Extraskeletal tumoral calcifications (TC) may occur in patients with end-stage renal disease. The TC usually develop in the presence of secondary hyperparathyroidism or a high calcium × phosphate product, while other factors have been also occasionally implicated in their development. At present, no uniformly accepted effective treatment has been described for this condition. We describe a 58-year-old female patient with end-stage renal disease who 7 years after the onset of dialysis presented with pain and movement restriction of various joints. A skeletal X-ray showed huge amounts of periarticular TC. The TC occurred in the absence of hyperparathyroidism or a high calcium × phosphate product as evidenced by hormonal and biochemical examination as well as by a bone biopsy specimen that revealed an adynamic bone disease with significant aluminum staining. Sodium thiosulfate, an inorganic salt that has been claimed to inhibit the formation and to favor the solubility and the mobilization of calcified masses, was administered to the patient, and after a long period of treatment considerable radiological regression of the TC with concurrent clinical recovery was noticed. Aluminum intoxication, along with other factors, was considered to be the cause of TC development. The use of sodium thiosulfate seemed to be a reasonable nonspecific therapeutic approach for the management of TC in this case.

Fifty-two British and 29 Greek idiopathic membranous nephropathy (IMN) patients were analysed for DRB, DQA1, DQB1 and DPB1 gene polymorphism using second exon amplification and sequence-specific oligonucleotides (SSO). In addition 100 British and 92 Greek controls were analysed. A highly significant increased frequency of the DRB1*0301 allele was found in IMN patients from Britain (80%), when compared to controls (27%, OR 10.6, P = 0.000004). A lower frequency of DRB1*0301 was observed in Greek IMN patients (33%), but this was just significant before correction, when compared to Greek controls (15%, OR 3, P = 0.02). The DRB3 allele most often associated with DRB1*0301 was DRB3*0101 (OR 4.2, P = 0.00025) in British patients and DRB3*0201/2 (OR 11, P = 0.006) in Greek patients. In Greek IMN patients a decrease in DR16 was found (OR 0.08, P = 0.004), and the overall incidence of DR2 was significantly lowered when both sets of IMN patients were combined (OR 0.21, chi 2 17.6, P = 0.00013). The incidence of DQA1*0501 was raised in both Greek (96% vs. 66%, OR 9.7, chi 2 6.9, P = 0.009) and British IMN (85% vs. 45%, OR 7.4, chi 2 20, P = 0.00007) patients. This gives some support to a proposal for a major role for this allele in IMN.(ABSTRACT TRUNCATED AT 250 WORDS)

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The absence of bcl-2 expression in normal and diseased glomeruli suggests and supports the reported notion that the mechanism of apoptosis may be available in the injured glomerulus. Moreover, bcl-2 expression in podocytes near intraglomerular fibrotic lesions and in epithelial cells of early adhesions and cellular crescents indicates the deregulation of apoptosis and its possible role in the progression of glomerular scarring. Key words: apoptosis; bcl-2 oncoprotein; glomerulonephritis; immunohistochemical; renal rejection.

Corticosteroids have the major role in the immunosuppressive treatment of patients who have received renal transplants. Despite their extensive use there is still debate about the appropriate dose that will prevent rejection of the renal allograft with the least morbidity. From March 1979 to November 1981 a randomised controlled trial of high (33 patients) v low oral dose (34 patients) of prednisolone along with azathioprine was conducted in recipients of first cadaveric transplants who had received a blood transfusion within six months of transplantation. The main difference in outcome between the two groups was a high incidence of some infections in the high dose group. Patient mortality, graft survival, transplant function, and number of rejection episodes were indistinguishable in the two groups, but rejection episodes tended to occur later in the high dose group.These findings suggest that the use of lower doses of corticosteroids soon after cadaveric renal transplantation does not jeopardise graft survival and results in lower patient morbidity.