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A patient, born in 1968, was found at the age of 9 years to have Alport's syndrome. In his 20th year, when in terminal renal failure, his father's kidney was transplanted into him. 14 months later there was a sudden worsening of his renal function after a varicella infection; for the first time antibodies against the glomerular basal membrane (GBM) were detected. Despite an increase in prednisolone dosage and 6 plasmaphereses chronic haemodialysis again became necessary. Renal biopsy revealed necrotizing intra- and extracapillary glomerulonephritis. Simultaneously there was a raised anti-NC-1-antibody titre (1:80) in the serum. After removal of the transplant the titre fell to normal. The NC-1 antigen, a component of the GBM in healthy persons, may be absent in Alport's syndrome. An analysis of the few cases of anti-GBM glomerulonephritis in renal transplants of patients with Alport's syndrome may make it possible to recognize factors which precipitate or favour this form of glomerulonephritis.

A pilot study of 21 patients (17 women; 4 men; mean age 35 [18-59] years), randomized into two groups, was undertaken to test how many cycles of intravenous pulse cyclophosphamide administration were required in lupus nephritis to achieve remission. It was planned that patients randomized to group A should be treated for 3 months, those in group B for over 12 months. In the first cycle the cyclophosphamide dosage was 500 mg/m2, in the subsequent cycles, 4 weeks apart, it was raised by 250 mg/m2 to a maximum of 1,000 mg/m2, if the WBC count was over 2,000/microliters. Three women in group B gave up treatment prematurely after 5-8 cycles, because a remission had occurred. In group A only one patient went into remission after only three cycles. Of the total of 18 patients in both groups whose data could be evaluated, 15 achieved remission after an average of 7.3 cycles and a cumulative total cyclophosphamide dosage of 9.3 g. The disease progressed in two patients, one died. No recurrence has so far been observed after a follow-up period of 1-41 months. Three patients had infections and two had developed leukopenia as side effects. Pulse cyclophosphamide has thus been shown to be an effective treatment in lupus nephritis, but it must be continued for more than 3 months.

A 58-year-old man developed continuous fever of around 40 degrees C and a macular rash on the trunk and limbs one week after an eight-day visit to the island of Rhodos. Typhus was diagnosed on the basis of the clinical findings, the characteristic rash and a rise in antibody titre against Rickettsia prowazekii and mooseri (1:1280). The fever subsided and the patient's general state markedly improved within three days of starting antibiotic treatment with doxycycline. Five days after hospital admission renal function deteriorated, serum creatinine rising from 1.7 to maximally 8.7 mg/dl. Renal biopsy on the eighth day of illness revealed, in concordance with the diagnosis of a rickettsial infection, acute granulomatous interstitial nephritis. Doxycycline administration was continued for a total of 18 days and renal function improved. Two weeks after discharge serum creatinine had fallen to 1.8 mg/dl and to 1.2 mg/dl after 6 months. The antibody titre against Rickettsia prowazekii had fallen to 1:20 about 12 weeks after discharge. Early antibiotic treatment of typhus is of importance to avoid irreversible renal damage.

Tubulointerstitial nephritis caused by polyomavirus of the subtype BK (BK virus nephropathy, BKN) is an important cause of deterioration of renal allograft function after kidney transplantation. In 3 cases of BKN diagnosed at our center, the suspected diagnosis made on the basis of urine cytology and serum PCR was confirmed by electron microscopy and immunohistology of the renal graft biopsy. In 1 patient, stable renal function without further virus detection was seen after reduction of the immunosuppression. In 2 further patients there was loss of graft function. BKN is an important differential diagnosis of unclear deterioration of renal graft function. The risk is particularly high with use of tacrolimus and mycophenolate mofetil (MMF). Urine cytology and serum PCR are suitable screening tests, histology provides conclusive evidence. The only therapeutic option available at present is reduction of immunosuppressive therapy.

This report concerns 6 patients with renal involvement in sarcoidosis. Two of the patients had no clinical symptoms at all. In 3 patients, no extrarenal organ manifestation was found. All 6 patients had elevated levels of serum creatinine, 2 were hypercalcemic. Five patients manifested with mild proteinuria, but in none of the cases was a nephritic sediment with erythrocytes found. Kidney biopsies in 5 patients showed epitheloid cell granulomatous interstitial nephritis, and 1 patient presented with nephrocalcinosis. All patients were treated with corticosteroids. The serum creatinine levels decreased significantly in 4 patients (> 50% decrease), and slightly in 2 patients, elevated serum calcium levels were normalized. Thus, even in the absence of other organ manifestations, sarcoidosis can be the cause of renal insufficiency, and it responds well to corticosteroid treatment. These patients demonstrate the importance of kidney biopsy in the unexplained deterioration of renal function.