SAT-363 Renal Papillary Necrosis Associated with Normocalcemic Hyperparathyroidism

IntroductionHypercalciuria is generally considered to be the most common identifiable metabolic risk factor for calcium nephrolithiasis. Important renal manifestations of primary hyperparathyroidism (PHPT) include asymptomatic nephrolithiasis, hypercalciuria, nephrocalcinosis, and chronic renal insufficiency. However renal papillary necrosis (RPN) occurring in PHPT has not been reported previously. We report a 50-year-old woman who manifested RPN associated with hypercalciuria and normocalcemic PHPT. Case ReportA 50-year-old Caucasian woman was evaluated in 2006 for hypercalcemia. She had no history of nephrolithiasis, fractures, or symptoms of hypercalcemia. Laboratory: serum calcium 11.8 mg/dL, ionized calcium 6.3 mg/dL, phosphorus 1.8 mg/dL, intact PTH 98 pg/mL (ref 15–65), urine calcium 543 mg/24 hrs (ref <235). Renal ultrasound showed no evidence of nephrocalcinosis or nephrolithiasis. A parathyroid scan was consistent with a left superior parathyroid adenoma. Patient underwent parathyroidectomy and became normocalcemic with normal serum PTH levels postoperatively. One year later she was diagnosed with a left sided bronchial carcinoid tumor. Surveillance Gallium-68 PET/CT scan done 2 years later was negative for any metastases. Twelve years later she reported to our clinic for follow up. She had no symptoms of hypercalcemia, fractures, nephrolithiasis, history of pyelonephritis, diabetes mellitus, analgesic use, or hypertension. Serum calcium was 9.1 mg/dL, serum phosphorous 3.8mg/dL, PTH 82 pg/mL, 25-OH vitamin D 34 ng/mL, 1,25-vitamin D 38 pg/mL, and a urorisk panel was normal except for a 24-hour urine calcium of 410 mg. However renal ultrasound showed bilateral RPN and this diagnosis was also confirmed by a CT scan. A urinalysis showed only microalbuminuria with no red cells. She had no history of any analgesic drug abuse, pyelonephritis, sickle cell disease, or diabetes mellitus. A glucose tolerance test was completely normal. Discussion RPN is characterized by coagulative necrosis of the renal medullary pyramids and papillae brought on by several associated disorders and toxins that exhibit synergism toward the development of ischemia. Although the initial kidney US was normal, a repeat US done 12 years later showed evidence of RPN. This finding along with hypercalciuria and a diagnosis of normocalcemic PHPT suggests that RPN may be associated with hypercalciuria and normocalcemic PHPT. Furthermore she had no other risk factors for RPN. Additional studies with large number of patients are needed to confirm the association between these 2 disorders.