A group of renal pathologists, nephrologists, and transplant surgeons met in Banff, Canada on August 2-4, 1991 to develop a schema for international standardization of nomenclature and criteria for the histologic diagnosis of renal allograft rejection. Development continued after the meeting and the schema was validated by the circulation of sets of slides for scoring by participant pathologists. In this schema intimal arteritis and tubulitis are the principal lesions indicative of acute rejection. Glomerular, interstitial, tubular, and vascular lesions of acute rejection and "chronic rejection" are defined and scored 0 to 3+, to produce an acute and/or chronic numerical coding for each biopsy. Arteriolar hyalinosis (an indication of cyclosporine toxicity) is also scored. Principal diagnostic categories, which can be used with or without the quantitative coding, are: (1) normal, (2) hyperacute rejection, (3) borderline changes, (4) acute rejection (grade I to III), (5) chronic allograft nephropathy ("chronic rejection") (grade I to III), and (6) other. The goal is to devise a schema in which a given biopsy grading would imply a prognosis for a therapeutic response or long-term function. While the clinical implications must be proven through further studies, the development of a standardized schema is a critical first step. This standardized classification should promote international uniformity in reporting of renal allograft pathology, facilitate the performance of multicenter trials of new therapies in renal transplantation, and ultimately lead to improvement in the management and care of renal transplant recipients.

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To measure the rate of histopathologically identified ocular surface squamous neoplasia (OSSN) in pterygium specimens. Methods: All pterygium specimens collected from consecutive patients between April 8, 2003, and February 6, 2008, were submitted for histopathologic examination, and the rate of OSSN was calculated. Results: The rate of OSSN was 9.8% (52 of 533) in sequential pterygium specimens. Conclusions: This rate of unsuspected OSSN suggests that all specimens of pterygium should be submitted for histopathologic examination and that patients in whom OSSN is noted should be examined at more frequent intervals so any clinical OSSN that develops can be identified at an early stage.

Madin-Darby canine kidney (MDCK) cells exhibit many of the characteristics of cells of the cortical collecting tubule. Since hypotheses concerning the development of gouty and uric acid nephropathy involve a reaction between such cells and crystals, either of monosodium urate monohydrate (MSUM) or uric acid, the reaction between MDCK cells in culture and the above crystals was studied, both morphologically and functionally. In monolayer cultures, reaction sites developed within four hours of exposure to urate crystals. These increased in number for up to 72 hours and subsided gradually after removal of the crystals. At these reaction sites, crystals were observed to have passed beneath the cell surface and could be demonstrated both within intra-cellular lysosomes as well as within the inter-cellular spaces. When the MDCK cells were maintained as single cells in suspension, phagocytosis of crystals by the majority of the cells could be observed, but the response was much more rapid than in monolayers. During the cell/crystal reaction, significant amounts of lysosomal enzymes and prostaglandin E2 were released and, to a less significant degree, cytosolic enzymes, presumably due to cell lysis. This enzyme release did not occur in MDCK cells grown in protein-free medium, and protein coating of the crystals was necessary for reactivity with cells. In this regard, coating with IgG or lysozyme was more effective than albumin. The reaction with uric acid crystals revealed a reactivity which was lesser in degree but qualitatively similar to that of urate crystals.(ABSTRACT TRUNCATED AT 250 WORDS)

Apoptotic cell death plays an important role in the pathogenesis of renal atrophy in diseases of the kidney involving chronic mild ischemia. The present study constitutes an in vitro model of these diseases and assesses the modes of cell death involved after hypoxic treatment of renal epithelium. Cultures of MDCK cells or primary cultures of rat renal parenchymal tubules were treated in either a physiological or a hypoxic atmosphere. Cultures were collected before treatment and at 24 h and 48 h, for morphological and biochemical studies. Both apoptosis and necrosis were observed at significantly increased levels by 48 h of hypoxia in the MDCK cell cultures. DNA gel electrophoresis patterns supported these findings. Experiments using tubule cultures demonstrated that, during the 48 h of study, tubular epithelial cells in the center of the control tubule structures died by apoptosis, possibly as a result of mild oxygen and/or nutrient depletion. With added hypoxic treatment, however, the entire tubule structure became necrotic. Results are similar to those found during in vivo studies, thus providing in vitro models that may be developed further to define factors in the pathogenesis of some renal diseases.

Scrotal calcinosis is a rare benign disorder considered idiopathic by most recent authors, although an origin from dystrophic calcification of epidermoid cysts has been proposed. In 3 of 4 cases which were otherwise typical of scrotal calcinosis, there was calcification of the contents of small cysts lined by stratified squamous epithelium. These structures were identified as eccrine duct milia because some of them communicated with eccrine ducts and there were ultrastructural features of eccrine duct differentiation in one case. The eccrine nature of the milia was confirmed using the immunoperoxidase technique for the demonstration of carcinoembryonic antigen (CEA) which serves as a marker of eccrine sweat glands. Since a transition could be seen between degenerating calcified milia and typical nodules, it appeared that the calcific deposits of scrotal calcinosis result from the breakdown of such lesions. Staining of deposits unassociated with cyst walls with the technique for the demonstration of CEA supported this conclusion. An advanced stage of evolution of the disease could account for the absence of visible cysts in many cases. We propose the term "hidrocalcinosis of the scrotum" for this distinctive form of cutaneous calcification.

Acute inflammatory polyneuropathy or Guillain-Barre syndrome may be associated with glomerulonephritis, especially membranous nephropathy. This paper details the case of a 73-year-old woman presenting with acute onset of Guillain-Barre syndrome associated with an abnormal urinary sediment and significant proteinuria. Renal biopsy was consistent with focal segmental glomerulosclerosis. Despite an initial response to plasmapheresis, the patient’s polyneuropathy deteriorated and subsequently improved with corticosteroid therapy. Simultaneously, her proteinuria and urinary sediment also improved. This implies that this was not a chance association. A brief discussion of the association between Guillain-Barre syndrome and glomerulopathies is undertaken.