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Background: Gentamicin has been increasingly used instead of cephalosporins for surgical prophylaxis in an attempt to reduce the rate of "Clostridium difficile" infection. There are limited data regarding nephrotoxicity related to gentamicin in these patients. Methods:We have conducted a systematic review and meta-analysis to evaluate the risk of acute kidney injury (AKI) in gentamicin-containing surgical prophylactic regimens, compared to regimens without gentamicin, in several types of surgery. Electronic searches were performed using PubMed and Embase, including terms for "AKI, gentamicin, and surgical prophylaxis" with and without MeSH/EMTREE functions. Statistical analysis was then performed using a random-effect model; risk ratios (RR), risk differences (RD) and heterogeneity (I 2 ) were calculated. Funnel plot was used for assessment of publication bias.Results: Eleven studies with fifteen cohorts with 18,354 patients were included in the analysis. Subgroup analysis was performed according to surgery type. We have found that antibiotic prophylaxis with gentamicin containing regimen has significant risk for developing postoperative AKI in orthopedic surgery (RR 2.99; 95% CI: 1.84, 4.88). The results were inconclusive in other types of surgery. Funnel plot indicates potential publication bias.Conclusions: Gentamicin-induced AKI is significant in patients undergoing orthopedic surgery.Physicians should consider risks and benefits of using this regimen in individual patients.

Pauci-immune crescentic glomerulonephritis (PICGN) is most commonly associated with antineutrophil cytoplasmic antibodies (ANCA). We report a case of chronic, sclerosing ANCA-negative PICGN discovered when a patient presented with multiple myeloma. A 57-year-old woman presented with complaints of nausea, emesis and weakness. She was found to be in renal failure with a serum creatinine of 9.4 mg/dl, mild hyperkalemia and acidosis. She was noted to have normochromic, normocytic anemia with normal platelet and white cell counts, normal plasma proteins and serum protein electrophoresis. Further studies revealed increased concentrations of κ and λ light chains in a ratio of 34.89; a bone marrow biopsy found 12% plasma cells. Serum protein electrophoresis revealed no spike. ANCA, anti-glomerular basement membrane, antineutrophil antibody, hepatitis panel and serum complements were normal. A kidney biopsy result showed chronic sclerosing PICGN plus tubular necrosis, severe tubular atrophy, interstitial fibrosis and severe arteriosclerosis. Congo red stains were negative and electron microscopy showed no intraglomerular deposits. The patient was subsequently treated for myeloma with bortezomib and dexamethasone with good hematologic response but never recovered renal function. She remains on outpatient hemodialysis. Renal manifestations of myeloma often involve glomerular deposition disease, tubulointerstitial disease, with characteristic proteinaceous casts, or both. In contrast, our patient demonstrated neither of these findings but had chronic sclerosing PICGN. Crescentic glomerulonephritis occurring in patients with plasma cell dyscrasias has been previously reported, but the association remains extremely rare.

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