Progression of renal failure

Arterial hypertension

Doctors have long identified the relationship between Bright's disease and an enlarged cardiac muscle. AH is both the cause and the effect of the affected kidneys. With AH, the development of renal failure occurs as a result of vascular damage and hypertensive nephroangiosis.

If healthy kidneys are present in the body, then AH does not develop. With excess intake of sodium in the body, the kidneys develop in the kidneys, which contributes to the rapid removal of excess. At the same time, BP quickly returns to normal. If the kidneys are unhealthy, then AG is called. On the other hand, if there is AH, then it contributes to kidney disease. The most important risk factor, in which progression of kidney failure progresses, is AH as a consequence of kidney disease. This situation requires regular preventive manipulation to prevent diseases of both kidney and AH.

Progression of renal failure is mainly based on secondary hemodynamic and metabolic factors. The definition of such mechanisms as glomerular hypertrophy, progressive development of hypertension and / or hyperfiltration in them is very important for preventing the appearance and minimization by surgical operation.

As is known, mechanisms of kidney damage are different. If there are chronic diseases, then the pressure in the capillaries of the glomeruli increases. With intramedular hypertension, the function of filtering proteins through the basal membrane increases substantially. The endothelium is damaged, cytokines are isolated, as well as other soluble mediators. As a consequence, replacement of normal renal tissue with fibrous tissue occurs. The leading role is performed by angiotensin II( A-II).This is one of the most powerful pressor factors of the body. In the presence of this factor, an increase in cell proliferation occurs, inflammation occurs, and the mesangial matrix accumulates.

It has been proved by repeated experiments that the drug reduction of systemic blood pressure significantly helps to reduce the intra-cerebral pressure and at the same time significantly slow the rate of progression of renal failure.

It should be noted that inhibitors of angiotensin-converting enzyme( ACE inhibitors) are much more effective than drugs of other groups. This is due to the function of reducing the induced A-II resistance for the glomerular arteriolus of the renal glomerulus.

As the tonus of the efferent arteriolus decreases, the blood flows out of the glomerulus and the pressure in the capillary loops decreases. It does not matter which systemic blood pressure. It should be assumed that the creation of a local AP is essential. The majority of patients with CRF have a circulating lower or lower normal level.

If drugs from another group( hydralazine, b-blockers, diuretics) are used, they will be less effective because of less effect on the tone of the outgoing arteriol. To all, hydralazine and nifedipine, significantly reduce the tonus of the leading arterioles, this worsens the mechanism of autoregulation functioning, initially changed in renal failure. In this case, drug-induced vasodilation can cause the renin-angiotensin system and raise the tonus of the efferent arteriolus with an increase in intraluminal pressure.

In non-hydropyridine calcium channel blockers( this is verapamil and diltiazem), in contrast to nifedipine - the vasodilating properties are not so strong and they can, like an ACE inhibitor, lower the tone of the outgoing arteriol. These drugs potentiate the action of the ACE inhibitor. Drugs to stop the progression.

We can use two types of drugs that fulfill the task we need. These are antagonists of A-P receptors and inhibitors of renin. Since the second drugs have minimal accessibility, the antagonists of A-P receptors have found wide application in the treatment of renal failure. Much time passed until the moment when the clinic proved experimentally the effectiveness and expediency of using these drugs. Recently, the results of tests of patients with type 2 diabetes have been published: IRMA2.According to these data, a slowdown in the progression of microalbuminuria to an expanded diabetic nephropathy by 70%.Data from other sources( Diabetic Nephropathy( IDNT, RENAAL)) showed a significant reduction in the risk of developing kidney failure. Even there have been cases of reduced cardiac complications.

If we consider again the mechanism of proteinuria decrease, then it must be remembered that protein excretion decreases not by jerks, but gradually, within several weeks, sometimes months, while the hemodynamic effect of ACE inhibitors occurs soon enough.

If you try to inject AP in critical pharmacological tests, then proteinuria does not increase, even with an increase in the tone of the kidney and peripheral vessels. This suggests that there are other mechanisms. Here comes the improved permeability of the basal membrane, which prevents the diffusion of macromolecules into the mesangial space.