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 authors studied the assimilation of nitrogen preparations--moriamin S-2 and "improved" caseine hydrolysate in parenternal administration to 100 albino rats. Healthy animals and those with toxic affection of the liver induced with CCl4 were experimented upon. In healthy animals administration of nitrogen preparations led to the change of negative nitrogen balance into a positive one, normalized the content of blood and tissue amine nitrogen deranged in protein deficiency. Assimilation of nitrogen preparations fell considerably in toxic hepatitis. An 8-day parenteral nutrition failed to change the negative nitrogen balance into positive, and did not eliminate hypoproteinemia; however, it normalized the amine nitrogen concentration in the blood and tissues.
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PMID:[Anabolic effectiveness of nitrogenous preparations for parenteral nutrition in the presence of toxic liver damage]. 9 94

In most cases hypoproteinemia of our patients is a result of the disease leading to hospitalization. Moreover, it may also be a consequence of unappropriate nutrition, so that it has to be pointed out with emphasis that clinics being able to furnish a great number of ferment analysis should be in a position to answer the simple question: are patients receiving adequate nutrition or not? Necessary assumption for this purpose is-besides analyses of serum-protein-in acute cases the control of nitrogen excretion in urine and in case of exact balances also in stool, in order to exactly answer the question, whether the nitrogen supply will suffice special requirements.
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PMID:[Hypoproteinemia--consequence of cause of diseases, particularly in long-term hospitalized patients]. 103 22

Oak poisoning occurred in crossbred cattle due to eating immature tender oak (Quercus incana) leaves. Mortality was 70%. The animals exhibited anorexia, severe constipation and brisket edema. The feces were hard, pelleted and coated with blood and mucous. Significant reductions in blood hemoglobin and mean corpuscular hemoglobin, and significant elevations in serum bilirubin were observed. Serum urea nitrogen and creatinine were greatly increased. There was bilirubinuria, proteinuria, hypoproteinemia and hypocalcemia, and greatly increased activities of serum aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. The levels of tannins and condensed tannins were 97.7 mg tannic acid equivalent and 5.8 mg catechin equivalent/g of dry leaves. There was extensive nephro- and hepatotoxicity in the affected cattle due to hydrolysable tannins and simple phenols in the oak leaves.
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PMID:Oak (Quercus incana) leaf poisoning in cattle. 150 80

High dietary protein intake, in the past recommended for nephrotic syndrome, does not improve hypoproteinemia and may accelerate progressive renal damage. In contrast, low-protein diets reduce proteinuria and preserve renal function in experimental renal models of nephrotic syndrome. In this study, 20 steroid-resistant, nephrotic patients were treated with a pure vegetarian, low-protein diet, supplemented with essential amino acids and ketoanalogues (supplemented vegan diet, SVD) for 4.6 +/- 3.1 months. Before the study, these patients followed an unrestricted protein, low-sodium diet (LSD). Proteinuria, daily urea nitrogen excretion and creatinine clearance decreased significantly on SVD. A similar lowering effect of SVD was observed on serum total cholesterol. Seven of the 20 patients changed from LSD to SVD and vice-versa on 3 occasions, and in all cases, we found an increase of proteinuria during the LSD period. Serum albumin, HDL cholesterol, triglycerides and anthropometric measurements did not change on SVD. Our data suggest that SVD exerts a favorable effect on proteinuria and hypercholesterolemia in nephrotic patients, without inducing clinical or laboratory signs of malnutrition.
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PMID:A special, supplemented 'vegan' diet for nephrotic patients. 180 35

The effects of 40 days of treatment with Cyclosporine A (CSA) on plasma and urine free amino acids were investigated in sham-operated (C) and partially nephrectomized (Pnx) female Fischer 344 rats. High Dose CSA (30 mg/kg/day ip) was associated with reduced weight gain, increased plasma urea nitrogen, and hypoproteinemia in C and Pnx animals. These animals also demonstrated increased plasma levels of alanine, markedly reduced levels of tryptophan, and an increase in urinary excretion of methylhistidines. C but not Pnx animals also showed a significant increase in plasma serine and a decrease in plasma taurine. CSA treatment of group C resulted in a progressive aminoaciduria involving substrates of the neutral and acidic renal amino acid transport systems; however, the renal excretion of taurine and beta-alanine by these animals was markedly reduced as compared to vehicle treated controls. High dose CSA exacerbated aminoaciduria in Pnx animals, but in this group, the excretion of beta amino acids was also increased. Our findings demonstrate that chronic CSA toxicity in rodents with normal renal function is characterized by increased muscle protein catabolism, significant reductions in plasma tryptophan, and an apparent decrease in whole body taurine pools. With the exception of the taurine abnormalities. CSA treatment had similar effects on Pnx animals; however, in this group, CSA-induced pathological changes were superimposed on the changes due to renal insufficiency per se. CSA toxicity as identified by the parameters investigated in this study was no more severe in Pnx animals with moderate chronic renal insufficiency than in controls with intact renal function.
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PMID:Free amino acids during chronic cyclosporine A toxicity in intact and partially nephrectomized rats. 188 71

The dose dependency of germanium dioxide(GeO2)-induced nephrotoxicity was investigated experimentally in rat groups orally treated with high (150 mg/kg/day), moderate (75 mg/kg/day), or low (37.5 mg/kg/day) doses of GeO2, and in an untreated group. Renal dysfunction, indicated by the increase of blood urea nitrogen and the decrease of creatinine clearance, and systemic toxicity by weight loss, anemia, and hypoproteinemia were more apparent in rats treated with higher dose of GeO2. Urinalysis including daily urinary protein excretion did not reveal any abnormalities in any of the groups. Urinary excretion and renal-tissue content of Ge were significantly elevated in the group of the higher dose of GeO2. Light microscopically, vacuolar degeneration and depositions of granules positive for periodic acid-Schiff in distal tubules were predominant in the higher-dose group of GeO2. The present study demonstrates that GeO2-induced nephrotoxicity develops dose dependently.
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PMID:Dose dependency of germanium-dioxide-induced nephrotoxicity in rats. 201 77

Clinico-pathological studies were made on rats with polycystic kidney disease (PCK), a congenital renal disorder transmitted as an autosomal recessive trait and characterised by facial and skeletal anomalies, with the results summarised as follows: 1) Affected animals had a poor weight gain and slightly increased urinary excretion of low molecular weight protein from 2 months after birth, and developed polyuria and hypocalciuria 5 months postnatally. They had elevation of serum urea nitrogen, increased urinary excretion of urea nitrogen and hypoproteinemia 8 months postnatally though without showing elevated serum creatinine and died around 10 months of life. 2) Kidneys of chin rats appear granular in surface, enlarge little by little while preserving the entire kidney morphology; a small cyst is formed in the renal medulla 2 months postnatally, then enlarges gradually to encroach upon the cortex and grows to involve all cortical layers by 8 months of life. This cyst was revealed by lectin staining to be derived from the collecting ducts and was assumed to correspond, both morphologically and clinically, to the infantile or juvenile form of PCK in humans. Pathogenetic factors of the characteristic facies and skeletal abnormalities were also investigated.
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PMID:[A study of an autosomal recessive polycystic kidney disease with facial and skeletal abnormalities in rat]. 208 54

In this problem-oriented review of abnormalities associated with cancer, we have emphasized distinctive diagnostic points related to pathogenesis for each condition and outlined how the approach to management is determined by pathogenesis. For abnormalities of the complete blood count, it is important to distinguish between abnormalities directly related to marrow malignancy and abnormalities associated with extramarrow malignancy. Hemopoietic tumors consist of developmentally deficient blood cells produced by a clonal population of malignant stem cells. Tumors infiltrating marrow cause overcrowding in the limited marrow microenviroment. Extramarrow malignancies cause blood abnormalities, but the potential for normal marrow function is present. Abnormalities of blood cells secondary to therapy are usually clearly identified by consideration of clinical history. The initial differential diagnosis for hypercalcemia is malignancy. An aggressive diagnostic approach may be needed to identify the neoplasm, and therapy should incorporate measures to prevent renal failure. Hypoproteinemia and hyperproteinemia may be caused by neoplasia. Monoclonal gammopathies should be identified and may be associated with hyperviscosity syndrome. Hypoglycemia in the adult animal is most frequently caused by insulin-secreting tumors, but it has also been associated with hepatic and other tumors. Increased blood urea nitrogen, creatinine, lipase, amylase, and liver enzyme activities may also be caused by malignancy. Inadequate urine concentrating ability may be caused by hypercalcemia or malignancy-associated renal insufficiency. Hematuria in older animals is suggestive of urinary tract neoplasia. Exfoliated tumor cells may be identified in the urine sediment of these patients.
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PMID:Laboratory abnormalities in patients with cancer. 219 37

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

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


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