Immune complex tubulointerstitial nephritis due to antibodies to brush border antigens of the proximal tubule has been demonstrated experimentally and rarely in humans. Our patient developed ESRD and early recurrence after transplantation. IgG and C3 deposits were conspicuous in the tubular basement membrane of proximal tubules, corresponding to deposits observed by electron microscopy. Rare subepithelial deposits were found in the glomeruli. The patient had no evidence of SLE and had normal complement levels. Serum samples from the patient reacted with the brush border of normal human kidney, in contrast with the negative results with 20 control serum samples. Preliminary characterization of the brush border target antigen excluded megalin, CD10, and maltase. We postulate that antibodies to brush border antigens cause direct epithelial injury, accumulate in the tubular basement membrane, and elicit an interstitial inflammatory response.

Because of its rarity, together with the variability and nonspecificity of its signs and symptoms, pheochromocytoma, a tumor arising from chromaffin cells, creates an unlucky paradox: it is often missed but only rarely found. Besides the association with arterial hypertension, often in the form of paroxysmal attacks, pheochromocytoma may also be associated, in up to 40% of cases, with orthostatic hypotension which, when present, provides a clue to the diagnosis of the tumor. Far more rare (about 2% of cases) is the clinical presentation in the form of shock, a possibility that, among other attributes, justifies the epithet “the great mimic” applied to the neoplasia. The authors report the case of a 51-year-old hypertensive woman whose death was erroneously attributed to septic shock. Autopsy disclosed an unsuspected left adrenal bulky pheochromocytoma with areas of hemorrhage and extensive central necrosis, pronounced pulmonary edema, left ventricular mural thrombus, and histological evidence of acute myocardial injury.

A 57-year-old man presented with bilateral leg swelling, myal-gia, weight gain, and reduced urine output for three months. He exhibited no signs and symptoms of urinary tract infection or sexually transmitted disease (STD). He reported a past medical history of diabetes mellitus and hypertension for 20 years, and bariatric surgery and abdominoplasty from about five years ago. Blood cell count was normal. Serum creati-nine and creatinine clearance were 1.9 mg/dL and 49 mL/min, respectively. A 24-h urine collection revealed 19 g of protein. These results were consistent with nephrotic syndrome. Sero-logical tests for hepatitis and HIV were negative and the venereal disease research laboratory (VDRL) test was positive with a titer of 1:1024. The ultrasound showed normal kidney size with some suggestive features of acute parenchy-mal disease. He was treated with losartan, furosemide,

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