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Introduction Zoledronate is an intravenous bisphosphonate that is commonly used to decrease bone resorption in patients with osteoporosis. The incidence of acute tubular necrosis (ATN) using zoledronate in patients with normal renal function is rare. Herein, we report the occurrence of severe ATN following treatment with a single zoledronate infusion in a patient with osteoporosis and normal renal function. Case Presentation A 51-year-old female with hypertension, well-controlled type 2 diabetes c/b gastroparesis without nephropathy(HbA1c6.8%), status-post hysterectomy, and bilateral oophorectomy, who was recently diagnosed with osteoporosis. Bone densitometry with Hologic revealed T scores of -2.8 at the spine and a T score of - 0.9 at the left hip. Her medications included lisinopril, metformin, and empagliflozin. Due to a history of gastroparesis, zoledronate was chosen as the preferred treatment. Pre-infusion blood work showed: a creatinine of 0.92 (0.5-1.1 mg/dl), 25-hydroxyvitamin-D 37.8 (30-100 NG/ml), calcium 8.9 (8.5-10.5mg/dl) and urine microalbumin 14 ( Discussion Zoledronate is widely used at low doses in the treatment of osteoporosis. ATN due to zoledronate infusion has been described in patients with pre-existing renal dysfunction and those receiving large and frequent doses for malignancy but rarely reported with the lower doses used to treat patients with osteoporosis and normal renal function. Zoledronate is believed to cause ATN by internalization in the renal tubular cells via the process of fluid-phase endocytosis. The intracellular accumulation of zoledronate may act as an epithelial toxin inducing tubular cytotoxicity. Interestingly, our patient had normal renal function without diabetic nephropathy and did not use nephrotoxic medications prior to the infusion. Conclusion We report a case of severe ATN due to a single dose of zoledronate in a patient with osteoporosis and previously normal renal function. This case highlights the need to be aware of the potential nephrotoxicity of zoledronate even in patients with normal renal function at baseline. Presentation: No date and time listed

Background Primary hyperparathyroidism (PHP) during pregnancy is rare with a reported incidence of 1%, although the true incidence is unknown. It is associated with increased morbidity and mortality for both mother and fetus. Most reported cases of PHP during pregnancy are due to small adenomas causing mild hyperparathyroidism. Surgical management is recommended if the calcium level is >11mg/dL (2.75mmol/L) or the patient has symptomatic hypercalcemia. It is generally recommended that surgery be performed in the second trimester due to the risk of miscarriage in the first trimester, and preterm labor in the third trimester. Case A 29-year-old woman presented to our emergency department at 10 weeks’ gestation with nausea and vomiting. She also reported constipation and fatigue. On examination, she was euvolemic, awake and alert, with no neurological symptoms or signs. The suspected diagnosis was hyperemesis gravidarum until her laboratory evaluation revealed marked hypercalcemia [15.6mg/d (3.9mmol/L)]. Further labs revealed hypophosphatemia [1.2mg/dL (0.39mmol/L)], hypokalemia [3.3mEq/L], hypomagnesemia [1.4mEq/L], low 25-hydroxy vitamin D [16.2ng/mL (40.44pmol/L)], and elevated intact parathyroid hormone (iPTH) [573pg/mL], 1,25-dihydroxy vitamin D [251.1pg/mL (626.75pmol/L)], and 24 hour urinary calcium [448mg/24 hours (11.2mmol/24 hours]. On cardiac evaluation, her QTc was normal. The patient was given intravenous hydration with normal saline, which reduced the calcium to 13.6mg/dL (3.4mmol/L) after 48 hours. She remained symptomatic and severely hypercalcemic, so calcitonin 4 IU/kg every 12 hours was added, while a neck ultrasound was performed to localize the parathyroid adenoma. Her calcium level decreased to 10.7mg/dL (2.7mmol/L) after calcitonin, but rapidly rebounded to 13.3mg/dL (3.3mmol/L) along with hypophosphatemia and hypokalemia. Intravenous potassium phosphate was initiated and her calcium decreased to 11.8mg/dL (2.95mmol/L). The neck ultrasound did not identify a parathyroid adenoma, but identified a 2.5×1.5×3.3 cm right mixed cystic/ solid thyroid nodule. An MRI of the neck revealed two right thyroid nodules. The decision was made to perform a neck dissection given the persistent severe hypercalcemia after a multidisciplinary team evaluation, and extensive discussion with the patient. The surgical exploration of the right neck identified a giant parathyroid adenoma that weighed 11.3g. The intraoperative PTH levels reduced from 804pg/mL to 60.7pg/mL. Her calcium normalized immediately postoperatively and she was discharged home without complication. At the time of last follow up, she was 18 weeks’ gestation and a fetal ultrasound was normal. Discussion This case had three unusual features: PHP causing severe hypercalcemia during pregnancy; a giant parathyroid adenoma; and parathyroid adenoma masquerading as a thyroid nodule on imaging. This case highlights the importance of a multidisciplinary team approach in optimizing the care of such complicated patients, along with the need for definitive surgical intervention. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Acute pancreatitis is a common reason for hospitalization in the United States and can have a high degree of morbidity and mortality if not treated appropriately. Establishing the diagnosis and following guideline-directed medical therapy are both important. In the Western world, the most common causes include acute alcohol overuse, hypertriglyceridemia, gallstone pancreatitis, post-instrumentation including endoscopic cholangiopancreatography, and medication side effects. Our team describes the case of an 84-year-old male that was found to have acute pancreatitis secondary to repaglinide, a commonly used medication for the management of diabetes mellitus. The diagnosis was made based on the imaging findings, physical examination, and the corresponding laboratory markers. The patient was also found to have a blood-alcohol level at baseline and triglyceride levels within normal range. The patient’s symptoms resolved with the cessation of repaglinide administration. Our team hopes to make the medical community more aware of the potential association between repaglinide and the potentially rapidly debilitating disease.

Hyperkalemia is potentially a life-threatening electrolyte disorder. Recently published Mehandru Syndrome, reveals novel cases of Pseudohypoaldosteronism with new classification as PHA-M/Mehandru Syndrome, where patients with isolated hyperkalemia were successfully managed with low potassium diet. These case reports in the above mentioned syndrome were extension of the previously reported cases in August 2017 as the “Atypical Presentation of Gordon Syndrome and Its Management”. We report three additional cases in which Patiromer was administered to aid patients unable to adhere to our standard eight week low-potassium diet protocol. Patiromer protocol was established with the objective of lowering high serum potassium without inducing hypokalemia. In our case reports, two females (ages 56 and 68, respectively) and a male (age 64) presented with unexplained hyperkalemia (6.3 mEq/L, 5.5 mEq/L, and 5.8 mEq/L respectively). Similar to patients previously reported with Mehandru Syndrome, two of our three patients presented with normal to slightly-elevated blood pressures with no other reported complaints. There were no other suspected causes for hyperkalemia, such as diabetes mellitus or the use of NSAIDs, Beta Blockers, ACEIs, ARBs, potassium supplementation, potassium sparing diuretics, or unusually high potassium diets. The prevalence of individuals presenting with Mehandru Syndrome from just our solo practice urges us to disseminate our findings with the larger medical community, with the goal of discovering and helping treat thousands of undiagnosed or misdiagnosed, hyperkalemic individuals. There is a potential that our findings will help hyperkalemic individuals who have been misdiagnosed Type IV Renal Tubular Acidosis (RTA), and those who remain in the category of unknown etiology. Mehandru Syndrome appears to affect individuals with an average age of 53 years, irrespective of gender bias, and predominantly affecting those who are Caucasian.

Platypnea-orthodeoxia syndrome (POS) has been defined as shortness of breath and hypoxemia in the upright position that improves with dorsal decubitus. This is a rare disorder caused by right-to-left shunts due to a persistent foramen ovale or pulmonary arteriovenous malformations. Hepatopulmonary syndrome can present with POS in the presence of pulmonary vasodilation and pulmonary arteriovenous communications in patients with liver disease. We report a case where the diagnosis of POS was made incidentally in a patient with cryptogenic liver cirrhosis. After other causes of hypoxemia were excluded, the diagnosis of right-to-left pulmonary shunt was confirmed by late opacification of the left heart chambers seen in a transthoracic echocardiogram. Interestingly, computerized tomography (CT) of the chest with contrast demonstrated a very prominent pulmonary vascular pattern extending to the periphery of the lungs. POS is a rare cause of hypoxemia that requires a high level of suspicion, and exclusion of more common causes of hypoxemia.

93 Background: Tumor mutational load (TML) has been proposed as a biomarker of responsiveness to novel immune checkpoint inhibitors (ICIs) due its association with increased neoantigen formation and tumor immunogenicity. Gastrointestinal cancers (GICs) are generally insensitive to ICIs; therefore the aim of this study was to evaluate the TML, clinically relevant genomic alterations (CRGAs), and PDL-1 status of GIC patients (pts). Methods: We analyzed samples of pts with GICs using a multiplatform profiling tool (Caris Life Sciences, Phoenix, AZ). TML and CRGAs were calculated based on next generation sequencing and mutational load was stratified as high (≥17 mut/Mb), intermediate (8-16 mut/Mb), and low (≤ 7 mut/Mb). PD-L1 status was determined by IHC. Descriptive statistics and simple linear regression were used for analysis. Results: A total of 85 pts with GICs were analyzed. The median pt age was 65. 53% were males and 47% were females. Tumors were colorectal 51%, pancreatic 13%, esophageal 13%, gastric 9%, hepatobiliary 11%, anal canal 4%, and small intestine 1%. 80 cases (94%) had an adequate sample for profiling and TML was available in 59 cases (74%). Cases were 5% TML-high, 56% TML-intermediate, and 39% TML-low. The median TML was 9 mut/Mb and median CRGAs was 3. The most commonly detected CRGAs were TP53 (56%), APC (44%), KRAS (40%), ATM (18%) and PTEN (6%). A positive but very weak correlation was found between TML and number of CRGAs (R2 = 0.3). PD-L1 status was available in 74 cases (93%) with 86% being PD-L1 negative and 14% PD-L1 positive. PD-L1 expression was most commonly seen in esophageal (50%) and anal canal (30%) cancers. Among 57 tumors tested for both biomarkers, no correlation was found between a high TML and PD-L1 expression. Conclusions: TML varies among GICs, and higher TML scores were not associated with PD-L1 expression, but there was a weak correlation between TML and the number of CRGAs. Further analysis by stratification of GIC type and prognostic analysis to assess the correlation between TMB and response to ICIs is warranted.