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Etiology of renal damage in hypertension

2017-01-08 16:16

Etiology summary:

The etiology of hypertensive renal damage is mainly pided into 3 aspects: in the general population, the level of blood pressure is associated with the mortality of fatal and non fatal cardiovascular disease. The pathogenesis of essential hypertension is not clear, mainly related to nervous, humoral, endocrine abnormalities. Renal damage caused by essential hypertension is commonly referred to as benign renal sclerosis.

Renal damage in hypertensive patients:

Epidemiology of renal damage in hypertension

In the general population, the level of blood pressure was associated with a mortality rate of fatal and nonfatal cardiovascular disease. In patients with hypertension, high blood pressure and target organ damage or clinical events, especially cardiovascular disease (CVD), cerebrovascular disease, chronic kidney disease (CKD) and peripheral arterial disease and retinopathy related. Studies have shown that elevated serum creatinine is associated with a significant increase in blood pressure, and an increase in age and mean arterial pressure is an independent risk factor for the decline in renal function. Epidemiological studies have also shown that SBP increased from 120mmHg to 130mmHg, and the risk of end-stage renal disease (ESRD) was significantly increased. CKD, which is caused by high blood pressure, has become the second or the third cause of ESRD in developed countries. According to Beijing in recent years, dialysis registration data show that renal damage caused by high blood pressure is also the third cause of ESRD.

Pathogenesis of hypertensive renal damage

The pathogenesis of essential hypertension is not fully understood. It is thought to be related to the nervous, humoral and endocrine abnormalities. The kidney plays an important role in the occurrence and development of hypertension, which can be adversely affected by the occurrence of hypertension. In addition to systemic blood pressure to the kidney damage, but also through the medium of norepinephrine and renal adrenergic receptors, direct contraction of renal vessels, the renal vascular resistance, increased renal blood flow decreased, renal ischemia, single CO oxidation should be increased, but to promote the release of renin from the juxtaglomerular apparatus, through further tension with the interaction of renin angiotensin system promotes vascular hypertension. In addition, the activation of renal sympathetic nerve can also be connected with the stimulation of proximal tubule Na+ reabsorption, resulting in sodium and water retention, increased circulating capacity. Hypertensive patients often accompanied by the renin-angiotensin system (RAS) activity, angiotensin II (AT II) pro increased, also increased the sensitivity by tube feedback effects on aldosterone, and directly promote the proximal tubular sodium reabsorption in the kidney, causing contraction of blood vessels, which caused the increase of decreased kidney blood flow and renal vascular resistance, glomerular pressure also increased, mesangial cell contraction, resulting in selective permeability to protein increased, and can activate the growth factor associated with fibrosis. In the short term GFR increased or remained unchanged, but proteinuria, glomerulosclerosis, and renal failure occurred over a long period of time. In addition, the renal damage of hypertension has a certain genetic susceptibility, and the proportion of renal damage and progression to ESRD is different in different races. Research Report shows that African Americans than Caucasians are more susceptible to hypertension, and more prone to kidney damage at the same level of blood pressure, due to hypertensive renal damage caused ESRD in the proportion of African Americans is far higher than that of caucasian. The condition of hypertension and increased glomerular glomerular arteriolar resistance before the internal pressure in a variety of factors, the nerve endocrine, paracrine function, hypertension and kidney interact continuously, continue to promote disease progression.

Pathological features of hypertensive renal damage

Renal damage caused by essential hypertension is commonly referred to as benign renal sclerosis (benignnephrosclerosis). It is the first to affect the glomerulus of the artery, mainly the human small artery and interlobular artery. Vascular smooth muscle cells in the small arteries are replaced by connective tissue, and the accumulation of hyaline material (plasma protein) in the intima (hyaline degeneration) is also observed. As associated with vascular lesions of glomerulus and renal tubule interstitial appeared ischemia, showed glomerular basement membrane ischemic shrinkage, vacuolization and granular degeneration of renal tubular epithelial cells, focal atrophy. Interstitial multifocal lymphoid and mononuclear cell infiltration, with fibrosis. The renal damage of hypertension lesions can be seen later glomerular sclerosis and severe interstitial renal tubular injury, namely multifocal and patchy atrophy, part compensatory hypertrophy of renal interstitial fibrosis. Immunofluorescence showed no specific expression, and there was no deposition of immunoglobulin and complement, and sometimes weak IgM deposition in glomeruli and arterioles. Electron microscopic examination was consistent with light microscopy. When patients with malignant hypertension, renal pathology was significant proliferative vascular lesions can appear arterial intimal thickening change in onion skin, can have glomerular segmental fibrinoid necrosis.


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