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The report describes 22 cases of lupus nephritis (20 diffuse and 2 mesangial) showing frequent tubuloreticular inclusions (TRI) in the glomerular and peritubular capillary endothelial cells as well as cylindric confronting cisternae (CCC) mainly in interstitial infiltrating cells. Ten other cases of lupus nephritis that were actively treated or were in the sclerosing stage and did not show CCC were also studied. The presence of cytoplasmic inclusions correlated with various clinical and histologic parameters. Cytoplasmic inclusions, especially CCC, are associated with clinically active, minimally treated renal disease of recent onset and histologically with active diffuse glomerular and acute interstitial lupus nephritis with many immune deposits.

Three patients are presented, who by electron microscopy, showed prominent fibrillary deposits in the glomeruli, and in two, also around the tubules. By immunohistology these two cases had no immunoglobulins in either glomeruli or around the tubules. In the third case, which probably represents a slightly different form of the disease, minor deposits of IgM were found in the glomeruli, while fibrillary deposits were extensive and widespread. It is suggested that precursors of fibrillary deposits may not be the same in all cases.

We encountered 4 individuals with Marfan syndrome who presented with microhematuria and proteinuria. In 2 of them, a renal biopsy was performed. The predominant glomerular change by light microscopy was a focal segmental increase in mesangial matrix with early sclerotic lesions. Ultrastructurally, there was variable subendothelial widening containing haphazardly arranged microfibrils, 10-13 nm in diameter. Changes in small arteries present in the biopsies were mild in case 1 and more striking in case 2 which consisted of elastolysis and fragmentation and focal disruption of internal elastic lamina, and focal degenerative changes in the media. In light of observations on the abnormalities of microfibrillar protein (fibrillin) in the microfibrillar-fiber system and the presence of abnormal type IV collagen in the connective tissues in Marfan syndrome, the glomerular basement membrane alterations may be related to these defects and lead to microhematuria and proteinuria.

The clinical and pathologic features of progressive renal disease in 4 patients with Down’s syndrome are described. All patients were male, between 20 and 30 years of age at the time of clinical presentation. Three out of 4 had proteinuria, and 2 had hematuria. Serologic tests for hepatitis B virus infection and antinuclear antibodies performed in 2 patients were negative. Examination of renal tissue from biopsy and/or from autopsy revealed mesangiocapillary glomerulonephritis (MCGN), type 1. While an increased incidence of congenital heart disease and acute leukemias has been documented in Down’s syndrome, an association with MCGN has not been reported previously to our knowledge. This probably represents a form of idiopathic MCGN and may be related to the long survival of these individuals.

This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.

The induction of heat shock (stress) proteins (HSP) is a response by cells due to a variety of physical, chemical, and infectious agents. They have a significant role as cytoprotectants, in the regulation of cellular functions, and in the recovery after sublethal injury. Using antibody to mammalian HSP 72/73, we have performed an immunohistological study of human renal tissue in normal and diseased states, including idiopathic nephrotic syndrome, proliferative and crescentic glomerulonephritis, and interstitial nephritis. A significant increase of HSP expression was noted in certain segments of the tubule in acute interstitial nephritis and in glomerulonephritis accompanied by active interstitial inflammation. A possible role by the inflammatory mediators in the induction of HSP in those cases is suggested.