Early and late humoral rejection: a clinicopathologic entity in two times.

Humoral rejection is an important cause of early and late graft loss. The late variant is difficult to diagnose and treat. There is a close correlation between sclerosing nephropathy and anti-HLA antibodies. We analyzed 113 renal allograft recipients between August 2004 and April 2007. Acute humoral rejection was defined as acute graft dysfunction in presence of donor-specific antibodies (DSA) detected by flow panel reactive antibodies (PRA) and/or C4d positive pericapilary tubules (PTC) detected histopathologically by immunofluorescent or immunoperoxidase at less than 3 months postransplantation. Late humoral rejection was defined as dysfunction occurring after 3 months postransplantation with histopathologic glomerulopathy or vasculopathy and positive C4d PTC. We included all patients who were diagnosed with early or late graft dysfunction and underwent biopsy, all of which were examined for C4d. Four patients had acute humoral rejection treated with IVIG or plasmapheresis. The patient and graft survivals were 100% and serum creatinine averaged 1.7 mg/dL. Three recipients experienced late humoral rejection at 3 to 10 years posttransplantation All received high-dose IVIG; one also was treated with thymoglobulin. Immunosuppression was switched to tacrolimus, mycophenolate mofetil, and steroids. Only one patient recovered renal function; the others returned to dialysis. Among seven patients only one had an actual PRA (>20%) and three showed 10% to 20%. However, six had a positive historical PRA of 10% to 50%. In conclusion, Recognition of acute humoral rejection has contributed to graft rescue by controlling alloantibody production through new specific immunosuppressive therapies in contrast with the clinical response to acute therapy, treatment of a chronic entity has shown poor outcomes, probably because antibody mediated chronic graft damage is already present when the late diagnosis is established by biopsy.

[Renal transplantation in patients with neurogenic bladder]. / Transplante renal en pacientes con vejiga neurogénica.

BACKGROUND: Renal transplantation can be done in patients with neurogenic bladder and clean intermittent self catheterization maintains renal function AIM: To retrospective assess the results of renal transplantation in patients with neurogenic bladder. PATIENTS AND METHODS: The medical records of seven patients aged 10 to 22 years old (3 female) followed during 7 to 32 months were reviewed. All patients had urinary tract infection, prior to transplantation, were instructed on self catheterization and received tri-associated immunosuppression. RESULTS: Grafts came from alive related donors in 5 patients and from cadavers in two. Prior to transplantation, three patients were subjected to nephrectomy and three to bladder enlargement, leaving a pigtail catheter. After transplantation, one lymphocele was drained, one uretherostomy due to an impacted lithiasis and one nephrectomy plus vesical enlargement due to intravesical pressures over 40 cm H2O, were done. One uretheral stricture was treated with dilatation. Seven episodes of pyelonephritis, 19 urinary tract infections and 77 asymptomatic bacteriurias were documented. Serum creatinine at the end of follow up ranged from 0.7 to 2.1 mg/dl. There were 0.7 acute rejection episodes per patient and all grafts survived. CONCLUSIONS: Renal transplantation in patients with neurogenic bladder is feasible, performing a vesical enlargement. There is however a high frequency of infectious episodes.

Vitamin and mineral nutrition in chronic alcoholics including patients with Korsakoff's psychosis.

1. A group of 129 patients with chronic alcoholism were assessed for their nutritional status with respect to certain minerals and vitamins, and compared with control subjects. 2. In all subjects the plasma values were normal for calcium, magnesium and zinc. 3. As in other studies a seasonal variation was found in the plasma levels of 25-hydroxyvitamin D in the control subjects and the alcoholic subjects; in all seasons lower levels were found in the alcoholics than in the controls, but none of the alcoholic patients had results in the range found in osteomalacia. 4. The alcoholic subjects had low levels of ascorbic acid both in the plasma and in the leucocytes. 5. Although vitamin A and beta-carotene levels were within the reference range, the results in alcoholics were found to be lower than in the control subjects. 6. We suggest that subclinical vitamin deficiencies other than thiamine deficiency contribute to the cerebral impairment frequently found in alcoholism.