Albumin and Nutritional Œdema

Golden, Michael; Golden, Barbara E.; Jackson, A. A.

doi:10.1016/s0140-6736(80)90603-0

Cited by 61 publications

(45 citation statements)

References 21 publications

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“…We [42] calculated the perivascular space from simultaneous measurement of PV and RCV and Ht, and found a value of 14.6 ±9.7 ml/kg lean body mass in patients with the NS that does not differ signifi cantly from the normal mean (13.3 ±3.3) either. In addi tion, the observation that the interstitial albumin concen tration was greatly diminished in nephrotic patients [46,86] as well as the decrease of the extravascular proportion of albumin seen in the NS [59] argue against increased extra vascular deposition of albumin in this condition. On these grounds it may be concluded that values for PV and BV in nephrotic subjects, obtained either by measurement of labeled RBC or by the human albumin method, reflect the 'true' volume to the same extent as in normals.…”

Section: Methods To Estimate Pv and Bvmentioning

confidence: 99%

Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Mees

Geers

Koomans³

1984

Nephron

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Section: Methods To Estimate Pv and Bvmentioning

confidence: 99%

Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Mees

Geers

Koomans³

1984

Nephron

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“…The period of low protein feeding was cautiously extended and the children improved remarkably, with a lowered mortality, on a diet supplying less protein than they were calculated to have had before admission. During this time, they lost all their oedema without any change in their serum albumin level 27 ; the rate of loss of oedema was entirely independent of the protein content of the diet 28 . The early argument that kwashiorkor was due to protein deficiency because of the response to diets rich in protein is fallacious: is a headache due to aspirin deficiency because it is cured by aspirin?…”

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confidence: 90%

Oedematous malnutrition

Golden

1998

British Medical Bulletin

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Oedematous malnutrition in the child or adult is not caused by protein deficiency; such a concept can lead to fatal therapeutic error in oedematous malnutrition treatment. On the other hand, deficiency of protein, or the other type II nutrients, is common and causes stunting and wasting. In kwashiorkor, the deficiency is more likely to be due to one or several type I nutrients, particularly those involved with anti-oxidant protection.

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“…Under these circumstances a low plasma albumin has been seen as a response to metabolic stress, and an intrinsic part of the acute phase response, rather than as an indication of a speci®c protein de®ciency which requires direct treatment (Golden et al, 1980). Despite the success of this approach to care, it has Limits of adaptation to high dietary protein intakes AA Jackson S49 not found wide acceptance, and the important lessons have not, in general, been extrapolated to adult care (Bredow & Jackson, 1994;.…”

Section: High Protein Intakes In Therapymentioning

confidence: 99%

Limits of adaptation to high dietary protein intakes

1999

Eur J Clin Nutr

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Ingested protein is made available to the body following digestion and absorption as amino acids and contributes to the body's demand for amino acids for protein synthesis and other metabolic pathways. As the pattern of amino acids required for metabolism is substantially different from that ingested, extensive metabolic interchange serves to improve the match. As a matter of course oxidation of amino acids contributes to satisfying the energy needs of the body. Amino acids in excess of immediate requirements follow degradative pathways and if the capacity of these pathways is exceeded adverse consequences ensue. In pathological states, such as inborn errors of metabolism, there is an obvious constraint on metabolic¯ow with serious sequelae. Pathways may be constrained to a lesser extent due to genetic polymorphisms, metabolic programming, limitation of cofactors or lack of associated substrates. Any of these can result in metabolic derangements, which do not manifest as overt disease, but limit normal function. There is the need to determine the dose response to increases in dietary protein and amino acid availability, using critical metabolic intermediates as outcome indices in order to clarify the upper limit of intake with which the body can cope under a range of physiological and pathological states.

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Albumin and Nutritional Œdema

Cited by 61 publications

References 21 publications

Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Blood Volume and Sodium Retention in the Nephrotic Syndrome: A Controversial Pathophysiological Concept

Oedematous malnutrition

Limits of adaptation to high dietary protein intakes

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