Baylor University Medical Center Proceedings July 2017 - 371

his skin and joint ﬁndings were attributed to an acute gouty
attack. This is apparently not uncommon, and this diagnosis is
certainly in the diﬀerential in patients presenting with metastatic
calcinosis cutis. No mention is made whether a joint or nodule
was aspirated: ﬁnding uric acid crystals under polarizing microscopy is the gold standard of making the diagnosis of acute
or tophaceous gout and would have been very helpful here in
guiding the clinicians in the correct direction.
A unique aspect of this case report is the extent and severity
of the skin and soft tissue calciﬁcations. We do not typically
see such severe calcinosis cutis even in patients who present de
novo to our renal service with profound uremia, often requiring
urgent initiation of hemodialysis as a life-saving measure. These
patients also have signiﬁcant hyperphosphatemia and elevated
PTH levels, but not nearly in the 5000 to 6000 range as in this
case. Likely this patient had uncontrolled hyperphosphatemia
for a prolonged period of time, and perhaps he had other unique
genetic factors that predisposed him to the development of
tertiary hyperparathyroidism.
The increased incidence of calciphylaxis in our CKD and
end-stage renal disease patients has rekindled interest in not
only metastatic calcinosis cutis, but also in abnormal calcium
deposits in blood vessels. This entity usually presents initially
with exquisitely painful noninﬂammatory, retiform purpuric
skin lesions with surrounding induration that commonly aﬀect
the fatty areas of the thighs, abdomen, and buttocks, though
acral and penile involvement can more rarely arise. These lesions
may rapidly progress to deep ulcers with a black eschar. It is
now appreciated that this condition can also occur with normal
renal function in patients who have primary hyperparathyroidism, alcoholic liver disease, diabetes mellitus, and malignancies.
These patients tend to have a less aggressive course and better

July 2017

prognosis. In addition, exposure to a variety of medications has
been implicated as well, including warfarin, vitamin D, calciumbased phosphate binders, iron therapy, and corticosteroids (3).
The case report by Jaeger and colleagues reminds us of the
many challenges still ahead as we attempt to fully explain the
complex interplay between several hormones in calcium and
phosphorus homeostasis in both normal physiologic conditions and in the pathologic states. With the identiﬁcation of
new hormones and their physiologic actions, we are in a better
position to tailor therapy to our complex patients with CKD
and end-stage renal disease who are living longer with the help
of newer technologies.
-Andrew Z. Fenves, MD
Department of Medicine, Massachusetts General
Hospital and Harvard Medical School, Boston, Massachusetts
E-mail: afenves@mgh.harvard.edu
-Daniela Kroshinsky, MD, MPH
Department of Dermatology, Massachusetts General
Hospital and Harvard Medical School, Boston, Massachusetts
Lever WF, Elder DE. Lever's Histopathology of the Skin, 9th ed. Philadelphia:
Lippincott Williams & Wilkins, 2005:444-447.
2. Nigwekar SU. Multidisciplinary approach to calciﬁc uremic arteriolopathy.
Curr Opin Nephrol Hypertens 2015;24(6):531-537.
3. Nigwekar SU, Kroshinsky D, Nazarian RM, Goverman J, Malhotra R,
Jackson VA, Kamdar MM, Steele DJR, Thadhani RI. Calciphylaxis: risk
factors, diagnosis and treatment. Am J Kidney Dis 2015;66(1):133-146.
4. Jaeger VA, Newman GM, Mirkes CR. Metastatic calcinosis cutis in
end-stage renal disease. Proc (Bayl Univ Med Cent) 2017;30(3):368-
369.
5. Bushinsky DA. Phosphate and its binders. NephSAP 2008;7(5):295-298.
6. Jamal SA, Miller PD. Secondary and tertiary hyperparathyroidism. J Clin
Densitometry 2013;16(1):64-68.
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Table of Contents for the Digital Edition of Baylor University Medical Center Proceedings July 2017
