Somatostatin mediates inhibitory functions through five G protein–coupled somatostatin receptors (sst1-5). We used immunohistochemistry, immunofluorescence, and RT-PCR to determine the presence of somatostatin receptors sst1, sst2A, sst2B, sst3, sst4, and sst5 in normal and IgA nephropathy human kidney. All somatostatin receptors were detected in the thin tubules (distal convoluted tubules and loops of Henle) and thick tubules (proximal convoluted tubules) in the tissue sections from nephrectomy and biopsy samples. Immunopositive sst1 and sst4 staining was more condensed in the cytoplasm of tubular epithelial cells. In normal kidney tissue sections, podocytes and mesangial cells in the glomeruli stained for sst1, sst2B, sst4 and sst5, and stained weakly for sst3. In IgA kidney tissue, the expression of somatostatin receptors was significantly increased with particular immmunopositive staining for sst1, sst2B, sst4, and sst5 within glomeruli. In the epithelial cells, the staining for sst2B and sst4 in proximal tubules and sst1, sst2B, and sst5 in distal tubules was increased. The mRNA expression of sst1-5 was also detected by RT-PCR. Somatostatin and all five receptor subtypes were ubiquitously distributed in normal kidney and IgA nephropathy. The increased expression of somatostatin receptors in IgA nephropathy kidney might be the potential pathogenesis of inflammatory renal disease.

One hundred and six bladders were removed at autopsy from adult women dying of diseases unrelated to the urinary tract. A fixative solution had been introduced into the bladder as soon as possible after death. The naked-eye appearances were recorded before and after application of Lugol's iodine solution and the trigones then submitted to histological examination. Vaginal metaplasia of the trigone was present in the majority (72%) of bladders, a similar incidence being found in both pre-menopausal and post-menopausal age groups. Histological evidence of chronic inflammation was found significantly more frequently in bladders showing vaginal metaplasia and it is suggested that vaginal metaplasia is not a consequence of chronic inflammation but that its surface characteristics may predispose to chronic infection. Its purported hormonal aetiology does not explain all observed features. Prominent venous channels within the tunica propria around the urethral orifice were a constant feature in all bladders studied. Two of the 76 bladders showing vaginal metaplasia also displayed atypical hyperplasia of this squamous epithelium, a previously unrecorded observation. The possible implications of such atypical hyperplasia are briefly discussed.

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Xanthogranulomatous inflammation is a rare clinico-pathological condition involving many organ systems. Breast involvement with this rare condition reported from a few cases of mastitis has been limited to only microscopic involvement on histology. We would like to report an unusual presentation of this inflammatory process presenting as a solid lump mimicking malignancy in latissimus dorsi donor site scar and implant-based breast reconstruction as a result of a ruptured silicone gel implant. To our knowledge there have been no previous reports on similar presentation published in the literature. This case highlights a rare complication of a leaked silicone gel implant triggering a xanthomatous response in the absence of the usual infective or obstructing etiologies. This condition is of benign nature with complete clearance on surgical excision and excellent clinical prognosis reported from other organ involvement.