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Objectives: To calculate the incidence of nondiagnostic (ND) colorectal (CR) polyp cases in which deeper tissue sectioning rendered new diagnostic information—particularly adenomas—in 2 laboratories staffed by the same pathologists. Methods: After initial diagnosis, 100 ND CR polyps from each laboratory were reexamined with 3 deeper levels to establish rates of diagnostic conversion based on biopsy specimen location and original observation(s). Results: Deeper sectioning rendered new diagnostic information in 43 (21.5%) of 200 biopsy specimens and specifically adenomas in 16 (8.0%) of 200 biopsy specimens. Conclusions: These results support routine ordering of deeper levels on ND CR polyps to improve adenoma detection rates, especially those cases without any histologic abnormality. If another biopsy in the same case already is adenomatous, examination of deeper levels may not be necessary, as it may not have any significant effect on the clinical management of the patient.

Background. The aetiological and clinical associations of collapsing focal segmental glomerulosclerosis (cFSGS) following kidney transplantation (KTx) are poorly described. In this study, post-transplant cFSGS and non-collapsing FSGS (ncFSGS) were compared in recent KTx recipients. Evidence for intragraft viral infection was sought. Methods. Twenty-nine cases of post-KTx FSGS were identified and classified as cFSGS (n ¼ 10) or ncFSGS (n ¼ 19). Biopsies were scored using Banff ‘97 criteria and subjected to in situ hybridization (ISH) for parvovirus B19 (pvB19), simian virus 40 (SV40) and BK virus (BKV). Results. cFSGS and ncFSGS patients were comparable for age, gender, weight, delayed function, human leucocyte antigen (HLA) matching, acute rejection and median time to diagnosis. Deceased donor source was more common among cFSGS cases (70 vs 32%, P ¼ 0.05). FSGS was recurrent in 2/10 cFSGS cases compared with 8/19 ncFSGS (P ¼ NS). cFSGS was associated with more proteinuria (11.9 vs 7.2 g/day, P ¼ 0.05) and higher serum creatinine (4.2 vs 1.9 mg/dl, P ¼ 0.0001) at diagnosis. Plasmapheresis was used in two out of 10 cFSGS and seven out of 19 ncFSGS cases with treatment response in 0 of two and three of seven, respectively. Graft loss was more rapid with cFSGS compared with ncFSGS (P ¼ 0.02). Histologically, cFSGS was associated with more severe chronic vascular abnormalities. All biopsies were negative for pvB19, SV40 and BKV by ISH. Conclusions. cFSGS following KTx presents with higher proteinuria, diminished renal function, more severe vascular disease and higher rate of graft loss compared with the non-collapsing form. There was no evidence for infection by pvB19 or polyomaviruses.

Anti-glomerular basement membrane (anti-GBM) glomerulonephritis is a rare disease caused by IgG autoantibodies against the glomerular basement membrane. We describe clinical and pathologic findings in a series of renal biopsy specimens from 80 patients. The patients ranged in age from 16 to 87 years. The age distribution was bimodal, with one peak at a young age predominated by males and a second peak in the sixth to eighth decades with females predominating. Most patients (70 [88%]) had severe necrotizing glomerulonephritis with crescents in more that 50% of glomeruli. The fraction of crescentic glomeruli in biopsy specimens correlated well with serum creatinine levels but not with serologic titers for anti-GBM antibodies. Interstitial fibrosis was uncommon and, when present, minimal to mild. Linear IgG deposition defines this entity, but immunofluorescent costaining for other immunoglobulins and complement is found frequently. To our knowledge, this is the largest series of renal biopsy specimens with anti-GBM glomerulonephritis studied to date.

Metanephric metaplasia of the parietal epithelium of the Bowman capsule is a rare pathologic finding of unknown pathogenesis that has occurred in patients with widespread malignant neoplasms of various types. We report this finding in a 25-year-old woman with partial expression of the Carney triad who died of a disseminated gastrointestinal stromal tumor, specifically a gastric stromal sarcoma. The metaplasia involved both kidneys diffusely. It originated in the parietal epithelium of the Bowman capsule, extended into the proximal tubules, and focally surrounded the glomeruli in a semicircular manner. Immunohistochemical analysis revealed that the cells of metanephric metaplasia expressed the Wilms tumor gene product, bcl-2 protein, and CD57 and cytokeratin 7 and keratin AE1/AE3 focally, but not CD56. This immunophenotype parallels that of metanephric adenoma, Wilms tumor, and nephrogenic rests and overlaps with antigen expression in certain periods of renal development.

Wegener’s granulomatosis (WG) is a systemic disease characterized pathologically by necrotizing granulomatous inflammation of the respiratory tract and generalized vasculitis involving mediumand smallsized vessels. Kidney involvement is usually manifested as a focal segmental necrotizing glomerulonephritis, with crescents [1]. Anti-neutrophil cytoplasm antibody (ANCA) testing has provided a very useful diagnostic aid. The majority of patients with WG have antibodies towards proteinase 3 (PR3-ANCA) (>70%), but antibodies towards myeloperoxidase (MPO-ANCA) is seen in 20% of cases. A few patients (

We studied 4 new cases of juxtaglomerular cell tumor and compared their morphologic and immunohistochemicalfeatures with 2 renal hemangiopericytomas and 5 cutaneous glomus tumors. The juxtaglomerular tumors were resectedfrom 2 males and 2 females (mean age at diagnosis, 23 years). Three patients manifested with severe hypertension. Tumors ranged from 2.2 to 8.0 cm and were well circumscribed. The tumors consisted of solid sheets and nodules of variably sized tumor cells with round, oval, and spindled nuclei alternating with edematous microcystic foci. Nuclear atypia, present in all tumors, was a prominent feature in 2. Mitotic activity was not identified. All cases showed hemorrhage, numerous mast cells, and thick-walled blood vessels. Unusual features included coagulative tumor necrosis, a hemangiopericytoma-like vascular pattern, and hyalinized stroma. All tumors were immunoreactive for CD34 and actin. Ultrastructural analysis revealed the presence of rhomboid-shaped renin protogranules. Patients were treated by partial or radical nephrectomy and followed up for 14 to 48 months. There were no recurrences or metastases. The characteristic clinical and morphologic features of juxtaglomerular cell tumor permit distinction from renal hemangiopericytoma and other renal tumors.

C.V. is a 22-year-old woman, who presented to the emergency room (ER) with shortness of breath, coughing and frank haemoptysis. She had been seen in the ER twice over the previous 3 weeks for similar symptoms, but with only mild blood-tinged sputum. Chest X-ray showed bilateral infiltrates. She was treated with Zithromax and subsequently Biaxin for a presumed pneumonia. There was no history of fevers, chills or weight loss. However, the haemoptysis persisted with increasing shortness of breath, forcing her back to the ER. Her history was significant in that she is a smoker and works as a bartender in a smoky restaurant. Laboratory investigations at admission: haemoglobin 10 gm/dl, platelet count 309 10/ml, sodium 138mEq/l, potassium 3.8mEq/l, serum creatinine 0.7mg/dl, blood urea nitrogen 11mg/dl, total bilirubin 1.5mg/dl, PCO2 34, PO2 48. Urinalysis was unremarkable. Chest X-rays showed worse diffuse alveolar infiltrates compared with the previous X-rays. The clinical diagnosis was that of acute interstitial lung disease with haemoptysis and included a differential diagnosis Wegner’s granulomatosis, lupus, sarcoidosis, pneumonitis, Goodpasture’s disease, etc. Titres for anti-GBM antibodies returned high positive (>32U/ml, normal

Fifty-seven cases of acute myeloid leukemia (AML), which had been subtyped by French-American-British morphologic and cytochemical criteria as myeloid (M1, M2) or monocytic (M4, M5), were retrieved from the files of the Division of Hematopathology, University of Iowa. Corresponding immunophenotyping data were reviewed with attention to the expression of CD14 (MY4) and CD24 (BA-1). Of 20 cases expressing CD24, 19 were M4 or M5, whereas all 14 cases expressing CD14 were of monocyte lineage. Therefore, CD14 was a highly specific (100%) but only moderately sensitive (58%) marker for distinguishing classes M1 or M2 from M4 or M5. By contrast and unexpectedly, CD24 was nearly as specific (97%), but more sensitive (79%) in marking M4 or M5 cells. This appears to be true even though CD24 is apparently not expressed on normal monocytes. When positive staining for either or both antibodies (CD24 or CD14) was considered indicative of a monocytic leukemia, the sensitivity of immunophenotyping in distinguishing M4/M5 from M1/M2 AML rose to 92%, while maintaining 97% specificity. The authors discuss a recent observation that may help explain the unexpected expression of CD24 in monocytic AML. They conclude that the usefulness of CD24 in identifying monocytic AML may exceed that of CD14, and that the use of CD24 and CD14 in combination improves the ability of flow cytometry to distinguish myeloid from monocytic acute leukemias.

Immunoperoxidase strains for prostate-specific antigen (PSA), prostatic acid phosphatase (PAcP), epithelial membrane antigen (EMA), and cytokeratins (MAK 6 and CK-KES) were performed on 1 case of squamous cell carcinoma of the prostate and on 13 cases of squamous metaplasia of prostatic epithelium in an effort to demonstrate prostatic origin of the neoplastic and metaplastic cells and to differentiate them from primary or metastatic well-differentiated squamous cell carcinoma. The authors found no specific staining of the metaplastic or neoplastic cells for PSA and only focal single cell PAcP positivity in three cases of squamous metaplasia. All cases showed strong staining of surrounding normal glandular epithelium for both antigens. In all but one case, both the metaplastic and glandular epithelium had positive results for MAK 6 and CK-KES. EMA was expressed strongly in ten cases, was weak or variable in two, and had negative results in two cases of squamous metaplasia. In only four cases did the glandular epithelium have positive results for EMA. The remaining cases showed no staining. PSA and PAcP marking, therefore, may not be useful for separating atypical squamous metaplasia from well-differentiated squamous cell carcinoma or even primary prostatic from metastatic squamous cell carcinoma. These findings suggest that although prostatic glandular epithelial cells retain their ability to express some prostate-associated antigens, this ability is greatly reduced, lost, or not developed in cells that undergo metaplasia into squamous cells or that develop into squamous cell carcinoma.