Kidney diseases articles within Nature Communications

Featured

  • Article
    | Open Access

    Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) is a lipid raft enzyme known to affect membrane lipid composition. Here, Mitrofanova et al. show that increased expression of SMPDL3b in diabetes impairs insulin signaling and ceramide-1-phosphate (C1P) availability in podocytes, and that C1P supplementation protects mice from diabetic kidney disease.

    • A. Mitrofanova
    • , S. K. Mallela
    •  & A. Fornoni

  • Article
    | Open Access

    Patients with diabetes commonly develop diabetic kidney disease (DKD). Here Gluck et al. identify a set of probes differentially methylated in renal samples from patients with DKD, and find that inclusion of these methylation probes improves current prediction models of renal function decline.

    • Caroline Gluck
    • , Chengxiang Qiu
    •  & Katalin Susztak

  • Article
    | Open Access

    Angiotensin II is known to cause renal inflammation and fibrosis. Here Lu et al. show that levels of circulating miR-103a-3p are elevated in hypertensive nephropathy patients and in an animal model of angiotensin II-induced renal dysfunction, and that miR-103a-3p suppresses SNRK expression leading to the activation of the pro-inflammatory NF-κB pathway in glomerular endothelial cells.

    • Qiulun Lu
    • , Zejun Ma
    •  & Ming-Hui Zou

  • Article
    | Open Access

    Polycystin-2 (PC2) is an ion channel commonly found mutated in autosomal dominant polycystic kidney disease. Here Arhatte et al. identify transmembrane protein 33 (TMEM33) as a regulator of PC2 function at the endoplasmic reticulum, and find that deletion of TMEM33 protects mice from acute kidney injury.

    • Malika Arhatte
    • , Gihan S. Gunaratne
    •  & Amanda Patel

  • Article
    | Open Access

    Estimated glomerular filtration rate (eGFR) is a measure of kidney function and used to characterize chronic kidney disease. Here, Graham et al. identify 53 novel loci for eGFR in a GWAS meta-analysis, a subset of which are associated with other common diseases, such as diabetes and hypertension, based on PheWAS.

    • Sarah E. Graham
    • , Jonas B. Nielsen
    •  & Cristen J. Willer

  • Article
    | Open Access

    Diabetes is a major cause of kidney disease. Here Kikuchi et al. show that phenol sulfate, a gut microbiota-derived metabolite, is increased in diabetic kidney disease and contributes to the pathology by promoting kidney injury, suggesting phenyl sulfate could be used a marker and therapeutic target for the treatment of diabetic kidney disease.

    • Koichi Kikuchi
    • , Daisuke Saigusa
    •  & Takaaki Abe

  • Article
    | Open Access

    Accurate monitoring of chronic kidney disease (CKD) progression is essential for efficient disease management. Here Chen et al. identify five serum metabolites in patients with stage 1–5 CKD whose levels associate with disease progression, and find that 5-methoxytryptophan and its regulatory enzyme TPH-1 exert anti-fibrotic effects in mouse models of kidney injury.

    • Dan-Qian Chen
    • , Gang Cao
    •  & Ying-Yong Zhao

  • Article
    | Open Access

    Vascular calcification is a hallmark of end stage renal disease. Here, Cheng et al. show that poly(ADP-ribose) polymerase (PARP) activity is increased in calcified arteries in patients and uremic rats, and that PARP1 promotes vascular calcification by suppressing miR-204 expression via IL-6/STAT3 signaling, thus relieving repression of the osteogenic regulator Runx2.

    • Cheng Wang
    • , Wenjing Xu
    •  & Kai Huang

  • Article
    | Open Access

    Allograft can induces local chronic inflammation, but how this feeds back to regulating late immunity is still not clear. Here the authors show, by charactering B cell transcriptome landscape dynamic in human allografts and in mouse kidneys transitioning from acute to chronic injury, that late B cell activation is associated with renal dysfunction and inflammation.

    • Pietro E. Cippà
    • , Jing Liu
    •  & Andrew P. McMahon

  • Article
    | Open Access

    The molecular mechanisms that underlie associations in GWAS, incl. chronic kidney disease (CKD), are largely unknown. Here, the authors perform an integrative analysis of genetic, transcriptomic and epigenomic data from human kidney to pinpoint plausible molecular pathways of CKD genetic associations.

    • Xiaoguang Xu
    • , James M. Eales
    •  & Maciej Tomaszewski

  • Article
    | Open Access

    Suppression of gene expression due to aberrant promoter methylation contributes to organ fibrosis. Here, the authors couple a deactivated Cas9 to the TET3 catalytic domain to induce expression of four antifibrotic genes, and show that lentiviral-mediated delivery is effective in reducing kidney fibrosis in mouse models.

    • Xingbo Xu
    • , Xiaoying Tan
    •  & Michael Zeisberg

  • Article
    | Open Access

    Mutations in the cation channel PKD2 cause human autosomal dominant polycystic kidney disease but its channel function and gating mechanism are poorly understood. Here authors study PKD2 using electrophysiology and cryo-EM, which identifies hydrophobic gates and proposes a gating mechanism for PKD2.

    • Wang Zheng
    • , Xiaoyong Yang
    •  & Xing-Zhen Chen

  • Article
    | Open Access

    Patients suffering from congenital nephrogenic diabetes insipidus (NDI) fail to concentrate urine due to mutations in vasopressin type 2 receptor (V2R). Here Ando et al. show that agents disrupting the interaction between PKA and AKAPs restore aquaporin-2 activity downstream of V2R, offering a therapeutic approach for the treatment of NDI.

    • Fumiaki Ando
    • , Shuichi Mori
    •  & Shinichi Uchida

  • Article
    | Open Access

    The recovery of function upon acute kidney injury is thought to involve tubular cell dedifferentiation and proliferation. Here the authors show that Pax2+ progenitors regenerate tubules via cell division while other tubular cells support function recovery by undergoing hypertrophy through endoreplication.

    • Elena Lazzeri
    • , Maria Lucia Angelotti
    •  & Paola Romagnani

  • Article
    | Open Access

    Polycystic kidney disease (PKD) is characterized by the formation of large fluid-filled cysts. Here Flowers and colleagues show that loss of Lkb1, downregulated in PKD, renders kidney cells dependent on glutamine for growth, and suggest that inhibition of glutamine metabolism may prevent cyst development in PKD.

    • Ebony M. Flowers
    • , Jessica Sudderth
    •  & Thomas J. Carroll

  • Article
    | Open Access

    In a lupus environment, basophils accumulate in secondary lymphoid organs where they affect pathogenesis by stimulating autoantibody production. Here the authors show this accumulation is driven by PGD2-induced CXCR4 surface expression and trafficking of basophils.

    • Christophe Pellefigues
    • , Barbara Dema
    •  & Nicolas Charles

  • Article
    | Open Access

    Nephropathic cystinosis is a lysosomal storage disease characterized by proximal tubular cell dysfunction. Here Festa and colleagues show that these lysosomal alterations lead to defective autophagic clearance of mitochondria and increased oxidative stress that, in turn, activates the transcription factor ZONAB leading to impaired cell differentiation.

    • Beatrice Paola Festa
    • , Zhiyong Chen
    •  & Alessandro Luciani

  • Article
    | Open Access

    Crescentic rapidly progressive glomerulonephritis is a severe form of glomerula disease characterized by podocyte proliferation and migration. Here Henique et al. demonstrate that inhibition of miRNA-92a prevents kidney failure by promoting the expression of CDK inhibitor p57Kip2 that regulates podocyte cell cycle.

    • Carole Henique
    • , Guillaume Bollée
    •  & Pierre-Louis Tharaux

  • Article
    | Open Access

    Renal angiomyolipomas (AML) contain a mix of clonal tumour cells. Here, through reverse tumour engineering experiments, mouse genetics and analyses of human AML tumours, the authors provide evidence that these mesenchymal tumours originate from renal proximal tubule epithelial cells.

    • Ana Filipa Gonçalves
    • , Mojca Adlesic
    •  & Ian J. Frew

  • Article
    | Open Access

    The formation mechanism of abundant calcium oxalate biomaterials is unresolved. Here the authors show the early stages of calcium oxalate formation in pure and citrate-bearing solutions by using a titration set-up in conjunction with solution quenching, transmission electron microscopy and analytical ultracentrifugation.

    • Encarnación Ruiz-Agudo
    • , Alejandro Burgos-Cara
    •  & Carlos Rodriguez-Navarro

  • Article
    | Open Access

    Autosomal dominant polycystic kidney disease (ADPKD) is a life-threatening genetic disease that leads to renal failure. Here Hajarniset al. show that miR-17 modulates cyst progression in ADPKD through metabolic reprogramming of mitochondria and its inhibition slows cyst development and improves renal functions.

    • Sachin Hajarnis
    • , Ronak Lakhia
    •  & Vishal Patel

  • Article
    | Open Access

    The polyol pathway, which converts glucose into sorbitol and fructose, is active in chronic conditions like hepatic steatosis and chronic kidney disease. Here, Andres-Hernandoet al. show that fructose production promotes renal injury and fructokinase inhibition protects against kidney damage during ischaemic acute kidney disease.

    • Ana Andres-Hernando
    • , Nanxing Li
    •  & Miguel A. Lanaspa

  • Article
    | Open Access

    Acute kidney injury can progress to chronic kidney disease. Here Dehnadiet al. develop a post-ischaemic chronic kidney disease model in cynomolgus monkeys and show that prophylactic inhibition of CD11b/CD18 leukocyte receptor via a monoclonal antibody inhibits progression of kidney disease and fibrosis.

    • Abbas Dehnadi
    • , A. Benedict Cosimi
    •  & M. Amin Arnaout

  • Article
    | Open Access

    Nephropathy is a common and hard-to-treat consequence of diabetes. Here Kato et al. show that a megacluster of microRNAs regulates early development of diabetic nephropathy in mice, and that inhibition of the cluster's host long non-coding RNA transcript attenuates disease symptoms, suggesting a new therapy for diabetic nephropathy.

    • Mitsuo Kato
    • , Mei Wang
    •  & Rama Natarajan

  • Article
    | Open Access

    Using forward genetic screen in fetal mice, Gregory Pazour and colleagues describe mutants affecting kidney/urinary tract development. The authors also show that mutants that cause kidney defects overlaps with those leading to congenital heart defects, thus linking renal anomalies and congenital heart disease.

    • Jovenal T. San Agustin
    • , Nikolai Klena
    •  & Gregory J. Pazour

  • Article
    | Open Access

    Polycystic kidney disease (PKD) is a ciliopathy resulting from defective localization of membrane proteins such as PC-1 to the primary cilium, resulting in renal cysts, and is associated with another cystic genetic disease called tuberous sclerosis complex (TSC). Here the authors use kidney-specific Tsc1 and Pkd1 mice to show that mTORC1 signalling inhibits PC-1 biogenesis as a potential mechanism of TSC/PKD contiguous gene syndrome.

    • Monika Pema
    • , Luca Drusian
    •  & Alessandra Boletta

  • Article
    | Open Access

    Steroid-sensitive nephrotic syndrome (SRNS) can cause CKD and necessitate kidney transplant. Here the authors identify FAT1 mutations by homozygosity mapping and whole-exome sequencing in families with SRNS and provide functional mouse and zebrafish evidence that FAT1 is required for normal glomerular and tubular function and that FAT1 mutations can cause SRNS.

    • Heon Yung Gee
    • , Carolin E. Sadowski
    •  & Friedhelm Hildebrandt

  • Article
    | Open Access

    Kidney stone disease is caused by accumulation of oxalate crystals, which trigger tissue injury, inflammation and cell death. Mulay et al. show that crystals induce cell death in the kidney through necroptosis, and propose that this pathway may be a target for the treatment of crystal-induced disease.

    • Shrikant R. Mulay
    • , Jyaysi Desai
    •  & Hans-Joachim Anders

  • Article
    | Open Access

    Proteinuria promotes chronic kidney disease progression. Karoui et al. show that proteinuria stimulates overexpression of iron transporting protein lipocalin-2 via Ca2+release-induced ER stress, which leads to tubular apoptosis, and that inhibition of this pathway by PBA delays renal deterioration in proteinuric mice.

    • Khalil El Karoui
    • , Amandine Viau
    •  & Fabiola Terzi

  • Article
    | Open Access

    Generating organized kidney tissues from human pluripotent stem cell is a major challenge. Here, Freedman et al. describe a differentiation system forming spheroids and tubular structures, characteristic of these kidney structures, and using CRISPR/Cas9, delete PKD1/2, to model polycystic kidney disease.

    • Benjamin S. Freedman
    • , Craig R. Brooks
    •  & Joseph V. Bonventre

  • Article
    | Open Access

    Kidney stone formation is influenced by genetic factors and recurrent stone formation places a significant burden on health care systems. Here Oddsson et al.perform a large-scale genome-wide association study and uncover new genetic variants associated with kidney stone susceptibility and associated biochemical traits.

    • Asmundur Oddsson
    • , Patrick Sulem
    •  & Kari Stefansson

  • Article
    | Open Access

    ER stress is associated with the pathogenesis of chronic kidney disease (CKD) and new CKD therapies are needed. Here the authors show that expression of Rtn1 can control severity of renal disease and that inhibition of its expression can attenuate ER stress and CKD.

    • Ying Fan
    • , Wenzhen Xiao
    •  & John C. He

  • Article
    | Open Access

    IgA nephropathy is a major cause of end-stage renal disease in China, occurring at a high frequency in Asian populations. Here Li and colleagues conduct a four-stage genome-wide association study in a Chinese population, identifying novel loci and variants associated with disease risk.

    • Ming Li
    • , Jia-Nee Foo
    •  & Jian-Jun Liu

  • Article
    | Open Access

    Diabetic kidney disease is associated with ER stress in podocytes. Here the authors use various genetically modified mouse models to study ER-stress-related signalling pathways and propose a mechanistic framework that links insulin signalling with ER stress in podocytes of diabetic mice.

    • Thati Madhusudhan
    • , Hongjie Wang
    •  & Berend Isermann

  • Article |

    The Notch signalling pathway is normally inactive in adult kidneys, but reactivated in kidney diseases. Here the authors show that activation of Notch2 receptors protects renal podocytes from apoptosis, which contrasts with the known detrimental effects of Notch1 signalling on the progression of kidney disease.

    • Eriko Tanaka
    • , Katsuhiko Asanuma
    •  & Yasuhiko Tomino

  • Article |

    Loss-of-function mutations in PKD1, the gene encoding the plasma membrane receptor Polycystin-1, lead to renal cyst formation in polycystic kidney disease. Here, Castelli et al. show that Polycystin-1 interacts with the Par3 polarity complex and has a role in the morphogenesis of kidney tubules during mouse development.

    • Maddalena Castelli
    • , Manila Boca
    •  & Alessandra Boletta

  • Article |

    Polycystic kidney disease family proteins form heteromeric complexes with transient receptor potential channel subunits of the TRPP subfamily. Yu and colleagues find that the polycystic kidney disease protein, PKD1L3, is an ion channel pore-forming subunit in the acid-sensing PKD1L3/TRPP3 complex.

    • Yong Yu
    • , Maximilian H. Ulbrich
    •  & Jian Yang

  • Article
    | Open Access

    Hyperuricemia, or gout, is thought to arise either from urate overproduction or from decreased renal excretion of urate. Ichidaet al. show that the extra-renal excretion of urate also has a role in the pathogenesis of hyperuricemia, and propose a new classification for patients with this disease.

    • Kimiyoshi Ichida
    • , Hirotaka Matsuo
    •  & Hiroshi Suzuki

  • Article
    | Open Access

    Magnesium is an essential element of the diet and is a cofactor for many enzymes. In this study, the channel kinase TRPM7 is shown to be essential for magnesium homeostasis, and heterozygous mice lacking the kinase domain show a defect in absorption of magnesium from the diet.

    • Lillia V. Ryazanova
    • , Lusliany J. Rondon
    •  & Alexey G. Ryazanov

Browse broader subjects

Browse narrower subjects

Browse Kidney diseases across other nature.com journals