NoFMBER, 5967

SPECIFIC NEPHROCALCINOSIS OF CHRONIC

GLOMERULONEPHRITIS
B,y WILLIAM J. ESPOSITO, M.D.
Downloaded from www.ajronline.org by 182.1.21.21 on 02/01/20 from IP address 182.1.21.21. Copyright ARRS. For personal use only; all rights reserved

SUMMIT, NEW JERSEY

A R ENC HY N RI . calcification is de- ported and even more that are not appre-
tectable in most, if not all, kidneys ciated aS examples of this entity.
whether normal or pathologic. The major- The total available data on nepilrocal-
ity of these are microscopic but in some cinosis, in general, have never been suitably
patients the calcifications are roentgeno- collected or classified.
graphi cally demonstrable. Renal tubular The ctlrrent report atids 2 cases to the 7
calcification of such magnitude (excluding cited above.
dystrophic renal calcification of neoplasms
REPORT OF CASES
and tuberculosis) is termeti nephrocal-
cinosis. The name was coineti by Aibright CASE I. H.C., white male, age 32. Atimitted
eta!.’ in 1934 and at that time the condition on lantiarv 24, 1964 with clinical itnti labor:t-

was thought to be tiiagnostic of hyperpara- tory evidence ot urenlia. Blood urea nitrogen
on admission was 226 111g. PC cent anti the
thyroidism. One year later Lightwood’#{176}
blood pressure rangeti from 19OI4O to 190/130.
provided autopsy evidence of renal par-
Pertinent I)reiotss history reveabeti scarlet
enchymal calcifications in a patient with
fever at 10 years of itge.
normal parathyroiti glands, indicating that Clinical tiiagnosis ot chronic gbomeruboneph-
hyperparathyroitiiSnl was not the sole
cause of nephrocalcinosis. Since then tile
following disorders have also been inlpli-
cated : hyperchloremic acidosis, rnedullarv
sponge kidney, chronic pyelonephritis, vita-
mm D intoxication, sarcoidosis, idiopathic
hypercalciu ri a, chronic glomerulonephri tis
and carcinomatosis.
Of the causes enumerated above, chronic
glomerulonephritis is one of the least
freqti en t.

HISTORY AND INCIDENCE

A single case was reported in 1947 by

Vaughan et a/.’ Geraci and his associates7
tiescribed an essentially itientical patient
in 1950. Mortensen et al.’2 founti 6 in-
stances of nephrocalcinosis of which i was
associateti Wi th chronic glomertilonephri tis.
.Arons et (11.2 atltled 4 cases to the literature
in 1955.

It has been estimated that chronic glom-

erulonephritis accounts for 3 per cent of
cases of nephrocalcinosis.’4 However, the
true incitlence is tluite tincertain. ‘Fiie
paucity of reported cases is probably not a
FIG. I. Case i. Illere is an increase in renal density’
valid reflection of its true incidence. Un- caused by’ the granular calcifications in the par-
doubtedly there are many cases not re- enchyma. Note small regular renal outlines.

688
 VOL. 101, No. 3 Specific Nephrocalcinosis of Chronic Glomerulonephritis 689

ntis was made in 1958. A plain roentgenogram

of the al)domen showed small kidneys contain-
ing many granular calcifications in cortical
areas (i’ig. I
). Retrograde pveiography revealed
normal ot the collecting tracts
Downloaded from www.ajronline.org by 182.1.21.21 on 02/01/20 from IP address 182.1.21.21. Copyright ARRS. For personal use only; all rights reserved

it ilppeitritnce
(l”ig. 2).
‘I’here were ; short term atimissions t()r pen-
toneal tiialvsis earls’ In 1964. In Nlarch 1964

w.
adhesions preven ted further (iiiti ysis from
being accomplished. A Barr’ plastic cannula
wits inserteti anti tiialvsis re-established. -
T_II .l.

‘l’hree tiavs later he was sent to New York

City where, with his mother acting as donor, a
ren al transpbtn tation was performed. There was
1”ic. 3. Case s. 1-lyalinization of gbomeruli. Note ex-
ho urinary Ot1tlUt during the first 24 hours; tensive calcification in ttibules.
this was attril)utetl to rejection phenomenon.
I)espite 1T1tnV heroic measures, including 6-
rnercaptoptz
capstzbotomv
ri Il e
itOd
adflhili
corticosteroids,
istration , irradiation,
the patient
fl,*-
,‘

-‘ -
stzcctsnibed. bile postmortem sttitly confirmeti
the tliagnosis of chronic gbomerubonephritis
(l”ig. ,fl.

CASE II. 1\I.C.’I’., Negro male, age 47. FAltered

with complaint of recurrent headaches that had 1.,t
become )rogressivelV more severe titiring the
past , ‘ears.

Fic. . Case lintlings essentially identical to

1..T
is.
those in Case i. There are innumerable granular
calcitications that are primarily cortical in boca-
ti on.

Aibuminuria was first detected in 19c3 tiuring

a. hospitalization for pneumonia.
Ill 1963 he first developed severe parietal and
occipital headaches. ‘Ehe pittient wits hyperten-
sive and a “chronic renal disease” wits diag-
noseti.
1)uning admission in August i 966 the 1)100(1
pressure was 204.’ 130, urine specific gravity
I.ooc, blood urea nitrogen 100 mg. per cent,
24 hour urine for prteis 4 gm. and creatinine
I I .2 mg. per cent.
A plain roentgenogram of the abdomen re-
vealed innumerable tiny punctate calcifications
diffusely scattereti throtighout the renal par-
enchvma (i”ig. 4). A roelltgenoiogic diagnosis

I of
File
chronic
patient
giomeruionephritis
wits placed (Ml a 500
was
111g.
offered.
sotiiulll
11G. 2. Case i. Normal appearance of the collecting diet 1)tlt the bbooti tirea nitrogen rose to 141 mg.
systems dem onstrated 1y’ retrograde pyebograph y. per Cent. At this time he wits placed Ofl essential
 690 William J. Esposito NOVEMBER, 1967

amino acid diet containing oo gm. protein and tis is associated with larger deposits and a
800 mg. of sodium. The blood urea nitrogen more unequal distribution than is seen in
then decreased and was 63 mg. per cent at the the above conditions.
time of the discharge.
He was re-admitted in December 1966 corn-
Downloaded from www.ajronline.org by 182.1.21.21 on 02/01/20 from IP address 182.1.21.21. Copyright ARRS. For personal use only; all rights reserved

FEATURES OF CHRONIC
plaining of headache and epistaxis. He expired GLOMERULONEPHRITIS
on December 26, 1966 of uremia and acute
pulmonary edema. Chronic glomerulonephritis is rarely ac-
Chronic glomerubonephritis was found at companied by visible calcification. How-
autopsy. ever, when present, its characteristics
enable the radiologist to make a histologic
DISCUSSION
diagnosis on a plain roentgenogram of the
Ordinarily one is unable to establish an abdomen. In Case ii the diagnosis was first
etiologic basis for renal lithiasis by roentgen suggested by the radiologist.
methods. On the other hand, in the ma- The kidneys retain a normal shape but
jority of instances, the radiologist can are uniformly small, the longitudinal axis
ascertain the cause of nephrocalcinosis rarely exceeding io cm. The calcifications
when the roentgenologic and clinical lea-. are granular, innumerable and diffusely
tures are correlated. scattered throughout the cortices. It is
Hyperparathyroidism, hyperchioremic the cortical location that distinguishes this
acidosis, chronic pyelonephritis, and medul- type of nephrocalcinosis from the others;
lary sponge kidneys account for approxi- no other condition presents stlch a pre-
mately 8o per cent of all cases. Less com- dominantly cortical localization.
mon causes are idiopathic hypercalciuria, Microscopically, most of the calcium is
chronic glomerulonephri tis, sarcoidosis, in the lumina of the tubules. Some is in the
carcinomatosis and vitamin D intoxication. epithelial lining cells of the loop of Henle,
Detailed roentgen features of the com- the distal convoluted tubules and the col-
mon causes of nephrocalcinosis have been lecting tubules. Occasionally, calcification
presented elsewhere, but a brief review is present in cortical interstitial tissues and
follows. In hyperparathyroidism renal lithi- medullary collecting tubules. The glomeruli
asis is much more common than renal may be hyalinized but they do not contain
calci nosis. However, when nephrocalci nosis calcium.
occurs, it is manifest by millet seed den-
sities confineti to the medulla. Occasionally, S UM MARY

larger pyramidal calcifications are present. Nephrocalcinosis associated with chronic

Fine streaks along the ducts of Bellini are glomerulonephritis is rare. Only 7 docu-
seen infrequently. Hellstr#{246}m8 reviewed 70 mented cases have been reported in the
cases of primary hyperparathyroidism; English language literature. The detection
he feels that tubular calcification is a pre- of 2 cases in 2 years in a relatively small
requisite to the formation of renal calculi, radiology practice indicates that it is con-
believing that the latter arise from ex- siderably more common than the literature
truded tubular debris. Similar calcifica- suggests.
tions are found in hyperchloremic acidosis. The roentgen features are described and
They may coalesce to form deposits of 2 additional cases are presented.
considerable size. As with hyperparathy-
151 Summit Avenue
roidism, the calcinosis may give rise to Summit, New Jersey 07901
renal lithiasis. The calcifications of medul-
lary sponge kidneys are small round or REFERENCES
oval deposits in the papillary portions of I. ALBRIGHT, F., BAIRD, P. C., COPE, 0., and
the pyramids. The involvement may be BLOOMBERG, E. Studies on physiology of
unilateral or bilateral. Chronic pyelonephri- parathyroid glands. IV. Renal complications
 VOL. 501, No. 3 Specific Nephrocalcinosis of Chronic Glomerulonephritis 691

of hyperparathyroidism. Am. 7. Med. Sc., mation in series of seventy cases of primary

1934, 187, 49-65. hyperparathyroidism. Brit. 7. Urol., 1955,
2. ARONS, W. L., CHRISTENSEN, W. R., and Sos- 27, 387-393.
MAN, M. C. Nephrocalcinosis visible by x-ray 9. KREEL, L. Radiological aspects of nephrocal-
associated with chronic glomerubonephri tis. cinosis. Clin. Radio!., 1962, 13, 218-223.
Downloaded from www.ajronline.org by 182.1.21.21 on 02/01/20 from IP address 182.1.21.21. Copyright ARRS. For personal use only; all rights reserved

Ann. mt. Med., 1955, 42, 260-282. 10. LIGHTWOOD, R. British Pediatric Association
3. BATESON, E. M. Nephrocalcinosis in children: Proceedings of Eighth Annual General Meet-
review of literature and report of case corn- ing. Arch. Dis. Childhood, i 35, JO, 205-206.
plicated by’ Wilms’ tumour. C/in. Radio!., II. MORTENSEN, J. D., BAGGENSTOSS, A. H.,
1962, 13, 231-237. POWER, M. H., and PUGH, D. G. Roentgeno-
4. BURNETT, C. H., COMMONS, R. R., ALBRIGHT, F., graphic demonstration of histologically iden-
and HOWARD, J. F. Hypercalcemia without tifiable renal calcification. Radiology, 1954.
hypercalciuria or hypophosphatemia, cal- 62, 703-712.
cinosis and renal insufficiency: syndrome fob- 12. MORTENSEN, J. D., and EMMETT, J. L. Nephro-
lowing prolonged intake of milk and alkali. calcinosis : collective and clinicopathobogic
New Englandj. Med., 1949, 240, 787-794. study. 7. Urol., 1954, 7!, 398-406.
5. EMMETT, J. L. Clinical Urography. Second cdi- 13. RICHARDSON, R. E. Nephrocalcinosis with spe-
tion. W. B. Saunders Company, Philadelphia, cial reference to its occurrence in renal tubular
1964, f3D. 489-496. acidosis. Clin. Radio!., 1962, 13, 224-230.
6. ENGEL, W. J. Nephrocalcinosis. 7.A.M.A., i5i, 14. PYRAH, L. N., and HODGKINSON, A. Nephro..
‘45, 288-294. calcinosis. Brit. 7. Urol., 1960,32, 361-373.
7. GERACI, J. E., HARRIS, H. W., and KEiTH, N. 15. VAUGHAN, J. H., SOSMAN, M. C., and KINNEY,
M. Bilateral diffuse nephrocalcinosis: report T. D. Nephrocalcinosis. AM.J. ROENTGENOL. &
ot two cases. Proc. Staff Meet. Mayo Clin., RAD. THERAPY, 1947,58, 33-45.
1950, 25, 305-315. 16. WOHL, H. Nephrocalcinosis: case report. 7.
8. HELLSTR#{246}M, J. Calcification and calculus for- Pediat., 1942, 2!, 382-385.