Gastrointestinal Protein Loss in the Nephrotic Syndrome Studied with &lt;sup&gt;51&lt;/sup&gt;Cr-Albumin

Schultze, G; Ahuja, Santosh; Faber, Ulrike; Molzahn, M

doi:10.1159/000181844

Cited by 16 publications

(6 citation statements)

References 7 publications

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“…In addition, the GI albumin clearance in nephrotic syndrome patients varies from negligible in about half of the patients 54 up to values of about 3.5 g/day. 55 Thus, nephrotic syndrome should induce a severe strain on albumin synthetic capacity of the body if the C P were to remain normal.…”

Section: Renal Albumin Clearancementioning

confidence: 99%

Human serum albumin homeostasis: a new look at the roles of synthesis, catabolism, renal and gastrointestinal excretion, and the clinical value of serum albumin measurements

Levitt¹,

Levitt²

2016

IJGM

512

403

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Serum albumin concentration (CP) is a remarkably strong prognostic indicator of morbidity and mortality in both sick and seemingly healthy subjects. Surprisingly, the specifics of the pathophysiology underlying the relationship between CP and ill-health are poorly understood. This review provides a summary that is not previously available in the literature, concerning how synthesis, catabolism, and renal and gastrointestinal clearance of albumin interact to bring about albumin homeostasis, with a focus on the clinical factors that influence this homeostasis. In normal humans, the albumin turnover time of about 25 days reflects a liver albumin synthesis rate of about 10.5 g/day balanced by renal (≈6%), gastrointestinal (≈10%), and catabolic (≈84%) clearances. The acute development of hypoalbuminemia with sepsis or trauma results from increased albumin capillary permeability leading to redistribution of albumin from the vascular to interstitial space. The best understood mechanism of chronic hypoalbuminemia is the decreased albumin synthesis observed in liver disease. Decreased albumin production also accounts for hypoalbuminemia observed with a low-protein and normal caloric diet. However, a calorie- and protein-deficient diet does not reduce albumin synthesis and is not associated with hypoalbuminemia, and CP is not a useful marker of malnutrition. In most disease states other than liver disease, albumin synthesis is normal or increased, and hypoalbuminemia reflects an enhanced rate of albumin turnover resulting either from an increased rate of catabolism (a poorly understood phenomenon) or enhanced loss of albumin into the urine (nephrosis) or intestine (protein-losing enteropathy). The latter may occur with subtle intestinal pathology and hence may be more prevalent than commonly appreciated. Clinically, reduced CP appears to be a result rather than a cause of ill-health, and therapy designed to increase CP has limited benefit. The ubiquitous occurrence of hypoalbuminemia in disease states limits the diagnostic utility of the CP measurement.

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Section: Renal Albumin Clearancementioning

confidence: 99%

Human serum albumin homeostasis: a new look at the roles of synthesis, catabolism, renal and gastrointestinal excretion, and the clinical value of serum albumin measurements

Levitt¹,

Levitt²

2016

IJGM

512

403

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“…It has been suggested that in these patients there is not only an increased permeability of the glomeruli for proteins but a generalized increase in permeability of all capillaries, resulting in increased filtration in the interstitium [10]. Increased capillary "permeability" has been attributed to a generalized loss of membrane negative charge in minimal lesions NS (MLNS) [11].…”

Section: The Capillariesmentioning

confidence: 99%

Pathogenesis of edema formation in the nephrotic syndrome

Walle

Donckerwolcke

2001

Pediatric Nephrology

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Based on observations in 110 children with nephrotic syndrome (NS) and data from the literature, existing concepts on the pathogenesis of edema formation in the NS have been modified. The data suggest that the basic abnormality is a primary disturbance in renal sodium excretion. Depending on the stage in the development of the NS, the rate of progression in the development of hypoproteinemia, and the absolute levels of plasma oncotic pressure, functional hypovolemia may develop, resulting in stimulation of hemostatic mechanisms and secondary sodium retention. This applies as much to patients with minimal change NS as to patients with histological lesions. Alterations in kidney function (glomerular filtration rate, renal plasma flow, filtration fraction) in the NS cannot be explained by hypo- or hypervolemia, but reflect variations in plasma oncotic pressure and glomerular basement membrane permeability. These abnormalities will also influence sodium excretion. Evaluation of the presence of functional hypovolemia will have therapeutic consequences. A quick diagnosis can be made by assessment of FENa+ and UK+/ (UK+ + UNa+) Sodium retention associated with increased distal Na/K exchange indicates functional hypovolemia, and may be treated by albumin infusion if clinically required.

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“…Direct measurement of red-cell surface charge showed no difference between nephrotic children and controls [7]. Studies on gastrointestinal protein loss in the nephrotic syndrome also yielded controversial results [8,9]. A study analysing saliva from adult patients with various forms of glomerulopathies showed no difference in the absolute concentration of salivary albumin compared with controls [12].…”

Section: Discussionmentioning

confidence: 99%

“…The selectivity of proteinuria was originally interpreted in terms of size selectivity of glomerular filtration, although it has long been appreciated that impairment of charge selectivity of the glomerular capillary wall may also play an important role [1][2][3][4]. It is still controversial whether the alteration of size and charge selectivity of capillary permeability in SSNS is confined to the glomerular capillary wall in the kidney, or is more widespread [5][6][7][8][9][10]. Direct sampling of interstitial fluid to ascertain this point is not possible, but saliva and cerebrospinal fluid may offer indirect evidence.…”

Section: Introductionmentioning

confidence: 99%

Salivary excretion of endogenous proteins in nephrotic syndrome in children

Neuhaus¹,

Shah²,

Barratt³

1997

Pediatric Nephrology

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Size and charge selectivity of capillary permeability in the salivary glands of nephrotic children were investigated by measuring salivary excretion of endogenous plasma proteins of different size and charge. We examined 10 children with steroid-sensitive nephrotic syndrome (SSNS) in relapse and subsequent remission, 11 with steroid-resistant nephrotic syndrome, and 11 healthy children (controls). Albumin [mol. wt. 66 kilodaltons (kDa), isoelectric point (pI) 4.9] was measured by radio-immunoassay, transferrin (mol. wt. 77 kDa, pI 5.9) and immunoglobulins IgG1 (mol. wt. 150 kDa, pI 7-9) and IgG4 (mol. wt. 150 kDa, pI < 6) by enzyme-linked immunoabsorbent assay. In saliva, no significant differences were found between the four groups of children for any of the four proteins. Also, the saliva/plasma ratios of the four proteins were not different among the four groups. From these data, we conclude that in subjects with SSNS in relapse, neither size nor charge selectivity of salivary gland capillary permeability are affected.

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Gastrointestinal Protein Loss in the Nephrotic Syndrome Studied with <sup>51</sup>Cr-Albumin

Cited by 16 publications

References 7 publications

Human serum albumin homeostasis: a new look at the roles of synthesis, catabolism, renal and gastrointestinal excretion, and the clinical value of serum albumin measurements

Human serum albumin homeostasis: a new look at the roles of synthesis, catabolism, renal and gastrointestinal excretion, and the clinical value of serum albumin measurements

Pathogenesis of edema formation in the nephrotic syndrome

Salivary excretion of endogenous proteins in nephrotic syndrome in children

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