FISIOLOGIA RENAL VANDERS PDF

Fisiologia Renal de Vander – Ebook download as PDF File .pdf) or read book online. Conciso e didático, este livro explora os aspectos fundamentais da fisiologia renal que são essenciais para o bom entendimento da medicina clínica. : FISIOLOGIA RENAL DE VANDER 6TA. EDIC. by EATON DOUGLAS C. () by Douglas C. Eaton and a great selection of similar.

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Fisiología renal de Vander – Douglas C. Eaton, John P. Pooler – Google Books

Renal physiology in the healthy oldest old has the following characteristics, in comparison with the renal physiology in the young: All physiological changes of the aged kidney are the same in both genders.

Even nowadays the limits that separate the changes considered typical of the normal ageing process of those patients who suffer from high prevalent illnesses characteristic of this period are not clear. In the present review article, we explain in detail the characteristics of the creatinine, urea, uric acid, sodium, water, and potassium renal handling in the very old healthy people taking the younger group years as a parameter.

Additionally, it is important to point out that there are no significant physiological differences related to gender in both age populations. Creatinine clearance measured without CC or with cimetidine CCWCwhich is almost the same as inuline clearance due to the blocking effect that cimetidine has on the proximal tubular secretion of creatinine, has proved to be significantly lower in the very old healthy people in comparison to that documented on the younger population[ 12 ]: The observed difference in the creatinine filtration between the studied age groups could be justified as a consequence of the decrease in the number of glomerular units secondary to their obliteration due to the glomeruloscrerosis which accompanies ageing[ 3 – 5 ].

Even though, the above mentioned creatinine renal filtration difference between the age groups, there is no significant difference regarding their serum creatinine value between them.

This phenomenon can be explained as the decrease in the creatine levels due to the senile diminution in lean body mass tissues from where creatinine comes [ 6 ]. The procurement of a ratio between the CC and the CCWC allows for the evaluation of the net tubular handling of this substance: These finding could be interpreted as the fact that the dehydration over expresses the habitual senile creatinine back-filtration.

It could be hypothesized that the phenomenon of net creatinine tubular vandesr documented on very old people could be explained due to the senile structural tubular changes atrophy, etc.

Something similar was documented in the newborns but in this case it was attributed to tubular immaturity since this finding disappeared as they grew older[ 89 ].

Clinical consequences[ 13 ]: It is already known that there is a significant difference between urea and uric acid renal handling in very old healthy people. On one hand, it has been documented that fractional excretion of urea, in volume contraction as well as in volume expansion, was significantly higher than the one reached by the young: Due to the fact that a reduction in the number of urea channels UT1 has been documented in the collecting tubules of very old rats, it could be suggested that the senile increase in urea excretion may be the consequence of a lower reabsorption of urea at the distal tubules[ 17 ].

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This increase in the urea urinary excretion, as well as the low protein diet that aged people usually have, both explain the normal serum urea value characteristically found in the elderly, despite of their reduced glomerular filtration rate[ 17 ]. Additionally, the high urea urinary excretion documented in the very old could be one of the factors which explains the senile medullar hypotonicity reduced urea medullar content and the nocturia urea osmotic diuresis usually found in the very old patients[ 1516 renxl.

On the other hand, serum uric acid level and fractional excretion of uric acid FEUAc do not differ between very old healthy people in comparison with healthy young ones. Since uric acid is mainly handled in the proximal tubule, a segment that suffers practically no functional changes with ageing, perhaps this could explain the above mentioned phenomenon[ 14 ]. Avnders tubular sodium handling in the oldest old, it has been documented that the selective fisiolovia of sodium at the proximal tubule, evaluated using the Chaimowitz test, shows that it remains in the normal range: Additionally, it has also been documented a decrease in sodium reabsorption in the thick ascending loop of Henle in very old healthy people[ 20 ].

This lower local sodium reabsorption, leads to the following alterations[ 8 ]: Studies in old rats have documented a significant reduction in the number of co-transporters NKCC2 in comparison with young ones. This phenomenon could explain the lower sodium reabsorption at the TALH in very old healthy people[ 1421 – 23 ]. Besides, it has been documented that free water clearance a marker of TALH function is considerably lower in the very old in comparison with the young: As regards the maximum tubular dilution capacity, another of the parameters which Chaimowitz test can evaluate, it has been reported that such dilution is significantly reduced in the very old in comparison with the young: This has been attributed to the senile medullar hypotonicity[ 324 ].

The lower reabsorption of sodium in TALH is translated into a lower medullar concentration of sodium, which causes senile medullar hypotonicity and as a consequence to a reduction in the urinary concentration capacity, which can be the cause of dehydration in the old in situations of high loss of water or low intake[ 13 ].

Furosemide intravenous infusion furosemide test shows that fractional excretion of sodium FENa post-furosemide infusion is significantly lower in the very old group in comparison with the young one: Since furosemide stimulates sodium loss due to the inhibition of its reabsorption at the level of the TALH, the lower increase in soduria after furosemide infusion in the very old in comparison with the young could be explained by the functional reduction in the TALH furosemide blocking site due to the senescence process[ 23 – 25 ].

From the clinical point of view, the above mentioned reduction in the tubular capacity to reabsorb sodium fosters sodium depletion and its clinical consequences: The collecting tubules are the nephronal segment where potassium secretion, and sodium and water reabsorption take place[ 9 ].

Aldosterone bioactivity in this segment is studied using the furosemide test, which ultimately generates a discrete hypovolemia that stimulates the release of this hormone, which in turn stimulates the secretion of potassium in the collecting tubules. In this test, it is observed that the basal fractional excretion of potassium FEK before furosemide infusion is not significantly different in the young and the very old group, whereas the highest FEK post-infusion of furosemide is significantly lower in the very old group in comparison with the young one: The values of aldosterone post-infusion of furosemide are significantly higher in the very old group in comparison with the young: The previously described physiological alterations also show that the characteristic senile sodium urinary loss depends not only on the reduced sodium reabsorbed in the TALH but also in the collecting tubules[ 24 ].

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The information obtained by means of the furosemide test senile hyposecretion of potassium explains why the tubular handling of potassium measured as FEK and transtubular potassium gradient: TTKG in basal situation, does not show any significant difference between the very old group and the young one, despite the existence of lower glomerular filtration in the very old, which ultimately accounts for the relatively reduced cation excretion in the very old, since it is known that the potassium excretion tends to increase paralelly to the reduction of glomerular filtration: Renal handling of many substances creatinine, urea, sodium, water, potassium significantly differs between very old healthy people and young one, while there is no change in uric acid renal handling between these groups.

National Center for Biotechnology InformationU. Journal List World J Nephrol v. Published online Oct 6. Author information Article notes Copyright and License information Disclaimer.

All authors contributed to this manuscript. This article has been cited by other articles in PMC. Abstract Renal physiology in the healthy oldest old has the following characteristics, in comparison with the renal physiology in the young: Cimetidine improves the reliability of creatinine as a marker of glomerular filtration.

Examination of kidney function.

Martinus Nijhoff Publisher; Geriatric nephrology and the ‘nephrogeriatric giants’. Anatomical changes in the aging kidney. The aging kidney in health and disease. Renal senescence in Feed-back between geriatric syndromes: Rennke H, Denker B. Creatinine reabsorption by avnders aged kidney. Creatinine reabsorption by the newborn rabbit kidney. Inhibition of renal reserve in chronic renap disease. Renal reserve in the oldest old. Aging and physiological changes of the kidneys including changes in glomerular filtration rate.

Rev Esp Geriatr Gerontol. Renal physiology in the oldest old: Fractional excretion of urea in severely dehydrated elderly with dementia.

Physiology of the healthy ageing kidney. Renal handling of uric acid, magnesium, phosphorus, calcium, and acid base in the elderly. Biology, functions and diseases.

FISIOLOGIA RENAL

Renal handling of sodium in old people: Dysfunction of the thick loop of Henle and senescence: Fractional excretion of K, Na and Cl following furosemide infusion in healthy, young and very old people. The normal ageing kidney—morphology and physiology. Support Center Support Center. Please review our privacy policy.