Antibrush border antibody (ABBA) disease is a rare cause of kidney disease characterized by progressive renal tubular injury associated with immune complex deposition along the basement membranes of the proximal tubule and circulating autoantibodies to brush border antigens. Several antigens have been identified as targets of autoantibodies in this disease, including low-density lipoprotein receptor related protein 2 (LRP2), cubilin, and amnionless proteins. We present 9 patients from 2 academic medical centers and describe the clinicopathologic characteristics and outcome data. All patients presented with acute kidney injury and proteinuria. Pathology confirmed immune complex deposition along proximal tubular basement membranes in all patients, but the majority (6/8) also showed segmental glomerular subepithelial immune complexes. Two of 3 patients treated with rituximab demonstrated stabilization of kidney function; 1 of these patients had mantle cell lymphoma. One patient with lung cancer showed stabilization of disease after treatment of the malignancy. The remaining patients progressed to end-stage kidney disease with either conservative therapy (3 patients) or immunosuppression with glucocorticoids (2 patients). This series highlights the poor prognosis of ABBA disease, but a potential benefit of anti-B cell therapy or treatment of an underlying malignancy in some cases.

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The safety of contemporary volatile anesthetic agents with respect to kidney function is well established, and growing evidence suggests that volatile anesthetics even protect against ischemic nephropathy. However, studies examining effects of volatile anesthetics on kidney function frequently demonstrate transient proteinuria and glycosuria following exposure to these agents, although the cause of these findings has not been thoroughly examined. We describe the case of a patient who underwent a neurosurgical procedure, then experienced glycosuria without hyperglycemia that resolved within days. Following a second neurosurgical procedure, the patient again developed glycosuria, now associated with ketonuria. Further examination demonstrated nonalbuminuric proteinuria in conjunction with urinary wasting of phosphate and potassium, indicative of proximal tubule impairment. We suggest that transient proximal tubule impairment may play a role in the proteinuria and glycosuria described following volatile anesthetic exposure and discuss the relationship between these observations and the ability of these agents to protect against ischemic nephropathy.