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Recurrent focal segmental glomerulosclerosis (FSGS) after kidney transplantation is a serious concern with poor allograft outcomes. Possible circulating permeability factors are postulated as pathogenetic factors leading to recurrence. Genetic FSGS is said to have a negligible risk of posttransplant recurrence. Here, we describe an unfortunate patient of genetic FSGS (pathogenic genetic variant) who had a recurrence within hours after transplant and presented with a sudden onset of anuria. The patient did not respond to plasma exchange and subsequently underwent allograft nephrectomy.

Abstract The gut microbiome influences the pathogenesis and course of metabolic disorders such as diabetes. While it is likely that duodenal mucosa associated microbiota contributes to the genesis and progression of increased blood sugar, including the pre-diabetic stage, it is much less studied than stool. We investigated paired stool and duodenal microbiota in subjects with hyperglycemia (HbA1c ≥ 5.7% and fasting plasma glucose > 100 mg/dl) compared to normoglycemic. We found patients with hyperglycemia (n = 33) had higher duodenal bacterial count (p = 0.008), increased pathobionts and reduction in beneficial flora compared to normoglycemic (n = 21). The microenvironment of duodenum was assessed by measuring oxygen saturation using T-Stat, serum inflammatory markers and zonulin for gut permeability. We observed that bacterial overload was correlated with increased serum zonulin (p = 0.061) and higher TNF-α (p = 0.054). Moreover, reduced oxygen saturation (p = 0.021) and a systemic proinflammatory state [increased total leukocyte count (p = 0.031) and reduced IL-10 (p = 0.015)] characterized the duodenum of hyperglycemic. Unlike stool flora, the variability in duodenal bacterial profile was associated with glycemic status and was predicted by bioinformatic analysis to adversely affect nutrient metabolism. Our findings offer new understanding of the compositional changes in the small intestine bacteria by identifying duodenal dysbiosis and altered local metabolism as potentially early events in hyperglycemia.

Abstract Heterogeneity in the Diabetic Kidney Disease (DKD) diagnosis makes its rational therapeutics challenging. Although albuminuria characterizes DKD, reports also indicate its prevalence among non-proteinuric. Recent understanding of disease progression has thus inclined the focus on proximal tubular cell damage besides the glomeruli. A non-invasive approach exploiting exosomal miRNA derived from human kidney proximal tubular cell line was, hence, targeted. Upon miRNA profiling, three miRNAs, namely, hsa-miR-155-5p, hsa-miR-28-3p, and hsa-miR-425-5p were found to be significantly upregulated, while hsa-miR-663a was downregulated under diabetic conditions. Among these, hsa-miR-663a downregulation was more pronounced in non-proteinuric than proteinuric DKD subjects and was thus selected for the bioinformatics study. Ingenuity Pathway Analysis (IPA) narrowed on to IL-8 signaling and inflammatory response as the most enriched ‘canonical pathway’ and ‘disease pathway’ respectively, during DKD. Further, the putative gene network generated from these enriched pathways revealed experimentally induced diabetes, renal tubular injury, and decreased levels of albumin as part of mapping under ‘disease and function’. Genes target predictions and annotations by IPA reiterated miR-663a’s role in the pathogenesis of DKD following tubular injury. Overall, the observations might offer an indirect reflection of the underlying mechanism between patients who develop proteinuria and non-proteinuria.

The occurrence of venous aneurysms (VAs) is very rare, and VAs have been seldom reported in the existing literature. The etiology leading to the formation of VAs has not yet been determined. The presentation can range from asymptomatic to painful thrombosis of the sac, with rare events of pulmonary embolism. We have reported the case of a patient who had had a large cephalic vein aneurysm that was treated successfully. A 39-year-old man had presented with swelling in the left forearm that had progressively increased in size for 2 years and was associated with discomfort. On examination, a 5 × 5-cm soft compressible lesion was present over the mid-forearm that disappeared with raising of the arm. Contrast-enhanced magnetic resonance imaging showed a well-defined lesion arising from the cephalic vein. Under local anesthesia, after proximal and distal ligation, the aneurysm was excised. The histopathologic examination showed a thinned out smooth muscle wall and multifocal absence of the smooth muscle layer. The patient was doing well at 1 year of follow-up with no further degeneration in the vein wall. The formation of VAs might result from endophlebohypertrophy and endophlebosclerosis of the veins at the site of recurrent stress. Surgical excision should be considered when the patient is symptomatic, cosmetic disfigurement is present, and/or complications such as venous thrombosis, pulmonary embolism, and/or nerve compression have developed.

Abstract Isolated external iliac artery aneurysm is a rare occurrence. These aneurysms have varied presentations depending on size and proximity. Both open surgical and endovascular modalities can be used for treatment depending upon presentation, aneurysmal anatomy, and patient condition. Preservation of at least one internal iliac artery is important to prevent post-repair hypogastric ischemia. There are no previous reports of IgG4-related disease (IgG4-RD) as etiology of these aneurysms. A 32-year-old male patient presented with a left lower abdominal lump and was found to have a left external iliac artery aneurysm on computed tomography angiography. The patient underwent iliofemoral bypass with an 8 mm polyester graft. Histopathological examination of the aneurysm wall suggested IgG4-RD. The patient fulfilled the 2020 Revised Comprehensive Diagnostic Criteria for IgG4-RD. An 18-Fluorodeoxyglucose-Positron Emission Tomography scan performed in the postoperative period showed no active disease, hence medical therapy was not instituted. The patient is doing well at 1 year.

Background: Gastrointestinal tuberculosis (GITB) and Crohn's disease (CD) are close mimickers and difficult to discriminate. Recent work has focused on the immunological differences between GITB and CD based on cytokines related to T-regulatory cells and Th17 cells. In the present cross-sectional study, suspected cases of GITB or CD underwent extensive clinical, radiological, endoscopic, histological, and microbiological assessment. The diagnosis was based on standard criteria and response to antitubercular therapy endoscopically. Methods: Interleukin (IL)-10, transforming growth factor-β (TGF-β), and IL-17 were measured and compared between GITB and CD along with other parameters. Fisher's exact test and Mann–Whitney U test were used as per the data type. Results: Of the 27 patients, 11 had CD, 9 had GITB, and 7 had other conditions. Chronic diarrhea, involvement of left and long segments of the colon, and aphthous ulcers were significantly more frequent in CD; however, transverse ulcers were in GITB. IL-10 was reduced in both GITB (median-interquartile range [IQR] 9.54 [3.65–24.04]) and CD (median-IQR 13.28 [6.91–22.50]) compared to control (median-IQR 26.72 [10.34–35.43]). TGF-β showed little variation, but IL-17 was below the detection limit in most cases. None of these cytokines were significantly different between CD and GITB. The sensitivity and specificity of multiplex Mycobacterium tuberculosis-polymerase chain reaction were 44.44% and 100%, respectively. Conclusion: Serum cytokine profiling (IL-10, IL-17, and TGF-β) could not significantly differentiate GITB and CD. Moreover, extensive molecular, transcriptomic, chemokines, and cytokine analyses may shed light on these aspects.

Primary membranous nephropathy (PMN) is a common cause of adult-onset nephrotic syndrome. Anti-M-type phospholipase A2 receptor (PLA2R) antibodies are pathogenic and correlate with clinical outcomes. The role of anti-PLA2R in recurrent PMN is unclear. In the present manuscript, we report five cases of PMN who underwent kidney transplantation (KT) with varying titers of anti-PLA2R pre-kidney transplantation (KT). Two patients with anti-PLA2R in the second and third tertiles had a recurrence of PMN, whereas patients with a negative or anti-PLA2R in the first tertile had no recurrence. The report signals a heightened risk of PMN recurrence in patients with elevated anti-PLA2R antibody titer at KT.

Background. Ex vivo normothermic machine perfusion (NMP) has improved organ preservation and viability assessment among heart, liver, and lung transplantation. However, literature regarding the application of NMP in human clinical kidney transplantation remains limited. Numerous kidneys, especially from donors with stage 3 acute kidney injury (AKI), are not utilized concerning the high rate of delayed graft function (DGF) and primary nonfunction. The present study investigated the impact of NMP (135–150 min) on short-term outcomes after kidney transplantation from deceased donors with AKI. Methods. Graft outcomes of NMP kidneys were compared with contralateral kidneys stored in static cold storage (SCS) from the same donor with AKI during December 2019–June 2021. The study’s primary aim is to assess the safety and feasibility of NMP in deceased donors with AKI. The primary outcome was DGF. Secondary outcomes were duration of DGF, biopsy-proven rejection, postoperative intrarenal resistive index, postoperative infections, hospital stay duration, primary nonfunction, and kidney function estimated glomerular filtrate rate at discharge, 3 mo, and 1 y. Results. Five pairs of AKI kidneys (NMP versus SCS) were included in the final analysis. The results show no statistically significant differences in clinical outcomes between NMP versus SCS kidneys; however, NMP kidneys demonstrated slightly improved estimated glomerular filtrate rate at 3 mo (59.8 ± 5.93 [59] versus 75.20 ± 14.94 [74]) mL/min/1.73 m2 (P < 0.065) and at the last follow-up (12–29 mo) (72.80 ± 10.71 [75]) versus (94 ± 22.67 [82]) mL/min/1.73 m2 (P < 0.059) as compared with SCS kidneys. A higher proportion of NMP kidneys had normal intrarenal resistive index (0.5–0.7) and mild acute tubular injury on protocol biopsy, suggesting NMP is safe and feasible in deceased donors with acute kidney injury. Conclusions. NMPs of AKI donor kidneys are safe and feasible. A larger cohort is required to explore the reconditioning effect of NMP on AKI kidneys.

Renal lymphangiectasia (RL), also known as renal lymphangiomatosis, is a rare benign condition characterized by ectasia of peripelvic, perirenal and intrarenal lymphatic vessels. It accounts for approximately 1% of all lymphangiomas.1 The pathophysiology of renal lymphangiectasia remains unclear. However, it is hypothesized that the failure of draining into the larger retroperitoneal lymphatic channels causes abnormal cystic dilatation of the peripelvic, perirenal and intrarenal lymphatic ducts.2 RL can manifest at any age, with males and females equally affected. Lymphangiectasia can involve both kidneys, albeit unilateral involvement is common. Patients may be asymptomatic or present with flank pain, abdominal distention, lower limb oedema, hematuria and hypertension. Extreme presentation such as renal failure has also been documented. Due to the classical imaging features, computed tomography (CT) scan becomes the best diagnostic modality for the diagnosis, which can be confirmed by aspiration of chylous fluid.3 In the pediatric patient, the differential diagnosis includes cystic diseases of the kidney, nephroblastomatosis, and hydronephrosis with perinephric urinoma. Depending on the presentation, the management varies, including conservative, percutaneous aspiration, marsupialization, and nephrectomy.4 We describe gross and microscopic features of renal lymphangiectasia in a 4-year-old male child who presented with gradually progressive abdominal distension for one month with accompanying vague flank pain and fatigue. No hematuria or bladder bowel complaints were noted. Family and perinatal history were not significant. An ill-defined large mass of approximately 20x10cm occupying the left flank and hypochondrium was palpable on bimanual palpation. The renal function test was within normal limits for this age. Ultrasonography (USG) abdomen revealed bilateral multi-loculated, anechoic, cystic lesions in the perirenal and parapelvic region. Raised cortical echoes indicated the loss of corticomedullary distinction. CT scan revealed bilateral non-enhancing multiloculated cystic collection in the perirenal and parapelvic locations. Exploratory laparotomy showed a well-defined thick-walled sac of 20x15cm encasing the left kidney. Intraoperatively, the left kidney was hard to feel, and the architecture was distorted. A Left nephroureterectomy was done and submitted for histopathological evaluation. The kidney with perinephric fat measures 15x9x5.5cm, and the ureter was 5cm in length. The perinephric fat showed multiple collapsed cysts that enclosed the whole kidney ranging in size from 4 to 8cm in the largest dimension. The cut surface of the kidney exhibited well-demarcated multiloculated cysts in the cortex and medulla. The cysts are of variable size measuring 0.5 to 4cm in maximum dimension and shows thickness of 0.2cm and intervening thin septa (Figure 1A). The luminal aspect appeared smooth, contained brownish serous fluid, and did not show any papillary excrescences or growth. The adjacent spared kidney showed indistinct cortico-medullary junction and focal thinning of the cortex (0.3 to 0.4cm). Microscopically, numerous and variably sized cystic spaces were present in the cortex, medulla, pelvis, and perinephric fat (Figure 1B). Glomeruli and tubules in the intervening renal parenchyma showed no abnormal pathology on microscopy; however, the interstitium appears oedematous containing dilated lymphatic channels (Figure 1C). Cystic spaces were lined by a discontinuous layer of flat endothelial cells as highlighted by D2-40 (Figure 1D), CD31, and CD34 immunostains. Neuromatoid hyperplasia was seen in the sections from renal pelvis. Following clinical-radio-pathological correlation, a diagnosis of renal lymphangiectasia was offered. The patient was on close imaging follow-up to keep track of the right kidney.

The Indian Association of Pathologists and Microbiologists (IAPM) and Indian Society of Gastroenterology (ISG) decided to make a joint consensus recommendation for handling, processing, and interpretation of SI biopsies for the diagnosis and management of celiac disease (CD) recognizing the inhomogeneous practice of biopsy sampling, orientation, processing, and interpretation. A modified Delphi process was used to develop this consensus document containing a total of 42 statements and recommendations, which were generated by sharing the document draft, incorporating expert's opinion, followed by three cycles of electronic voting as well as a full-day face-to-face virtual ZOOM meeting and review of supporting literature. Of the 42 statements, 7 statements are on small intestinal (SI) biopsy in suspected patients of CD, site and the number of biopsies; 7 on handling, fixative, orientation, processing, and sectioning in pathology laboratories; 2 on histological orientation; 13 statements on histological interpretation and histological grading; 3 on the assessment of follow-up biopsies; 2 statements on gluten-free diet (GFD)-nonresponsive CD; 4 on challenges in the diagnosis of CD; 2 statements each on pathology reporting protocol and training and infrastructure in this area. The goal of this guideline document is to formulate a uniform protocol agreed upon both by the experienced pathologists and gastroenterologists to standardize the practice, improve the yield of small bowel biopsy interpretation, patients' compliance, overall management in CD, and generate unified data for patient care and research in the related field.

Background: In vitro allo-specific cytokine response to prospective allograft antigens might provide a means to identify patients at risk to adverse clinical endpoints/graft failure and predict allograft survival after transplantation. Methods: Cytokine profiles of recipient's peripheral blood mononuclear cells cocultured with allograft antigen-pulsed recipient macrophages were studied in 49 renal transplant recipients, 19 of which has acute rejection-12 with acute cellular rejection (ACR) and 37 non-ACR allografts. Cytometric bead array was used to analyze 18 cytokines/chemokines in the culture supernatants of graft antigen-pulsed and un-pulsed cultures. The mean increment in cytokine expression in stimulated versus unstimulated cultures was calculated. Results: Interleukin 6 (IL-6) (2336.42 ± 213.4 vs. 1244.06 ± 224 fg/ml; P = 0.0070), IL-1α (28.3 ± 7.451 vs. 16.78 ± 5.513 fg/ml; P = 0.0417), IL-17A (201 ± 96.73 vs. 28.91 ± 18.45 fg/ml; P = 0.0262), and MIP-1α/CCL3 (2682.25 ± 1013 vs. 1748.99 ± 780.4 pg/ml; P = 0.0383) were found to be high in rejection compared to stable allografts. Similarly, IL-6, IP-10/CXCL10, MIP-1α, and MCP-1 were increased in ACR, whereas granzyme B (11.36 ± 7.974 vs. 28.71 ± 9.393 pg/ml; P = 0.0011) and RANTES/CCL5 were higher in the non-ACR group. Conclusion: Distinct allo-specific in vitro cytokine profiles correlated with the occurrence of posttransplantation rejection episodes in the cohort, which indicated the feasibility of this in vitro model to predict transplant outcomes.

Sensitized patients, who constitute a considerable proportion of kidney-transplant recipients, often have poor allograft outcomes. Only cell-based complement-dependent cytotoxicity (CDC) assays are typically used to quantify donor-specific antibodies (DSAs) in patients in developing nations, owing to financial restraints. We report the clinical outcomes of ten sensitized patients who were stratified and managed based on Luminex single-antigen beads (SAB) method for the DSA detection in a cost-limited set-up. Sensitization events included a history of blood transfusion, multiple pregnancies, and previous allograft loss. Anti-human leukocyte antigen antibodies, measured by SAB and reported as mean fluorescence intensity (MFI), were considered positive if the value was > 1000 MFI for single antigen. Three best approaches, (1) cadaveric transplants using virtual cross-match for kidney allocation in five patients, (2) desensitization before living donor transplants for four donor–recipient pairs with immunological incompatibility (high DSAs but cross-match compatible), and (3) combined kidney paired exchange with desensitization for one donor–recipient pair with cross-match incompatibility (positive CDC cross-match), resulted in successful allograft outcomes in all the 10 patients during follow-up (range: 3–55 months). DSA by SAB to assess pretransplant immunological risk (in a sensitized recipient) is useful even in cost-limited settings, largely due to reduction of posttransplant rejection rates and avoidance of mortality while on the waitlist.

Background. Allograft rejection postkidney transplantation (KTx) is a major clinical challenge despite increased access to a healthcare system and improvement in immunosuppressive (IS) drugs. In recent years, mesenchymal stromal cells (MSCs) have aroused considerable interest in field of transplantation due to their immunomodulatory and regenerative properties. This study was aimed at investigating safety, feasibility, and immunological effects of autologous MSCs (auto-MSCs) and allogeneic MSCs (allo-MSCs) as a complement to IS drug therapy in KTx patients. Methods. 10 patients undergoing KTx with a living-related donor were analysed along with 5 patients in the control group. Patients were given auto-MSCs or allo-MSCs at two time points, i.e., one day before transplant (D-0) and 30 days after transplant (D-30) at the rate of 1.0-1.5×106 MSCs per kg body weight in addition to immunosuppressants. Patients were followed up for 2 years, and 29 immunologically relevant lymphocyte subsets and 8 cytokines and important biomarkers were analysed at all time points. Results. Patients displayed no signs of discomfort or dose-related toxicities in response to MSC infusion. Flow cytometric analysis revealed an increase in B regulatory lymphocyte populations and nonconventional T regulatory cells and a decrease in T effector lymphocyte proportions in auto-MSC-infused patients. No such favourable immune responses were observed in all MSC-infused patients. Conclusion. This study provides evidence that auto-MSCs are safe and well tolerated. This is the first ever report to compare autologous and allogeneic MSC infusion in KTx patients. Importantly, our data demonstrated that MSC-induced immune responses in patients did not completely correlate with clinical outcomes. Our findings add to the current perspective of using MSCs in KTx and explore possibilities through which donor/recipient chimerism can be achieved to induce immune tolerance in KTx patients.

Blunt chest trauma (BCT) is one of the rarest causes of acute myocardial infarction (AMI). This paper reports the case of a young married man who suffered from AMI due to BCT sustained in a fight with his wife. The histopathology examination revealed a rupture of atherosclerotic plaque with superimposed thrombus in the proximal left anterior descending artery. This report also reviews previously reported BCT-induced AMI cases in the literature.

Intestinal involvement in Behcet's disease (BD) is uncommon. Differentiating it from close mimics like Crohn's Disease is difficult. Further, in asymptomatic cases, diagnostic challenges posed is still greater. A 17‐year‐old boy had history of recurrent oro‐genital ulcers, papulo‐pustular skin eruptions, ocular lesions and had presented with recent onset perianal abscess. Fecal calprotectin was elevated, and ileo‐colonoscopy showed ileocolonic ulcers of inflammatory nature. Clinical diagnosis of intestinal BD was made. Patients with BD having mucosal lesions may harbor asymptomatic intestinal lesions. Screening them with fecal calprotectin levels and if positive, with subsequent imaging and endoscopic biopsy with timely initiation of appropriate treatment in such asymptomatic cases help to control overall disease activity.

Transplantation-associated thrombotic microangiopathy (TMA) is one of the most disastrous complications of renal transplantation. It may be either de novo (more common with a poor prognosis) or recurrent (with genetic background due to underlying mutations). Varied presentation mandates a high index of clinical suspicion, and the diagnosis usually requires allograft biopsy demonstrating TMA with or without underlying etiology. It has never been reported to mimic hyperacute rejection. In this context, we describe an end-stage renal disease patient with underlying IgA nephropathy, who underwent blood group incompatible renal transplant following successful desensitization and after that had systemic TMA in the 1st-h posttransplant itself, with allograft biopsy revealing florid TMA with no evidence of rejection, tacrolimus toxicity, or infection. Etiology remained elusive despite exhaustive workup and all possible attempts to salvage the allograft went in vain, with subsequent graft nephrectomy at 3 months. The patient after that has undergone a blood group compatible deceased-donor renal transplant and fortunately has normal graft function at 2 years follow-up, enthralling us to hypothesize possible interaction between the endothelial cells of renal allograft and anti-donor hemagglutinin antibodies; a mechanism already avowed for graft loss in blood group incompatible liver transplantation. We, therefore, suggest that patients willing for blood group incompatible renal transplantation need to be counseled beforehand about this, although a rare but devastating entity.

Snake bite envenomation is common in tropical countries during the summer. Snake bite-induced acute kidney injury (AKI) has varied histopathological manifestations such as acute cortical necrosis, acute tubular necrosis (ATN), and acute interstitial nephritis. However, snake bite-induced renal medullary angiitis has rarely been reported. We describe a nine-year-old child with AKI following viperine snake bite and renal biopsy revealed pigment cast nephropathy, ATN and medullary angiitis.

Acute kidney injury (AKI) occurs in about 1% of cases of malaria; however, in these cases, the mortality rate can be as high as 45%. Thrombotic microangiopathy (TMA) as a cause of AKI in malaria is rare with only a handful cases documented in literature so far. Alternate complement pathway (ACP) dysregulation as a major mechanism of injury in the development of thrombotic microangiopathies is well known. It is proposed that patients with preexisting defects in ACP are usually clinically silent, until stress condition such as infections help manifest them. Herein, we describe the presence of two complement factor H (CFH) variants in an 8-year-old female with vivax malaria associated TMA. The complement workup confirmed dysregulated ACP and revealed two single-nucleotide polymorphisms in CFH gene, i.e. exon-7 rs1061147 (p.Ala243Ala) and exon-9 rs1061170 (p.His402Tyr) which predisposed this patient to develop TMA precipitated by vivax malaria.

Introduction: Treatment options for recurrent C3 glomerulopathy (C3G) are not explored in large trials. Only Eculizumab has been successfully used to improve the renal function in patients with recurrent C3G. In the current report, we are sharing our experience with plasma exchange (PLEX) in the management of early recurrent C3G post-renal transplantation. Materials and Methods: A total of four patients underwent PLEX. Time to recur was less than two weeks in all the patients. Serology levels, autoantibody testing and limited genetic workup was done in all the four patients. The clinical details of patients were recorded. Results: All the patients underwent 5 PLEX (40 ml/kg/session) with fresh frozen plasma as the replacement. The median time for post-transplant recurrence was 3-days. Immediate reduction in serum creatinine was seen in three (75%) patients. After a median last follow-up of 8.5 (range: 4-18) months, two (50%) patients achieved remission and the other two (50%) had resistant disease resulting in graft loss. Three patients tested positive for autoantibodies (two cases had positive C3-nephritic factor and one had anti-complement factor-H autoantibodies. Complement factor H gene analysis revealed rs1061170; p.His402Tyr (missense variant), rs1061147; p.Ala307= (synonymous variant) and rs2274700; p.Ala473= (synonymous variant) in three cases. All the three patients who had immediate response to PLEX had positive autoantibodies against complement pathway regulators. Conclusion: In the present report, we performed extensive workup for complement pathway abnormality and found that patients with recurrent C3G following transplantation having autoantibodies benefited with PLEX.

Aim: Recurrence of focal segmental glomerulosclerosis (FSGS) in the post-transplant setting is variable with high rates of graft loss. Risk factors of recurrence include young age and Caucasian race. Data on outcome of recurrent FSGS from South Asia is scanty. We describe our experience of managing adults with recurrent FSGS with different therapies. Settings and Design: The study was conducted at the Department of Nephrology and Renal transplant surgery, Post Graduate Institute of Medical education and Research Institute, Chandigarh, India, and this was an observational study. Methods: We analyzed outcomes of patients with biopsy-proven recurrent FSGS over the last 5 years (2012–2017). Recurrence was defined as significant proteinuria (albuminuria ≥ 3+) and a demonstrable FSGS lesion on light microscopy and/or electron microscopy suggestive of diffuse foot process effacement. Results: Thirteen patients with 14 recurrences of FSGS post-renal transplant were identified. Mean age of the patients was 33.15 (±8.32) years. Median time to recurrence of FSGS was 45 days. Plasma exchange (PLEX) alone was used in two patients with 50% in remission. Combined PLEX and rituximab were used in six recurrences with remission in 83.3% of them. Five recurrences were treated with only angiotensin-converting enzyme inhibitor/angiotensin receptor blockade (ACEi/ARB) due to financial constraints. Of them, 4 (80%) achieved remission in proteinuria. One patient did not receive any therapy and expired in the 1st month of follow-up. Conclusion: The present series is one of the largest reports of recurrent FSGS from South Asia. Furthermore, the current report strengthens the use of ACEi/ARB in patients with recurrent FSGS.

Both cCTX/GCs and CNIs are recommended as first-line agents in the management of PMN. The present study is an extended report of patients randomized to receive TAC/GCs or cCTX/GCs at 2 years post randomization. Methods: Seventy patients enrolled in the clinical trial Tacrolimus Combined With Corticosteroids Versus Modified Ponticelli Regimen in Treatment of Idiopathic Membranous Nephropathy: Randomized Control Trial were followed quarterly between 12 and 24 months. At the end of 24 months, 3 patients were lost to follow-up. Results: At 18 months, 66% and 89% (P = 0.04) were in remission in TAC/GCs and cCTX/GCs groups, respectively. At 18 and 24 months, 60% and 86% (P = 0.03) of cases were in remission in the TAC/GCs and cCTX/GCs groups, respectively. At 18 months, 57% and 83% (P = 0.03) of the patients in TAC/GCs and cCTX/GCs groups were in remission without need of any additional immunosuppression (persistent remission) and, at 24 months, 43% and 80% (P = 0.002) were in persistent remission in TAC/GCs and cCTX/GCs groups, respectively. Relapse rate after any remission was 40% and 6.7% in TAC/GCs and cCTX/GCs groups, respectively (P = 0.007). There was an association of aPLA2R titers with remission or resistance (P = 0.006) in relapsing PMN. The significant decrease in eGFR after 12 months of TAC/GCs therapy normalized at 18 and 24 months. Discussion: At 2 years after randomization, relapse rates are higher for TAC/GCs compared with cCTX/GCs in PMN patients. Thus, cCTX/GCs are better than TAC/GCs in the longer term in PMN patients.

Background: Viral infections cause significant morbidity and mortality in post-transplant period. A highly sensitive and specific detection tool if used may help in early diagnosis and better management in these patients. The study aimed to assess the utility of quantitative real-time polymerase chain reaction (qRT-PCR) as a diagnostic and monitoring tool for viral infections in post renal transplant patients. Methods: A quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect EBV and CMV infection in 50 patients on 1st, 2nd, 3rd, and after 6 months of renal transplantation. Results: CMV infection was found in 34%, EBV in 28% of recipients, and 17% showed dual infection. Viruses were detectable after the first month of transplantation followed by symptomatic infections within first three months of follow-up, with diarrhea being the commonest symptom. These patients were also at high risk for developing other infections. Anti-thymocyte globulin (ATG) induction was a definitive risk factor for CMV/EBV infection in post operative period. Conclusion: Renal transplant patients frequently develop one or more viral infections at a time. Regular monitoring with qRT-PCR and prompt antiviral therapy with reduction in immunosuppression may be an ideal approach for management of these patients.

Granulomatous interstitial nephritis (GIN) is reported in 0.9% of the native renal biopsies. GIN occurrence in renal allograft is rare and a proton-pump inhibitor-induced GIN is infrequent. Our patient, a 36-year-old renal transplant recipient (2002), on triple immunosuppression with normal renal function, after 16 years of renal transplant, presented with raised serum creatinine (1.9 mg/dl), biopsy revealed GIN, workup for secondary causes were negative, on detailed inquiry, the patient was receiving pantoprazole for the last 1 month on the prescription of his primary physician for dyspeptic symptoms. On stopping pantoprazole, serum creatinine reduced to baseline (1 mg/dl) at 15 days, confirming the diagnosis of pantoprazole-induced GIN.

Introduction: The clinical course of ulcerative colitis (UC) ranges from a mild course with prolonged periods of remission to severe disease requiring long-term immunosuppression for disease control. There is limited data on the predictors of need for immunosuppression at presentation. Objective: The aim was to evaluate clinical, endoscopic and histopathological parameters at presentation in patients with UC that predict the need for long-term immunosuppressive therapy. Materials and Methods: We studied 81 patients (males; 40; mean age 38.69 ± 12.90 years) with UC (41 prospectively and 40 retrospectively). The clinical presentation, duration, extra-intestinal features, extent of disease, haematological and biochemical features, histology and outcome (drugs, surgery, and mortality) were recorded and analyzed. Subgroup analysis was done after dividing the patients into two groups depending upon whether they needed long term immunosuppressants or not. Results: The presenting symptoms were bloody stools (100%), mucus in stools (98.8%), abdominal pain (35.8%), anorectal pain (14.8%) and extra-intestinal symptoms (4.9%). Of these 81 patients, 7 (8.6%) patients required surgery and 2 (2.4%) patients died. Long term immunosuppressants were used in 19 patients (Azathioprine 16, Mycophenolate mofetil 2 and Tacrolimus 1). The patients who received immunosuppressants had a higher prevalence of pancolitis (47.4% vs. 16.1%, P = 0.005). Other clinical, hematological and histological parameters such as inflammatory grade, chronicity grade, cellular infiltrates, submucosal fibrosis, Paneth cell metaplasia, and the presence of neuronal cells were similar in the two groups. Conclusion: Of the clinical, biochemical, endoscopic and histological features at presentation only the presence of pancolitis predicts the need for long term immunosuppressants in ulcerative colitis.

Colorectal polyps may be detected incidentally on a screening colonoscopy or when they present with symptoms like anemia or gastrointestinal bleeding. Early recognition and prompt management of polyps can cure the primary disease and prevent future risk of malignancies in the patient and provide an opportunity to screen the families in cases of inherited polyposis syndromes. We report a case of rectal bleeding due to colorectal polyps of varying histology. Histology showed hyperplastic polyp, juvenile polyps (JP) with focal dysplasia, adenomatous polyp and villous adenoma with dysplasia. He underwent total proctocolectomy with ileal pouch anal anastomosis (J-pouch) (TP-IPAA). Mixed polyposis syndrome is a rare entity. (J Dig Endosc 2013;4(2):39-41)