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Year : 2017  |  Volume : 15  |  Issue : 2  |  Page : 144-145

Calcium in the kidney

Department of Nephrology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India

Date of Web Publication18-May-2017

Correspondence Address:
Anna T Valson
Department of Nephrology, Christian Medical College and Hospital, Vellore - 632 004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cmi.cmi_31_17

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How to cite this article:
Valson AT. Calcium in the kidney. Curr Med Issues 2017;15:144-5

How to cite this URL:
Valson AT. Calcium in the kidney. Curr Med Issues [serial online] 2017 [cited 2022 May 24];15:144-5. Available from: https://www.cmijournal.org/text.asp?2017/15/2/144/206521

  Case Scenario Top

A 56-year-old female presented with polyuria, constipation, and generalized weakness. On evaluation, she was found to have normal fasting and postprandial blood sugar, serum creatinine 1.3 mg/dL, serum calcium 12 mg/dL, and serum phosphorus 2 mg/dL. Serum 25(OH) Vitamin D was 30 ng/mL (normal >30 ng/mL) and serum parathyroid hormone (PTH) was 80 pg/mL (normal range: 8–64 pg/mL). Physical examination was normal. X-ray of the kidney-ureter-bladder (KUB) is shown in [Figure 1].
Figure 1: X-ray kidney-ureter-bladder of the patient.

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  Questions Top

  1. Describe the findings on the X-ray KUB
  2. Why is the pathophysiology of this condition?
  3. What diseases can be associated with this finding?
  4. What is your diagnosis in this case?

  Answers Top

  1. Nodular calcifications in the region of the renal pyramids (blue arrow) with radio-opaque shadows in the pelvicalyceal system (white arrow). This condition is called medullary nephrocalcinosis, and in this case, it is associated with renal calculi
  2. Nephrocalcinosis refers to the deposition of calcium oxalate and/or calcium phosphate salts along the renal pyramids. It is caused by increased urinary excretion of calcium, phosphate, and/or oxalate such that the concentration of these salts in the urine exceeds the saturation point.[1] Since the renal medulla is exposed to a hypoxic, hyperosmolar environment, and tubular flow is most turbulent in the medullary loop of Henle, precipitation of salts most commonly occurs here, extending into the interstitium, collecting ducts, and the renal papillae, when it becomes radiologically evident. A low urine volume and low urine concentration of crystal inhibitors such as magnesium, citrate, and proteins such as Tamm–Horsfall protein accelerate this process [2]
  3. The causes of medullary nephrocalcinosis can be classified based on laboratory parameters, into four broad categories. (1) Conditions that cause hypercalciuria with hypercalcemia, for example, primary hyperparathyroidism, Vitamin D intoxication, and sarcoidosis. (2) Conditions that cause hypercalciuria without hypercalcemia, for example, distal renal tubular acidosis, medullary sponge kidney, loop diuretics, Bartter syndrome, and Dent's disease. (3) Conditions that cause hyperphosphaturia, for example, X-linked, autosomal-dominant, and autosomal recessive hypophosphatemic rickets, tumor lysis, and acute phosphate nephropathy due to sodium phosphate-containing bowel preparations. (4) Conditions that cause hyperoxaluria, for example, primary hyperoxaluria, fat malabsorption due to pancreatic insufficiency, inflammatory bowel disease, and bowel resection or bypass. Out of these, primary hyperparathyroidism, distal renal tubular acidosis, and medullary sponge kidney are the most common causes of medullary nephrocalcinosis [3]
  4. When hypercalcemia coexists with elevated PTH or PTH in the high normal range, the diagnosis is primary hyperparathyroidism [4] – an excessive production of PTH by one or more of the four parathyroid glands. A parathyroid adenoma is the most common cause of primary hyperparathyroidism,[5] and hypercalcemia is the result of increased osteoclastic bone resorption and intestinal calcium absorption. The function of PTH is to maintain serum calcium within the normal range, and in the setting of hypercalcemia, PTH release from the parathyroid gland would normally undergo feedback inhibition. However, an adenomatous or hyperplastic parathyroid gland becomes autonomous and resistant to feedback inhibition, leading to the finding of hypercalcemia and high or high normal PTH level.[5] The diagnosis can be confirmed by ultrasound of the neck or parathyroid radionuclide scintigraphy using technetium-99m sestamibi. Renal involvement in the form of nephrocalcinosis or renal calculi is an indication for parathyroidectomy even in the absence of symptoms of hypercalcemia.[4]

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There are no conflicts of interest.

  References Top

Sayer JA, Carr G, Simmons NL. Nephrocalcinosis: Molecular insights into calcium precipitation within the kidney. Clin Sci (Lond) 2004;106:549-61.  Back to cited text no. 1
Shavit L, Jaeger P, Unwin RJ. What is nephrocalcinosis? Kidney Int 2015;88:35-43.  Back to cited text no. 2
Wrong O. Nephrocalcinosis. In: Davison A, Cameron JS, Grünfeld J, editors. Oxford Textbook of Clinical Nephrology. Oxford: Oxford University Press; 2005. p. 1375.  Back to cited text no. 3
Khan AA, Hanley DA, Rizzoli R, Bollerslev J, Young JE, Rejnmark L, et al. Primary hyperparathyroidism: Review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus. Osteoporos Int 2017;28:1-19.  Back to cited text no. 4
Bilezikian JP, Cusano NE, Khan AA, Liu JM, Marcocci C, Bandeira F. Primary hyperparathyroidism. Nat Rev Dis Primers 2016;2:16033.  Back to cited text no. 5


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