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Affinity purified immunoglobulin G (IgG) fractions from systemic lupus erythematosus (SLE) patients positive for anti-endothelial cell antibodies (AECA) bind human umbilical vein endothelial cell (HUVEC) monolayers. In vitro incubation of serial protein concentrations of SLE AECA IgG induces a dose-dependent endothelial activation: i) increase of functional adhesion of the monocytic cell line U937; ii) upregulation of E-Selectin, ICAM-1, VCAM-1 expression evaluated by a cell solid-phase enzyme linked immunoassay; and iii) increased secretion of interleukin (IL)-6 in the culture supernatants. Control experiments carried out with HUVEC monolayers incubated with IgG fractions from normal healthy controls or from AECA negative SLE sera do not affect at all endothelial adhesion molecule expression or pro-inflammatory cytokine secretion. The AECA IgG effects are not related to both anti-phospholipid or anti-DNA activities. Taken together the findings suggest that these autoantibodies might be important in recruiting and in activating mononuclear leukocytes responsible for vessel wall infiltration and raise the possibility that AECA might display a pathogenic role in SLE vessel damage.

To assess the sensitivity and specificity of third-generation assays for antibody to hepatitis C virus (anti-HCV), sera from 244 renal transplant patients (113 positive for anti-HCV enzyme-linked immunosorbent assay [ELISA]2) were studied. Hepatitis C virus RNA was detected by a reverse-transcripted nested polymerase chain reaction. Antibody to HCV was detected by ELISA-3 in 108 (96%) ELISA-2-positive samples. Five (4%) ELISA-2-positive sera were negative by both ELISA-3 and polymerase chain reaction. In the anti-HCV-negative group, six (5%) additional cases were ELISA-3-positive; three of these were confirmed by recombinant immunoblot assay-3 (RIBA-3) and polymerase chain reaction. Recombinant immunoblot assay-3 was used to resolve 82 RIBA-2-indeterminate and three RIBA-2-negative sera. Using RIBA-3, 49 (60%) RIBA-2-indeterminate samples were positive, five (6%) ELISA-3-negative samples were negative, and 28 (34%) were remained indeterminate. Recombinant immunoblot assay-2-negative samples were indeterminate with RIBA-3. Hepatitis C virus RNA was detected in all RIBA-3-positive and 58% of the RIBA-3-indeterminate samples. Third-generation assays for anti-HCV are more sensitive and specific than second-generation assays in renal transplant patients.

It is still uncertain which, if any, immunologic parameters may help diagnose a renal flare of lupus nephritis. Anti-C1q antibody (Ab) titers have been elevated in patients with lupus with renal involvement, but little information is available on whether the titers are different in quiescent and active phases of lupus nephritis. In this study, we compared anti-C1q Ab titers with other serological test results in 48 patients with biopsy-proven lupus nephritis to assess which parameter could offer the best reliability for differentiating between quiescent and active phases of lupus nephritis. Serum C3 and C4 levels, as well as anti-double-stranded DNA, antiendothelial cell, anti-C1q, and antiphospholipid Ab titers, were evaluated in patients with quiescent renal disease (38 samples) and those with clinical evidence of renal activity (23 samples). Only anti-C1q Ab titers correlated with active renal disease in both univariate (P < 0.0001) and multivariate analysis (P < 0.0001), with a sensitivity of 87% and a specificity of 92%. In six patients, immunologic parameters were measured serially. In all patients, the high anti-C1q Ab titers returned to normal values after treatment-induced remission. The other serological parameters did not show a significant association with renal disease activity. In patients with biopsy-proven lupus nephritis, anti-C1q Ab titers appear to be strongly related to renal disease activity. Their measurement may be useful for confirming the diagnosis of renal flares of lupus nephritis.

BACKGROUND Phosphate-induced hyperparathyroidism still represents an intriguing problem in dialysis patients. Postprandial hyperphosphataemia is considered to be the main stimulus to parathyroid hyperfunction, and therefore many efforts have focused on the use of phosphate binders to prevent phosphate absorption. METHODS We investigated whether the pH-mediated gastric ionization of calcium phosphate dietary salts is necessary for its intestinal absorption. In eight normal subjects we measured 24-h urinary calcium phosphate excretion and the postprandial blood calcium phosphate profile after a meal containing 1 g of calcium and 2 g of phosphate salts in a crossover placebo-omeprazole study. On two occasions the subjects received either placebo or omeprazole 60 mg/day 2 days before and during the day test. RESULTS Serum gastrin levels were measured as an indicator of achlorhydria and were 13.7 +/- 1 pg/ml after placebo and 30.4 +/- 4.7 after omeprazole (P < 0.003). Postprandial plasma phosphate profiles were not significantly different between the two studies (+36 +/- 8% after placebo and +24 +/- 8% after omeprazole, NS), while plasma calcium increased by +6.1 +/- 1% after placebo and decreased by -4.2 +/- 0.7% after omeprazole (P < 0.01). The 24-h urinary phosphate excretion was 1068 +/- 85 mg after placebo and 773 +/- 55 after omeprazole (P < 0.002), while the 24-h urinary calcium excretion was 360 +/- 21 after placebo and 238 +/- 15 after omeprazole (P < 0.0001). A negative relationship was observed between absolute changes in plasma gastrin and those in urinary calcium (P < 0.009) and phosphate (P < 0.05). CONCLUSIONS The inhibition of gastric acid secretion by omeprazole significantly reduces both urinary phosphate and calcium excretion after an oral load. The behaviour of the postprandial calcium-phosphate plasma profile suggests that gastric acid inhibition is more effective in reducing calcium rather than phosphate dietary salts absorption in normal subjects.

• The long-term clinical course of 11 adults with hemolytic-uremic syndrome (HUS) is reported. All patients were treated with heparin and antiplatelet drugs, and ten required dialysis. One patient died after 38 days; the others recovered from anuria after seven to 400 days. One patient was resubmitted to regular dialysis five years later, and another died because of cerebral hemorrhage. Among the remaining eight patients, four show renal failure and four have normal renal function after one to ten years of observation. All but three require vigorous antihypertensive therapy. It is concluded that in adults with HUS (1) recovery may occur even after a prolonged anuria; (2) severe hypertension and progressive renal failure may appear later in apparently recovered patients; and (3) heparin and antiplatelet drugs seem to be beneficial in reversing acute renal failure. ( Arch Intern Med 140:353-357, 1980)