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BACKGROUND: Helicobacter pylori has been identified as a possible cause of vitamin B12 deficiency in the general population. We assessed any potential relationship between low cyanocobalamin serum levels and Helicobacter pylori status in hemodialysis patients and subsequently correlated these results with the existence of anemia (a common complication in hemodialysis patients), and macrocytosis. METHODS: In 29 chronic hemodialysis patients, active H. pylori infection was diagnosed using two different methods regardless of digestive symptoms: by searching for bacterial antigens in stools and by the detection of urea breakdown through breath testing. If these results were non-coincident, gastroscopy was performed and antral biopsies obtained. Patients were subsequently divided into group A (H. pylori-positive, n = 8, 28%) and group B (H. pylori-negative, n = 21, 72%). The corresponding initial values of erythrocytic folic acid, vitamin B12 and homocysteine prior to the first hemodialysis session of each patient were retrospectively collected. RESULTS: Vitamin B12 levels (normal 200- 900 pg/ml) were significantly lower in group A compared to group B (225.4 +/- 111.9 vs. 707.9 +/- 258.3 pg/ml, p < 0.011). In group A, 5 patients (63%) had vitamin B12 deficiency (154 +/- 24.6 pg/ml). Baseline hematocrits, erythrocyte folic acid and serum homocysteine levels were not different between the groups, but mean corpuscular volumes were significantly higher in group A compared to group B (109.7 +/-14.1 vs. 91.8 +/- 8.8 fl, p = 0.002). CONCLUSIONS: H. pylori-positive chronic hemodialysis patients may present with lower vitamin B12 blood levels and macrocytosis. H. pylori infection should be suspected in this population when low or low-normal vitamin B12 levels or macrocytosis exist.

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BACKGROUND: Oxidative stress has been implicated in the development of endothelial damage in hemodialysis (HD). We have assessed the effects of N-acetylcysteine (NAC), a compound with antioxidant effects, on malondialdehyde (MDA), a marker of oxidative stress on lipid peroxidation. METHODS: A clinical trial was conducted in which 24 chronic HD patients were divided into 2 groups according to gender, age, time on HD and cause of renal failure. The NAC group (n = 12) received 600 mg of NAC twice a day for 30 days. The remaining patients constituted the control group (n = 12). MDA levels were measured pre- and post-dialysis at the beginning of the study (baseline) and on day 30 (30 days). RESULTS: Baseline pre- and post-dialysis MDA levels were not different between both groups and were above normal values. A significant decrease was found in the NAC group when either pre- or post-dialysis MDA levels were compared to the corresponding control group levels on day 30 (pre-dialysis NAC vs control group 3.01 +/- 0.6 vs 4.5 +/- 0.73 micromol/l, p < 0.0001, post-dialysis NAC vs control group 2.76 +/- 0.5 vs 4.39 +/- 0.7 micromol/l, p < 0.0001). Only in the NAC group were pre-dialysis MDA 30-day levels different from pre-dialysis baseline levels (3.01 +/- 0.6 vs 5.07 +/- 1.6 micromol/l, p < 0.002). Post-dialysis MDA 30-day concentrations were significantly lower than post-dialysis MDA baseline levels (2.76 +/- 0.5 vs 4.32 +/- 0.7 micromol/l, p < 0.002) and pre-dialysis MDA 30-day measurements (2.76 +/- 0.5 vs 3.01 +/- 0.6 micromol/l, p < 0.011). CONCLUSIONS: MDA levels are elevated in chronic HD patients and are not significantly reduced by HD. NAC significantly reduces malondialdehyde levels in chronic HD patients.

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The immune response has largely been implicated in the pathogenesis of inflammatory bowel disease (ulcerative colitis and Crohn's disease) and immunoglobulin A nephropathy. We present a 26-year-old woman with a long past history of asymptomatic macroscopic hematuria who later developed several episodes of bloody stools and abdominal pain. A colonic biopsy disclosed ulcerative colitis and a renal biopsy was consistent with immunoglobulin A nephropathy. Immunoglobulin A nephropathy is the most common glomerulonephritis, being end-stage renal disease a rare but the most serious complication. It can be primary or secondary, but the association between both entities is unusually observed. We discuss the possible immunologic mechanisms involved and believe the initial immunologic derangement originates in the bone marrow. We suggest both conditions must be considered when either a patient with ulcerative colitis and micro- or macrohematuria or with renal involvement and a past history of diarrhea or abdominal pain presents.

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Cytomegalovirus (CMV) is the most important viral agent in kidney transplantation. Clinical manifestations of CMV disease in transplantation include hepatitis, pneumonitis, pancreatitis, kidney allograft dysfunction, colitis, and meningoencephalitis. However, skin involvement is rare. We describe a severely compromised cadaveric-kidney transplant recipient who developed renal failure, colonic ulcers, and a maculopapular rash accompanied by fever and malaise 4 months after transplantation. Only the skin biopsy was diagnostic and consistent with CMV disease. Intravenous ganciclovir administration resulted in clinical improvement of CMV-induced skin lesions; kidney function normalized and the patient became asymptomatic after 14 days of ganciclovir therapy. Nephrologists should consider the diagnosis of CMV disease in the febrile immunosuppressed patient with skin involvement. Skin biopsy must be considered as a useful and safe procedure in patients with a rash to obtain a prompt diagnosis and efficiently treat this immunocompromised population.

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