Lipid peroxidation products, both lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS) were determined in the plasma of 31 uremic patients treated with maintenance hemodialysis. Whereas patients had significantly elevated TBARS compared to 93 healthy controls (4.25 ± 1.53 vs. 1.66 ± 0.50 μmol/l; p < 0.01) lipid hydroperoxides were not detected in the plasma of patients before dialysis. After hemodialysis, a slight increase in TBARS was observed (4.50 ± 1.97 μmol/l, p > 0.01). However, when the TBARS were corrected for hemoconcentration by relating TBARS to the plasma cholesterol concentrations a statistically significant decrease of TBARS was observed (1.02 ± 0.63 μmol TBARS/mmol cholesterol vs. 0.84 ± 0.60 μmol TBARS/mmol cholesterol; p < 0.01) after 240 min of hemodialysis. There was no evidence for the formation of plasma lipid hydroperoxides in the extracorporeal circulation. It is therefore suggested that elevated TBARS in chronic renal failure are not caused by the dialysis therapy.

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Veno-occlusive disease (VOD) developed in a 4 5-year-old white male 2 years after cadaveric kidney transplantation while receiving combined immunosuppressive therapy with prednisone and azathioprine. Early clinical signs at presentation included ascites and tender hepatomegaly. The diagnosis of VOD was established at laparoscopy and by histological examination of liver biopsies. Azathioprine was discontinued. Gross ascites refractory to medical treatment and decreasing liver function required surgical treatment by portacaval shunt. Transient postoperative complications were hepatic encephalopathy and considerable hyperbilirubinaemia. 8 months later the patient is well, with stable renal function and no clinical signs of hepatic disease.

A new method was applied to isolate a polypeptide hormone from human blood. The polypeptides from 1,000 1 of hemofiltrate with a molecular weight lower than 20 kDaltons were adsorbed to 2.5 kg alginic acid, then eluted, precipitated, and desalted on a G-25 Sephadex column, thus obtaining a crude lyophilised plasma polypeptide extract. These polypeptides were further submitted to ion-exchange chromatography. Thereafter, two steps of HPLC were carried out to purify a distinct polypeptide which was the circulating form of cardiodilatin (CDD) in this case. The amino acid analysis, C-terminal enzymatic cleavage by carboxypeptidase A, and sequence analysis showed that the only form of circulating cardiodilatin is the 28 amino acid residue containing molecule, cardiodilatin-99-126 cleaved from the C-terminus of cardiodilatin-126 and identical with alpha-ANP (alpha atrial natriuretic polypeptide). Other bioactive molecular forms of the polypeptide hormones of the cardiodilatin family were not detected in the hemofiltrate. The isolation procedure was followed up by a bioassay using in vitro vascular smooth muscle relaxation.

A patient with typical features of late onset McArdle's disease is described. During forearm ischemic work test the patient exhibited an exaggerated increase in ammonia release, largely exceeding normal values. It is suggested, that this is due to an activation of the myokinase/myoadenylate deaminase pathway. Besides lack of lactate release increased ammonia release during ischemia may be a typical feature of McArdle's disease.