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Safeguarding dialysis services during the COVID-19 pandemic
Mayuri Trivedi
doi : 10.1038/s41581-021-00448-w
Nature Reviews Nephrology volume 17, page569 (2021)
Clinical versus research genomics in kidney disease
Andrew J. Mallett, Nine Knoers, John Sayer & Zornitza Stark
doi : 10.1038/s41581-021-00436-0
Nature Reviews Nephrology volume 17, pages570–571 (2021)
Calcium phosphate crystals: targets for renoprotection
Monica Wang
doi : 10.1038/s41581-021-00472-w
Nature Reviews Nephrology volume 17, page572 (2021)
Protective circulating proteins in DKD
Susan Allison
doi : 10.1038/s41581-021-00467-7
Nature Reviews Nephrology volume 17, page572 (2021)
KIM-1 targeted extracellular vesicles for AKI
Susan Allison
doi : 10.1038/s41581-021-00468-6
Nature Reviews Nephrology volume 17, page572 (2021)
Kidney involvement in COVID-19
Susan Allison
doi : 10.1038/s41581-021-00469-5
Nature Reviews Nephrology volume 17, page572 (2021)
Daratumumab for AL amyloidosis
Susan Allison
doi : 10.1038/s41581-021-00470-y
Nature Reviews Nephrology volume 17, page572 (2021)
A new era of treatment for primary hyperoxaluria type 1
Florian Erger & Bodo B. Beck
doi : 10.1038/s41581-021-00449-9
Nature Reviews Nephrology volume 17, pages573–574 (2021)
Nitric oxide signalling in kidney regulation and cardiometabolic health
Mattias Carlström
doi : 10.1038/s41581-021-00429-z
Nature Reviews Nephrology volume 17, pages575–590 (2021)
The prevalence of cardiovascular and metabolic disease coupled with kidney dysfunction is increasing worldwide. This triad of disorders is associated with considerable morbidity and mortality as well as a substantial economic burden. Further understanding of the underlying pathophysiological mechanisms is important to develop novel preventive or therapeutic approaches. Among the proposed mechanisms, compromised nitric oxide (NO) bioactivity associated with oxidative stress is considered to be important. NO is a short-lived diatomic signalling molecule that exerts numerous effects on the kidneys, heart and vasculature as well as on peripheral metabolically active organs. The enzymatic L-arginine-dependent NO synthase (NOS) pathway is classically viewed as the main source of endogenous NO formation. However, the function of the NOS system is often compromised in various pathologies including kidney, cardiovascular and metabolic diseases. An alternative pathway, the nitrate–nitrite–NO pathway, enables endogenous or dietary-derived inorganic nitrate and nitrite to be recycled via serial reduction to form bioactive nitrogen species, including NO, independent of the NOS system. Signalling via these nitrogen species is linked with cGMP-dependent and independent mechanisms. Novel approaches to restoring NO homeostasis during NOS deficiency and oxidative stress have potential therapeutic applications in kidney, cardiovascular and metabolic disorders.
Liquid biopsies: donor-derived cell-free DNA for the detection of kidney allograft injury
Michael Oellerich, Karen Sherwood, Paul Keown, Ekkehard Schütz, Julia Beck, Johannes Stegbauer, Lars Christian Rump & Philip D. Walson
doi : 10.1038/s41581-021-00428-0
Nature Reviews Nephrology volume 17, pages591–603 (2021)
In kidney transplantation, the use of minimally invasive damage biomarkers that are more sensitive and specific than plasma creatinine will be crucial to enable early, actionable detection or exclusion of structural kidney damage due to acute or chronic rejection. Donor-derived cell-free DNA (dd-cfDNA), which can be quantified, for example, through next-generation sequencing, droplet digital PCR and quantitative PCR, is a candidate biomarker with great potential for enabling comprehensive monitoring of allograft injury. dd-cfDNA has a favourable overall diagnostic performance for the detection of rejection and its high negative predictive value might be especially useful for avoiding unnecessary biopsies. Elevated dd-cfDNA levels have been shown to be detectable before graft injury can be clinically identified using current diagnostic methods. Moreover, dd-cfDNA falls rapidly to baseline levels after successful treatment for rejection owing to its short half-life. dd-cfDNA can detect graft injury caused by immune activation owing to insufficient immunosuppression and might therefore also help guide immunosuppression dosing. The fractional abundance of dd-cfDNA can be affected by changes in the recipient cfDNA (for example, due to infection or physical exercise) but the use of absolute quantification of dd-cfDNA overcomes this limitation. Serial dd-cfDNA determinations might therefore facilitate cost-effective personalized clinical management of kidney transplant recipients to reduce premature graft loss.
Postoperative acute kidney injury in adult non-cardiac surgery: joint consensus report of the Acute Disease Quality Initiative and PeriOperative Quality Initiative
John R. Prowle, Lui G. Forni, Max Bell, Michelle S. Chew, Mark Edwards, Morgan E. Grams, Michael P. W. Grocott, Kathleen D. Liu, David McIlroy, Patrick T. Murray, Marlies Ostermann, Alexander Zarbock, Sean M. Bagshaw, Raquel Bartz, Samira Bell, Azra Bihorac, Tong J. Gan, Charles E. Hobson, Michael Joannidis, Jay L. Koyner, Denny Z. H. Levett, Ravindra L. Mehta, Timothy E. Miller, Michael G. Mythen, Mitra K. Nadim, Rupert M. Pearse, Thomas Rimmele, Claudio Ronco, Andrew D. Shaw & John A. Kellum
doi : 10.1038/s41581-021-00418-2
Nature Reviews Nephrology volume 17, pages605–618 (2021)
Postoperative acute kidney injury (PO-AKI) is a common complication of major surgery that is strongly associated with short-term surgical complications and long-term adverse outcomes, including increased risk of chronic kidney disease, cardiovascular events and death. Risk factors for PO-AKI include older age and comorbid diseases such as chronic kidney disease and diabetes mellitus. PO-AKI is best defined as AKI occurring within 7 days of an operative intervention using the Kidney Disease Improving Global Outcomes (KDIGO) definition of AKI; however, additional prognostic information may be gained from detailed clinical assessment and other diagnostic investigations in the form of a focused kidney health assessment (KHA). Prevention of PO-AKI is largely based on identification of high baseline risk, monitoring and reduction of nephrotoxic insults, whereas treatment involves the application of a bundle of interventions to avoid secondary kidney injury and mitigate the severity of AKI. As PO-AKI is strongly associated with long-term adverse outcomes, some form of follow-up KHA is essential; however, the form and location of this will be dictated by the nature and severity of the AKI. In this Consensus Statement, we provide graded recommendations for AKI after non-cardiac surgery and highlight priorities for future research.
Therapeutic trials in adult FSGS: lessons learned and the road forward
An S. De Vriese, Jack F. Wetzels, Richard J. Glassock, Sanjeev Sethi & Fernando C. Fervenza
doi : 10.1038/s41581-021-00427-1
Nature Reviews Nephrology volume 17, pages619–630 (2021)
Focal segmental glomerulosclerosis (FSGS) is not a specific disease entity but a lesion that primarily targets the podocyte. In a broad sense, the causes of the lesion can be divided into those triggered by a presumed circulating permeability factor, those that occur secondary to a process that might originate outside the kidneys, those caused by a genetic mutation in a podocyte or glomerular basement membrane protein, and those that arise through an as yet unidentifiable process, seemingly unrelated to a circulating permeability factor. A careful attempt to correctly stratify patients with FSGS based on their clinical presentation and pathological findings on kidney biopsy is essential for sound treatment decisions in individual patients. However, it is also essential for the rational design of therapeutic trials in FSGS. Greater recognition of the pathophysiology underlying podocyte stress and damage in FSGS will increase the likelihood that the cause of an FSGS lesion is properly identified and enable stratification of patients in future interventional trials. Such efforts will facilitate the identification of effective therapeutic agents.
