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Chronic kidney disease

Abstract

Chronic kidney disease (CKD) is defined by persistent urine abnormalities, structural abnormalities or impaired excretory renal function suggestive of a loss of functional nephrons. The majority of patients with CKD are at risk of accelerated cardiovascular disease and death. For those who progress to end-stage renal disease, the limited accessibility to renal replacement therapy is a problem in many parts of the world. Risk factors for the development and progression of CKD include low nephron number at birth, nephron loss due to increasing age and acute or chronic kidney injuries caused by toxic exposures or diseases (for example, obesity and type 2 diabetes mellitus). The management of patients with CKD is focused on early detection or prevention, treatment of the underlying cause (if possible) to curb progression and attention to secondary processes that contribute to ongoing nephron loss. Blood pressure control, inhibition of the renin–angiotensin system and disease-specific interventions are the cornerstones of therapy. CKD complications such as anaemia, metabolic acidosis and secondary hyperparathyroidism affect cardiovascular health and quality of life, and require diagnosis and treatment.

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Figure 1: The KDIGO classification of CKD.
Figure 2: Global prevalence of renal replacement therapy.
Figure 3: GFR with ageing and effect of LBW on progression of CKD.
Figure 4: Injury, hyperfiltration and hypertrophy of the nephron.
Figure 5: Interstitial fibrosis.
Figure 6: Contributing factors to nephron loss.
Figure 7: The earlier, the better.
Figure 8: Haemodialysis and peritoneal dialysis.
Figure 9: Targeting kidney regeneration.

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Acknowledgements

P.R. is supported by the European Research Council under the Consolidator Grant RENOIR (ERC-2014-CoG), grant number 648274. G.R. and H.-J.A. have received support from the European Union's research and innovation programme (under grant agreement Horizon 2020, NEPHSTROM No. 634086). Z.M. has received research grants from the French government (the Investisssement d'Avenir programme). H.-J.A. has received support from the Deutsche Forschungsgemeinschaft (AN372/16-2, 23–1 and 24–1). The views expressed here are the responsibility of the authors only. The EU Commission takes no responsibility for any use made of the information set out.

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All authors contributed equally to all sections of the Primer, with H.-J.A. coordinating the project.

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Correspondence to Hans-Joachim Anders.

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R.G. has received speaker honoraria from Genentech and consultancy honoraria from Bristol Myers Squibb; he has conducted compensated editorial tasks for the American Society of Nephrology and Karger and Wolters-Kluwer; and he owns stock in Reata. Z.M. has received grants for research from Amgen, Baxter, Dohme-Chibret, Fresenius Medical Care, GlaxoSmithKline, Lilly, Merck Sharp, Otsuka, and Sanofi-Genzyme; and has received personal fees and grants to charities from Amgen, Bayer and Sanofi-Genzyme. The other authors declare no competing interests.

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Romagnani, P., Remuzzi, G., Glassock, R. et al. Chronic kidney disease. Nat Rev Dis Primers 3, 17088 (2017). https://doi.org/10.1038/nrdp.2017.88

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