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Review
. 2021 Oct;36(10):2997-3006.
doi: 10.1007/s00467-020-04849-0. Epub 2021 Jan 7.

Acute kidney injury and aging

Monica Chang-Panesso  1
Affiliations
Review

Acute kidney injury and aging

Monica Chang-Panesso. Pediatr Nephrol. 2021 Oct.

Abstract

Our aging population is growing and developing treatments for age-related diseases such as Alzheimer's and Parkinson's disease has taken on an increasing urgency and is accompanied by high public awareness. The already high and rising incidence of acute kidney injury (AKI) in the elderly, however, has received relatively little attention despite the potentially fatal outcomes associated with an episode of AKI in this age group. When discussing AKI and aging, one should consider two aspects: first, elderly patients have an increased susceptibility to an AKI episode, and second, they have decreased kidney repair after AKI given the high incidence of progression to chronic kidney disease (CKD). It is unclear if the same factors that drive the increased susceptibility to AKI could be playing a role in the decreased repair capacity or if they are totally different and unrelated. This review will examine current knowledge on the risk factors for the increased susceptibility to AKI in the elderly and will also explore potential aspects that might contribute to a decreased kidney repair response in this age group.

Keywords: Acute kidney injury; Aging; Chronic kidney disease; Elderly; Renal aging; Senescence.

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Figures

Figure 1.
Figure 1.. Risk factors for increased susceptibility to AKI in the elderly.
Epidemiological studies have highlighted the increased incidence of AKI in elderly patients and their poor outcomes. Comorbidities, medications, age-related hemodynamic changes and intrinsic aging of the kidney are some of the possible risk factors for the increased susceptibility of elderly patients to AKI.
Figure 2.
Figure 2.. Factors that might contribute to decreased repair in the aging kidney.
It is well-established from clinical studies that elderly patients are at higher risk of progression to CKD after an episode of AKI. This risk is likely due to decreased repair capacity after injury, although it is unclear what the drivers for this failed repair are. Possible mechanisms driving this failed repair include impaired angiogenesis, decreased proliferation, cellular senescence, and impaired immune response.
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