Nephrol Dial Transplant (2002) 17: 677-678
© 2002 European Renal Association-European Dialysis and Transplant Association
Nephroquiz
Hypercalcaemia-induced renal failure—a mystery
(Section Editor: M. G. Zeier)
Department of Nephrology, Klinikum der Universität Heidelberg, Bergheimer Strasse 56a, D-69115 Heidelberg, Germany Email: daniel_henriquez{at}med.uni-heidelberg.de
An 80-year-old male patient was admitted with a 2-week medical history of progressive weakness, anorexia, pollakisuria and subsequent oliguria.
The patient was slightly disoriented and a detailed history was difficult to obtain. His private physician reported a history of arterial hypertension, dyslipidaemia, atrial fibrillation and thyroidectomy because of suspected (but disproven) thyroid malignancy. On admission the patient was hypotensive (90/60 mmHg). Hypotension promptly responded to intravenous (i.v.) saline. Laboratory investigation revealed acute renal failure, with serum creatinine 3.65 mg/dl, urea 123 mg/dl, uric acid 7.1 mg/dl and metabolic acidosis.
The patient had hypercalcaemia, a serum calcium of 3.11 mmol/l, serum phosphorus of 1.20 mmol/l and serum albumin of 4.6 g/dl. Serum PTH and PTH-related peptide were low (Table 1
). Urinalysis was unremakable (no haematuria or proteinuria). Ultrasonography showed normal sized kidneys, no renal calculi and no nephrocalcinosis.
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Serum chemistry was otherwise normal, including 25 OH-vitamin D3, 1,25 OH-vitamin D2, ACE (angiotensin converting enzyme), PSA (prostate specific antigen), and immunelectrophoresis. Urinary immunelectrophoresis did not reveal any abnormal immunoreactive protein.
Questions
What is the diagnosis?
What further possibilities would you explore?
Answer to the quiz on the preceding page
Because of PTH suppression and no evidence of malignancy (including PTH-related peptide concentration) the patient was treated empirically with i.v. saline, and the administration of loop diuretics (furosemide) and corticosteroids (Table 2). The patient responded slowly to treatment and serum calcium returned to the upper normal range within 10 days.
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The patient was still confused, but reported that following thyroidectomy he had episodes of tetany and received medication.
An interview with the former physician who had taken care of the patient up until a year previous revealed that he had received the vitamin-D analogue dihydrotachysterol (AT-10) (Figure 1). The patient had faithfully continued to take the drug. It is of note that the concentration of dihydrotachysterol is not detected by the 25 OH-vitamin D3 assay [1].
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The diagnosis was dihydrotachysterol intoxication with hypercalcaemia and subsequent acute renal failure [2–4]. More recently, the patient was doing well and his serum creatinine was below 2 mg/dl but still not within the normal range.
This case illustrates that for an inclusive history of potentially prescribed drugs, not only the referring physician, but also his predecessors should be consulted.
Notes
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Suggested Reading
- Schwartzman MS. Vitamin D toxicity complicating the treatment of senile, postmenopausal and glucocorticoid-induced osteoporosis. Am J Med1987; 82: 224–230[Medline]
- Earm JH. Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts in poliuric hypercalcemic rats. J Am Soc Nephrol1998; 9: 2181–2193[Abstract]
- Mawer EB. Vitamin D metabolism in patients intoxicated with ergocalciferol. Clin Sci1985; 68: 135–141[Medline]
- Chapuy MC. Metabolic basis of Vitamin D intoxication. In: Cohen RD, Lewis B, Alberti KG, Denman AM, eds. The Metabolic and Molecular Basis of Acquired Disease. Bailliere Tindall, London, 1990; 11: 1824–1834
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