Ricin induces glomerular thrombotic microangiopathy, closely resembling that which occurs in verocytotoxin-producing E. coli-induced HUS. As in HUS, high concentrations of proinflammatory cytokines are present, which are probably a result of cytokine superinduction by the toxin.

Plasma immunoreactive human atrial natriuretic peptide (Ir-ANP) levels were measured in eight patients with chronic renal failure who were volume-expanded and during treatment by sequential ultrafiltration and haemodialysis. One patient was studied at two separate treatment sessions. Plasma Ir-ANP levels were raised in all patients (mean +/- SE 184 +/- 44 pmol/l, n = 9) compared with healthy controls (11 +/- 1.4 pmol/l), but showed considerable inter-patient variability. Plasma Ir-ANP levels fell with fluid removal during ultrafiltration (123 +/- 30 pmol/l, n = 9, P less than 0.02) and again as fluid was removed during haemodialysis (76 +/- 20 pmol/l, n = 9, P less than 0.02). Seven patients studied 48 h later, before their next dialysis treatment, had regained weight and showed a coincident rise in circulating plasma Ir-ANP (130 +/- 33 pmol/l, n = 7). Our data would support the hypothesis that the secretion of ANP is determined by volume or by a stimulus related to volume. However, it does not exclude the possibility that a factor other than extracellular fluid volume expansion contributes to the raised plasma Ir-ANP levels in chronic renal failure.

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1. Plasma and urinary aluminium levels, and renal function, were investigated in a control group of rats (n = 5) and in two groups that received an intravenous bolus dose of aluminium chloride (either 25 micrograms or 800 micrograms of aluminium, n = 7 and 5, respectively). 2. In the control group (plasma aluminium concentration 76.8 +/- 14.2 ng/ml), 59.4 +/- 3.5% of the plasma aluminium was ultrafilterable. The percentage ultrafilterable after the administration of 25 micrograms of aluminium was 41.9 +/- 7.8 (plasma concentration 154.3 +/- 18.6 ng/ml). However, after administration of 800 micrograms of aluminium, to give a plasma concentration of 19,800 +/- 2956 ng/ml, only 1.06 +/- 0.13% was ultrafilterable. 3. Such results have generally been interpreted as indicating an increase in protein-binding of aluminium with increasing aluminium concentration. In buffered aqueous solutions of aluminium chloride at pH 7.4, with an aluminium concentration of 189 +/- 6 ng/ml, 96.12 +/- 0.02% was ultrafilterable (n = 6). This concentration is comparable with that attained in the low-dose (25 micrograms) aluminium group of animals and suggests that the difference between the ultrafilterable percentage of aluminium in plasma compared with that in aqueous solution is indeed due to the binding of aluminium to high Mr material (proteins). In contrast, however, in an aqueous buffered (pH 7.4) solution containing 28,200 ng of aluminium/ml, only 1.05 +/- 0.09% was ultrafilterable. This indicates insolubility (i.e. colloid formation) of the aluminium at this high concentration. The same percentage (1.06 +/- 0.13) was ultrafilterable from plasma from the high-dose (800 micrograms) aluminium group with a plasma aluminium concentration of 19,800 +/- 2956 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)