No abstract

The pathophysiology of post-renal transplantation phosphorus wasting is complex and to date is still not fully recognized. Further studies of the regulatory mechanism of fibroblast growth factor-23 and its metabolism may offer additional insights into phosphorus homeostasis and its clinical application in the post-renal transplantation population.

Background Observational studies examining the role of estrogen in the risk of kidney stone formation have shown conflicting results. However, randomized trial evidence on nephrolithiasis risk with estrogen therapy in postmenopausal women is lacking. Methods We reviewed the incidence of nephrolithiasis in the Women’s Health Initiative estrogen-alone and estrogen plus progestin trials conducted at 40 US clinical centers. A total of 10 739 postmenopausal women with hysterectomy were randomized to receive 0.625 mg/d of conjugated equine estrogens (CEE) or placebo, and 16 608 postmenopausal women without hysterectomy were randomized to receive placebo or estrogen plus progestin given as CEE plus medroxyprogesterone acetate (2.5 mg/d). The incidence of nephrolithiasis was determined for an average follow-up of 7.1 years for the CEE trial and 5.6 years for the estrogen plus progestin trial. Results Baseline demographic characteristics and risk factors for nephrolithiasis were similar in the placebo and treatment arms. Estrogen therapy was associated with a significant increase in nephrolithiasis risk from 34 to 39 cases per 10 000 person-years (hazard ratio, 1.21; 95% confidence interval, 1.03-1.44). Censoring data from women when they ceased to adhere to study medication increased the hazard ratio to 1.39 (95% confidence interval, 1.08-1.78). The increased nephrolithiasis risk was independent of progestin coadministration, and effects did not vary significantly according to prerandomization history of nephrolithiasis. Conclusions These data suggest that estrogen therapy increases the risk of nephrolithiasis in healthy postmenopausal women. These findings should be considered in decision making regarding postmenopausal estrogen use. The mechanisms underlying this higher susceptibility remain to be determined.

Presentation C.S., a previously healthy 26-year-old Cantonese woman, presented with 6 days of nausea, vomiting, occasional fevers, and nonspecific abdominal pain that progressed to myalgias, polyuria, polydipsia, fatigue, and delirium. She had been asleep in bed for many hours preceding admission. Her only medication was an oral contraceptive, and she did not use herbals or alcohol. Her father had type 2 diabetes. In the emergency room, she was mildly delirious, hyperventilating, afebrile, and dehydrated. She weighed 133 lb, her pulse was 110 bpm, and her blood pressure was 102/62 mmHg. The physical exam was otherwise normal. Urinalysis revealed 4+ glucose and ketones, large blood without red blood cells, and no infection. The urine was tea-colored. Plasma glucose was 809 mg/dl, betahydroxybutyrate 6.9 mmol/l, lactate 3.2 mmol/l, sodium 126 mmol/l, potassium 4.9 mmol/l, creatinine 2.2 mg/dl, carbon dioxide 9 mmol/l, leukocytes 24,800/ml, arterial pH 7.06, and partial pressure of arterial carbon dioxide (PaCO 2) was 15 mmHg. Toxicology screen was negative, phosphate was 3.0 mmol/l, alanine aminotransferase was 299 IU/l, and aspartate aminotransferase was 782 IU/l, with normal bilirubin and alkaline phosphatase levels. Creatine kinase (CK) was 46,305 IU/l. Troponin I peaked at 5.8 ng/ml, but C.S. reported no chest pain, and electrocardiogram showed only sinus tachycardia. Islet cell, insulin, and glutamic acid decarboxylase antibodies were negative. Her hemoglobin A 1c was 6.7%.

Amiodarone is a class III antiarrhythmic drug widely used for both ventricular and supraventricular tachyarrhythmias. Due to its high iodine content and structural similarity to thyroxine, abnormalities in thyroid function are common in patients taking amiodarone, especially with long-term use. Both hypo- and hyperthyroidism have been associated with amiodarone, with the former far more common in the United States. We present a patient with medically refractory amiodarone-induced thyrotoxicosis after a 2-year history of amiodarone use, resulting in cardiac arrest and encephalopathy. The patient ultimately required total thyroidectomy for symptomatic control.