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Prabhat Chauhan and Raja Ramachandran

The prevalence of malignancy in patients with membranous nephropathy (MN) ranges from 4% to 10% (1, 2). In adults, MN is the most common cause of nephrotic syndrome outside of diabetes and is well described but not well studied in patients with cancer.

In a recent article by Thet and colleagues (3) in Translational Oncology, the authors impart on an update on cancer risks in patients with a glomerular diseases. Thet et al. (3) used MN as a prototype to understand malignancy-related glomerular disease. Malignancy-related MN is a disease of

Sheila Bermejo

Cancer is a worldwide epidemic that has increased its prevalence exponentially over the last decades. In 2020, 19.3 million new cases of cancer were diagnosed, and there were 10 million deaths from cancer worldwide (1). Cancer patients are susceptible to chemotherapy and immunotherapy treatments that can cause renal complications, such as acute kidney injury (secondary to glomerular disease, acute interstitial nephritis, or acute tubular necrosis), electrolyte disorder, proteinuria, and others (2). Additionally, a higher prevalence of cancer has been demonstrated in patients with chronic kidney disease from various types, those with a kidney transplant, and patients

Paul E. Hanna and Meghan E. Sise

Important decisions about diagnosing kidney disease, managing drug dosing, and considering kidney replacement therapy rely on an accurate estimation of the glomerular filtration rate (GFR), especially in patients with cancer (1, 2). Despite its continued use, the Cockcroft-Gault equation (3), originally created to assess kidney function based on serum creatinine in 1976, has significant limitations that may be even greater in patients with cancer who have sarcopenia. To address this, Costa E Silva and colleagues (4) compared the measured GFR using chromium-51-labeled ethylenediamine tetraacetic acid (51Cr-EDTA) clearance in 1200 patients

Insara Jaffer Sathick and Aisha Shaikh

Pseudo-electrolyte disorders are laboratory artifacts, and failure to recognize this entity can lead to inadvertent treatment. The hallmark of pseudo-electrolyte disorders is that the patient does not exhibit classic signs or symptoms of the underlying electrolyte abnormality. This should prompt clinicians to rule out pseudo-electrolyte disorders before initiating therapy. Here, we highlight pseudo-electrolyte disorders seen in onconephrology practice.

Pseudo-hyponatremia

A falsely low sodium level is seen in conditions that reduce the water content of a given volume of plasma, such as 1) severe hyperproteinemia due to paraproteinemia, hypergammaglobulinemia, or intravenous immunoglobulin (IVIG) administration; 2) severe hyperlipidemia due to

Pooja Amarapurkar, Pooja Kalantri, Levard Roberts, and Jose Navarrete

Sickle cell disease and sickle cell trait are associated with several kidney abnormalities. The inner medullary environment of the kidney with low oxygen tension, hyperosmolarity, and acidemia is an ideal setup for hemoglobin polymerization and sickling. Repeated hemolysis, vaso-occlusive episodes, subsequent reperfusion injury, oxidative stress, and inflammation lead to acute and chronic kidney disease (CKD) (1, 2). The various kidney manifestations of sickle cell disease are summarized in Table 1.

Kidney manifestations of sickle cell disease

Glomerular hyperfiltration and lower mean arterial pressure occur in early years of life. With advancing age,

Jermaine G. Johnston and Elinor C. Mannon

The start of a new year often signals a time for reflection. As we move through 2022, we again may find ourselves asking: What is the state of nephrology research? How are trainees fairing as they build their own independent careers in this field? There are many sources of support that assist trainees at all levels as they hone the skills necessary for scientific investigation. However, this career path is not without challenges, including, but not limited to, scientific investigation funding, time that is dedicated for investigation, support to build a professional network, and the current lack of diversity in

Keisa W. Mathis, Corey L. Reynolds, and Clintoria R. Williams

According to surveys conducted by the Association of Chairs of Departments of Physiology, the percentage of Black faculty has averaged 1% for the past 20 years (1). This same trend in lack of representation exists for the trainee (graduate student and postdoc) level as well, further complicating the recruitment and retention of the next generation of Black physiologists. It was due to these defaults in the system that in the summer of 2020, Black in Physiology (BiP), an organization committed to nurturing and celebrating Black excellence throughout the physiology community, was created by four charter members. Currently, two

Koki Abe and Tomokazu Souma

Cell death is a fundamental biological process underlying normal development, homeostasis, and diseases. Regulated cell death is defined as a molecularly controlled cell death that can be modulated (either promoting or preventing) by specific interventions (1). Although apoptosis has been the focus of interest regarding research on regulated cell death and has been historically considered a major cell death pathway in kidney disease processes, there are surprisingly many other ways cells end their lives in a molecularly regulated manner, such as necroptosis, pyroptosis, ferroptosis, and others. Among them, ferroptosis is attracting attention as a critical contributor and a

Jianxiang Xue and Timo Rieg

A series of clinical trials demonstrated promising outcomes of sodium glucose co-transporter 2 (SGLT2) inhibitors, a novel class of anti-diabetic drugs, in patients with heart failure (HF), with either reduced ejection fraction or preserved ejection fraction. Of note, these positive outcomes are irrespective of the diabetic status and with rapid onset, suggesting the clinical benefits of SGLT2 inhibition are not fully attributable to glycemic control. Based on various experimental studies, a substantial number of hypotheses have been proposed to explain the beneficial effects of SGLT2 inhibition in HF. These effects can be divided into two groups: indirect systemic effects and

Jeanne A. Ishimwe, Valentina Kon, and Annet Kirabo

Persistent systemic inflammation is a hallmark of chronic kidney disease (CKD) and several of its risk factors, including diabetes and hypertension. The gut microbiome is defined as the microorganisms and their genetic material in the intestinal tract. Emerging evidence has substantiated the gut microbiome as a key mediator of inflammation in various pathophysiologic states, including kidney diseases (1, 2). Patients with kidney failure on dialysis also exhibit bacterial translocation from the intestines to the circulation, contributing to microinflammation (3). Bacterial translocation is reported in other pathologies, including hypertension and autoimmunity (4,