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On the one hand, renal dysfunction and particularly renal disease can cause an increase in blood pressure, while on the other hand, high blood pressure accelerates loss of function of the diseased kidney. Transplantation studies, both in experimental animals and humans, documented that blood pressure goes with the kidney : a normotensive recipient of a kidney genetically programmed for hypertension will become hypertensive, while conversely hypertensive patients with renal failure receiving the kidney of a normotensive donor may become normotensive.

• Betegség diabetes étkezési kezelés
• Orv Hetil ; 12 :03

Family studies showed higher blood pressure values and more frequent hypertension in first degree relatives of patients with primary glomerulonephritis or what antihypertensive is best for diabetics nephropathy, suggesting that genes coding for hypertension increase also the risk of renal disease. The mechanisms through which blood pressure increases in renal disease comprise: salt and water retention, inappropriate activity of the renin angiotensin system RAS and of the sympathetic nerve what antihypertensive is best for diabetics as well as impaired endothelial cell-mediated vasodilatation.

There is ample evidence, both in primary renal disease and in nephropathy of type 1 or type 2 diabetes, that pharmacological blockade of the RAS by angiotensin converting enzyme inhibitors ACEI or angiotensin II type 1 receptor blockers ATRB has blood pressure-independent renoprotective effects, and may reduce proteinuria.

Since, according to recent concepts, proteinuria is a nephrotoxin, apart kezelése sarok homlok diabetes blood pressure, proteinuria is a further and partially blood pressure independent indication for antihypertensive treatment using ACEI or ATRB for patients with diabetic nephropathy or primary renal diseases. Brenner 1 proposed the hypothesis, that deviations of the kidney structure are found in patients with so called essential hypertension i.

This hypothesis is supported by a number of experimental and clinical observations.

Absztrakt:

Stereologic investigation of the kidney revealed significant glomerular enlargement 2. Similarly, in the bacground of spontaneous hypertension, proteinuria, and glomerulosclerosis of MWF rats, a reduced nephron number was detected with stereologic methods 3.

The number of glomeruli and glomerular volume were investigated stereologically with a modified Gundersen fractionator method. A significantly lower number of glomeruli per kidney was noted in hypertensive individuals than in the matched controls Figure 1.

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At the same time, the glomerular volume was significantly greater in hypertensive individuals than in matched controls Figure 1. Such increase in glomerular volume may constitute a compensatory mechanism.

Of course it was important to exclude one artefact, i. In this study there was no histological evidence of glomerular loss hypertensive nephropathy.

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The findings of this postmortal human study fits nicely with a series of animal experiments which have shown that hypertension and normotension can be transferred from a donor to a recipient by transplanting a kidney, i.

The most elegant studies on this topics were reported by Rettig et al 6.

- Böngészés - szerző: "Gesztelyi, Rudolf"

He showed that, transplantation of a kidney from a genetically hypertensionprone donor rat, even when it had been kept normotensive from weaning cukorbetegség kezelés hatásokkal antihypertensive medication, caused a progressive increase of blood pressure in a recipient animal which was immunologically manipulated to prevent rejection. This finding is extremely interesting: a kidney genetically programmed to develop high blood pressure forces an organism programmed for normotension to develop hypertension, although the recipient s central nervous system, volume control systems, sympathetic nervous system, prosztatagyulladás diabetes function etc are all geared for normotension.

In contrast, and quantitatively less impressive, transplantation of a kidney from a donor genetically programmed for normotension lowered blood pressure in the recipient 7. Although animal experiments are very nice, most reader of this paper deal with hypertensive patients and not hypertensive rats.

Absztrakt:

Is the above experimental observation also true for humans? Of course, no controlled studies are available where kidneys from patients with essential hypertension were transplanted to normotensive recipients or conversely. However uncontrolled data strongly suggest that recipients of kidneys from donors with essential hypertension develop hypertension more frequently than recipients of kidneys from normotensive donors 8, 9.

It has also been shown that kidney graft recipients required more antihypertensive medication if the grafts had been obtained from genetically hypertension-prone donors 8.

In particular, recipients of kidneys from donors dying from cerebral hemorrhage, presumably caused by hypertension, had a higher risk to develop hypertension 9. Because of numerous scores ±0. However, Curtis et al 11 showed very convincingly, that conversly, the transplantation of a kidney from a normotensive donor can permamently normalise the blood pressure of recipients with essential hypertension.

He studied 6 black patients with essential hypertension of unknown origin who became dialysis dependent as a result of hypertensive nephrosclerosis without any histologic signs of primary kidney disease.

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After these patients had received a kidney from a normotensive donor, all of cukorbetegség okozta kiütések became normotensive and this persisted during a 4.

There was evidence of reversal of hypertensive damage to the heart and retinal vessels, and of completely normal blood pressure responses to salt deprivation and salt loading. Diabetes care factors, genetic or environmental, could be potentially responsible for the hypertensinogenic effects of the kidney and, according to Brenner s hypothesis for so called nephron underdosing?

Since the pioneering experiment of Weitz in the ies of the last century we know that genetic factors play a key role in essential hypertension We must, therefore, suppose that the number of functional nephrons is genetically determined.

This hypothesis is what antihypertensive is best for diabetics supported by the race dependent differences in glomerular count in humans However, there are what antihypertensive is best for diabetics many animal experiments and human studies which suggest that during the fetal period environmental factors may also influence renal 0. Langley et al 14 have shown that dietary protein restriction of pregnant rats caused high blood pressure in the offspring.

In humans Merlet-Benichou et al 15 showed that newborns with lower birth weight as an indirect sign of fetal malnutrition had a lower nephron number than newborns with normal birth weight.