Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Mar;25(2):166-180.
doi: 10.1053/j.ackd.2017.12.005.

Acute Kidney Injury and Progression of Diabetic Kidney Disease

Samuel Mon-Wei Yu  1 , Joseph V Bonventre  2
Affiliations
Review

Acute Kidney Injury and Progression of Diabetic Kidney Disease

Samuel Mon-Wei Yu et al. Adv Chronic Kidney Dis. 2018 Mar.

Abstract

Diabetic kidney disease, commonly termed diabetic nephropathy (DN), is the most common cause of end-stage kidney disease (ESKD) worldwide. The characteristic histopathology of DN includes glomerular basement membrane thickening, mesangial expansion, nodular glomerular sclerosis, and tubulointerstitial fibrosis. Diabetes is associated with a number of metabolic derangements, such as reactive oxygen species overproduction, hypoxic state, mitochondrial dysfunction, and inflammation. In the past few decades, our knowledge of DN has advanced considerably although much needs to be learned. The traditional paradigm of glomerulus-centered pathophysiology has expanded to the tubule-interstitium, the immune response and inflammation. Biomarkers of proximal tubule injury have been shown to correlate with DN progression, independent of traditional glomerular injury biomarkers such as albuminuria. In this review, we summarize mechanisms of increased susceptibility to acute kidney injury in diabetes mellitus and the roles played by many kidney cell types to facilitate maladaptive responses leading to chronic and end-stage kidney disease.

Keywords: Acute kidney injury; Diabetic kidney disease; End-stage kidney disease.

PubMed Disclaimer

Figures

Figure
Figure. Scheme of relationship between diabetic nephropathy (DN) and acute kidney injury (AKI)
Diabetic nephropathy ensues from chronic hyperglycemia via several mechanisms, such as worsening hypoxic status, chronic inflammation, mitochondrial dysfunction, increasing mTOR signaling, and exposure to advanced glycation endproduct (AGE). Diseased kidney cells are more susceptible to acute kidney injury (AKI), and vice versa these damaged cells from DN can hasten the damage during each AKI episode. As traditional paradigm of DN has been expanded from glomerulus (podocyte)-centered to other cell types, the crosstalk among different kidney cells are revealed to be crucial in DN development. After diabetic kidneys undergo repetitive AKI, maladaptive repair occurs from acute renal insults, and irreversible tubulointerstitial fibrosis accumulates and eventually lead to chronic kidney disease (CKD) and end-stage kidney disease (ESKD).
See this image and copyright information in PMC

References

    1. Saran R, Robinson B, Abbott KC, et al. US Renal Data System 2016 Annual Data Report: Epidemiology of Kidney Disease in the United States. Am J Kidney Dis. 2017;69(3S1):A7–A8. - PMC - PubMed
    1. Gregg EW, Li Y, Wang J, et al. Changes in diabetes-related complications in the United States, 1990–2010. N Engl J Med. 2014;370(16):1514–1523. - PubMed
    1. Badal SS, Danesh FR. New insights into molecular mechanisms of diabetic kidney disease. Am J Kidney Dis. 2014;63(2 Suppl 2):S63–83. - PMC - PubMed
    1. Bojestig M, Arnqvist HJ, Hermansson G, Karlberg BE, Ludvigsson J. Declining incidence of nephropathy in insulin-dependent diabetes mellitus. N Engl J Med. 1994;330(1):15–18. - PubMed
    1. Hovind P, Tarnow L, Rossing K, et al. Decreasing incidence of severe diabetic microangiopathy in type 1 diabetes. Diabetes Care. 2003;26(4):1258–1264. - PubMed

MeSH terms