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Mayuri Trivedi

Recently, the world of nephrology rejoiced at another “positive” trial in nephrology: Dapagliflozin in Patients with Chronic Kidney Disease (DAPA-CKD) (1). But in India and other nations in the South Asian subcontinent we also are deeply concerned by the fact that the sodium glucose cotransporter-2 inhibitors (SGLT2i) are scarcely available and, when they are, place a huge financial burden on our patients who manage to procure them. Dapagliflozin costs the US dollar equivalent of $0.89 for a 10-mg tablet in India (compared to one 75-mg tablet of aspirin [ASA] at $0.038 and one 10-mg tablet of atorvastatin 10

Mayuri Trivedi and Zaheer Virani

Membranous nephropathy (MN) is a common cause of adult nephrotic syndrome, which may present as a sub-nephrotic or nephrotic range proteinuria with hypoalbuminemia, hyperlipidemia, and edema. It is an immune-mediated glomerular disease that is pathologically characterized by glomerular intra-membranous and sub-epithelial immune complex deposits (immunoglobulin G4 [IgG4] and complement 3 [C3]) causing membrane thickening.

The pathophysiology of MN was first described by the Heymann nephritis rat model in 1959 (1). Although the target antigen described in that model was “megalin,” which does not play a major role in humans, it set the path for subsequent discoveries of many

Raja Ramachandran and Mayuri Trivedi

Podocytopathies are a group of kidney diseases caused by direct or indirect injury to the glomerular podocytes, resulting in proteinuria. Examples of podocytopathies are minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and collapsing glomerulopathy (CG) (1). T-regulatory cell dysfunction and the podocyte proteins CD80 (2)/angiopoietin-like protein 4 (Angptl4) (3) have been shown to participate in the pathogenesis of MCD. An insult to the network of the visceral and parietal epithelial cells of the glomerulus by the immune system or a genetic defect is thought to be responsible for the development of primary FSGS

Mayuri Trivedi and Vivekanand Jha

The unfolding story of COVID-19 in India has shown how a narrative can change quickly. It was only a few months ago that experts around the world were wondering what explained India's relatively cheap escape (until then) from the ravages of the COVID-19 pandemic. India is now back in the news, but this time, the reports are highlighting the utter collapse of the healthcare system, shortage of critical supplies and hospital beds, people dying on the curbsides, and striking images of over-busy cremation and burial grounds. Amid this chaos, care of patients with chronic illnesses like kidney diseases has been

Mayuri Trivedi and Sanjeev Nair

Mineral bone disease (MBD) has proven to be a Pandora’s box for most clinicians treating chronic kidney disease (CKD), including end-stage kidney disease (ESKD). Although the body of literature highlighting the various bone metabolic abnormalities associated with ESKD as definite risk factors for mortality, cardiovascular disease, increased risk of fractures, and other musculoskeletal complications grows stronger, the therapeutic agents to deal with these abnormalities continue to keep us on edge (Table 1).

Reasons for skepticism among nephrologists regarding novel drugs for MBD

MBD = mineral bone disease

In recent years, a few novel agents have

Kenar Jhaveri and Mayuri Trivedi

Traditionally, the field of hematology-oncology has elicited a feeling of despair and morbidity in many until a few years ago. However, with the growing advances in the field of oncology, there are a larger number of patients who are being diagnosed with cancers and an even larger number surviving cancer. With this change in the field of oncology, we—as nephrologists—encounter many patients who develop kidney diseases due to cancer or the therapy used for the treatment of cancer.

From electrolyte and acid-base imbalance to acute and chronic kidney disease, including glomerular diseases, nephrologists are seeing a growing number of patients

Kenar D. Jhaveri and Mayuri Trivedi

In 1914, Volhard and Fahr (1) described the first-ever classification of glomerular diseases. It was simple: inflammatory, degenerative, or related to arteriosclerosis (Table 1). Since then, diseases of the glomerulus have always held a special place of interest for nephrologists. On closer inspection, the science and knowledge of the glomerulus have revealed much of the beauty and complexity of this structure. From the 1900s to 2021, we have come a long way with advances in genetics in the discovery of APOL1 polymorphisms associated with focal segmental glomerulosclerosis (FSGS), multiple monogenic causes of FSGS and other primary

Mayuri Trivedi and Kirk N. Campbell

Novel biomarkers have been changing our understanding of glomerular disease physiology by improving our diagnostic and prognostic capabilities while opening the door to more precise therapeutic options. Most notably, the discovery of the anti-phospholipase receptor-2 antibody (anti-PLA2R Ab) in 2009 has facilitated diagnostic algorithms where some patients with high PLA2R titers may not need a kidney biopsy. Titer levels are followed clinically to monitor response to treatment and risk of relapse, whereas novel therapeutics are being developed to specifically inhibit presumed pathogenic properties of PLA2R Abs (1).

Nephrin, an important component of the slit diaphragm, has been one