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In 3 patients rapidly progressive glomerulonephritis revealed plasma cell dyscrasia in 2 cases and Waldenstrom's macroglobulinemia in the 3rd. Renal biopsy showed proliferative glomerulonephritis with marked endo- and extracapillary (crescentic) proliferation. In case 1, corticosteroids and cyclophosphamide favorably influenced the course of the disease. The 2nd patient was not treated and went on to maintenance hemodialysis. In the 3rd case, plasma exchange and cytotoxic drugs allowed discontinuation of hemodialysis. Thirteen other cases of proliferative glomerulonephritis associated with monoclonal gammapathies have been described in the literature, including 3 with crescents. B-cell dyscrasia should be considered a possible etiology in a patient with crescentic glomerulonephritis. In such case we show that treatment of the hematologic disorder can be followed by a dramatic improvement of renal function.

Three women with adenocarcinoma of cardia, adenocarcinoma of liver or ileum carcinoid tumor, respectively, were treated with mitomycin C (MMC) and 5-fluoro-uracil (5-FU). Two patients had renal impairment 6 and 11 months, the third as early as 8 weeks after initiation of MMC therapy. In the three cases, blood transfusions appeared to play an aggravating role inducing respiratory distress, microangiopathic hemolytic anemia and thrombocytopenia, and to accelerate progression of renal failure. Death occurred in the first patient; terminal renal insufficiency necessitated hemodialysis treatment in the second, and after 10 plasma exchanges, renal failure remained stable in the third. Light and electron microscopy study of the kidney revealed renal lesions compatible with thrombotic microangiopathy in all cases. Mesangiolysis with swollen nuclei of endothelial cells in most glomeruli was also seen in two cases. We compared our observations with the findings found in 30 previously reported cases. These observations substantiate the renal toxicity of mitomycin C.

Histological changes in bone marrow reticulin were studied in 68 patients with adult acute leukaemia. Biopsies were performed on diagnosis and during the subsequent course of the disease. Marrow fibrosis was seen in 40% of the patients, with no predilection for morphological type of leukaemia. In most cases fibrosis was mild-to-moderate, diffuse, of the reticulin type and showing a fine regular fibre network. Pronounced fibrosis with signs of collagenization was rare. Complete regression of marrow fibrosis coincided with complete remission, and reappearance of fibrosis with relapse. The clinical and haematological course of acute leukaemia is not affected by marrow fibrosis, with the exception of more frequent bone pain and dry taps. Complete remission rate, remission induction time and mean survival time show little difference between patients with and without marrow fibrosis.