Leukocyte CMV antigen levels in renal allograft recipients

Thirty-eight [38] new kidney recipients, and 12 normal controls were included in this study to determine the value of various immunologic parameters in the early monitoring of active CMV infection. CMV antigen and IgG and IgM antibodies were measured weekly in both recipient and control groups. In addition, the level of Soluble Interleukin 2 Receptor [SIL2R] and T cell subsets were measured at monthly intervals. This was correlated to their clinical condition. Eight [8] of the 38 recipients became positive for CMV antigen in peripheral blood leukocytes. This usually preceded the appearance of CMV IgM antibodies by at least one week. On further follow-up, CMV IgM decreased to normal levels in 4 to 6 weeks in 5 recipients. The remaining 3 died from CMV syndrome. In addition, the serum SIL2R level in the recipients before transplantation was significantly higher than in the control group. One month after transplantation, the CMV negative antigen group showed a significant lowering of the SIL2R level, while the CMV positive group showed a significant rise in this level. One month later, SIL2R decreased significantly. Finally, T cell subset determination in the CMV positive group showed a slight lowering of helper T cells and a marked elevation of the suppressor cells compared to the CMV negative group. This was also associated with a significant decrease in the helper/suppressor ratio. CMV antigenaemia is a sensitive and specific marker of CMV infection that significantly precedes the appearance of CMV antibodies. It is of great value in the monitoring of renal transplant recipients who are at high risk of CMV infection

Study of urinary excretion of leukotriene B4 and prostaglandin E2 in patients with glomerulonephritis and bilharziasis

Estimation of urinary excretion of prostaglandin E2 [PGE2] and leukatriene B4 [LTB4] was studied in chronic liver disease patients with and without chronic glomerulonephritis [GN]. 44 chronic liver disease patients [Schistosomal or non-schistosomal] were divided into two groups: group A [21 patients] associated with chronic glomerulonephritis; group B [23 patients] without detectable urinary abonrmality. 10 adults [group C] served as healthy controls. PGE2 and LTB4 were estimated in 24 hours urine by radioimmunoassay technique. Urinary PGE2 was significantly higher in liver disease patients associated with chronic glomerulonephritis [group A] than patients with liver disease only [group B]. The latter group showed a significant higher PGE2 than the normal controls. Increased urinary LTB4 excretion was found in chronic liver disease patients associated with chronic glomerulonephritis compared to nromal adults. While no detectable difference was found in LTB4 excretion between patients with liver disease [group B] compared to normal adults. We concluded that urinary PGE2 and LTB4 excretion increase with the development of G.N yet the explanation for this increase is postulated to be different. Increased manry PGE2 excretion is a translation to an endosgenous renal protective mechanism, while the increase in LTB4 excretion reflects the severity of the inflammatory process of the kidney