Patients with end-stage renal disease (ESRD) develop hemostatic disorders mainly in the form of bleeding diatheses. Hemorrhage can occur at cutaneous, mucosal, or serosal sites. Retroperitoneal or intracranial hemorrhages also occur. Platelet dysfunction is the main factor responsible for hemorrhagic tendencies in advanced kidney disease. Anemia, dialysis, the accumulation of medications due to poor clearance, and anticoagulation used during dialysis have some role in causing impaired hemostasis in ESRD patients. Platelet dysfunction occurs both as a result of intrinsic platelet abnormalities and impaired platelet-vessel wall interaction. The normal platelet response to vessel wall injury with platelet activation, recruitment, adhesion, and aggregation is defective in advanced renal failure. Dialysis may partially correct these defects, but cannot totally eliminate them. The hemodialysis process itself may in fact contribute to bleeding. Hemodialysis is also associated with thrombosis as a result of chronic platelet activation due to contact with artificial surfaces during dialysis. Desmopressin acetate and conjugated estrogen are treatment modalities that can be used for uremic bleeding. Achieving a hematocrit of 30% improves bleeding time in ESRD patients.

Donor-specific alloantibodies (DSA) to HLA-DP may cause antibody-mediated rejection (AMR), especially in re-transplants. We describe the immunization history of a patient who received 3 kidney transplants; the 3rd kidney was completely matched except at DPA1 and DPB1. Prior to the 3rd transplant, single antigen bead analysis (SAB) showed DSA reactivity against DPA1 shared by the 1st and 3rd donors, but B and T flow crossmatch (FXM) results were negative. Within 11 days the 3rd transplant underwent acute C4d+ AMR which coincided with the presence of complement (C1q)-binding IgG1 DSA against donor DPA1 and DPB1. Using HLAMatchmaker and SAB, we provide evidence that eplet (epitope) spreading on DPA1 and eplet sharing on differing DPB1 alleles of the 1st and 3rd transplants was associated with AMR. Since weak DSA to DPA1/DPB1 may induce acute AMR with negative FXM, donor DPA1/DPB1 high resolution typing should be considered in sensitized patients with DP-directed DSA.

Henoch-Schonlein purpura (HSP) is an acute leukocytoclastic vasculitis that primarily affects children but also affects approximately 1% of adults. We discuss a case of HSP that started after pantoprazole ingestion. Clinical manifestation included terminal ileitis and rapidly progressing glomerulonephritis. To our knowledge, this is the first reported case of HSP secondary to pantoprazole ingestion. The patient presented with renal failure requiring hemodialysis and was initially unresponsive to intravenous pulse steroids. The patient was treated with mycophenolate mofetil, and his renal function recovered. There are limited data regarding use of mycophenolate mofetil for treating crescentic glomerulonephritis secondary to HSP.

Hydralazine is a commonly used drug for treatment of hypertension and is known to cause drug-induced lupus erythematosus. It has rarely been reported to cause anti neutrophil cytoplasmic antibody positive vasculitis, a life-threatening complication. Presentation could be extremely variable delaying diagnosis. Although drug-induced vasculitis has been infrequently associated with rapidly progressing glomerulonephritis, pulmonary involvement presenting as pulmonary renal syndrome is extremely rare. We report a case of hydralazine-induced vasculitis presenting as pulmonary renal syndrome with fatal outcome even after aggressive treatment. Numerous antibodies are associated with hydralazine including anti myeloperoxidase antibody, anti-nuclear antibody, anti-histone antibody, and anti-elastase antibody. Additionally, we also report the presence of anti-phospholipid antibodies specific to anti-cardiolipin, anti-beta2 glycoprotein, and anti-phosphatid that have not been previously reported. We conclude that early diagnosis and prompt discontinuation of the drug is necessary for the treatment of hydralazine-induced anti neutrophil cytoplasmic antibody vasculitis.

Gastrointestinal (GI) complication used to be the second most common complication in renal transplant patients after infection (Bardaxoglou et al. in Transpl Int 6(3):148-152, 1993). Review of transplant registry reveals that GI complication is no longer the second most common type of complication after renal transplant, but that it is still a common cause of significant amount of deaths in renal transplant recipients (De Bartolomeis et al. in Transpl Proc 37(6):2504-2506, 2005). In a study of 1,515 adults with severe GI complication after renal transplant, Sarkio et al. (Transpl Int 17(9):505-510, 2004) reported that gastroduodenal ulcers followed by colon perforation were the two biggest groups of GI complications during the first year after renal transplantation. Colonic perforation is estimated to occur in about 1 % of all cases of renal transplant patients, and it does predispose to potentially fatal complication. About 50 % of all colonic perforation is due to complication of acute inflammation of diverticular disease (Bardaxoglou et al. in Transpl Int 6(3):148-152, 1993; Guice et al. in Am J Surg 138(1):43-48, 1979; Koneru et al. in Arch Surg 125(5):610-613, 1990; Coccolini et al. in Transpl Proc 41(4):1189-1190, 2009). This is particularly so because these patients were previously exposed to uremia before transplantation which alters their protein metabolism hence interfering with tissue healing there after (Carson et al. in Ann Surg 188(1):109-113, 1978). GI complications including colon perforation after renal transplantation have effect on a patient's long-term survival (Gil-Vernet et al. in Transpl Proc 39(7):2190-2193, 2007). Despite this, the role of renal transplantation medication compared to anatomic anomaly in GI complication has been equivocal.