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)

The purpose of this investigation was to determine the effect of nephrotic syndrome (NS) on the pharmacodynamics of a barbiturate. NS was induced in male rats by puromycin aminonucleoside; it caused hypoproteinemia, increased liver and kidney weight and elevated serum creatinine and urea nitrogen concentrations. Serum albumin concentration decreased from 3.5% in controls to 0.90% in NS animals. The rats were infused i.v. with heptabarbital, 1 mg/min, until they lost their righting reflex. The total dose (mean +/- S.D.) required by rats with NS, 40.2 +/- 4.2 mg/kg, was substantially lower than that required by normal animals (68.6 +/- 6.2 mg/kg, P less than .001). Serum protein binding of heptabarbital was reduced from 49% in controls to 26% in NS rats. However, the drug concentration in cerebrospinal fluid (CSF) at the pharmacologic endpoint was not significantly different in controls and NS rats (18.9 +/- 1.5 vs. 18.3 +/- 1.4 mg/l). Serum, CSF and the brain contained appreciable concentrations of a metabolite of heptabarbital. To determine if the metabolite contributes to the pharmacologic effect of the parent drug, rats received an i.v. injection of 46, 60 or 100 mg/kg of heptabarbital. Concentrations of heptabarbital in CSF at return of righting reflex (which occurred after 15, 25 and 50 min, respectively) were independent of dose whereas metabolite concentrations increased with increasing dose. Thus, the metabolite of heptabarbital in male rats is pharmacologically inactive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of drug action in disease states. XXIX. Effect of experimental nephrotic syndrome on the pharmacodynamics of heptabarbital: implications of severe hypoalbuminemia. 256 85

Impairments of protein metabolism, expressed as predominance of catabolism over anabolism and hypoproteinemia, were observed in one month old rats with experimental burns of the IIIA-IIIB degree, when 20-25% of a body surface was impaired. After administration of steroid drugs (retabolyl at a dose of 1 mg/100 g of body mass or oxymetacyl--4-methyl-5-oxyuracil---at a dose of 5 mg/100 g of body mass) content of protein and urea normalized in blood serum, activity of cathepsin D decreased in tissues, the rate of 35S-methionine incorporation into tissue proteins increased. The pyrimidine derivative oxymetacyl exhibited higher effect on protein metabolism in burns of preadolescent rats as compared with retabolyl.
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PMID:[Effect of retabolyl and oxymetacyl on protein metabolism in experimental burns in immature rats]. 344 45

Amyloidosis was diagnosed in 6 Holstein cows that were examined because of chronic intractable diarrhea. Besides diarrhea, the chief finding was a nephrotic-like syndrome, in that there was edema, hypoproteinemia, and proteinuria. Other consistent clinicopathologic abnormalities were hyperfibrinogenemia, low-normal serum calcium content or hypocalcemia, hypomagnesemia, prolonged bromosulphalein half time, high serum urea nitrogen concentration, high serum creatinine concentration, and low urine specific gravity. Foci of inflammation including traumatic reticuloperitonitis, traumatic pericarditis, salpingitis, mastitis, and metritis were found. There was histologic evidence of amyloid in the kidneys, liver, adrenal glands, and spleen. The iodine-sulfuric acid test for amyloid was positive in 2 cows. The Congo red dye test for amyloid was positive in 2 other cows. In spite of supportive care, all the cows either died naturally or were euthanatized. Because foci of inflammation were found in each cow, it was concluded that the most likely classification of amyloidosis in these cases would be reactive systemic amyloidosis and that the major amyloid fibril protein would be type AA.
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PMID:Amyloidosis in six dairy cows. 651 26

In a group of 18 infants with birth weights of 1,500 gm or less, either preterm transitional or mature human milk was given during the time of initial hospitalization. Half of the infants were given protein supplement isolated from mature human milk which increased the protein content of the ingested milk by 0.8 gm/dl. The protein intake of these infants was increased by 0.6 to 1.6 gm/kg/day between two and 12 weeks after birth. The infants in the unsupplemented group developed hypoproteinemia at 8 to 12 weeks of age whereas those who received protein supplementation did not. We conclude that the hypoproteinemia resulted from nutritional lack of protein and did not represent a physiologic phenomenon of preterm development. There was no difference in the growth of the two groups. There was no evidence of any imbalance in amino acid metabolism even though there were significant correlations between individual protein intakes and plasma concentrations of tyrosine and phenylalanine. Protein intake of more than 3 gm/kg/day resulted in a mean serum urea nitrogen concentration of more than 15 mg/dl at 2 weeks of age, indicating that excessive protein intake should be avoided soon after birth.
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PMID:Human milk protein supplementation for the prevention of hypoproteinemia without metabolic imbalance in breast milk-fed, very low-birth-weight infants. 709 22

This clinical investigation was carried out in order to determine whether the 10-12 hr food and fluid restrictions imposed before elective operations have detrimental effects on older patients according to various metabolic parameters. Thirty male urological patients aged between 60 and 90 years were chosen for study (group I 60-70 years, group II 70-80 years, group III 89-90 years). The following parameters were measured at 7 p.m. the evening before the operation, and at 7. a.m. on the morning of operation: body weight, hematocrit, blood-gas analysis, electrolytes, serum osmolality, urea, creatinine, total protein with electrophoresis and blood glucose. Urine was collected during the period of abstinence and osmolality, electrolytes, total nitrogen, creatinine and urea were estimated. All patients showed a reduced creatinine clearance to a degree that was expected for their age. In all three groups a significant weight reduction (p less than 0,001) occurred during the time of observation. The 12 hr urine volume increased from one age group to the next whereas perspiration decreased, indicating deficient thermal regulations in older patients. The hypohydration on the morning of operation, especially in group II and III, marked a relatively lower hematocrit and hypoproteinemia. In all three groups the urea and creatinine values were slightly lower in the morning than in the evening before, indicating the occurrence of further hypohydration due to fasting. The low elimination of total nitrogen, urea, and creatinine in the urine could be an indication that the 12 hr food and fluid restriction caused no marked catabolism. Our study shows that geriatric patients are indeed able to compensate for a 12 hr-period of abstinence. When however, these patients also have to undergo an operation, possibly associated with a considerable loss of body fluids or when restriction of oral intake extends to 16-20 hrs, decompensation may rapidly occur leading to deleterious consequences.
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PMID:[The effect of preoperative food and fluid restrictions on various metabolic parameters in geriatric patients]. 730 24

Magnesium lithospermate B, a compound newly isolated from Dan Shen, was given orally to rats for 70 days after excision of five-sixths of their kidney volume. As a result, mesangial proliferation, tubulo-interstitial lesions and glomerular sclerotic lesions, which were conspicuous in rats that were not given magnesium lithospermate B after nephrectomy, were inhibited. Furthermore, a decrease in blood urea nitrogen, improvement of hypoproteinemia, hypoalbuminemia and hypercholesteremia, and inhibition of urinary protein excretion were observed. The levels of creatinine, methylguanidine and guanidino-succinic acid, which accumulate in the blood with the progress of renal failure, were decreased significantly in rats given magnesium lithospermate B. These results indicate that magnesium lithospermate B, a component of an Oriental medicine has potential as a new therapeutic agent for inhibiting the progression of renal dysfunction.
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PMID:Effects of a Dan Shen component, magnesium lithospermate B, in nephrectomized rats. 775 1

We analyzed the serum anion gap (AG = sodium plus potassium minus chloride plus bicarbonate, N = 11-21 mEq/l), serum uric acid and urea concentrations in hyponatremia of various origins. We found that characteristic chemical patterns emerged in association with different hypotonic states: Low uric acid concentration was typically observed in the SIADH and in hyponatremia related to hypopituitarism. The same observation was also frequently noted in hyponatremia secondary to diuretics or to polydypsia. In the SIADH, we observed a decrease in the AG but to a greater extent (-26%) than one would expect from the simple dilutional effect (-16%). Fifty percent of the patients presented an AG lower than 11 mEq/l. In patients with diuretic-related hyponatremia, one group presented an hypouricemia and a low AG as in SIADH (reflecting volume expansion), in the other group the AG was normal or increased as was uric acid concentration (reflecting volume depletion). In adrenocorticotropin deficiency, hyponatremia was typically associated with a low bicarbonate concentration, a normal AG and hypouricemia. In polydypsic patients with hyponatremia, the AG was usually normal or increased despite sometimes very low sodium levels. Uric acid levels were highly variable, most often decreased. We also noted in these patients that the serum urea levels were correlated with urine osmolality (R = +0.8; p < 0.001), and in 40% of them we observed very low blood urea concentration (0.5-2 mmol/l) at the admission time. In hyponatremia related to cardiac failure or cirrhosis, the AG was usually normal despite mild hypoproteinemia.
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PMID:Uric acid, anion gap and urea concentration in the diagnostic approach to hyponatremia. 852 2

Characteristic alterations in the serum and urine biochemical profiles of Doberman Pinschers with congestive heart failure (CHF) resulting from idiopathic dilated cardiomyopathy were determined. We compared these alterations with those observed in 2 other models of CHF: rate overload induced by rapid ventricular pacing in dogs, and biventricular hypertrophy and dilatation induced in turkey poults by furazolidone toxicosis. Serum and urine biochemical changes in both models of CHF in dogs were mild to moderate in degree, and were moderately consistent. They could be attributed to secondary neurohumoral, hepatic, and renal effects of heart failure. The most marked and consistent changes observed were mildly decreased anion gap that developed, in part, because of decreased serum sodium concentration, moderately increased catecholamine concentrations, moderate lactaciduria, hyposthenuria, and mildly increased urea concentrations and liver enzyme activities. In birds with furazolidone cardiomyopathy, we observed mild increases in serum urate concentration, liver and muscle enzyme activities, but moderately increased sodium concentration with decreased chloride concentration. In the pacing and furazolidone models, in which CHF was rapidly induced, moderate to marked hypoproteinemia was attributable to decreases in albumin and globulin concentrations. Using the avian model we found that the hypoproteinemia could be largely attributed to blood volume expansion, and to a lesser extent, inanition. Development of hypoalbuminemia during rapid ventricular pacing and furazolidone treatment may contribute to the effects of rate overload or drug toxicity in the pathogenesis of CHF, because hypoalbuminemia may contribute to altered hemodynamics and neuroendocrine system activation. Our data indicate that clinical biochemical analysis of serum and urine may be useful for assessing progression of CHF.
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PMID:Clinical pathologic profiles of dogs and turkeys with congestive heart failure, either noninduced or induced by rapid ventricular pacing, and turkeys with furazolidone toxicosis. 842 73

Seven related Bernese Mountain Dogs developed a syndrome Characterized by progressive cerebellar and hepatic disease. Clinically, stiffness in the hind limbs, mild incoordination, and a slight head tremor were first noticeable when pups were 4 to 6 weeks old. The condition progressed, causing pups to assume a wide-based stance. Other signs included head bobbing, spontaneous nystagmus, and, finally, paresis. Hematologic findings included leukocytosis with a left shift; normocytic, normochromic anemia; hypoproteinemia, low serum creatinine, and urea nitrogen concentrations; excessive fasting plasma ammonia concentration; and an increase in concentration of serum bile acids. Portal venography performed on 1 dog revealed a small liver and extensive extrahepatic varicosities. Necropsy revealed cerebellar hypoplasia, nodular liver, extensive abdominal varicosities, and ascites. Histologically, degeneration and depletion of Purkinje's cells and vacuolation, degeneration, and nodular regeneration of hepatic tissues were evident. Preliminary analysis of the pedigree was suggestive of an autosomal recessive pattern of inheritance.
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PMID:Clinical, hematologic, and biochemical features of a syndrome in Bernese mountain dogs characterized by hepatocerebellar degeneration. 863 71

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55


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