Kaplan-Meier survival plots revealed significantly lower event free survival in CML and B-ALL patients that were carriers of 3435TT genotype (p  less then  0.05). Multivariate analysis considered 3435TT genotype as independent risk factor for imatinib resistance in CML cases (HR 6.24, p = 0.002) and increased relapse risk in B-ALL patients (HR 4.51, p = 0.03). The current study provides preliminary evidence of a significant association between variant TT genotype and increased B-ALL risk. Also, results suggest that ABCB1 3435TT genotype increases imatinib resistance in CML and influence therapeutic outcome in B-ALL.B cell lineage acute lymphoblastic leukemia is the most common leukemia occurring in children and young adults and is the leading cause of cancer related deaths. The 5 year overall survival outcome in children with B-ALL has improved significantly in the last few decades. In the past, the discovery of various genetic alterations and targeted therapy have played a major role in decreasing disease-related deaths. In addition, numerous advances in the pathogenesis of B-ALL have been found which have provided better understanding of the genes involved in disease biology with respect to diagnostic and prognostic implications. Present review will summarize current understanding of risk stratification, genetic factors including cytogenetics in diagnosis and prognosis of B-ALL.Atypical hemolytic uremic syndrome is a rare form of thrombotic microangiopathy caused by complement pathogenic variants. We describe a case of a 33-year-old woman who presented as rapidly progressing renal failure requiring dialysis and had anemia, microhematuria, low C3, normal C4 levels, and normal platelet count. Renal biopsy revealed arteriolar thrombotic microangiopathy and acute tubular injury. Patient was treated with plasma exchange and hemodialysis as required. This resulted in partial recovery at 1 month. Genetic workup by multiplex ligation-dependent probe amplification revealed a 1.5 times higher signal intensity on downstream region of CFH gene and 50% reduced intensity of exon 6 of CFHR1 gene, suggesting a gene conversion event, similar to those previously reported from Spain and Portugal.Central venous stenosis (CVS) refers to a significant stenosis of a large intrathoracic vein, such as the subclavian, brachiocephalic, or the superior vena cava (hemodialysis, HD). Percutaneous transluminal angioplasty (PTA) with or without stent placement has been the recommended as the preferred approach to CVS. A total of 10 consecutive HD patients with documented CVS over a 2-year time period from April 2017-April 2019 underwent percutaneous angioplasty and stent insertions under sedation. The procedure was performed by the interventional cardiologist in the institute. One patient underwent only PTA, whereas nine (90%) had PTA with primary stent insertion. Primary patency was 90% at 3 months, 80% at 6 months while at 12 months, it was 70% and remained at 70% at 24 months. We did not find any association between age, gender, diabetic status, dialysis vintage, or previous catheter infection with procedural patency. Central venous stenosis can be treated successfully with percutaneous angioplasty and primary stenting. Despite advances, prevention of CVS should be the primary approach.Drug induced acute interstitial nephritis is an idiosyncratic reaction following a drug exposure. The commonest drugs implicated are nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and proton pump inhibitors. Renal cortical necrosis is a rare cause of acute kidney injury caused by severe and sustained vasoconstriction of small renal vessels. There is a change in the epidemiology of acute kidney injury especially in developing countries where drug induced acute kidney injury is becoming increasingly common. Naproxen is known to cause renal failure by renal papillary necrosis, tubular damage and acute interstitial nephritis. We present a case of Naproxen induced acute interstitial nephritis with acute cortical necrosis. To the best of our knowledge this is the first documented case of Naproxen induced renal cortical necrosis.Invasive fungal infections are a significant cause of morbidity and mortality in patients systemic lupus erythematosus. The case illustrates the autopsy findings in a patient with systemic lupus erythematosus complicated by multiple fungal infections. Rare, uncommon manifestations of SLE such as mesenteric panniculitis and rhabdomyolysis were also present. High index of suspicion with timely intervention with aggressive antifungal was life-saving.We present this rare case of hyperhomocysteinemia due to a mutation in methylene-tetrahydrofolate-reductase (MTFHR) combined with plasminogen activator inhibitor deficiency, causing bilateral renal artery thrombosis. This case highlights the importance of genetic screening in individuals with a family history of thrombotic diseases. There seems to be a role of intervention, even in the setting of renal infarction. Collapsing glomerulopathy (CG) is a distinct morphologic pattern of proliferative renal parenchymal injury. It differ from focal segmental glomerulosclerosis (FSGS) by clinicopathologic pattern and its adverse outcome. The clinical significance of CG in renal allograft biopsies is not yet clear due to scant data and less occurrence of CG in renal transplant recipients. https://www.selleckchem.com/products/GDC-0449.html We conducted this single-center retrospective study to evaluate the prevalence, clinicopathological features, and outcome of post renal transplant CG. We studied 127 renal allograft biopsies performed over a period of 45 months (Jan 2015-Oct 2018). A diagnosis of CG was made if at least one glomerulus demonstrated global or segmental collapse of the glomerular capillary walls, associated marked hyperplasia, and hypertrophy of the overlying visceral epithelial cells. We analyzed clinical, biochemical, and pathological characteristics and its impact on renal allograft outcome. Statistical analysis was performed and continuous variables were eroteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients. CG presents with moderate to severe proteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients.