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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 96-99

Acute Kidney Injury Due to Hypervitaminosis D in an Infant


Department of Paediatrics, Army College of Medical Sciences, New Delhi, India

Date of Submission18-Nov-2014
Date of Acceptance17-Feb-2015
Date of Web Publication20-May-2015

Correspondence Address:
Dr. Bindu Thankamany Nair
Department of Paediatrics, Army College of Medical Sciences, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2384-5147.157435

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  Abstract 

We report here a case of bilateral pelviureteric junction stones in a 2 months old baby who presented with acute onset anuria and sepsis. The baby was diagnosed to have acute postrenal failure due to obstructive bilateral ureteric stones based on the findings of ultrasound scan. This was a rare case of drug-induced hypercalcemia resulting from inappropriate iatrogenic supplementation of calcium and Vitamin D. Baby later developed hydrocephalus as sequelae to meningitis. Magnetic resonance imaging of brain showed periventricular calcification probably a sequelae to hypercalcemia. Our case emphasizes the need for considering iatrogenic hypercalcemia as a cause of urolithiasis and other forms of calcification in infants.

Keywords: Acute kidney injury, hypercalcemia, periventricular calcification, urolithiasis, Vitamin D and calcium supplements


How to cite this article:
Nair BT, Sanjeev RK, Surendran S. Acute Kidney Injury Due to Hypervitaminosis D in an Infant. Sub-Saharan Afr J Med 2015;2:96-9

How to cite this URL:
Nair BT, Sanjeev RK, Surendran S. Acute Kidney Injury Due to Hypervitaminosis D in an Infant. Sub-Saharan Afr J Med [serial online] 2015 [cited 2024 Feb 26];2:96-9. Available from: https://www.ssajm.org/text.asp?2015/2/2/96/157435


  Introduction Top


Urolithiasis has varied prevalence in different countries. In Western countries, the prevalence of urolithiasis in adults is relatively higher than in the Eastern hemisphere. The reported prevalence of urolithiasis is 1-5% in Asia, 5-9% in Europe, 12% in Canada, and 13-15% in the USA. [1] Although even in some Asian countries, such as Saudi Arabia, there is a very high reported prevalence of 20.1%. [2] Children represent 2-3% of the total population of patients with urolithiasis. [3]

We report a case of urolithiasis due to hypervitaminosis D presenting as acute kidney injury (AKI) in a baby <2 months of age. This would perhaps be the youngest case of AKI due to urolithiasis in world literature. Vitamin D toxicity is a known cause of hypercalcemia leading to metastatic calcification, including urolithiasis and perivascular calcifications in various parts of the body. Although Vitamin D has a wide therapeutic index, its toxicity is well known due to off the counter usage of various calcium and Vitamin D supplements, self-medication, and malpractice.


  Case Report Top


A term male infant was brought to our hospital at 58 days of age with a history of not having passed urine for 3 days. The baby was the first product of a nonconsanguineous marriage with normal antenatal ultrasonography. Anthropometry at delivery was appropriate for the gestational age. There was no history of perinatal asphyxia or TORCH infection in the mother. There was also no history of excessive irritability, rash, seizures or any history of ureteric calculus in the family. The baby had a normal urinary stream after birth.

On admission, baby had pallor and generalized edema. His pulse rate was 130 beats/min, respiratory rate was 60 breaths/min and blood pressure was 130/82 mm Hg (>99 th centile). Abdominal examination revealed hepatomegaly and bilateral ballotable masses. In view of the moribund condition of the baby, he was shifted to the pediatric intensive care unit with a suspected diagnosis of late onset sepsis with AKI.

Blood investigations showed hemoglobin- 7.4 g/dL (12-14 g/dL), total leucocyte count-22,400/mm 3 (4000-11000/mm 3 ) with 79% neutrophils, platelets-1,64,000 (1,50,000-4,00,000/mm 3 ), blood urea-84.5 mg/dL (10-40 mg/dL), creatinine-3.4 mg/dL (0.5-1.4 mg/dL), sodium 117 mEq/L (130-149 mEq/L), potassium 6.4 mEq/L (3.5-5.5 mEq/L), serum calcium 12.5 mg/dL (9.5-11.5 mg/dL), and serum phosphorus 5.4 mg/dL (3.5-5.5 mg/dL). Arterial blood gas analysis showed mild metabolic acidosis and C-reactive proteins was positive. Peripheral blood smear showed microcytic hypochromic anemia with toxic granules. Chest X-ray was normal. Kidney ultrasound was urgently done to see the echogenicity and corticomedullary differentiation of the kidneys. Surprisingly we found that the cause of AKI was bilateral pelviureteric junction obstruction with calcareous debris within the dilated system and there was also bilateral hydronephrosis? Pyonephrosis.

The baby was treated with initially fluid restriction and broad-spectrum antibiotics. Emergency peritoneal dialysis was started. On the next day of admission, bilateral ureterolithotomy was done under general anesthesia and bilateral nephrostomy drains were inserted [Figure 1]. High urine flow was promptly achieved after the procedure, and the serum creatinine level dropped quickly from 3.4 to 0.5 mg/dl. Baby was on ventilator support for 3 days. The nephrostomy drain tubes were removed on 8 th postoperative day and the antibiotics were continued for 3 weeks. Urine output gradually improved. After intensive supportive treatment the patient's condition improved.
Figure 1: The infant on ventilator with bilateral nephrostomy tubings

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On further workup, it was found that urinary calcium creatinine ratio was 0.92 (normal <0.8), serum parathyroid hormone (PTH) levels - 5.50 pg/ml (N-15-68 pg/ml), Serum 25-hydroxy Vitamin D3-228.92 nmol/L (intoxication >200 nmol/L). Thyroid function test was normal and serum Vitamin A or retinol was 37 μg/dL (normal reference interval 38-106). Metabolic screening by way of tandem mass spectrometry and gas chromatography-mass spectrometry (GC/MS) was normal. Stone analysis (Fourier transform infrared spectroscopy) of the sandy stones [Figure 2] which were removed through the nephrostomy tubes showed it to be carbonate apatite and traces of Weddellite.
Figure 2: Urine from nephrostomy tubing showing calcareous sandy stones

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On further enquiry to find out the cause of hypercalcemia, the parents informed that the baby had received injections of Vitamin D, 6,00,000 IU twice in 2 months during his hospitalization in a rural hospital (for suspected sepsis). Furthermore, the baby was prescribed two different preparations of calcium phosphate and one preparation of calcium carbonate thrice daily post discharge from the hospital. In addition to this, baby was also taking two multivitamin preparations daily. Thus, the baby received 5000 IU of Vitamin D against a daily requirement of 400-600 IU. The amount of calcium taken was also much higher than the recommended dietary allowances (RDA). The likelihood of hypercalcemia precipitated by over-ingestion of Vitamin D and calcium was suspected as there was severe hypercalcemia with concomitantly normal serum phosphorous, appropriately suppressed, PTH and raised serum 25 (OH)Vitamin D.

The patient completely recovered in 4 weeks and had normal serum calcium, parathyroid hormone and phosphorous level at 3-month follow-up. The serum calcium and renal functions remained normal on follow-up. However, after 2 months of follow-up the patient was seen to have noncommunicating hydrocephalus, probably due to postmeningitic sequelae and a VentriculoPeritoneal shunt was inserted for the same. A magnetic resonance imaging (MRI) done at this stage showed bilateral symmetric calcification in the periventricular white matter. As patient was asymptomatic, only treatment for primary condition and supportive care was given.

As other secondary causes like primary hyperparathyroidism, malignancy, sarcoidosis, etc. were ruled out, an excessive intake of Vitamin D along with calcium supplements was considered as the cause of hypercalcemia. The findings of excessive metastatic calcification from the MRI scan may be an indirect clue towards excessive calcium and Vitamin D load over the past several days.


  Discussion Top


In this case report, we would like to emphasize the importance of urolithiasis in the differential diagnosis of AKI in young children. In children, stone formation is less common. There is always an underlying metabolic or anatomical abnormality in children who form stones. [2] These include obstructions of the kidney or ureter and diseases such as spina bifida and bladder exstrophy. These anatomical problems make the treatment of stones in children more complicated. [4]

Urolithiasis may only cause nonspecific symptoms in children. [5] An early diagnosis with prompt treatment and a close follow-up are the key to achieve the best long-term outcome. Bilateral ureteral obstruction in children is a rare condition related to several medical or surgical pictures. It needs to be promptly suspected in order to attempt a quick renal function recovery. It is a rare event but is required to be kept in mind. [6]

Iatrogenic hypercalcemia, though rare, should also be kept in mind as a metabolic cause of urolithiasis in children. Administering high doses of inappropriate medications and inadequate follow-up is the commonest error of iatrogenic hypercalcemia. The highest chronic daily oral intake of Vitamin D that will pose no risk of adverse effects for most healthy infants has not been elucidated. [7] Our patient had received daily Vitamin D of 5000 IU every day for the last 2 months since his birth as against RDA of 400-800 IU/day. This emphasizes the need to regularly assess the patients suspected of taking multiple off the counter medications.

Vitamin D intoxication can be accidental [8] or due to self-medication [9] or induced by diet or over the counter supplements [10],[11],[12] or iatrogenic in some unusual cases. [13] It is a common practice for physicians to prescribe Vitamin D preparations for assumed nutritional deficiency and nonspecific body and leg pains which are partly believed to be due to Vitamin D deficiency. The overzealous use of Vitamin D in India due to the fear of rickets can also lead to Vitamin D intoxication. [14],[15]

Metastatic calcification as seen in our case is frequently described in hypercalcemia due to hypervitaminosis of Vitamin D. Metastatic calcium is found in many forms including carbonate, phosphate, oxalate, whitlockite, and apatite. [16],[17] Autopsies have shown metastatic calcification in large, medium, and small arteries, lungs, liver, spleen, kidneys (as calculi and nephrocalcinosis), adrenals, and mesentery. [18],[19]

Our case report emphasizes the consideration of Vitamin D overdose in young infants presenting with hypercalcemia. A careful enquiry into drug history and appropriate biochemical tests can unravel a treatable cause, generally considered rare in an area of florid Vitamin D deficiency. [20] Treatment consists of withdrawing Vitamin D and drugs that exacerbate its effects on serum calcium and renal function.

Physicians need to be wary of prescribing Vitamin D in high doses without monitoring and must be sensitive to the potential toxic effects of a seemingly innocuous "vitamin." [21] Pre-treatment and follow-up Vitamin D levels should be done for appropriate evidence-based treatment. Thus, this report highlights the life-threatening perils of indiscriminate and often excessive intake of Vitamin D and calcium-containing supplements.

 
  References Top

1.
Ramello A, Vitale C, Marangella M. Epidemiology of nephrolithiasis. J Nephrol 2000;13:45-50.  Back to cited text no. 1
    
2.
López M, Hoppe B. History, epidemiology and regional diversities of urolithiasis. Pediatr Nephrol 2010;25:49-59.  Back to cited text no. 2
    
3.
Schwarz RD, Dwyer NT. Pediatric kidney stones: Long-term outcomes. Urology 2006;67:812-6.  Back to cited text no. 3
    
4.
Alaya A, Nouri A, Najjar MF. Paediatric renal stone disease in Tunisia: A 12 years experience. Arch Ital Urol Androl 2008;80:50-5.  Back to cited text no. 4
    
5.
Sternberg K, Greenfield SP, Williot P, Wan J. Pediatric stone disease: An evolving experience. J Urol 2005;174:1711-4.  Back to cited text no. 5
    
6.
Daudon M. Component analysis of urinary calculi in the etiologic diagnosis of urolithiasis in the child. Arch Pediatr 2000;7:855-65.  Back to cited text no. 6
    
7.
Hathcock JN, Shao A, Vieth R, Heaney R. Risk assessment for Vitamin D. Am J Clin Nutr 2007;85:6-18.  Back to cited text no. 7
    
8.
Ozyurek HE. Iatrogenic Vitamin D intoxication. Yeni Týp Derg 2001;22:22-3.  Back to cited text no. 8
    
9.
Chambellan-Tison C, Horen B, Plat-Wilson G, Moulin P, Claudet I. Severe hypercalcemia due to Vitamin D intoxication. Arch Pediatr 2007;14:1328-32.  Back to cited text no. 9
    
10.
Kawaguchi M, Mitsuhashi Y, Kondo S. Iatrogenic hypercalcemia due to Vitamin D3 ointment (1,24(OH)2D3) combined with thiazide diuretics in a case of psoriasis. J Dermatol 2003;30:801-4.  Back to cited text no. 10
    
11.
Klontz KC, Acheson DW. Dietary supplement-induced Vitamin D intoxication. N Engl J Med 2007;357:308-9.  Back to cited text no. 11
    
12.
Koutkia P, Chen TC, Holick MF. Vitamin D intoxication associated with an over-the-counter supplement. N Engl J Med 2001;345:66-7.  Back to cited text no. 12
    
13.
Chiricone D, De Santo NG, Cirillo M. Unusual cases of chronic intoxication by Vitamin D. J Nephrol 2003;16:917-21.  Back to cited text no. 13
    
14.
Rudneva LF, Androsova LA. Long-term outcomes after acute Vitamin D3 intoxication. Vopr Pitan 2004;73:11-3.  Back to cited text no. 14
    
15.
Jones G. Vitamin D and health in the 21 st century: An update pharmacokinetics of Vitamin D toxicity. Am J Clin Nutr 2008;88:582-6.  Back to cited text no. 15
    
16.
Joshi R. Hypercalcemia due to hypervitaminosis D: Report of seven patients. J Trop Pediatr 2009;55:396-8.  Back to cited text no. 16
    
17.
Doneray H, Ozkan B, Ozkan A, Koþan C, Orbak Z, Karakelleoðlu C. The clinical and laboratory characteristics of Vitamin D intoxication in children. Turk J Med Sci 2009;39:1-4.  Back to cited text no. 17
    
18.
Allgrove J. Disorders of calcium metabolism. Curr Paediatr 2003;13:529-35.  Back to cited text no. 18
    
19.
Jones G. Pharmacokinetics of Vitamin D toxicity. Am J Clin Nutr 2008;88:582S-6.  Back to cited text no. 19
    
20.
Maji D. Vitamin D toxicity. Indian J Endocrinol Metab 2012;16:295-6.  Back to cited text no. 20
    
21.
Glade MJ. Vitamin D: Health panacea or false prophet? Nutrition 2013;29:37-41.  Back to cited text no. 21
    


    Figures

  [Figure 1], [Figure 2]



 

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