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The Key Advances in Nephrology collection offers a unique series of specially commissioned ‘Year in Review’ articles that highlight the key discoveries made each year. In these articles, leading experts in the field describe their pick of the top 3–5 key advances of the year, outlining their clinical impact and implications for current and future research.
The COVID-19 pandemic and the Movement for Black Lives have focused attention on racial disparities in kidney health outcomes. In 2020, kidney professionals highlighted threats posed by racism and other negative social drivers of kidney health, and proposed solutions to address these issues through scholarship and advocacy for social justice.
The consequences of the COVID-19 pandemic have been devastating; however, evidence suggests that patients with, or at risk of, kidney disease are disproportionally affected. Patients on dialysis and kidney transplant recipients are at higher risk of adverse outcomes from COVID-19, whereas, conversely, patients with severe COVID-19 are at increased risk of acute kidney injury, with short-term and possibly long-term consequences for nephrological care.
Sodium–glucose co-transporter 2 inhibitors offer impressive cardiac and kidney outcome benefits to people with type 2 diabetes mellitus (T2DM). These benefits now appear to extend to people without T2DM, according to three trials published in 2020.
Genetic research in nephrology is rapidly advancing. Key studies published in 2020 demonstrate that genetic findings can provide new tools for patient diagnosis and risk stratification as well as important insights into kidney physiology and disease mechanisms that could potentially lead to novel therapies.
Timely diagnosis and dialytic treatment of acute kidney injury (AKI) came to the forefront at the height of the coronavirus disease 2019 pandemic as admissions surged in intensive care units. Research on early diagnosis, timing of initiation of kidney replacement therapy, and appropriate post-hospitalization patient care remains essential to tackling the burden of AKI.
In 2020 a number of clinical trials have provided insights into therapeutic approaches for the treatment of anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis and lupus nephritis. Moreover, mechanistic insights have potential to open new therapeutic strategies in the future.
After nearly two decades, a new therapeutic agent, canagliflozin, received regulatory approval to prevent loss of kidney function, end-stage kidney disease, hospitalization for heart failure and cardiovascular death in patients with diabetic kidney disease. Nonetheless, the residual risk of kidney disease progression and complications remains high, underlining the importance of ongoing therapeutic development.
Acute kidney injury (AKI) is an important clinical problem that is associated with adverse short- and long-term outcomes. Studies published in 2019 provide new insights into the staging, risk stratification and subphenotyping of AKI as well as the adverse effects of AKI on the heart.
2019 saw advances in the generation of induced pluripotent stem cell (iPSC)-derived nephron progenitors and in our understanding of how nephrons form in a kidney organoid. Fundamental studies of regeneration in zebrafish continue to provide vital clues as to how we might use iPSC-derived cells to regenerate a human nephron in vivo.
Artificial intelligence is increasingly being used to improve diagnosis and prognostication for acute and chronic kidney diseases. Studies with this objective published in 2019 relied on a variety of available data sources, including electronic health records, intraoperative physiological signals, kidney ultrasound imaging, and digitized biopsy specimens.
Single-cell genomics provide a powerful approach to investigate the intrinsic complexity of the kidney and understand the diverse cell types and states that exist during kidney development, homeostasis and disease. Several advances were made in 2019 that enhance our understanding of kidney immune cell states in health and disease and the quality of current kidney organoid model systems for studying human diseases.
With many failures, a sense of helplessness has overshadowed the field of acute kidney injury (AKI). Publications in 2018 offer new hope: better drug targets, better end points and improved understanding of conditions that cause AKI and its complications bring promise that a drug will soon be available.
The function of polycystin proteins and the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD) are not well understood. Studies published in 2018 made important contributions to the understanding of genetic mechanisms, the structure of the polycystin complex and the roles of G-protein signalling and the immune system in ADPKD.
Numerous exciting studies that advanced our understanding of immune-mediated kidney disease were published in 2018. Whereas most of these studies analysed the role of pro-inflammatory mediators, several novel anti-inflammatory mechanisms were discovered that involve immune cells and mediators with previously unrecognized protective roles in renal disease.
In 2018, consolidating evidence for renoprotective benefits was seen with respect to sodium–glucose cotransporter 2 inhibitors and glucagon-like peptide 1 agonists, which are currently being incorporated into clinical practice. The focus now turns to novel therapeutic targets to optimize renoprotection as diabetic kidney disease grows to epidemic proportions worldwide.
Discoveries in 2018 using single-cell sequencing and gene-editing technologies have revealed their transformative potential for the investigation of kidney physiology and disease. Their promise is matched by the speed of their evolution.
Clinical trials have demonstrated that glucagon-like peptide 1 receptor (GLP1R) agonists have therapeutic benefits beyond glycaemic control. Here, the authors examine the protective effects of incretin-based therapies in patients with diabetic kidney disease and how the immunomodulatory and anti-inflammatory effects of GLP1 might underlie this protection.
This Review describes our current understanding of the pathogenic mechanisms involved in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the progression of coronavirus disease 2019 (COVID-19), focusing on the immunological hyper-response and the induction of widespread endothelial damage, complement-associated blood clotting and systemic microangiopathy, as well as the effects of these processes on the kidney. The authors also discuss therapeutic interventions that currently hold most promise.
COVID-19-associated AKI (COVID-19 AKI) is associated with high mortality and is an independent risk factor for all-cause in-hospital death in patients with COVID-19. This Consensus Statement from the Acute Disease Quality Initiative provides recommendations for the diagnosis, prevention and management of COVID-19 AKI and for areas of future research, with the aim of improving understanding of the underlying processes and outcomes for patients with COVID-19 AKI.
Working towards sustainable development is essential to tackle the rise in the global burden of non-communicable diseases, including kidney disease. Five years after the Sustainable Development Goal agenda was set, this Review examines the progress thus far, highlighting future challenges and opportunities, and explores the implications for kidney disease.
An increasing body of evidence suggests that genomic disorders and monogenic aetiologies contribute meaningfully to seemingly complex forms of chronic kidney disease (CKD). This Review describes rare genetic causes of CKD and the genetic and phenotypic complexity of this group of disorders, and discusses novel approaches to help to address the challenges posed by the complexity of CKD.
An episode of acute kidney injury (AKI) can predispose individuals to a variety of adverse clinical outcomes. In this Review, the authors discuss the potential long-term outcomes of AKI, as well as current and novel strategies to improve the follow-up care of AKI survivors.
Vallon and Thompson provide a tubule-centred view of diabetic kidney physiology. According to the tubular hypothesis of nephron filtration and diabetic kidney disease, early diabetes induces changes in renal tubules that alter interactions between the tubule and glomerulus, ultimately leading to diabetic kidney disease.