Short-term experience with early steroid withdrawal in African-American renal transplant recipients.

There are limited data on the results of early steroid withdrawal (ESW) in African-American (AA) renal allograft recipients. We examined short-term transplant outcomes in a retrospective, non-concurrent cohort study of 40 AAs who did not (ESW group), and 33 who did [steroid maintenance (SM) group] receive maintenance steroids after day 4 post-transplant. Patients received thymoglobulin (ATG) induction, mycophenolate mofetil, and tacrolimus or sirolimus. Data were analyzed using survival analysis methods and regression models. Patients in the ESW group were older, had lower current panel reactive antibody and fewer re-transplants, and received fewer doses of ATG. One-year graft survival and acute rejection (AR) rates were 100% and 13% in the ESW group and 97% and 15% in the SM group. After controlling for confounders, at 1 year, ESW was not associated with higher risk of graft loss, AR, or worse graft function, but was associated with less weight gain. The SM group had higher cholesterol levels at 3 months and higher risk of post-transplant diabetes mellitus. We did not observe any cases of subclinical rejection. This study suggests that ESW under modern immunosuppression is safe over the short term in at least a subset of AA recipients with risk profiles similar to those studied herein, and could be associated with improved outcomes.

Acute renal failure.

Acute renal failure is divided into its classic parts: prerenal azotemia, postrenal azotemia (obstruction), and renal azotemia (including acute tubular necrosis). The division of acute tubular necrosis into the ischemic and toxic varieties is supplemented by an analysis of toxic varieties into those caused by antibiotics, radiologic contrast agents, chemotherapeutic-immunosuppressive agents, heavy metals, organic solvents, etc. Acute tubular necrosis caused by hemoglobin and myoglobin is described in detail. The importance of urinalysis and the urinary indices in distinguishing prerenal azotemia from acute tubular necrosis is stressed. Finally, current prognosis and treatment are reviewed.

Leukocyte metabolism and function in uremia.

Leukocyte metabolism was studied in 13 non-diabetic hemodialysis patients, 8 clinically stable, nondiabetic transplant recipients, and 13 control subjects. Metabolic parameters included rates of oxygen consumption (nmoles/min/10(6) cells), glucose uptake, lactate production (nmoles/hr/10(6) cells), and 14C-l-glucose oxidation to 14CO2 (nmoles/hr/10(6) cells). Granulocyte metabolism was stimulated by phagocytosis of opsonized zymosan (Z) and by the membrane perturbing agent phorbol myristate acetate (PMA). Granulocyte motility in response to zymosan-activated plasma (ZAP) was also studied. Granulocytes from hemodialysis patients showed significantly impaired stimulated oxygen consumption (Z = 2.41 +/- 0.30 vs. 3.73 +/- 0.39; PMA = 2.63 +/- 0.33 vs. 3.67 +/- 0.19), resting glucose uptake (17.7 +/- 2.9 vs. 36.5 +/- 3.5), stimulated glucose uptake (Z = 44.2 +/- 7.1 vs. 71.8 +/- 5.3; PMA = 63.7 +/- 5.5 vs. 92.8 +/- 5.6), stimulated lactate production (Z = 68.4 +/- 5.1 vs. 97.5 +/- 9.3; PMA = 70.7 +/- 4.9 vs. 92.7 +/- 5.4), and ZAP-stimulated granulocyte motility (16 +/- 3 vs. 30 +/- 4 mu). Metabolic responses of granulocytes from transplant recipients were frequently intermediate between those of hemodialysis patients and controls, but not significantly different from controls. Abnormalities of glucose and oxygen metabolism in granulocytes from uremic patients may cause or contribute to granulocyte dysfunction and vulnerability to infection in such patients.

Lymphocyte and granulocyte function in zinc-treated and zinc-deficient hemodialysis patients.

Lymphocyte blast transformation and granulocyte motility were studied in 20 clinically stable hemodialysis patients, 10 of whom were receiving 50 mg of zinc (as zinc acetate) per day and 10 of whom were not. Plasma zinc concentration was significantly higher in zinc-treated than in untreated patients (108 +/- 5 vs. 82 +/- 2 micrograms/dl). Mononuclear cell subpopulation analysis showed equivalent proportions of T lymphocytes and monocytes in both groups, but B lymphocytes were reduced in untreated patients (10 +/- 0.7 vs 14 +/- 0.5%). Lymphocyte blast transformations in response to nonspecific mitogens, soluble antigen and mixed lymphocyte culture were not significantly different in the two groups, nor was lymphocyte zinc concentration. Zinc-treated patients showed significantly greater granulocyte responsiveness to zymosan-activated serum (21 +/- 1 vs. 14 +/- 2 mean), greater chemokinetic activity (50 +/- 4 vs. 27 +/- 3 mean) and higher granulocyte zinc concentration (114 +/- 6 vs. 47 +/- 2 micrograms/10(6) cells) than untreated patients. Granulocyte zinc correlated significantly with plasma zinc (r = 0.81, P less than 0.001) and with granulocyte motility (r = 0.63, P = 0.001). Moderate zinc deficiency in hemodialysis patients does not result in abnormal lymphocyte blast transformation in vitro, but it does result in granulocyte zinc depletion and impaired granulocyte motility.