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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.

Genes coding for CD66a (biliary glycoprotein), carcinoembryonic antigen (CEA) group member 2 (CGM2), and nonspecific cross-reacting antigen (NCA) are members of the human CEA gene subgroup. We investigated a series of 11 colorectal carcinomas by Northern blot and isotopic in situ hybridization (ISH), demonstrating underexpression of CD66a and CGM2 in the majority of the carcinomas as compared with the normal mucosa, whereas NCA was overexpressed. ISH for CD66a and CGM2 mRNA revealed that large areas of the carcinomas remained without or with only faint hybridization signals. However, in every carcinoma, at least some positive foci were observed, indicating remaining cell populations that actively transcribe CD66a and CGM2. In contrast, ISH for NCA displayed strong and extensive autoradiographic signals. By analysis of step sections, foci of CD66a and CGM2 expression were shown to co-localize. Furthermore, these foci contained relatively few nuclei immunohistochemically positive for the proliferation-associated nuclear antigen Ki-67. Our data indicate a dysregulation of the three genes possibly with a common transcriptional control for CD66a and CGM2 and a different control for NCA. The focal expression of CD66a and CGM2 could be interpreted as due to a focal, incomplete, and abortive differentiation or, alternatively, as a consequence of genetic heterogeneity with foci of slow-proliferating subclones.