Observations on the fate of cholesterol emboli

Gore, Ira; McCombs, H. L.; Lindquist, Ryan

doi:10.1016/s0368-1319(64)80055-7

Cited by 51 publications

(22 citation statements)

References 2 publications

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“…However, the contribution of CCs to inflammation and necrosis in CCE remains obscure to date, mostly owing to the lack of suitable animal models of the disease. Nevertheless, researchers have tried to mimic atheroembolic renal diseases in rabbits and rats by injecting human atherosclerotic material or CCs [11, 12]. These studies identified early neutrophilic reactions followed by recruitment of macrophages in response to the atherosclerotic material or CCs.…”

Section: Type 1 Crystalline Nephropathy: Renal Cholesterol Embolismmentioning

confidence: 99%

Novel Insights into Crystal-Induced Kidney Injury

Mulay

Shi

et al. 2018

Kidney Dis

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Background: The entity of crystal nephropathies encompasses a spectrum of different kidney injuries induced by crystal-formed intrinsic minerals, metabolites, and proteins or extrinsic dietary components and drug metabolites. Depending on the localization and dynamics of crystal deposition, the clinical presentation can be acute kidney injury, progressive chronic kidney disease, or renal colic. Summary: The molecular mechanisms involving crystal-induced injury are diverse and remain poorly understood. Type 1 crystal nephropathies arise from crystals in the vascular lumen (cholesterol embolism) or the vascular wall (atherosclerosis) and involve kidney infarcts or chronic ischemia, respectively. Type 2 crystal nephropathies arise from intratubular crystal deposition causing obstruction, interstitial inflammation, and tubular cell injury. NLRP3 inflammasome and necroptosis drive renal necroinflammation in acute settings. Type 3 is represented by crystal and stone formation in the draining urinary tract, i.e., urolithiasis, causing renal colic and chronic obstruction. Key Messages: Dissecting the types of injury is the first step towards a better understanding of the pathophysiology of crystal nephropathies. Crystal-induced activation of the inflammasome and necroptosis, crystal adhesion, crystallization inhibitors, extratubulation, and granuloma formation are only a few of certainly many involved pathomechanisms that deserve further studies to eventually form the basis for innovative cures for these diseases.

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Section: Type 1 Crystalline Nephropathy: Renal Cholesterol Embolismmentioning

confidence: 99%

Novel Insights into Crystal-Induced Kidney Injury

Mulay

Shi

et al. 2018

Kidney Dis

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“…[1][2][3][4] In studies 20,21,[37][38][39][40] in people and animals, results suggest that emboli produce a microcrystalline angiitis, characterised by an endothelial infl ammatory reaction developing in a stepwise pattern. Shortly after lodging, polymorpho-nuclear leukocytes and esosinophils infi ltrate the aff ected arterioles, preceding mononuclear-cell infi ltration and giant-cell formation.…”

Section: Search Strategy and Selection Criteriamentioning

confidence: 99%

Atheroembolic renal disease

2010

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Atheroembolic renal disease develops when atheromatous aortic plaques rupture, releasing cholesterol crystals into the small renal arteries. Embolisation often aff ects other organs, such as the skin, gastrointestinal system, and brain. Although the disease can develop spontaneously, it usually develops after vascular surgery, catheterisation, or anticoagulation. The systemic nature of atheroembolism makes diagnosis diffi cult. The classic triad of a precipitating event, acute or subacute renal failure, and skin lesions, are strongly suggestive of the disorder. Eosinophilia further supports the diagnosis, usually confi rmed by biopsy of an aff ected organ or by the fundoscopic fi nding of cholesterol crystals in the retinal circulation. Renal and patient prognosis are poor. Treatment is mostly preventive, based on avoidance of further precipitating factors, and symptomatic, aimed to the optimum treatment of hypertension and cardiac and renal failure. Statins, which stabilise atherosclerotic plaques, should be off ered to all patients. Steroids might have a role in acute or subacute progressive forms with systemic infl ammation.

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“…Cholesterol emboli may remain lodged for months because they are often resistant to scavenging by macrophages. 54 …”

Section: Inflammatory Responsementioning

confidence: 99%