Transition from paediatric to adult-focused care: unresolved issues

Maria E. Diaz-Gonzalez de Ferris, Michael Ted Ferris & Guido Filler

doi : 10.1038/s41581-021-00476-6

Nature Reviews Nephrology volume 17, pages705–706 (2021)

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DPEP1 and CHMP1A in kidney ferroptosis

Susan J. Allison

doi : 10.1038/s41581-021-00496-2

Nature Reviews Nephrology volume 17, page707 (2021)

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Targeting OSBPL7 restores cholesterol efflux

Monica Wang

doi : 10.1038/s41581-021-00492-6

Nature Reviews Nephrology volume 17, page707 (2021)

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Nanocapsule system tackles polymyxin B toxicity

Monica Wang

doi : 10.1038/s41581-021-00493-5

Nature Reviews Nephrology volume 17, page707 (2021)

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RBC mitochondria trigger interferon release

Monica Wang

doi : 10.1038/s41581-021-00494-4

Nature Reviews Nephrology volume 17, page707 (2021)

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Reducing stress-induced CHOP is renoprotective

Monica Wang

doi : 10.1038/s41581-021-00495-3

Nature Reviews Nephrology volume 17, page707 (2021)

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Potential cardiorenal benefits of efpeglenatide in diabetes

Jacques Ma & Mark E. Cooper

doi : 10.1038/s41581-021-00475-7

Nature Reviews Nephrology volume 17, pages708–709 (2021)

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Multi-omics integration in the age of million single-cell data

Zhen Miao, Benjamin D. Humphreys, Andrew P. McMahon & Junhyong Kim

doi : 10.1038/s41581-021-00463-x

Nature Reviews Nephrology volume 17, pages710–724 (2021)

An explosion in single-cell technologies has revealed a previously underappreciated heterogeneity of cell types and novel cell-state associations with sex, disease, development and other processes. Starting with transcriptome analyses, single-cell techniques have extended to multi-omics approaches and now enable the simultaneous measurement of data modalities and spatial cellular context. Data are now available for millions of cells, for whole-genome measurements and for multiple modalities. Although analyses of such multimodal datasets have the potential to provide new insights into biological processes that cannot be inferred with a single mode of assay, the integration of very large, complex, multimodal data into biological models and mechanisms represents a considerable challenge. An understanding of the principles of data integration and visualization methods is required to determine what methods are best applied to a particular single-cell dataset. Each class of method has advantages and pitfalls in terms of its ability to achieve various biological goals, including cell-type classification, regulatory network modelling and biological process inference. In choosing a data integration strategy, consideration must be given to whether the multi-omics data are matched (that is, measured on the same cell) or unmatched (that is, measured on different cells) and, more importantly, the overall modelling and visualization goals of the integrated analysis.

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Pro-resolving lipid mediators: regulators of inflammation, metabolism and kidney function

Eoin Brennan, Phillip Kantharidis, Mark E. Cooper & Catherine Godson

doi : 10.1038/s41581-021-00454-y

Nature Reviews Nephrology volume 17, pages725–739 (2021)

Obesity, diabetes mellitus, hypertension and cardiovascular disease are risk factors for chronic kidney disease (CKD) and kidney failure. Chronic, low-grade inflammation is recognized as a major pathogenic mechanism that underlies the association between CKD and obesity, impaired glucose tolerance, insulin resistance and diabetes, through interaction between resident and/or circulating immune cells with parenchymal cells. Thus, considerable interest exists in approaches that target inflammation as a strategy to manage CKD. The initial phase of the inflammatory response to injury or metabolic dysfunction reflects the release of pro-inflammatory mediators including peptides, lipids and cytokines, and the recruitment of leukocytes. In self-limiting inflammation, the evolving inflammatory response is coupled to distinct processes that promote the resolution of inflammation and restore homeostasis. The discovery of endogenously generated lipid mediators — specialized pro-resolving lipid mediators and branched fatty acid esters of hydroxy fatty acids — which promote the resolution of inflammation and attenuate the microvascular and macrovascular complications of obesity and diabetes mellitus highlights novel opportunities for potential therapeutic intervention through the targeting of pro-resolution, rather than anti-inflammatory pathways.

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Trajectories of kidney function in diabetes: a clinicopathological update

Megumi Oshima, Miho Shimizu, Masayuki Yamanouchi, Tadashi Toyama, Akinori Hara, Kengo Furuichi & Takashi Wada

doi : 10.1038/s41581-021-00462-y

Nature Reviews Nephrology volume 17, pages740–750 (2021)

Diabetic nephropathy has been traditionally diagnosed based on persistently high albuminuria and a subsequent decline in glomerular filtration rate (GFR), which is widely recognized as the classical phenotype of diabetic kidney disease (DKD). Several studies have emphasized that trajectories of kidney function in patients with diabetes (specifically, changes in GFR and albuminuria over time) can differ from this classical DKD phenotype. Three alternative DKD phenotypes have been reported to date and are characterized by albuminuria regression, a rapid decline in GFR, or non-proteinuric or non-albuminuric DKD. Although kidney biopsies are not typically required for the diagnosis of DKD, a few studies of biopsy samples from patients with DKD have demonstrated that changes in kidney function associate with specific histopathological findings in diabetes. In addition, various clinical and biochemical parameters are related to trajectories of GFR and albuminuria. Collectively, pathological and clinical characteristics can be used to predict trajectories of GFR and albuminuria in diabetes. Furthermore, cohort studies have suggested that the risks of kidney and cardiovascular outcomes might vary among different phenotypes of DKD. A broader understanding of the clinical course of DKD is therefore crucial to improve risk stratification and enable early interventions that prevent adverse outcomes.

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Pathophysiology of COVID-19-associated acute kidney injury

Matthieu Legrand, Samira Bell, Lui Forni, Michael Joannidis, Jay L. Koyner, Kathleen Liu & Vincenzo Cantaluppi

doi : 10.1038/s41581-021-00452-0

Nature Reviews Nephrology volume 17, pages751–764 (2021)

Although respiratory failure and hypoxaemia are the main manifestations of COVID-19, kidney involvement is also common. Available evidence supports a number of potential pathophysiological pathways through which acute kidney injury (AKI) can develop in the context of SARS-CoV-2 infection. Histopathological findings have highlighted both similarities and differences between AKI in patients with COVID-19 and in those with AKI in non-COVID-related sepsis. Acute tubular injury is common, although it is often mild, despite markedly reduced kidney function. Systemic haemodynamic instability very likely contributes to tubular injury. Despite descriptions of COVID-19 as a cytokine storm syndrome, levels of circulating cytokines are often lower in patients with COVID-19 than in patients with acute respiratory distress syndrome with causes other than COVID-19. Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury, as might endothelial injury and microvascular thrombi. Findings of high viral load in patients who have died with AKI suggest a contribution of viral invasion in the kidneys, although the issue of renal tropism remains controversial. An impaired type I interferon response has also been reported in patients with severe COVID-19. In light of these observations, the potential pathophysiological mechanisms of COVID-19-associated AKI may provide insights into therapeutic strategies.

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Aquaporin 2 regulation: implications for water balance and polycystic kidney diseases

Emma T. B. Olesen & Robert A. Fenton

doi : 10.1038/s41581-021-00447-x

Nature Reviews Nephrology volume 17, pages765–781 (2021)

Targeting the collecting duct water channel aquaporin 2 (AQP2) to the plasma membrane is essential for the maintenance of mammalian water homeostasis. The vasopressin V2 receptor (V2R), which is a GS protein-coupled receptor that increases intracellular cAMP levels, has a major role in this targeting process. Although a rise in cAMP levels and activation of protein kinase A are involved in facilitating the actions of V2R, studies in knockout mice and cell models have suggested that cAMP signalling pathways are not an absolute requirement for V2R-mediated AQP2 trafficking to the plasma membrane. In addition, although AQP2 phosphorylation is a known prerequisite for V2R-mediated plasma membrane targeting, none of the known AQP2 phosphorylation events appears to be rate-limiting in this process, which suggests the involvement of other factors; cytoskeletal remodelling has also been implicated. Notably, several regulatory processes and signalling pathways involved in AQP2 trafficking also have a role in the pathophysiology of autosomal dominant polycystic kidney disease, although the role of AQP2 in cyst progression is unknown. Here, we highlight advances in the field of AQP2 regulation that might be exploited for the treatment of water balance disorders and provide a rationale for targeting these pathways in autosomal dominant polycystic kidney disease.

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