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Background and Aim: Thrombotic microangiopathy (TMA) is a disease of microvasculature, triggered by numerous immunological and nonimmunological factors. The aim of this study is to identify the incidence, etiology, and clinical characteristics of posttransplant TMA in renal allografts and its impact on graft outcome. Patients and Methods: In this retrospective study, the records of patients who underwent renal transplantation between January 2013 and December 2017 were reviewed, and those recipients who had allograft biopsy-proven TMA were analyzed. Based on the clinical characteristics and investigations, the recipients were divided into two groups: those with systemic features of TMA and those with allograft-limited TMA. The clinical course and graft outcome of both the groups were compared and analyzed. Results: The number of patients who underwent renal transplantation during the study period was 212. Out of them, 16 patients had biopsy-proven TMA. Five patients had TMA with systemic features and the remaining 11 patients had allograft-limited TMA. In this study, the incidence of TMA among postrenal transplant recipients was 7.5%. The most common cause for TMA was acute antibody-mediated rejection (ABMR), followed by TMA due to tacrolimus toxicity. In one patient, TMA was secondary to disseminated tuberculosis (TB). TB as a cause of TMA is rarely reported. One-year graft survival in patients with allograft-limited TMA was 72.7% when compared to 50% in patients with systemic TMA, but this difference was statistically insignificant (P = 0.2). The graft loss was high in patients with TMA secondary to ABMR in both the groups. Conclusion: One-year graft survival is better in patients with allograft-limited TMA. Diligent search for an etiology for TMA should be made in all patients with TMA, as the treatment differs between each category.

The process of learning has been confined to the realms of educational institutions. Over the last ten years, the semantics of social media networks have evolved with the use of mobile gadgets. Consequently, nephrologists have realised the potential benefits of using these platforms for their educational and career development. Social media can change the horizon of nephrology education. The concept of bedside examination, teaching and sharing experiences have changed with the advent of Facebook, YouTube, Instagram and X (former Twitter). Other networking portals, such as WhatsApp, Telegram, X (former Twitter), and Pinterest, have also amassed the attention of selected users. Despite split opinions on the utility of social media, it is undeniable that it has influenced interaction between students and mentors. Resources ranging from online networks, blogs, visual aids, podcasts, online journal clubs, videos, live conference coverages, and tutorials have made it possible for nephrologists to stay informed and educated with recent updates. In this review, we discuss how social media can enrich nephrology academia, facilitate the sharing of research and access to fellowships and mentorship programs, provide career prospects to trainees, and broadcast scientific conferences while bringing nephrology societies together.

Molecular testing, including apolipoprotein L1 (APOL1) sequencing, has recently become more accessible for use in the clinical setting. Although there is a strong association between APOL1 and kidney disease, only a small minority of African American kidney disease patients are estimated to have an APOL1 high-risk genotype. In addition, the lifetime risk for developing kidney disease among individuals with two risk alleles is estimated to be very low. The low prevalence suggests that it follows a two-hit model, where a secondary factor, such as environmental or genomic modifiers, is required to develop kidney disease. We still have a limited appreciation of factors that can act as a “second hit,” and it is unclear whether the hyperfiltration that follows donor nephrectomy constitutes as a “second hit” for the disease. One does not yet know the burden of APOL1 risk alleles among prospective living donors. Now that APOL1 genetic testing is available, and in the absence of prospective data, the role of APOL1 genotyping in live kidney donor candidate selection remains uncertain. There are several ethical issues concerning the use of genetic testing to determine donor eligibility, which can impact the development of policy around APOL1 genetic testing, release of results, and counseling.

Infection-related glomerulonephritis (IRGN) results from an immune-mediated process in the occurrence of non-renal infection. Despite increased incidence of infections post-transplant, which is attributed to the immunosuppression, IRGN serves to be a rare cause of de novo GN. Here, we present a 43-year old male, a deceased donor renal transplant recipient, who presented with acute decline in allograft function that developed in association with IRGN five years after transplant. He continued to have renal allograft dysfunction despite treatment with antibiotics. We infer that IRGN must be thought of as a possible entity, although rare, in the diagnosis of de novo GN post-transplant. Furthermore, the absence of definitive treatment protocol makes this emerging cause of renal allograft dysfunction be associated with the poor prognosis.

Introduction: Acute kidney injury represents one of the most severe complications of rhabdomyolysis. Methods: We performed a prospective observational study to analyze the etiology, clinical manifestations, laboratory profile, and outcome in patients with biopsy-proven pigment-induced nephropathy between January 2017 and September 2019. History, clinical examination findings, laboratory investigations, and outcomes were recorded. Results: A total of 26 patients were included. Mean age was 34.81 ± 11.89 years. Mean peak serum creatinine was 6.79 ± 4.07 mg/dL. Median values of Creatine phosphokinase (CPK) and Lactate dehydrogenase (LDH) were 12500 U/L (3187, 17167.50) and 447 U/L (354.50, 908.75), respectively. Of the patients presenting with rhabdomyolysis, 12 patients (46%) had traumatic causes and 14 patients (54%) had nontraumatic causes. Nontraumatic etiology of rhabdomyolysis included seizures (1), wasp sting (1), paraphenylenediamine ingestion (2), rat killer ingestion (2), leptospirosis (2), dehydration (3), acute limb ischemia (1), Gloriosa superba ingestion (1), and prolonged immobilization (1). On renal biopsy, 16 patients had myoglobin cast nephropathy and one had immunoglobulin A deposits in addition to pigment nephropathy. Twenty (76.9%) were initiated on hemodialysis, and two patients (7.6%) were treated with peritoneal dialysis and four patients (15.5%) were treated with forced alkaline diuresis. A total of four patients died (15.4%) due to sepsis/disseminated intravascular coagulation and respiratory failure. At the mean follow-up of 6 months, two patients (7.7%) progressed to chronic kidney disease (CKD). Conclusions: Rhabdomyolysis-associated acute kidney injury is an important cause of renal failure requiring renal replacement therapy. In our study, it was more common in males. Traumatic and nontraumatic causes played an equal causative role. Most of the patients recovered from AKI. Forced alkaline diuresis was found useful in nontraumatic rhabdomyolysis AKI. [ABSTRACT FROM AUTHOR]

Although the vast majority of hypertension is "essential," some may be secondary. And, an accurate diagnosis of secondary cause of hypertension provides the treating clinician with a unique opportunity that renders dramatic response to the patient, either with pharmacologic therapy or surgery. One such secondary cause of hypertension is congenital adrenal hyperplasia due to 11 beta hydroxylase or 17 alpha hydroxylase deficiency. These inherited syndromes are caused by deficient adrenal corticosteroid biosynthesis, in which there is reduced negative feedback inhibition of cortisol and, depending on the steroidogenic pathway involved, an alteration in adrenal mineralocortiocoid and androgen secretion occurs. Here, we present, a young adult presented with hypertension, in association with hypokalemia and metabolic alkalosis, who was diagnosed with congenital adrenal hyperplasia (CAH) due to non-classical variant 11-beta hydroxylase deficiency, which responded dramatically to steroids therapy. Furthermore, we also report two new mis-sense mutations in CYP11B1 gene, a gene coding for 11-betahydroxylase enzyme. [ABSTRACT FROM AUTHOR]

Acute porphyrias are metabolic disorders resulting from deficiency of a specific enzyme involved in heme biosynthetic pathway. These deficiencies also affect normal renal physiology, as kidneys are also involved in heme synthesis. Sometimes, this could even lead to end stage renal disease. Acute Intermittent Porphyria, an autosomal dominant disorder arising from half-normal activity of hydroxymethylbilane synthase, is characterized by occurrence of vague neurovisceral attacks (abdominal pain, nausea, vomiting, constipation and neuropsychiatric symptoms), with urinary excretion of porphyrin precursors, such as 5-Amino-levulinic acid (ALA) and Porphobilinogen (PBG). Acute attacks are triggered by dehydration, diarrhea, steroids, low calorie diets. Treatment includes avoidance of precipitating factors, adequate hydration, high carbohydrate diet and heme replacement. Here, we present an adolescent female who had presented with recurrent abdominal pain, dyselectrolyemia with associated seizures, was diagnosed with Acute Intermittent Porphyria and recovered well with symptomatic management. [ABSTRACT FROM AUTHOR]