Belgyógyászati KlinikaBudapest, Korányi S. A társaságok tagjai számára ingyenes. A folyóiratban megjelenõ közleményekrõl külön lenyomat A folyóiratban valamennyi írásos és képi anyag közlési joga a szerkesztõséget illeti. A megjelent anyag, illetve annak egy részének bármilyen formában történõ másolásához, ismételt megjelentetéséhez a szerkesztõség hozzájárulása szükséges. 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.
Family studies showed higher blood pressure values and more frequent hypertension in first degree relatives of patients with primary glomerulonephritis or diabetic 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 system 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 from blood kezelése bodza cukorbetegségben, 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. 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.
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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. 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. 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. He showed that, transplantation of a kidney from a genetically hypertensionprone donor rat, even when it had been kept normotensive from weaning by antihypertensive medication, caused a progressive increase of blood pressure in a recipient animal which was immunologically manipulated to prevent rejection.
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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, heart 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 best diuretic for type 2 diabetes this paper deal with hypertensive patients and not hypertensive rats.
Is the above experimental observation also true for humans?
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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.
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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.
After these patients had received a kidney from a normotensive donor, all of them 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.
Which factors, genetic or environmental, could be potentially responsible for the hypertensinogenic effects of the kidney and, according to Brenner s hypothesis for best diuretic for type 2 diabetes 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 also supported by the race dependent differences in glomerular count in humans However, there are also 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.
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The role of the kidney in the pathogenesis of essential hypertension is probably not only due to potential structural alterations, such as lower nephron number, but also due to changes in kidney function. According to this concept, because the gain of the blood-pressure-natriuresis relationship overrides all other regulatory systems, the ultimate determinant of blood pressure must always be the renal handling of sodium.
It is interesting that renal function, as reflected by the blood pressure-natriuresis relationship, can be disturbed as a consequence of extrarenal causes. Lombardi et al 17 performed a very interesting experiment. However when normotensive rats had temporarily been rendered hypertensive by infusing angiotensin II and after they had subsequently become normotensive when angiotensin II infusion had been stopped, they had permanently become sodium sensitive.
The kidney remembered so to speak the injury induced by angiotensin II. If these animals were later exposed to a high sodium intake their blood pressure increased and they again developed hypertension. The shift of the blood pressure-natriuresisrelationship under hormonal influences such as mineralo and glucocorticoid excess 18testosteron 19 and estrogen 20 etc is well known. However it is also interesting that for example dietary factors such as high intake of unsaturated fatty acid 21or high potassium intake 22, 23 can shift this relationship.
These experimental findings prompted the DASH study, designed to investigate the új módszerek a diabétesz of such dietary factors on blood pressure in humans Which mechanisms cause the increase of blood pressure in kidney disease?
Elegant evidence for disturbed renal sodium excretion leading to hypervolemia was provided by Schmid et al In his study blood pressure of patients with polycystic kidney disease PKD was increased after a high sodium load, even when glomerular filtration was still normal.
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In PKD patients, concentrations of atrial natriuretic peptide ANP were higher indicating hypervolemia, both at low and high sodium intake. It is well known that in patients with primary renal disease the activity of the renin-angiotensin system is inadequately high.
Kuczera et al 26 showed in the isolated perfused hindlimb preparation of subtotally nephrectomized rats that this is true not only for the renal, but also for the local renin-angiotensin system of the vessel wall. In the kidney an important but not the sole mechanism, responsible for increased and unregulated renin secretion is luminal narrowing of preglomerular vessels because of vascular sclerosis. Consequently the baroreceptor will measure a falsely low perfusion pressure analogous to the kidney with a Goldblatt clip on the renal artery.
More renin will therefore be secreted. In subjects with healthy kidneys plasma renin activity falls asymptotically with increasing blood pressure. In contrast in patients with kidney disease renin secretion is inadequately suppressed and plasma renin activity remains inappropriately high.
In the past it was thought that the above two mechanisms i. Today we know that this concept is an oversimplification. DiBona et al 27 showed that the kidney contains chemoreceptors and baroreceptors. These receptors are stimulated in a diseased kidney Afferent signals then travel to the hypothalamus where the activity of the centers controlling sympathetic tone is increased This causes elevation of the efferent sympathetic nerve activity. This phenomenon is not only important for the development of high blood pressure, but also for progression of kidney disease.
Non-hypotensive doses cukorbetegség tüneteti the central sympathicoplegic agent moxonidine reduced the development of glomerulosclosis and of albuminuria in subtotally nephrectomized rats That this effect is not unique to the centrally acting drug moxonidine is shown by further experiments: metoprolol at doses which failed to affect systemic blood pressure 31or surgical denervation of the kidney had a similar renoprotective effects 28, This opens of course perspectives for the therapy of kidney diseases.
Is the sympathetic activity elevated in humans with kidney diseases as well? Converse et al 32 was the first to use microneurographic techniques and to document that sympathetic activity of the sural nerve was increased in dialysis patients. The number of discharges was doubled in hemodialyzed patients with chronic renal failure as compared to controls. On the other hand if the non-functional kidneys of medicine hírek cukorbetegség kezelésében patients had been removed by binephrectomy the frequency of discharges was completely normalized Recently, Hausberg et al 34 showed that correction of uremia by kidney transplantation did not normalise best diuretic for type 2 diabetes sympathetic nervous activity.
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It was normalized, however, by nephrectomy of the recipients own kidneys. These observations provide evidence that afferent signals emanating from the kidney cause sympathetic overactivity in humans as well. Interestingly there are interactions between the renin angiotensin system and sympathetic nerve system.
Ligtenberg et al 35 found that the elevated sympathetic activity of patients with chronic renal failure decreased after administration of an angiotensin converting enzyme inhibitor.