Acute Kidney Injury and Chronic Kidney Disease

Bydash, Jason R.; Ishani, Areef

doi:10.2215/cjn.09560911

Cited by 33 publications

(24 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Approximately 45% of critically ill patients and 20% of hospitalized patients develop AKI (40), which leads to increased hospital stays, infectious complications, and increased mortality, at significant cost (41,42). In addition, AKI has been associated with future development of chronic kidney disease (43). The leading cause of AKI in native as well as transplanted kidneys is ischemic AKI.…”

Section: Discussionmentioning

confidence: 99%

Elevated urinary CRELD2 is associated with endoplasmic reticulum stress–mediated kidney disease

Park¹,

Manson²,

Molina³

et al. 2017

JCI Insight

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Elevated urinary CRELD2 is associated with endoplasmic reticulum stress–mediated kidney disease

Park¹,

Manson²,

Molina³

et al. 2017

JCI Insight

View full text Add to dashboard Cite

“…[1][2][3][4][5][6] We modeled this clinical paradigm experimentally by inducing IRI in rats with prior RMR. 29 Rats with implanted BP transducers were subjected to IRI 2 weeks after sham surgery, unilateral nephrectomy (moderate RMR), or unilateral nephrectomy with surgical removal of 50% renal mass from the other kidney (severe RMR).…”

Section: The Ckd-aki-ckd Connection: Aki On Ckd Can Trigger Hemodynammentioning

confidence: 99%

“…[1][2][3][4][5][6] Kidneys from patients recovering from AKI exhibit chronic dysfunction, tubule atrophy, and interstitial fibrosis ( Figure 1, E and F). [7][8][9][10][11][12][13][14][15][16][17][18][19][20] Incomplete recovery from AKI in patients with CKD not only adds to preexisting pathology and dysfunction but also, may synergize with hemodynamic mechanisms of progression.…”

mentioning

confidence: 99%

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Venkatachalam

Weinberg

Kriz

et al. 2015

Journal of the American Society of Nephrology

591

454

View full text Add to dashboard Cite

The transition of AKI to CKD has major clinical significance. As reviewed here, recent studies show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic signaling along multiple pathways. Paracrine products derived therefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast transformation, proliferation, and fibrosis as well as capillary disintegration and rarefaction. Although signals from injured endothelium and inflammatory/immune cells also contribute, tubule injury alone is sufficient to produce the interstitial pathology required for fibrosis. Localized hypoxia produced by microvascular pathology may also prevent tubule recovery. However, fibrosis is not intrinsically progressive, and microvascular pathology develops strictly around damaged tubules; thus, additional deterioration of kidney structure after the transition of AKI to CKD requires new acute injury or other mechanisms of progression. Indeed, experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression. Continued investigation of these pathologic mechanisms should reveal options for preventing renal disease progression after AKI.

show abstract

“…Elevations in circulating IL-6 are also associated with the incidence of AKI in critically ill patients with sepsis [39]. …”

Section: Inflammation Acute Kidney Injury and Chronic Kidney Diseasementioning

confidence: 99%

Chronic Kidney Disease and the Foot in Diabetes - Is Inflammation the Missing Link?

2013

View full text Add to dashboard Cite

Diabetes is commonly complicated by the development of chronic kidney disease (CKD). Equally prevalent is the development of diabetic foot disease and it is now recognised that there is a higher risk of the development of foot disease and major amputation in those patients with CKD. This is particularly marked in those patients with end-stage kidney disease receiving renal replacement therapy for which there are many possible mechanisms, including the effect of dialysis on tissue hypoxia. What has been recognised recently is that the risk of the development of foot disease appears to start prior to the onset of renal replacement therapy. Whilst this may be due to the fact that the emphasis of care shifts towards the requirements of the patients' renal disease, here we discuss the possibility that the presence of a foot ulcer itself may contribute to the development or progression of CKD through repeated episodes of sepsis or chronic inflammation, or both.

show abstract

Acute Kidney Injury and Chronic Kidney Disease

Cited by 33 publications

References 9 publications

Elevated urinary CRELD2 is associated with endoplasmic reticulum stress–mediated kidney disease

Elevated urinary CRELD2 is associated with endoplasmic reticulum stress–mediated kidney disease

Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression

Chronic Kidney Disease and the Foot in Diabetes - Is Inflammation the Missing Link?

Contact Info

Product

Resources

About