Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty Chinchilla rabbits of both sexes were examined for changes in some parameters of protein, lipid and trace elements metabolism (total protein, protein fractions, urea, residual nitrogen in blood serum, lipids, total cholesterol, free cholesterol, diglycerides, phospholipids, triglycerides, free fatty acids and the trace elements selenium, iron, zinc and so forth in the liver) during the animals' poisoning with the defoliant magnesium chlorate. A study was made of the effect on these changes of the administration for 3 weeks of sodium selenite (15 micrograms/kg), vitamin E (25 mg/kg) and retabolil (2 mg/kg once a week). It has been established that the combined administration of these agents removes and prevents the changes in protein, lipid and trace elements (hypoproteinemia, dysproteinemia and impairment of the nitrous balance) and lipid metabolism because of the animals' poisoning with magnesium chlorate.
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PMID:[Anabolic effects of sodium selenite, vitamin E and retabolil in experimental hypotrophy induced by a pesticide]. 255 78

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.
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PMID:Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders. 295 52

We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2-83% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.
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PMID:Acid-base effects of altering plasma protein concentration in human blood in vitro. 310 Apr 99

We studied the effects of hypoproteinemia following 12 days of repeated plasmapheresis and low-protein diet on sodium balance, fluid volumes, and renal hemodynamics in six conscious dogs on 50 mmol sodium intake. Measurements during hypoproteinemia were obtained during a 5-day recovery period starting 20 h after the final plasmapheresis session, with continued low-protein diet. During the plasmapheresis period sodium was retained. Sodium balance became negative on the first recovery day when plasma protein was 29 +/- 1 g/l (control 60 +/- 2 g/l, P less than 0.01), and plasma colloid osmotic pressure (COP) was 9 +/- 1 mmHg (control 22 +/- 1 mmHg, P less than 0.01). Subcutaneous fluid COP was lowered from 14 +/- 1 to 4 +/- 1 mmHg (P less than 0.01). Blood volume, plasma renin activity, and aldosterone were unchanged. Glomerular filtration rate and effective renal plasma flow were slightly reduced (NS), and filtration fraction was unchanged. After a second plasmapheresis period in three of the dogs, plasma protein fell to 26 +/- 1 g/l and COP to 7 +/- 1 mmHg. Now sodium was retained on the first day after stopping plasmapheresis, and renin and aldosterone were high. The next day, when plasma protein was again 29 +/- 1 g/l and COP 8 +/- 1 mmHg, these three dogs were able to completely excrete an infusion of 130 mmol sodium. These data suggest that the level of plasma COP below which dogs on a medium-sodium intake would retain sodium averages 8 mmHg, which is considerably lower than generally thought.
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PMID:Hypoproteinemia and recovery from edema in dogs. 313 59

The pathophysiology of renal dysfunction in generalized sepsis remains unknown. In this study, 24 hours after surgical induction of peritonitis in 20 volume-loaded sheep, three patterns of renal function were seen. In group 1 (n = 8), glomerular filtration rate (GFR) decreased by 70%, urine volume by 85%, absolute sodium excretion by 95%, and fractional sodium excretion by 83%. Group 2 (n = 4) exhibited similar sodium retention but GFR did not fall. Group 3 (n = 8) showed no change in GFR or urine volume and only minimally reduced sodium excretion. Mean arterial pressure fell 17% in group 1 only; central venous pressure, pulmonary capillary wedge pressure, and plasma volume were maintained at or above presepsis values in all groups. Cardiac index was either increased or unchanged, and renal plasma flow was maintained in all groups; there was thus no hemodynamic evidence to suggest volume contraction. Histologic examination showed only minor changes with no consistent pattern. Renal functional changes correlated with other manifestations of severe sepsis--GFR and sodium retention correlated significantly with increased cardiac index, decreased systemic vascular resistance, pulmonary arterial hypertension, leukopenia, hypoproteinemia, and hypoglycemia. All of these changes were most marked in group 1. In groups 1 and 2, plasma renin activity (PRA) increased and urinary kallikrein excretion decreased. PRA correlated inversely with GFR, urine volume, and sodium excretion; urinary kallikrein excretion correlated positively with urine volume and sodium excretion. Urinary excretion of 6-keto-PGF1 alpha was increased in groups 1 and 2 and correlated inversely with mean arterial pressure in group 1 animals. During sepsis, urinary thromboxane B2 excretion continued at presepsis values in all groups. The results suggest that unusual reciprocal changes in activity of the renin-angiotensin and renal kallikrein-kinin systems may play a role in the renal response to sepsis. PGI2 synthesis is increased and may affect systemic hemodynamics and renal function; the role of thromboxane A2 in this context is unknown.
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PMID:Vasoactive hormones in the renal response to systemic sepsis. 327 70

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.
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PMID:Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume. 354 69

Edema formation in nephrotic syndrome has been attributed to intravascular volume depletion resulting from leakage of plasma water into the interstitial space and activating secondary renal sodium retention. However, clinical studies indicate that edematous patients with nephrotic syndrome may have normal or expanded plasma volumes. We evaluated the relationship between plasma volume and edema formation in control rats and rats with chronic renal failure (CRF) produced by 7/8 nephrectomy. In each group, plasma volume and 22Na space were measured during the control period and after induction of hypoalbuminemia from passive Heymann nephritis. Rats with CRF had expanded plasma volume during the initial period (4.23 +/- 0.46 vs. 3.32 +/- 0.68 ml/100 g body wt) that became significantly more expanded (to 5.44 +/- 1.16 ml/100 g body wt) when they became nephrotic as 22Na space also increased. Plasma volume and 22Na space did not change in the sham-operated rats when nephrosis was produced. Plasma renin activity was lower in the CRF rats during the control period than in the sham-operated rats and fell significantly during the nephrotic period when edema developed. Nonnephrotic rats had a plasma colloid osmotic pressure (COP) of 17.8 +/- 4.3 mmHg compared with 8.5 +/- 2.9 mmHg when nephrotic. Despite this large difference in COP, both nephrotic and nonnephrotic rats exhibited the same relationship between plasma volume and extravascular sodium space, a measure of edema formation. Hypoproteinemia is not sufficient for edema formation in the rat with passive Heymann nephritis; concomitant plasma volume expansion resulting from CRF is a necessary additional component.
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PMID:Plasma volume expansion is necessary for edema formation in the rate with Heymann nephritis. 397 Feb 14

Four cases of left-sided pleural hydrothorax in connection with severe pre-eclampsia are reported. In addition an increased formation of ascitic fluid was observed in the patients. A long-lasting bed rest in the left lateral recumbent position preceded the discovery of the roentgenologically verified pleural changes. Hypoproteinemia caused by the excretion of large amounts of protein in the urine seems to be a partial etiological factor aggravated by the renal retention of sodium and water. Pleural transudate disappeared spontaneously within two weeks from the delivery. In such cases, immediate diagnostic procedures, e.g. the exclusion of tuberculosis, are unnecessary. The authors think that the phenomenon is common in similar cases but usually remains undiagnosed.
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PMID:Left-sided hydrothorax in connection with severe pre-eclampsia. Case reports. 615 19

Oedema fluid was collected from the leg through a sterile 21 gauge needle inserted into the subcutaneous space in 12 patients with protein energy malnutrition, 12 with nephrosis, 5 with Indian childhood cirrhosis, 4 with acute nephritis, 4 with epidemic dropsy and 3 with congestive heart failure. The concentrations of protein, free amino acids and electrolytes were measured in plasma and oedema fluid. The plasma/oedema fluid ratios were 36:1, 49:1, 32:1 and 52:1 in protein energy malnutrition, nephrosis, Indian childhood cirrhosis and congestive heart failure. These ratios were significantly smaller in epidemic dropsy (4:1) and acute nephritis (21:1). The free alpha amino nitrogen concentrations in these two compartments were almost in equilibrium. This was also found for essential and non-essential amino acid distributions in protein energy malnutrition and nephrosis, whereas differences in amino acid patterns were found in nephritis and epidemic dropsy. Sodium and potassium concentrations varied substantially between diseases where the underlying cause was gross hypoproteinemia compared to non-hypoproteinemic conditions.
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PMID:Oedema fluid composition in childhood disorders. 641 20

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.
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PMID:Effects of hypoproteinemia on fluid volumes and arterial pressure. 688 62


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