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Hypertension
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Early in the development of hypertension, there are no pathologic changes, but when it is severe or prolonged, target organs are damaged. These are usually the cardiovascular system, brain, and kidneys. Damage increases risks for coronary artery disease (CAD), heart failure, myocardial infarction (MI), hemorrhagic and other types of stroke, renal failure, and death. Pathological damage occurs with general arteriolosclerosis, plus increased progression of atherogenesis. Arteriolosclerosis involves medial hypertrophy, hyalinization, and hyperplasia. It is obvious in small arterioles such as those of the eyes and kidneys. As the renal arteriolar lumen narrows, TPR increases.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Arteriolosclerosis (or age-related and vascular risk factor–related small-vessel diseases) is mainly characterized by loss of smooth muscle cells from the tunica media, deposits of fibrohyaline material, narrowing of the lumen, and thickening of the vessel wall. Other pathologic features may include fibrinoid necrosis, lipohyalinosis, microatheroma (distal manifestation of atherosclerosis), microaneurysms (elongated and dilated vessels: saccular, lipohyalinotic, asymmetric fusiform, bleeding globe), and segmental arterial disorganization. In addition to the brain, arteriolosclerosis also affects the kidney and retina. It is strongly associated with aging, hypertension, and diabetes (Table 12.27).
Atherosclerosis, Arteriolosclerosis and Vasculitis
Published in Jeremy R. Jass, Understanding Pathology, 2020
Arteriolosclerosis is a hyaline (glassy eosinophilic) thickening of the walls of arterioles that is age related but more severe and generalised in hypertensive subjects. Hypertension may be caused by a variety of hormone-secreting tumours, chronic renal diseases and vascular disorders including renal artery stenosis and polyarteritis nodosa. However, the essential cause is unknown in the vast majority of cases, although it is almost certainly polygenic (due to the interaction of several genes and environmental influences). The main complication of hypertension is accelerated atherogenesis leading to the outcomes described above. The major clinical sequelae are hemorrhagic stroke, aortic aneurysm and hypertensive and ischaemic heart disease.
Rituximab for the treatment of refractory anti-glomerular basement membrane disease
Published in Renal Failure, 2022
Xue-Fen Yang, Xiao-Yu Jia, Xiao-Juan Yu, Zhao Cui, Ming-Hui Zhao
Six of the 8 patients underwent kidney biopsy at diagnosis (Table 2), and typical linear deposits of IgG along GBM was demonstrated in all of them. All of the patients showed crescent formation with a median percentage of crescents in glomeruli of 85.3% (32 to 95.8%). Four of them (Patients 3, 4, 5 and 6) had diffuse crescents occupying >50% of the glomeruli. Three patients showed IgA deposition in the mesangium area by Immunofluorescence and electron dense deposits in the corresponding area under electron microscopy. All six patients showed tubular atrophy and interstitial fibrosis, interstitial inflammatory cells infiltration. One patient (Patient 1) showed arteriolosclerosis.
Intrarenal resistive index conundrum: systemic atherosclerosis versus renal arteriolosclerosis
Published in Renal Failure, 2019
Gabriel Ștefan, Cosmin Florescu, Alexandru-Anton Sabo, Simona Stancu, Gabriel Mircescu
Hyaline arteriolosclerosis is a common vascular lesion, found in many different situations, including aging, arterial hypertension, diabetes mellitus, focal and segmental glomerulosclerosis. It is generated by the accumulation of serum proteins in the subendothelial space, often extending into the media [16]. Arteriolosclerosis appears to be related to the loss of glomerular autoregulation and, furthermore, to participate in the pathogenesis of the associated glomerular lesions [17].