β2-microglobulin and other proteins in serum and urine during preeclampsia

Summary Serum and urine samples of 5 patients with preeclampsia, an equal number with preeclampsia superimposed upon chronic pyelonephritis, and 20 normal pregnant women were analysed for fibrin split products (immunoelectrophoresis) and other proteins (Oudin-method) including₂-microglobulin (radioimmunoassay).No fibrin split products could be detected in normal pregnant women or those with preeclampsia superimposed upon chronic pyelonephritis. Distinctly abnormal values were found, however, in the patients with preeclampsia (split D, 27.2±5.1 mg% (S.D.) in serum and 162±55mg/24 h (S.D.) in urine; split E, 0.3±0.1 mg% (S.D.) in serum and 4.2±3.1 mg%/24 h (S.D.) in the urine; fibrinogen in serum 532±146 mg% and in urine 340±78 mg/24 h (S.D.).Mean total protein excretion of patients with preeclampsia (1951±322 mg S.D./24 h) was not different from the value of patients with preeclampsia superimposed upon chronic pyelonephritis (1781±289 mg S.D./24 h).Urinary₂-microglobulin excretion of patients with simple preeclampsia (glomerular filtration rate 100 ml/min) was 4 to 5-fold increased at term but more than 100-fold in patients whose preeclampsia was superimposed upon chronic pyelonephritis (glomerular filtration rate 30–70 ml/min).The transient urinary excretion of fibrin split products and other proteins in patients with preeclampsia and normal glomerular filtration rate is an indication of a reversible glomerular lesion, whereas the increased₂-microglobulin excretion in this group of patients is due to a tubular lesion. In patients with preeclampsia superimposed upon chronic pyelonephritis the excretion of₂-microglobulin is further increased which may be explained by an additional lesion of the already impaired tubular function during delivery.In serum, prealbumin was decreased to about 55% and albumin to 60% in the patients with preeclampsia and preeclampsia superimposed upon chronic pyelonephritis which cannot be explained by renal loss alone but is very likely due to an inhibition of protein synthesis in the liver cell.Contains parts of the Doctoral Thesis of D. Prüfer