Acute rejection is an expected event after transplantation and has been associated with poor long-term kidney transplant outcome. The presence of B cells in the kidney graft with acute rejection is thought to be an omnious sign, as it has been associated with poor graft outcome. There is no definitive treatment for acute rejection with B cells in the graft. Rituximab, a humanized monoclonal antibody against CD20, has been used in the treatment of B cell lymphoma. We present the case of a 49-yr-old Caucasian male with early acute kidney allograft rejection that was refractory to high doses of steroids and rabbit anti-thymocyte globulin (thymoglobulin). Repeat renal biopsy revealed T cell and B cells in the kidney graft and responded to the combination of rituximab and muromonab (a mouse monoclonal antibody to CD3 receptor). Over 9 months post-transplant, the patient remains rejection free with a serum creatinine of 1.7 mg/dL.

Recovery from ischemic acute renal failure (ARF) involves a well-described regenerative process; however, recovery from ARF also results in a predisposition to a progressive renal disease that is not well understood. This study sought to identify alterations in renal gene expression in postischemic, recovered animals that might play important roles in this progressive disorder. RNA isolated from sham-operated control rats or rats 35 days after recovery from bilateral ischemia-reperfusion (I/R) injury was compared using a cDNA microarray containing approximately 2,000 known rat genes. A reference hybridization strategy was utilized to define a 99.9% interval and to identify 16 genes that were persistently altered after recovery from I/R injury (12 were upregulated and 4 were downregulated). Real-time PCR verified the altered expression of six of eight genes that had been positively identified. Several genes that were identified had not previously been evaluated within the context of ARF. S100A4, a specific marker of fibroblasts, was identified in a population of interstitial cells that were present postischemic injury. S100A4-positive cells were also identified in tubular cells at earlier time points postischemia. Genes associated with calcification, including osteopontin and matrix Gla protein, were also enhanced postischemic injury. Several proinflammatory genes were identified, including complement C4, were enhanced in postischemic tissues. Conversely, renal kallikrein expression was specifically reduced in the postischemic kidney. In summary, genes with known inflammatory, remodeling, and vasoactive activities were identified in rat kidneys after recovery from ARF, some of which may play a role in altering long-term renal function after recovery from ARF.

A 36-year-old man who was undergoing longterm hemodialysis was hospitalized with a twoday history of increasing dyspnea on exertion. He stated that he did not have cough, orthopnea, or night sweats.On examination, he was found to be in mild respiratory distress, with a blood pressure of 156/68 mm Hg, a respiratory rate of 22, a pulse of 80 per minute, and a temperature of 38.3°C (100.9°F). The site of entry of a right subclavian dialysis catheter appeared unremarkable. There was edema of the left hand and an audible bruit over an arteriovenous shunt in the left forearm. The heart and right lung were normal on examination, but the entire left hemithorax was dull to percussion, with decreased breath sounds. There was no ascites or pedal edema.A chest film revealed a massive, left-sided pleural effusion (Fig. 1). The blood urea nitrogen level was 73 mg per deciliter (26 mmol per liter), the serum creatinine level was 11.3 mg per deciliter (999 µmol per liter), and the hemoglobin level was 10.6 g per deciliter. Serum levels of potassium, sodium, and bicarbonate were normal. In arterial blood, the pH was 7.33, the partial pressure of carbon dioxide was 41 mm Hg, and the partial pressure of oxygen was 84 mm Hg.The New England Journal of Medicine Downloaded from nejm.org at HELSEBIBLIOTEKET GIR DEG TILGANG TIL NEJM on August 13, 2015. For personal use only. No other uses without permission.