Background: There is little information in literature on renal allograft biopsy findings in renal allograft dysfunction in live related renal transplant recipients. Material and Methods:A retrospective review of 1210 renal allograft biopsies from 575 renal transplant patients was carried out over a period of seven years from June 1997 till December 2004. The demographic, clinical, laboratory and biopsy findings were collected and analyzed.Results: A total of 1210 graft biopsies were performed on 575 patients. The mean age of recipients and donors was 29.2±9.7 years, and 35.7±10.5 years, respectively. The males were predominant among recipients (76.7 vs. 23.3%), while among donors they only slightly outnumbered females (51.8 vs. 48.2%).Regarding pathological lesions, acute rejection was seen in 292 (24%) cases, followed by acute tubular injury and cyclosporine A (CsA) toxicity, found in 281 (23.2%) and 134 (11%) cases respectively. Chronic allograft nephropathy (CAN) with variable degree of tubular atrophy was seen in 361 (29.8%) cases. Seventy nine cases (6.5%) of acute pyelonephritis were detected on graft biopsies. A number of rare lesions were also found, including 13 (1.07%) cases of recurrent/de novo renal disease, and 13 (1.07%) of polyoma virus infection. Five cases of CsA induced hemolytic uremic syndrome (HUS) were also noted. Conclusion:In conclusion, the incidence of acute rejection is low in our patients as compared to cadaveric renal transplant recipients as reported in Western studies and CsA toxicity is more common. Recurrent/de novo renal disease is uncommon in our patients.
Collapsing focal segmental glomerulosclerosis (cFSGS), also known as collapsing glomerulopathy is currently classified under the rubric of FSGS. However, its defining morphological features are in stark contrast to those observed in most other variants of FSGS. During the early stage of the disease, the lesion is characterized pathologically by an implosive segmental and/or global collapse of the glomerular capillary tufts, marked hypertrophy and hyperplasia of podocytes, and severe tubulointerstitial disease. With advancement of the disease, segmental and/or global glomerulosclerosis is also observed in association with the collapsing lesions. The etiology of this enigmatic disorder is still elusive, but a growing list of diseases/conditions is being reported in association with this morphological pattern of renal parenchymal injury. The pathogenesis of cFSGS involves discreet epithelial cell injury leading to cell cycle dysregulation and a proliferative cellular phenotype. From the clinical perspective, cFSGS is notorious for its propensity to affect black people, a high incidence and severity of nephrotic syndrome, marked resistance to empirical therapy, and rapid progression to end-stage renal disease. The lesion has also been reported in transplanted kidneys either as recurrent or de novo disease, frequently leading to graft loss. Most cases have been reported in western countries, but the lesion is also being increasingly recognized in the tropical regions. The recent increase in reporting of cFSGS partly reflects a true increase in the incidence and partly a detection bias. There is no specific treatment for the disorder at present. Newer insights into the pathogenesis may lead to the development of targeted and specific therapy in near future. There is an urgent need to increase awareness of the lesion among pathologists and nephrologists, especially those from developing countries, to ensure accurate diagnosis and appropriate managment. With the accumulation of more and more data, it is hoped that the prevailing confusion about the nosological identity of the lesion will also be resolved in a more logical way.
BACKGROUND Celiac disease (CD) is usually missed, if the serology is negative. We aimed to evaluate the clinicopathological characteristics of seronegative CD (SNCD) and its response to gluten-free diet (GFD) in adult patients. METHODS This observational study was carried out at the Department of Hepatogastroenterology, Sindh Institute of Urology and Transplantation, Karachi, Pakistan from 2009 to 2015. All consecutive adult patients (≥17 years) with features of marked villous atrophy (Marsh class≥III) on duodenal biopsy, negative tissue transglutaminase IgA and IgG antibodies (anti-tTg IgA and IgG) and human leukocyte antigen (HLA) DQ2 or DQ8 serotypes were studied. Clinical characteristics, laboratory parameters, and response to GFD were analyzed by SPSS software version 20. Median and interquartile range (IQR) were used for summarizing quantitative data. Frequency (percentages) was used for qualitative data. RESULTS A total of 12 patients with median age of 31.5 years (IQR: 19.75-46.75 years), of whom five (41.6%) were men were studied. The presenting complaints were: weight loss in 11 (91.6%) and abdominal pain in 9 (75%) patients. Anemia was observed in 10 (83.3%) patients with median hemoglobin of 9.5 g/dL (IQR: 6.3-13.25 g/dL). Median alanine transaminase (ALT) was 21 U/L (IQR: 13–27 U/L) and median albumin was 3 g/dL (IQR: 2.4-3.6 g/dL). Anti-tTg IgA and IgG were negative in all patients. HLA DQ serotyping showed homozygous DQ2 and DQ8 in four and one patients, respectively; while heterozygous DQ2 and DQ8 in five and two patients, respectively. All patients were advised to receive GFD. Nine (75%) patients showed complete clinical response. Two patients were non-compliant and one with non-alcoholic fatty liver disease (NAFLD)-related cirrhosis had partial clinical response. Out of the nine responders, two patients showed response within 6 months while the remaining showed improvement over a year period. CONCLUSION The diagnosis of SNCD is rewarding as it responds favorably to GFD in most patients. HLA serology provides an important tool for diagnosis of this entity.
Gastritis cystica profunda (GCP) is a rare, benign lesion of the stomach characterized by polypoid hyperplasia and/or ulcerated mucosal lesion and cystic dilatation of the gastric glands extending into the submucosa or muscularis propria of the stomach. Its etiology and pathogenesis are still incompletely understood. The most important factor is assumed to be a history of prior gastric surgery. We herein present a case of a young adult female with upper gastrointestinal (GI) symptoms. She underwent upper GI endoscopy twice, which revealed pyloric narrowing and intramural mass. Gastric endoscopic mucosal biopsies were performed, but no tumor was identified and her symptoms persisted. Imaging studies also revealed a mass lesion. Open laparotomy and partial gastrectomy with histopathology of the resected specimen revealed the true nature of the lesion. Surgery also improved her symptoms. GCP should be kept in the differential diagnosis of gastric mural mass lesions.
Signet ring adenocarcinoma of urinary bladder is a rare condition. Most cases reported in literature are primary and only one case of metastatic signet ring carcinoma has been reported. [1] This tumor has poor response to chemotherapy and radiotherapy, and is associated with dismal prognosis. [2] Here, we report a case of primary duodenal signet cell adenocarcinoma metastasizing to urinary bladder which is exceptionally rare and only one case is previously reported in literature. [3]
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