lohr, 0. W.:Oxalosis. PEDIATRiCS, 15 :383, 1955.
11. Dunn, H. C. : Oxalosis: report of case with
review of literature. Am.
J.
Dis. Child.,90:58,
1955.
12. Neustein, H. B., Stevenson, S. S., and
Kramer,
L.
: Oxalosis withrenal
calci-liosis due to calcium oxalate.
J.
Pediat., 47:642, 1955.13. Lund, T., and Reske-Nielsen, E. :
Nephroli-thiasis and nephrocalcinosis with
cal-cium oxalate crystals in the kidneys and
other organs: report of two cases. Acta
path.
et. microbiol. scandinav., 38:353,1956.
14. Archer, H. E., Dormer, A. E., Scowen, E. F., and Watts, R. W. E. : Primary
hvperoxaluria. Lancet, 2:320, 1957. 15. De Toni, C., Durand, P., and Rosso, C.:
L’assalosi : una nuova malattia del ricambio a carattere tesaurismotico: ossglosi con ittiosi, nanismo renale rene
a ferro
di cavallo,
nephrocalcinosi
insufli-cienza renal globale. Minerva pediat.,
9:623,
1957.16. Edwards, D. L. : Idiopathic familiar
oxalo-sis. Arch. Path., 64:546, 1957. 17. Lund, T. : Cited by Archer et
18. Simko, I.: Oxalosis. Ann. pediat., 189:1, 1957.
19. Cod’svin,
J.
T., Fowler, M. F., Dempsey,E. F., and Henneman, P. H. : Primary
hvperoxaluria
and
oxalosis.
New
Eng-land
J.
Med., 259:1099, 1958.20. Stuart, H. C. : Standards of physical
de-velopment
for reference in clinicalap-praisement; suggestions for their
pre-sentation and use.
J.
Pediat., 5:194, 1934.21. Stuart, H. C., and Meredith, H. V. : Use of
body measurements ill the school health
program. II. Methods to be followed in
taking and interpreting the measure-ments
and
norms
to
be
used.
Am.J.
Pub.
Health,
36:
1373, 1946.22. Owren, P. A.,
and
Aas,
K.: The controlof dicumarol therapy and the
quantita-tive determination of
prothrombin
and
proconvertin. Scandinav.
J.
Clin. & Lab.Invest.,
3:201,
1951.
23. Fowell, A. H.: Turbimetric method of fibrinogen assay. Am.
J.
Clin. Path., 25:340, 1955.
Sam-CERHART S. SCHWARZ, \I.D. melrohren-nekrosen ill der N ieren.
Frankfurt Ztschr. Path., 55:265, 1941. 25. Burke, E. C.: Oxalosis, in Modern
Prob-lems in Pediatrics, 3rd Ed., edited by
Freudenberg, E., and Hauser, F. New York, Karger, 1958, p. 314.
26. Arons, W. L., Christensen, W. R., and Sos-man, NI. C.: Nephrocalcinosis visible by
x-ray associated with chronic glomeru-lonephritis. Ann.
mt.
Med., 42:260,1955.
27. Albright, R., Sulkowitch, H. W., and Chute, H.: Non-surgical aspects of the kidney stone problem. J.A.M.A., 113:
2049, 1939.
28. Wohi, H.: Nephrocalcinosis; a case report.
J.
Pediat., 21:382, 1942.29. Jeghers, H., and Murphy, R.: Practical as-pects of oxalate metabolism. New
Eng-land
J.
Med., 233:208, 238, 1945. 30. Biggs, R., and MacFarlane, R. G.: HumanBlood Coagulation and Its Disorders, 2nd Ed. Oxford, Blackwell, 1957, p.
150.
31. Archer, H. E., Dormer, A. E., Scowen,
E. F., and Watts, R. W. E.: Aetiologv
of primary hvperoxaluria. Brit. NI.
J.,
1:175, 1958.
ROENTGENDIAGNOSTIK BEIf NEUCEBORENEN
UND SAUCLING, Hermann
C.
Wolf,
M.D.
Vienna, Wilhelm Maudrich Publisher,
1959, 317 pp., $23.60.
The author, an assistant at tile Vienna Uni-versity Children’s Clinic and chief of its
Roent-gen Station undertook to publish this book 3
years after Swoboda, his predecessor, had
brought out his book entitled “The Skeleton of the Child.” The author stresses the great
value of short simple radiographic procedures
OIL newborns and infants which lead often to immediate clarification of the problem and
re-suit in useful surgery despite the fact that it is impossible to communicate with the patient at
such an early age of life.
The book is divided into three parts: Skele-tal system, Thoracic organs and Abdominal organs. Each part is preceded b a
demonstra-tion of normal radiographs of the respective
region.
The material presented is entirely up-to-date
and contains a world bibliography of the past
10 ears. Its reader soon appreciates how much
the United States has contributed to modern pediatric radiology and in what high esteem
contemporar\ American pediatrics is held in Central Europe. The book thus fulfills two vai-uable missions: 1) It brings American pediatric
radiology home to European readers,
particu-larly those who read only Cerman; and 2) it bridges the large vacant gap between the
earlier tradition of the Vienna University Chil-dren’s Clinic, when contributions to pediatric radiology were the order of the day (Escherich,
Rach, Wimberger and Priesel, to mention but
a few) and the present time when new interest and activity are stirring in that city’s medical
climate.
The bibliography appears at the end of each of the three parts of the 1)00k. Though it is
sub-divided according to organs, the reader would
welcome its being distributed over the pages
so that each subdivision follows the subject to which it refers. The discussion of congenital
heart disease is very wisely restricted to four pages and based on scout films of the chest alone. Only a minimum of text is used which
is confined to the description of the radiographic
findings. The reader is expected to be familiar with the basic pathology of the condition
dis-cussed. This lends the book a semi-atlas quality which is very pleasing.
The selection of material amid the reproduc-tion of radiographs are excellent.
The book fills a definite need because its subject matter is limited to diseases of the new-born and infants. It is a very welcome addition
