A case of nephrocalcinosis

A 42-year-old Caucasian male was initially admitted with generalized weakness, malaise, poor oral intake, and occasional nausea and vomiting for 3 weeks. There was no history of gross hematuria or shortness of breath. Past medical history was notable solely for tobacco use (two packs per day for 20 years). There was no history of hypertension or diabetes and there was no family history of renal disease. The patient took no prescription medications but reported taking antacids as needed and occasional ibuprofen. Physical examination revealed a heart rate of 92 b.p.m., respiratory rate of 12 breaths per min, blood pressure of 108/62 mm Hg, and the absence of edema or cutaneous manifestations. Laboratory evaluation (Table 1) revealed acute kidney injury with a creatinine of 7.2 mg/dl, mild hypokalemia, hypercalcemia, mild hyperphosphatemia, a severe non-anion gap metabolic alkalosis, and a suppressed parathyroid hormone level. The patient reported having not seen a physician for 10 years, and no baseline laboratory values were available for comparison. Urinalysis revealed trace protein and a bland sediment with no red blood cells, white blood cells, or casts. The patient was found to have a urine protein-to-creatinine ratio of 0.37 (mg/mg). Serologic evaluation revealed normal C3 and C4 complement levels and no evidence of a monoclonal spike on serum or urine protein electrophoresis. The following serologies were negative: antinuclear antibody, antineutrophil cytoplasmic antibody, antistreptolysin O, antiglomerular basement membrane antibody, hepatitis B surface antigen, and antihepatitis C antibody. The kidneys measured 9 cm in length by ultrasound, with increased echogenicity but no evidence of obstruction. Two discreet areas of dystrophic calcification were noted within the interpolar region of the renal parenchyma and measured 6 and 3 mm. The patient was admitted and given intravenous normal saline with added potassium for treatment of hypercalcemia and hypokalemia, antiemetics, and a proton pump inhibitor. Over the course of 4 days, the patient's creatinine declined to 4 mg/dl and serum calcium and potassium levels normalized. The patient was discharged. Following discharge, the patient was feeling well and the creatinine declined over 2 weeks to 2.3 mg/dl. Five weeks later, the creatinine was 1.6 mg/dl. Two months after the initial presentation, repeat serum chemistries again revealed acute kidney injury with a creatinine of 5.4 mg/dl. At that time, the patient had a serum sodium of134 mmol/l, potassium 2.9 mmol/l, chloride 75 mmol/l, CO 2 44 mmol/l, calcium 12.8 mg/dl, and phosphorus 6.7 mg/dl. The patient reported no significant new symptoms although he did mention persistent 'heartburn'. On his own, he had discontinued taking the proton pump inhibitor and restarted antacids, without relief of symptoms. Similarly, he reported having to 'drink milk at night' to help the symptoms. Physical examination was unrevealing. Given the unclear etiology of the patient's acute kidney injury, a renal biopsy was performed.