Bocanegra Jesús, Alejandra

Guinetti Ortiz, Katia

Gómez de la Torre del Carpio, Andrea

Spanish

LAReferencia - Red Federada de Repositorios Institucionales de Publicaciones Científicas Latinoamericanas

Valvular calcifications in CKD: Mineral and bone disease or previous cardiovascular risk?

Repositorio Académico UPC - Universidad de Ciencias Aplicadas (UPC)

Alejandra Bocanegra-Jesús

Katia Guinetti-Ortiz

Andrea Gómez de la Torre-del Carpio

Directory of Open Access Journals

Nefrología

¿Calcificaciones valvulares en ERC: enfermedad mineral ósea o riesgo cardiovascular previo?

Nefrología (English Edition)

Bocanegra-Jesús, Alejandra

Guinetti-Ortiz, Katia

Gómez de la Torre-del Carpio, Andrea

Elsevier - Publisher Connector 

Valvular calcifications in CKD: Mineral and bone disease or previous cardiovascular risk? 

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en e f r o l o g i a. 2 0 1 5;3 5(6):597–601
Revista de la Sociedad Española de Nefrología
w w w.rev is tanef ro logia .com
etters to the Editor
alvular  calciﬁcations  in CKD:  Mineral  and bone disease  or
revious cardiovascular  risk?Calciﬁcaciones  valvulares  en  ERC:  enfermedad  mineral  ósea  o
r
1
2
3
4iesgo  cardiovascular  previo?
o the Editor,
e  read with great interest the article by Carmen Sánchez-
erales et al., recently published in Nefrología.1 In this study,
he authors analysed the presence of valvular calciﬁcation in
atients starting dialysis and its relationship to cardiovascular
vents and cardiovascular death. We would like to offer some
omments on the study.
Valvular calciﬁcation may occur in the presence or absence
f renal disease. In individuals without renal disease, calciﬁ-
ation is usually a result of a pro-inﬂammatory state caused
y other comorbidities such as diabetes, dyslipidaemia, and
ypertension. In individuals with chronic kidney disease
CKD), often it cannot be established with certainty whether
alciﬁcation is due to changes in bone mineral metabolism,
nﬂammation caused by comorbidities, or both.2
In the “methods” section of the study, the authors stated
hat they measured serum levels of phosphorus, calcium, and
arathyroid hormone (PTH). However, calcium and PTH were
ot included in the univariate analysis. We  think that the
tatistical analysis of these two variables would be relevant,
ecause the studies performed by Streja et al.3 and Floege
t al.,4 found that patients with serum values of intact PTH,
alcium, and phosphate outside the ranges recommended by
he Kidney Disease Outcomes Quality Initiative (KDOQITM)5
iPTH, 150–300 pg/mL; calcium, 2.10–2.37 mmol/L; and phos-
hate, 1.13–1.78 mmol/L) had a higher mortality risk than
atients with values within these ranges.
In the multivariate analysis by Sánchez-Perales et al.,
he authors state that the model was adjusted for factors
ith statistical signiﬁcance in the univariate analysis and for
ther factors that were potentially involved in the valvular
 Please cite this article as: Bocanegra-Jesús A, Guinetti-Ortiz K, Góm
nfermedad mineral ósea o riesgo cardiovascular previo? Nefrología. N
5calciﬁcation process. However, it was not clear why variables
associated with valvular calciﬁcation in patients with CKD
(PTH, calcium, and phosphate) were not included.
Finally, whilst the study demonstrates that the presence
of valvular calciﬁcation is a predictor of mortality, the anal-
ysis performed does not establish whether calciﬁcation is
secondary to atherogenic comorbidities or to an imbalance
of bone mineral metabolism. Future studies could further
explore this association.
 e  f  e  r  e  n  c  e  s
. Sánchez-Perales C, Vázquez Ruiz de Castroviejo E,
García-Cortés M, del Mar Biechy M, Gil-Cunquero J,
Borrego-Hinojosa J, et al. Las calciﬁcaciones valvulares al inicio
de diálisis predicen la aparición de eventos cardiovasculares
en la evolución. Nefrologia. 2015;35:157–63.
. Ruiz JL, Hutcheson JD, Aikawa E. Cardiovascular calciﬁcation:
Current controversies and novel concepts. Cardiovasc Pathol.
2015;24:207–12.
. Streja R, Wang HY, Lau WL,  Molnar MZ, Kovesdy CP,
Kalantar-Zadeh K, et al. Mortality of combined serum
phosphorus and parathyroid hormone concentrations and
their changes over time in hemodialysis patients. Bone.
2014;61:201–7.
. Floege J, Kim J, Ireland E, Chazot C, Drueke T, de Francisco A,
et al. Serum iPTH, calcium and phosphate, and the risk of
mortality in a European haemodialysis population. Nephrolez de la Torre-del Carpio A. ¿Calciﬁcaciones valvulares en ERC:
efrologia. 2015;35:597–598.
Dial Transplant. 2011;26:1948–55.
. National Kidney Foundation. K/DOQI clinical practice
guidelines for bone metabolism and disease in chronic kidney
disease. Am J Kidney Dis. 2003;42 Suppl. 3:S1–201.
598  n e f r o l o g i a. 2 0 1 5;3 5(6):597–601
Alejandra Bocanegra-Jesús ∗, Katia Guinetti-Ortiz,
Andrea Gómez de la Torre-del Carpio
Escuela de Medicina, Universidad Peruana de Ciencias Aplicadas,
Lima, Peru
∗ Corresponding author.
E-mail address: alejandrabocanegra@hotmail.com
(A. Bocanegra-Jesús).
2013-2514/© 2015 Sociedad Espan˜ola de Nefrol-
ogía. Published by Elsevier España, S.L.U. This is an
open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/).
http://dx.doi.org/10.1016/j.nefroe.2015.07.007
Lots  of steroids  and vitamins,  tons  of complications.
Hypercalcemia and  nephrocalcinosis  as important
complications of  performance-enhancing  drugs
Montones  de  esteroides  y  vitaminas,  toneladas  de  complicaciones.
Hipercalcemia  y  nefrocalcinosis  como  complicaciones  importantes
de  los  fármacos  para  mejorar  el  rendimiento
Dear Editor,
Chronic hypercalcemia can be an important complica-
tion of anabolic steroid and vitamin supplement abuse.
We report the case of a 30-year-old bodybuilder that for
more  than 4 years used injectable anabolic-androgenic
steroids (AAS) and one veterinary polyvitamin formulation
with vitamin A (2,100,000 IU), D (ergocalciferol: 60,000 IU),
and E (55 IU) on a monthly basis. He also reported self-
injecting mineral oil intramuscularly for esthetic purposes
for more  than 2 years. He presented to the emergency
room with an acute, severe epigastric pain, associated
with nausea and vomiting. Laboratory evaluation (Table 1)
demonstrated an elevated amylase 2500 IU/L (50–160 IU/L);
lipase of 612 IU/L (0–75 IU/L); a corrected serum calcium of
12.5 mg/dL (8.5–10.5 mg/dL); PTH of 73.2 pg/mL (15–68.3 pg/mL)
and 25(OH)D of 65.1 ng/mL (30–100 ng/mL). Serum creatinine
was 1.2 mg/dL (0.6–1.2 mg/dL). Abdominal ultrasound showed
a diffusely edematous pancreas, bilateral ureterolithiasis and
nephrocalcinosis. A high-resolution CT of the chest and
abdomen was performed and revealed absence of granulomas
and lymphadenopathies. He had a tormented clinical course,
with acute kidney injury (attributed to volume depletion
and renal vasoconstriction in the setting of hypercalcemia)
without the need of hemodialysis; protracted vomiting that
lead to a laparoscopic duodenum–jejunum anastomosis with
improvement of complains and multiple infectious compli-
cations. Serum calcium and PTH returned to normal levels
(9 mg/dL and 35 pg/mL, respectively) after vitamin D discon-
tinuation, vigorous venous hydration with 0.9% saline infusion
and therapy with furosemide and corticosteroids. After more
With the desire to improve performance, some athletes or
amateurs use performance-enhancing drugs. The widespread
use of these substances without medical prescription or clini-
cal follow-up can lead to serious health problems as described
on several reports.1–3 We believe that the main clinical fea-
tures seen in this patient are due to chronic hypercalcemia due
to multiple substance abuse and parafﬁnomas. The associa-
tion between focal segmental glomerulosclerosis and anabolic
steroids abuse may be explained by increase in lean body
mass and potential direct nephrotoxic effects of anabolic
steroids.1 Furthermore, this drug modulates steroid hydroxy-
lase activity predisposing to hypercalcemia.4 The association
of vitamin A toxicity and hypercalcemia is rare but well rec-
ognized. It is attributed to a direct effect on bone (activation
of bone reabsorption with increased osteoclast activity),5 on
the parathyroid, or in both.6 According to Chertow et al.,
vitamin A stimulate PTH secretion in bovine parathyroid
tissue and in men.6,7 The minimum dose of vitamin A
required to produce hypercalcemia cannot be stated with cer-
tainty; toxicity has been described from doses ranging from
50,000 to 500,000 IU/day.5 Although we did not measure the
value of vitamin A in blood, the patient injected more  than
2,100,000 IU/month (which correspond 70.000 IU of vitamin
A/day) for more  than 4 years, which is compatible with toxicity.
Hypercalcemia is a well-known but uncommon complication
of vitamin D intake.8 Usually results from doses that exceed
10,000 IU/day, and is generally associated with serum lev-
els of 25-hydroxyvitamin D that are well above 150 ng/mL.8
In this case, 60,000 IU of ergocalciferol were inject monthly
and serum vitamin D was in the upper limit of normal.
The tolerable upper level of daily vitamin D intake recentlythan 60 days of hospitalization he was discharged home hav-
ing made a full recovery.set by the Institute of Medicine is 4000 IU.8 Vitamin A and
D can act synergistically to cause hypercalcemia. Contrary


NEUROSURGERY ENTHUSIASTIC WOMEN SOCIETY

Repositorio Académico UPC

n e f  r  o l  o g i  a 2  0 1 5;3  5(6):597–601Revista de la Sociedad Española de Nefrologíaw w w.rev is tanef ro logia .comCartas al Director¿Calcificaciones  valvulares  en  ERC: enfermedad  mineralósea o riesgo cardiovascular  previo?Valvular  calcifications  in  CKD:  Mineral  and  bone  disease  or  previouscardiovascular  risk?Sr.  Director:Hemos leído con mucho interés el artículo de CarmenSánchez-Perales et  al., recientemente publicado en Nefrología1. En este estudio, los autores analizan la presenciade calcificaciones valvulares en el paciente que inicia diáli-sis y su relación con la presentación de eventos y  mortalidadcardiovascular en la evolución. Nos gustaría realizar algunoscomentarios.Se sabe que las calcificaciones valvulares pueden presen-tarse con o sin enfermedad renal. En aquellos sin esta, sueleproducirse por estados proinflamatorios debido a  otras comor-bilidades como diabetes, dislipidemia e hipertensión arterial,entre otras. Por otra parte, en personas con enfermedad renalcrónica (ERC) muchas veces no se logra saber con exactitudsi las calcificaciones se deben específicamente a  las altera-ciones del metabolismo mineral óseo, a la inflamación porcomorbilidades o  a  ambas2.En la sección de «métodos del estudio»,  se menciona que semidieron los niveles de fósforo, calcio y  paratohormona (PTH)séricos, sin embargo, en el análisis univariado estos 2 últimosno fueron incluidos. En  este sentido, consideramos que seríarelevante conocer el análisis estadístico de dichas variables.Esto debido a  que, en los estudios realizados por Streja et  al.3y Floege et al.4,  se encontró que los pacientes con valorespor encima o por debajo de los rangos recomendados por elKidney Disease Outcomes Quality Initiative (KDOQITM)5 dePTH intacta (iPTH) (150-300 pg/ml), calcio (2,10-2,37 mmol/l)y fosfato (1,13-1,78 mmol/l) séricos presentan mayor riesgode mortalidad comparado con aquellos pacientes dentro delrango.Por otro lado, en el análisis multivariado, se mencionaque el modelo fue ajustado por los factores con significaciónestadística en el análisis univariado, y otros con  poten-cial participación en el proceso de calcificación valvular. SinVéase contenido relacionado en DOI:http://dx.doi.org/10.1016/j.nefro.2015.08.005.embargo, no queda claro por qué las variables relacionadas acalcificaciones valvulares en pacientes con ERC  (PTH, calcio yfosfato) no fueron incluidas.Finalmente, si bien el estudio demuestra que la presenciade calcificaciones valvulares es un predictor de  mortalidad, elanálisis realizado no permite diferenciar si estas son secun-darias a comorbilidades aterogénicas o al disbalance en elmetabolismo mineral ósea. Futuros estudios podrían explorarmejor esta asociación.Conflicto  de interesesLas autoras declaran que no tienen conflictos de intere-ses potenciales relacionados con los contenidos de esteartículo.b i b l  i o  g r a  f  í  a1. Sánchez-Perales C, Vázquez Ruiz de  Castroviejo E,García-Cortés M, del Mar Biechy M, Gil-Cunquero J,Borrego-Hinojosa J, et al. Las calcificaciones valvulares al  iniciode diálisis predicen la aparición de  eventos cardiovascularesen  la evolución. Nefrologia. 2015;35:157–63.2. Ruiz JL, Hutcheson JD, Aikawa E. Cardiovascular calcification:Current controversies and novel concepts. Cardiovasc Pathol.2015;24:207–12.3. Streja R, Wang HY, Lau WL,  Molnar MZ, Kovesdy CP,Kalantar-Zadeh K, et al. Mortality of combined serumphosphorus and parathyroid hormone concentrations andtheir changes over time in hemodialysis patients. Bone.2014;61:201–7.4. Floege J, Kim J, Ireland E, Chazot C, Drueke T, de Francisco A,et al. Serum iPTH, calcium and phosphate, and the risk ofmortality in a  European haemodialysis population. NephrolDial Transplant. 2011;26:1948–55.598  n e f r  o l o g i  a 2 0 1 5;3  5(6):597–6015. National Kidney Foundation. K/DOQI clinical practiceguidelines for bone metabolism and disease in chronic kidneydisease. Am J  Kidney Dis. 2003;42 Suppl 3:S1–201.Alejandra Bocanegra-Jesús ∗, Katia Guinetti-Ortiz yAndrea Gómez de la Torre-del CarpioEscuela de Medicina, Universidad Peruana de Ciencias Aplicadas,Lima, Perú∗ Autor para correspondencia.Correo electrónico: alejandrabocanegra@hotmail.com(A. Bocanegra-Jesús).http://dx.doi.org/10.1016/j.nefro.2015.07.0090211-6995/© 2015 Sociedad Española de Nefrología. Publi-cado por Elsevier España, S.L.U. Este es un artículo OpenAccess bajo la licencia CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/).Lots  of  steroids  and  vitamins,  tons  of  complications.Hypercalcemia and nephrocalcinosis  as importantcomplications of performance-enhancing  drugsMontones  de  esteroides  y vitaminas,  toneladas  de  complicaciones.Hipercalcemia  y nefrocalcinosis  como  complicaciones  importantesde  los  fármacos  para  mejorar  el  rendimientoDear Editor,Chronic hypercalcemia can be an  important complica-tion of anabolic steroid and vitamin supplement abuse.We  report the case of a  30-year-old bodybuilder that formore than 4  years used injectable anabolic-androgenic ste-roids (AAS) and one veterinary polyvitamin formulationwith vitamin A  (2,100,000 IU), D (ergocalciferol: 60,000 IU),and E (55 IU) on a  monthly basis. He also reported self-injecting mineral oil intramuscularly for esthetic purposesfor more  than 2 years. He presented to the emergencyroom with an acute, severe epigastric pain, associatedwith nausea and vomiting. Laboratory evaluation (Table 1)demonstrated an  elevated amylase 2500 IU/L (50–160 IU/L);lipase of 612 IU/L (0–75 IU/L); a  corrected serum calcium of12.5 mg/dL (8.5–10.5 mg/dL); PTH of 73.2 pg/mL (15–68.3 pg/mL)and 25(OH)D of 65.1 ng/mL (30–100 ng/mL). Serum creatininewas 1.2 mg/dL (0.6–1.2 mg/dL). Abdominal ultrasound showeda diffusely edematous pancreas, bilateral ureterolithiasis andnephrocalcinosis. A  high-resolution CT of the chest and abdo-men  was performed and revealed absence of granulomas andlymphadenopathies. He had a tormented clinical course, withacute kidney injury (attributed to volume depletion and renalvasoconstriction in the setting of hypercalcemia) without theneed of hemodialysis; protracted vomiting that lead to a  lapa-roscopic duodenum–jejunum anastomosis with improvementof complains and multiple infectious complications. Serumcalcium and PTH returned to normal levels (9 mg/dL and35 pg/mL, respectively) after vitamin D discontinuation, vigo-rous venous hydration with 0.9% saline infusion and therapywith furosemide and corticosteroids. After more  than 60 daysof hospitalization he was discharged home having made a fullrecovery.With the desire to improve performance, some athletesor amateurs use performance-enhancing drugs. The wides-pread use of these substances without medical prescriptionor clinical follow-up can lead to serious health problems asdescribed on several reports.1–3 We believe that the mainclinical features seen in this patient are due to  chronic hyper-calcemia due to multiple substance abuse and paraffinomas.The association between focal segmental glomerulosclerosisand anabolic steroids abuse may be explained by increasein lean body mass and potential direct nephrotoxic effectsof anabolic steroids.1 Furthermore, this drug modulates ste-roid hydroxylase activity predisposing to hypercalcemia.4 Theassociation of vitamin A toxicity and hypercalcemia is rarebut well recognized. It is  attributed to a direct effect onbone (activation of bone reabsorption with increased osteo-clast activity),5 on the  parathyroid, or in both.6 According toChertow et al.,  vitamin A  stimulate PTH secretion in bovineparathyroid tissue and in men.6,7 The minimum dose of vita-min A required to produce hypercalcemia cannot be statedwith certainty; toxicity has  been described from doses rangingfrom 50,000 to 500,000 IU/day.5 Although we  did not measurethe value of vitamin A  in blood, the patient injected morethan 2,100,000 IU/month (which correspond 70.000 IU of vita-min A/day) for more  than 4 years, which is compatible withtoxicity. Hypercalcemia is a  well-known but uncommon com-plication of vitamin D intake.8 Usually results from doses thatexceed 10,000 IU/day, and is  generally associated with serumlevels of 25-hydroxyvitamin D that are well above 150 ng/mL.8In this case, 60,000 IU of ergocalciferol were inject monthlyand serum vitamin D was in the upper limit of normal. Thetolerable upper level of daily vitamin D intake recently setby the Institute of Medicine is 4000 IU.8 Vitamin A and Dcan act synergistically to cause hypercalcemia. Contrary to

¿Calcificaciones valvulares en ERC: enfermedad mineral ósea o riesgo cardiovascular previo? 

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hn e f r o l o g i a 2 0 1 5;3 5(6):597–601
Revista de la Sociedad Española de Nefrología
w w w.rev is tanef ro logia .com
artas al Director
Calciﬁcaciones  valvulares  en ERC:  enfermedad  mineral
sea o riesgo  cardiovascular  previo?alvular  calciﬁcations  in  CKD:  Mineral  and  bone  disease  or  previous
b
1
2
3
4. Floege J, Kim J, Ireland E, Chazot C, Drueke T, de Francisco A,ardiovascular  risk?
r. Director:
emos leído con mucho interés el artículo de Carmen
ánchez-Perales et al., recientemente publicado en Nef
ología1. En este estudio, los autores analizan la presencia
e calciﬁcaciones valvulares en el paciente que inicia diáli-
is y su relación con la presentación de eventos y mortalidad
ardiovascular en la evolución. Nos gustaría realizar algunos
omentarios.
Se sabe que las calciﬁcaciones valvulares pueden presen-
arse con o sin enfermedad renal. En aquellos sin esta, suele
roducirse por estados proinﬂamatorios debido a otras comor-
ilidades como diabetes, dislipidemia e hipertensión arterial,
ntre otras. Por otra parte, en personas con enfermedad renal
rónica (ERC) muchas veces no se logra saber con exactitud
i las calciﬁcaciones se deben especíﬁcamente a las altera-
iones del metabolismo mineral óseo, a la inﬂamación por
omorbilidades o a ambas2.
En la sección de «métodos del estudio», se menciona que se
idieron los niveles de fósforo, calcio y paratohormona (PTH)
éricos, sin embargo, en el análisis univariado estos 2 últimos
o fueron incluidos. En este sentido, consideramos que sería
elevante conocer el análisis estadístico de dichas variables.
sto debido a que, en los estudios realizados por Streja et al.3
 Floege et al.4, se encontró que los pacientes con valores
or encima o por debajo de los rangos recomendados por el
idney Disease Outcomes Quality Initiative (KDOQITM)5 de
TH intacta (iPTH) (150-300 pg/ml), calcio (2,10-2,37 mmol/l)
 fosfato (1,13-1,78 mmol/l) séricos presentan mayor riesgo
e mortalidad comparado con aquellos pacientes dentro del
ango.
Por otro lado, en el análisis multivariado, se menciona
ue el modelo fue ajustado por los factores con signiﬁcación
stadística en el análisis univariado, y otros con poten-
ial participación en el proceso de calciﬁcación valvular. Sin
Véase contenido relacionado en DOI:
ttp://dx.doi.org/10.1016/j.nefro.2015.08.005.embargo, no queda claro por qué las variables relacionadas a
calciﬁcaciones valvulares en pacientes con ERC (PTH, calcio y
fosfato) no fueron incluidas.
Finalmente, si bien el estudio demuestra que la presencia
de calciﬁcaciones valvulares es un predictor de mortalidad, el
análisis realizado no permite diferenciar si estas son secun-
darias a comorbilidades aterogénicas o al disbalance en el
metabolismo mineral ósea. Futuros estudios podrían explorar
mejor esta asociación.
Conﬂicto  de  intereses
Las autoras declaran que no tienen conﬂictos de intere-
ses potenciales relacionados con los contenidos de este
artículo.
 i  b  l  i  o  g  r  a  f  í  a
. Sánchez-Perales C, Vázquez Ruiz de Castroviejo E,
García-Cortés M, del Mar Biechy M, Gil-Cunquero J,
Borrego-Hinojosa J, et al. Las calciﬁcaciones valvulares al inicio
de diálisis predicen la aparición de eventos cardiovasculares
en la evolución. Nefrologia. 2015;35:157–63.
. Ruiz JL, Hutcheson JD, Aikawa E. Cardiovascular calciﬁcation:
Current controversies and novel concepts. Cardiovasc Pathol.
2015;24:207–12.
. Streja R, Wang HY, Lau WL,  Molnar MZ, Kovesdy CP,
Kalantar-Zadeh K, et al. Mortality of combined serum
phosphorus and parathyroid hormone concentrations and
their changes over time in hemodialysis patients. Bone.
2014;61:201–7.et al. Serum iPTH, calcium and phosphate, and the risk of
mortality in a European haemodialysis population. Nephrol
Dial Transplant. 2011;26:1948–55.
5598  n e f r o l o g i a 2 0 1 5;3  5(6):597–601
. National Kidney Foundation. K/DOQI clinical practice
guidelines for bone metabolism and disease in chronic kidney
disease. Am J Kidney Dis. 2003;42 Suppl 3:S1–201.
Alejandra Bocanegra-Jesús ∗, Katia Guinetti-Ortiz y
Andrea Gómez de la Torre-del Carpio
Escuela de Medicina, Universidad Peruana de Ciencias Aplicadas,
Lima, Perú
∗ Autor para correspondencia.
Correo electrónico: alejandrabocanegra@hotmail.com
(A. Bocanegra-Jesús).
http://dx.doi.org/10.1016/j.nefro.2015.07.009
0211-6995/© 2015 Sociedad Espan˜ola de Nefrología. Publi-
cado por Elsevier España, S.L.U. Este es un artículo Open
Access bajo la licencia CC BY-NC-ND (http://creativecommons.
org/licenses/by-nc-nd/4.0/).
Lots  of steroids  and vitamins,  tons  of complications.
Hypercalcemia and  nephrocalcinosis  as important
complications of  performance-enhancing  drugs
Montones  de  esteroides  y  vitaminas,  toneladas  de  complicaciones.
Hipercalcemia  y  nefrocalcinosis  como  complicaciones  importantes
de  los  fármacos  para  mejorar  el  rendimiento
Dear Editor,
Chronic hypercalcemia can be an important complica-
tion of anabolic steroid and vitamin supplement abuse.
We report the case of a 30-year-old bodybuilder that for
more  than 4 years used injectable anabolic-androgenic ste-
roids (AAS) and one veterinary polyvitamin formulation
with vitamin A (2,100,000 IU), D (ergocalciferol: 60,000 IU),
and E (55 IU) on a monthly basis. He also reported self-
injecting mineral oil intramuscularly for esthetic purposes
for more  than 2 years. He presented to the emergency
room with an acute, severe epigastric pain, associated
with nausea and vomiting. Laboratory evaluation (Table 1)
demonstrated an elevated amylase 2500 IU/L (50–160 IU/L);
lipase of 612 IU/L (0–75 IU/L); a corrected serum calcium of
12.5 mg/dL (8.5–10.5 mg/dL); PTH of 73.2 pg/mL (15–68.3 pg/mL)
and 25(OH)D of 65.1 ng/mL (30–100 ng/mL). Serum creatinine
was 1.2 mg/dL (0.6–1.2 mg/dL). Abdominal ultrasound showed
a diffusely edematous pancreas, bilateral ureterolithiasis and
nephrocalcinosis. A high-resolution CT of the chest and abdo-
men  was performed and revealed absence of granulomas and
lymphadenopathies. He had a tormented clinical course, with
acute kidney injury (attributed to volume depletion and renal
vasoconstriction in the setting of hypercalcemia) without the
need of hemodialysis; protracted vomiting that lead to a lapa-
roscopic duodenum–jejunum anastomosis with improvement
of complains and multiple infectious complications. Serum
calcium and PTH returned to normal levels (9 mg/dL and
35 pg/mL, respectively) after vitamin D discontinuation, vigo-
rous venous hydration with 0.9% saline infusion and therapy
With the desire to improve performance, some athletes
or amateurs use performance-enhancing drugs. The wides-
pread use of these substances without medical prescription
or clinical follow-up can lead to serious health problems as
described on several reports.1–3 We  believe that the main
clinical features seen in this patient are due to chronic hyper-
calcemia due to multiple substance abuse and parafﬁnomas.
The association between focal segmental glomerulosclerosis
and anabolic steroids abuse may be explained by increase
in lean body mass and potential direct nephrotoxic effects
of anabolic steroids.1 Furthermore, this drug modulates ste-
roid hydroxylase activity predisposing to hypercalcemia.4 The
association of vitamin A toxicity and hypercalcemia is rare
but well recognized. It is attributed to a direct effect on
bone (activation of bone reabsorption with increased osteo-
clast activity),5 on the parathyroid, or in both.6 According to
Chertow et al., vitamin A stimulate PTH secretion in bovine
parathyroid tissue and in men.6,7 The minimum dose of vita-
min  A required to produce hypercalcemia cannot be stated
with certainty; toxicity has been described from doses ranging
from 50,000 to 500,000 IU/day.5 Although we  did not measure
the value of vitamin A in blood, the patient injected more
than 2,100,000 IU/month (which correspond 70.000 IU of vita-
min  A/day) for more  than 4 years, which is compatible with
toxicity. Hypercalcemia is a well-known but uncommon com-
plication of vitamin D intake.8 Usually results from doses that
exceed 10,000 IU/day, and is generally associated with serum
levels of 25-hydroxyvitamin D that are well above 150 ng/mL.8
In this case, 60,000 IU of ergocalciferol were inject monthly
and serum vitamin D was in the upper limit of normal. Thewith furosemide and corticosteroids. After more  than 60 days
of hospitalization he was discharged home having made a full
recovery.tolerable upper level of daily vitamin D intake recently set
by the Institute of Medicine is 4000 IU.8 Vitamin A and D
can act synergistically to cause hypercalcemia. Contrary to


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Valvular calcifications in CKD: Mineral and bone disease or previous cardiovascular risk?

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