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The HBeAg/anti-HBe system was studied as a marker of infectivity and chronic progressive liver disease in 460 hemodialysis patients. The importance of HBeAg as an index of infectivity was confirmed in that it was present simultaneously with specific DNA polymerase (31 patients) and by the presence of widely diffuse core particles in the hepatocyte nuclei (revealed by biopsy in six patients). In contrast, HBeAg showed no useful correlation with progressive liver disease, the absence of which was confirmed in all cases by biochemical and histological studies.

A case of nonoliguric acute renal failure after treatment with piromidic acid and acetylsalicylic acid is reported. The histological picture of acute interstitial nephritis and a positive leukocyte in

2 cases of acute renal failure associated with diclofenac therapy are reported. In the 1st case no other risk factors but diclofenac administration were identified. Renal biopsy showed patchy interstitial infiltration of mononuclear cells and polymorphonuclear leukocytes. In the 2nd case preexisting nephropathy and heart failure were underlying illnesses. In both cases renal function returned to the basal values after stopping the drug.

In 20 patients with nephrotic syndrome (10 minimal change glomerulonephritis, MCN; 10 focal glomerulosclerosis, FGS) the peripheral blood lymphocytes showed a statistically significant increase in IgG-bearing cells (SIgG-C) in comparison with 30 patients with other histological types of primary glomerulonephritis with and without nephrotic syndrome (14 and 16, respectively). In the same MCN and FGS patients the serum IgG levels were slightly decreased. Furthermore, 5 cases of MCN in sustained remission for 1 year after steroid therapy showed normalization of the SIgG-C and the serum IgG levels. The possible significance of these phenomena in the pathogenesis of the hypo-IgG-globulinemia in MCN and FGS is discussed.

One hundred and one patients were treated for up to two years for three hours every other day (10.5 hr/week), or four hours thrice-weekly with conventional disposable 1m2 dialysers have been investigated. Rigorous control of water balance and the maintenance of predialysis serum K and PO4 within normal limits were the main criteria for judging the adequacy of the treatment. The results regarding blood pressure, phosphate problems, haematocrit, peripheral nerve status, pericarditis and range of rehabilitation are discussed.

The present paper reports some aspects of glycolipid metabolism observed during and after dialysis of varying duration, and the effects of glucose content in dialysis fluid. Some substances used in dialysis interfere with glycolipid metabolism: heparin (Robinson and French, 1960; Wolff and Wolff, 1960); sodium acetate (Bloch, 1947; Ghosal et al, 1969; Mion et al, 1964); and glucose in high (Leonards et al, 1961; Mendelssonhn et al, 1967) or low concentrations (Drukker et al, 1964; Hagstam et al, 1969) or, more recently, completely eliminated (Alwall et al, 1970; Hubner et al, 1971).

The clinical and bioptic aspects of 211 cases of primary mesangioproliferative glomerulonephritis with urinary abnormalities lasting mre than 1 year were reviewed. We observed the following clinical syndromes: 1) Persistent proteinuria, isolated or with microhematuria: - a) with latent onset: 39% with hypertension (H); 10% with renal failure (RF); - b) with acute nephritic syndrome at onset: 31% with H; 6% with RF; 2) Recurrent macroscopic hematuria: 26% with H; 10% with RF; 3) Nephrotic syndrome: 70% with H; 29% with RF. The histological lesions, diffuse in all cases, appeared unrelated to the clinical syndromes and/or immunofluorescent patterns. In 65 cases with prevalent mesangial deposits of IgA, 46% showed persistent proteinuria with latent onset, 23% persistent proteinuria with acute nephritic syndrome at onset, 28% recurrent hematuria and 3% nephrotic syndrome. 37% of such patients developed H, 14% RF and 6% remission (R). On the other hand in 65 patients with other deposits the clinical aspects were as follows: persistent proteinuria with latent onset: 46%; persistent proteinuria with acute nephritic syndrome at onset: 31%; recurrent hematuria: 17%; nephrotic syndrome: 6%. 35% of these cases displayed H; 9% RF and 8% R.primary mesangioproliferative glomerulonephritis appears to represent a heterogeneous group with only the morphological aspects in common and associated with one of the three above-mentioned clinical syndromes. Immunohistology shows different Ig and/or complement which bear no specific relationship with clinical courses. In particular IgA deposits are present in 50% of the cases and are only related to higher incidence of recurrent hematuria and abnormal IgA serum levels.

The plasma concentration and urinary excretion after a single 500 mg dose of Aminosidine have been studied in 12 patients with different degrees of renal failure and 4 normal subjects. In normal subjects the plasma half-life is 2.47 hr; in patients with creatinine clearance (Ccr) of 30-60 ml/min, its 6.7 hrs.; in patients with Ccr of 10-30 ml/min, it is 16.7hrs.; in patients with Ccr less than 10 ml/min, it is 36.6 hrs. A dose of 0.5 g of Aminosidine should be given to normal subjects every 12 hr. When renal function is reduced, the interval (in hr) between doses should be the following: Ccr 60-40 ml/min: 19-28;Ccr 40-30 ml/min; 28-35; Ccr 30-20 ml/min: 35-47; Ccr 20-10 ml/min: 47; Ccr less than 10 ml/min: 76.