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Edgar V. Lerma and Helbert Rondon-Berrios

The conventional first-line therapy for any patient presenting with hypotonic hyponatremia due to SIAD (syndrome of inappropriate antidiuresis) is that of fluid restriction. However, we recognize that fluid restriction alone does not always work. The Expert Panel Recommendations on Diagnosis, Evaluation, and Treatment of Hyponatremia, published in 2013, identified certain criteria that are predictive of which patients are less likely to respond to fluid restriction alone (1). These include a urine-to-plasma electrolyte ratio ([urine Na + urine K]/plasma sodium [PNa]) >1 or a high urine osmolality (>500 mOsm/kg H2O).

It has been suggested that those patients

Susan Murray and Matthew A. Sparks

The year 2019 proved an incredibly important year for the treatment of patients with diabetic kidney disease (DKD). The Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE) trial was a game changer; it demonstrated impressive cardiovascular- and kidney-protective effects of the sodium glucose co-transporter-2 (SGLT2) inhibitor canagliflozin in patients with DKD (1). CREDENCE was important because it was the first trial of SGLT2 inhibitors to include kidney endpoints as primary targets of the trial and led to the US Food and Drug Administration (FDA) extending the indication for canagliflozin specifically for reducing the risk

Katherine Kwon

Veverimer is a novel agent for the treatment of metabolic acidosis in chronic kidney disease (CKD). It is a nonabsorbable polymer that selectively binds hydrochloric acid, leading to excretion of excess acid via the gastrointestinal tract. Veverimer completed a phase 3 clinical trial, demonstrating correction of serum bicarbonate when compared to placebo (1). However, in August 2020, the US Food and Drug Administration (FDA) declined to approve veverimer, requesting additional information on the likelihood of clinical benefit. This prompted manufacturer Tricida to create the VALOR-CKD trial. This ongoing trial will evaluate veverimer’s efficacy against placebo on progression of

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

Edgar V. Lerma

Figure created using BioRender

Appropriate and timely management of hyperkalemia is an important component of a nephrology practice. Hyperkalemia can result from increased K+ intake in the diet, impaired distribution between intracellular and extracellular spaces, and decreased kidney excretion. Risk factors associated with the development of hyperkalemia include older age, male sex, diabetes, underlying kidney disease, as well as intake of certain medications that affect the renin angiotensin aldosterone system (RAAS).

Prior to the advent of sodium zirconium cyclosilicate (SZC) and patiromer, only sodium polystyrene sulfonate (SPS) was available as a potassium exchange resin (1). Approved by the

Samira S. Farouk

"Continue FK, MMF, pred."

Most nephrologists learn early in their training that the most common immunosuppressant regimen for patients with a kidney transplant consists of a calcineurin inhibitor (CNI), mycophenolic acid (usually mycophenolate mofetil [MMF]), with or without some corticosteroid. Let’s take a quick look at two emerging outside-the-box immunosuppression tools.

The new kid on the block

CNIs have long been a thorn in kidney transplantation’s side—with a laundry list of adverse effects ranging from tremors to electrolyte disturbances to paradoxical nephrotoxicity (1). One newer drug that has provided a CNI-free option in some patients is belatacept (approved

Sahar Semnani and Eugene Lin

The last two years have brought several promising trials with novel therapies for the treatment of membranous nephropathy, the most common etiology of nephrotic syndrome in adults (1, 2).

Currently, the mainstay of treatment is steroids in combination with alkylating agents (modified Ponticelli regimen) or calcineurin inhibitors (3). With the identification of auto-antibodies against the phospholipase-2 receptor (PLA2R) comes the potential for new therapies (4, 5), including monoclonal antibodies against CD20 on B-lymphocytes: rituximab and obinutuzumab (4).

In 2019, the MENTOR randomized controlled trial showed that rituximab was

Anna Gaddy

Ms. H is a 33-year-old Hispanic woman referred from a primary care clinic for proteinuria. Her only past medical history is hypertension on a single agent, amlodipine. She has had three children and had a tubal ligation for contraception. She reports that her pregnancies were uncomplicated with no history of preeclampsia or gestational diabetes. Her physical exam was unremarkable with blood pressure 130/70 mm Hg, and she has no edema.

Her laboratory data revealed a normal comprehensive metabolic panel with serum creatinine of 1.6 mg/dL and complete blood counts, although her serologies were noted for the following:

■ double-stranded DNA

Kenar D. Jhaveri

Drug discovery and development is a lengthy and expensive process. Testing new agents in humans at an early stage can reduce the time and costs involved in identifying drugs that are likely to succeed in clinical studies. Implementation of a new drug in practice also requires the development of useful biomarkers of disease and of the drug’s efficacy, as well as sensitive molecular imaging techniques.

Nephrology relied on only a handful of therapeutics during the 1970s to 2000s for managing anemia, bone-mineral disease, glomerular diseases, and transplantation-related events. In the past 2 decades, there has been a steady rise in

Mohammed Elsadany, Yifeng Yang, Sonali Gupta, and Joseph Mattana

It has been well known for many years that cardiovascular disease disproportionately affects patients with chronic kidney disease (CKD) and kidney failure, both through acceleration of atherogenesis as a consequence of reduced kidney function and through the various comorbidities with which our patients are frequently afflicted. Despite growing mechanistic insights into kidney–heart interactions, atherogenesis, cardiac hypertrophy, valvular heart disease, and other phenomena and into new therapies that are available, patients with kidney disease continue to experience an excessive burden of cardiovascular disease and events.

Cardiovascular disease, particularly coronary artery disease, is more often a condition of the older individual, but