Lipoma of the adrenal gland is rare with a reported incidence of between 2% to 4%. Improved imaging techniques have helped in the diagnosis of these lesions.

Chronic Renal Allograft Dysfunction (CRAD) is responsible for a large number of graft failures. We have abrogated acute T-cell rejections using Ahmedabad Tolerance Induction Protocol (ATIP) with hematopoietic stem cell transplantation (HSCT) under non-myeloablative conditioning pre-transplant. However B-cell mediated rejections and CRAD continue to haunt us. We carried out retrospective analysis of renal allograft biopsies performed in the last 4 years to evaluate the effect of ATIP on CRAD.

Recurrent or de novo glomerulonephritis are one of the well-known causes for renal allograft dysfunction in early and late period after renal transplantation. Focal Segmental Glomerulosclerosis (FSGS) is a devastating lesion of the renal allograft. De novo FSGS is uncommon compared to recurrent FSGS. To find out the incidence of de novo FSGS. A retrospective evaluation of renal allograft biopsies was performed from 2007 to 2015, by light microscopy and immunohistochemistry including patient-donor demographics. Graft function status in terms of serum creatinine (SCr) and proteinuria were evaluated. Out of 2,599 renal allograft biopsies performed, 1.6% biopsies were reported as de novo FSGS. Majority were live related females donors with mean age of 43.8 years. Mean time of biopsy was 1.1 years post-transplant with proteinuria of 2.95 grams/24 hours and SCr of 2.24 mg/dL. Histopathological variants were collapsing 47.6%, Not Otherwise Specified/ classical 35.7%, cellular 9.5% and perihilar 7.1% biopsies. Associated Antibody Mediated Rejection (AMR) with T-Cell Rejection (TCR) was observed in 35.7% biopsies, acute on chronic CNI toxicity (calcineurin inhibitor) in five biopsies. Majority of the patients were on CNI based maintenance immunosuppression regimen. Total 28.6% patients and 23.8% grafts were lost over a mean follow up of 2.40 years. The mean SCr of remaining patients was 1.98 mg/dL. De novo FSGS can occur after the first year of renal transplant with related Human Leukocyte Antigen (HLA)matched donors leading to poor allograft survival. Close monitoring of urinary proteinuria and evaluation of allograft biopsy help in appropriate therapeutic modification to improve long term outcome of graft function.

Adrenal gland is an endocrine organ comprising of an outer cortex and inner medulla. These secrete various hormones that have a vital role in maintaining the normal homeostasis of the body. Lesions of adrenal cortex are quite common to encounter and most of these are related to the hormones secreted by three layers of adrenal cortex: the zona glomerulosa, the zona fasciculata, and the zona reticularis. Also it is very infrequent to encounter metastatic lesions in the adrenal glands too. So it is very important as a part of a clinician as well as a pathologist to know the pattern in which these hormones are secreted along with their physiological roles. Thus this chapter includes the disease that are related to excess as well as deficiencies of the hormones secreted by adrenal cortex. The chapter also includes various genetic syndromes that are associated with the disorders associated with hormones of adrenal cortex. The last part of the chapter includes a brief description of various benign as well as malignant lesions, the pathological as well as the etiological aspects and the hormonal abnormalities associated. This chapter thus mainly focuses on the pathology associated with the adrenal cortex and hormones secreted by the various layers of adrenal cortex.

Atypical hemolytic uremic syndrome (aHUS) although rare is the commonest cause of acute renal failure (ARF) in children and has poor prognosis. We present single centre experience of aHUS. Thirty six children (29 males, 7 females) with mean age, 7.9 years presented with ARF, 2 children also had tonic–clonic type convulsions. Their hematology examination revealed hemolytic anemia with s. creatinine (SCr), 5.54 mg/dl. Acute HUS was observed in 75 %, acute on chronic HUS in 19.4 % and patchy cortical necrosis (PCN) in 5.6 % biopsies. Mean 5.4 plasma exchanges (PE) were carried out. Supportive management of anti-hypertensives and prednisone was also given. Recovery end points were establishment of urine output, improvement of SCr and hematological profile. Hematology and renal function profile improved variably in all children, 5.6 % died, relapse was observed in 80.5 % over mean 70 days; 13.9 % children are doing well over mean follow-up of 268.8 days. Thus poor prognosis was observed in 86.1 % children. Children with acute on chronic HUS and PCN did not recover. Six children who recovered had acute HUS. aHUS in Indian children occurs at an older age of around 8 years and chronic/irreversible changes on histopathology examination are harbingers of poor prognosis. PE is life-saving however further research for developing strategies to improve long-term survival is needed.