Baylor University Medical Center Proceedings July 2017 - 368

Metastatic calcinosis cutis in end-stage renal disease
Victoria A. Jaeger, DO, Megan G. Newman, MD, and Curtis R. Mirkes, DO

Alterations in calcium and phosphorus levels and joint pain are a common occurrence in end-stage renal disease patients. However, metastatic
calcinosis cutis is a rare diagnosis that often combines these two findings,
with extensive soft tissue calcification surrounding a large joint being
the hallmark of this disease. The exact mechanism behind this clinical
entity is unknown. The treatment and complications can be severe and
disabling. Here, we discuss the case of a 26-year-old man presenting
with unusually advanced skin and joint calcification of the shoulders,
neck, hand, and penis.

alcinosis cutis is an unusual disorder characterized by
large calcium phosphate deposition into cutaneous and
subcutaneous tissues. Five subtypes of calcinosis cutis
exist: dystrophic, metastatic, idiopathic, iatrogenic, and
calciphylaxis. The shoulders, elbows, and hips are typically the
joints aﬀected by these lesions. However, cases have been reported in various other periarticular areas of the body (1). Patients present with symptoms such as pain, joint stiﬀness, nerve
compression, inﬂammation, ﬁstula formation, infection, and
sometimes systemic symptoms such as fever (1, 2). Presenting
skin ﬁndings may be nodules with extrusion of a chalky while
substance. Here, we describe a patient who presented with advanced metastatic calcinosis cutis with multiple lesions of the
large joints, neck, hands, and penis.
CASE REPORT
A 26-year-old man with a history of focal segmental glomerulosclerosis and a congenital solitary kidney presented with
left hand pain and fatigue. He had been treated for presumed
gout aﬀecting the left hand 12 days prior to presentation at the
emergency department without resolution of his symptoms.
He appeared cachectic and ill, with multiple areas of calcium
deposits on the left hand, left shoulder, right axilla (Figure 1),
and penis. The left third digit was swollen with calciﬁc deposits
and nodules. The dorsal and left lateral penile shaft had hard,
nontender nodules without swelling. Initial laboratory values
were a calcium level of 9.7 mg/dL, phosphorus level of 10.6 mg/
dL, parathyroid hormone level of 5646 pg/mL, creatinine of
7.60 mg/dL, blood urea nitrogen of 124 mg/dL, and estimated
glomerular ﬁltration rate of 8.8 mL/min/1.73 m2. Computed

368

tomography without intravenous contrast showed extensive,
lobulated soft tissue calciﬁcations in both shoulders and the
left chest wall, extending into the neck (Figure 2). Findings
were consistent with metastatic calcinosis cutis secondary to
chronic kidney disease stage 5. Hemodialysis, cinacalcet, a renal
diet, and phosphate binders were started. A calcium-phosphate
product <50 was targeted. Sodium thiosulfate was given following dialysis, and a subtotal parathyroidectomy was ultimately
performed to resolve tertiary hyperparathyroidism.
DISCUSSION
Hundreds of cases of calcinosis cutis have been reported,
but only a small number have involved areas of the hand. The
typical sites of involvement are the superior and lateral shoulder,
posterior elbows, and lateral hip and gluteal regions (1). Other
areas such as hands, feet, spine, temporomandibular joint, and
knee have been observed. Our patient had extensive involvement of the usual shoulder regions, but also involvement of the
digits, neck, and genitals.
Five subtypes of calcinosis cutis exist. Our patient presented
with the subclass termed metastatic calcinosis cutis, which was
likely secondary to end-stage renal disease. Though rare, calcinosis cutis is a severe complication of chronic kidney disease
with an incidence of 0.5% to 3% (2). The subclass of calcinosis
cutis that our patient presented with is characterized by abnormal phosphorus or calcium metabolism resulting in widespread
deposition of calcium in the skin and soft tissues (3). Metastatic calcinosis cutis has been linked to other conditions such
as sarcoidosis, Albright hereditary osteodystrophy, neoplasms,
and hypervitaminosis D (3). The most common predisposing
condition, however, is chronic kidney disease. A mechanism of
pathogenesis of calcinosis cutis has been proposed. It is believed
that repeated small trauma occurs, which creates hemorrhages
in tissues surrounding the joints and initiates an inﬂammatory
response (1, 4).
From the Department of Internal Medicine, Baylor Scott and White Hospital and
Texas A&M Health Science Center College of Medicine, Temple, Texas.
Corresponding author: Megan G. Newman, MD, Department of Internal
Medicine, Baylor Scott and White Hospital, Texas A&M Health Science Center
College of Medicine, 2401 S. 31st Street, Temple, TX 76508 (e-mail: Megan.
Newman@BSWHealth.org).
Proc (Bayl Univ Med Cent) 2017;30(3):368-369

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