Immunological investigations in vernal eye disease.

A group of patients with vernal disease was investigated for serum IgE levels, specific antibody to external allergens in serum and tears, and the frequencies of the HL-A antigens. Biopsies taken from the conjunctiva were examined by means of light and electron microscopy for the presence of mast cells and other inflammatory cells. Serum IgE was elevated in 75 per cent of the patients, all of whom demonstrated positive prick tests to common allergens and specific antibody in their serum using the radio-allergosorbent test (RAST). Specific antibody was also demonstrated in tears using the same technique. The distribution of the HL-A antigens showed no difference in frequency when compared with controls. Conjunctival biopsies demonstrated numerous mast cells, the more superficial of which were degranulating in active disease. In control biopsy material, mast cells were densely packed with granules. The clinical manifestations in vernal disease together with the infiltration of the tarsal conjunctiva with many types of inflammatory cell, are possible caused by mediators which are known to be produced by degranulating mast cells when they are stimulated by allergens.

Human polyomavirus (BK) infection and ureteric stenosis in renal allograft recipients.

Human polyomavirus (BK) was detected in two renal allograft recipients as a result of routine examination of Papanicolaou-stained smears of urinary sediment in the light microscope. Infection with this recently identified virus was confirmed by virus isolation and electron microscopy. The cytological, histological, and ultrastructural changes due to the virus are described, and virus excretion is correlated with the clinical progress of the patients and the pathological findings. The transplant ureters in both patients were found to be ulcerated and stenosed, and virus-infected cells were observed in the ureteric epithelium. We suggest that the administration of high-dose steroids in transplantation may permit active infection with human polyomavirus to occur in ureteric epithelium which has been damaged by ischaemia or inflammation.

Human polyoma virus (HPV)--a significant pathogen in renal transplantation.

Routine cytological screening of Papanicolaou-stained smears of the urinary sediment from 57 renal allografts in 51 patients has resulted in the detection of seven cases of Human Polyoma Virus (HPV) BK infection--14% of the total number. Infection was confirmed by virus isolation and electron microscopy (EM). The cytological, histological and ultra-structural data are described and related to the clinical progress of the patient. Four out of the seven cases are discussed in more detail as histological material was available; in three of these, there was evidence of stenosis of the transplant ureter with virus infected cells in the ureteric epithelium and in one case also in the renal tubules. Administration of high dose steroids may provoke active infection with HPV in ureteric epithelium damaged by ischaemia and inflammation. The similarity between the clinical features of an HPV infection and a rejection episode make it imperative to confirm the diagnosis quickly and accurately. Cytological examination of the urinary deposit by light microscopy is a simple, inexpensive procedure which provides positive diagnosis of the typical virus inclusions within an hour of receiving the urine specimen in the laboratory. This can be confirmed by removing single cells from the original cytological slide preparation and processing them for EM using a technique described by Coleman et al [1].

Penicillamine nephropathy in rheumatoid arthritis. A clinical, pathological and immunological study.

Fourteen patients who developed persistent proteinuria while on penicillamine for rheumatoid arthritis, were collected over a period of one year. Eleven patients had a frank nephrotic syndrome and three had a lesser degree of proteinuria but no oedema. The patients had received penicillamine (mean daily dose 1015 mg) for less than one year (mean 7-5 months) when the nephropathy was detected. Clinical investigations have been correlated with renal biopsy material. Light microscopy detected no abnormalities except for minimal hypercellularity in a few patients. In markde contrast, the electron-microscope revealed numerous electron-dense deposits (EED's) in the outer layer of the basement membrane. Immunofluorescence showed the presence of IgG and complement in the basement membrane, the intensity of which correlated with the number of EED's. The pathological picture was essentially the same in those patients with the nephrotic syndrome and those with proteinuria. In this series, we found no evidence that penicillamine induced renal damage by any other mechanism except immune complex deposition. Serological tests revealed little evidence for complement activation or consumption and platelet aggregation was the only positive direct test for circulating immune complexes. Renal biopsies were performed at differing intervals after the cessation of penicillamine therapy, which allowed assessment of the natural history of the pathological lesion and revealed a striking persistence of EDD's in some patients. Two patients showed an almost identical picture initially and at re-biopsy one year later. Persistent proteinuria was also a feature of the group as a whole. The pathological picture has similarities with that of idiopathic membranous glomerulopathy. This study suggests that the use of penicillamine in rheumatoid arthritis may induce persistent renal damage.