Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The female patient initially showed the acquired type of total lipoatrophy at about 8 years of age. At 12 years of age, the onset of diabetes mellitus was speculated from advanced pyodermia and dedentition. At 29 years of age, glucosuria was found, and she developed proteinuria, ascites, and pretibial edema. The physical examination revealed: hepatosplenomegaly, complete absence of subcutanous fat, cutaneous xanthomas, and emaciated facies with pronounced zygomatic arches. Diabetic retinopathy was revealed in the ophthalmological examination, and nephropathy was evident in renal biopsy specimens. She also had peripheral diabetic neuropathy. No adipose tissue was found in the mesenterium under peritoneoscopy. The hepatic biopsy specimen revealed advanced portal liver cirrhosis. Laboratory findings included: hyperlipidemia, elevation of BMR without evidence of hyperthyroidism, impaired renal function, and undetected anti-insulin antibodies and anti-insulin antibodies. Endocrinological examinations revealed normal value, except for an impaired hGH response in the arginine test. C-peptide immunoreactivity was high. Her condition was fairly well controlled by 140 units of insulin injection daily.
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PMID:Lipoatrophic diabetes. Report of a case. 15 92

Serum lipids and their lipoprotein fractions were measured in 16 nephrotic syndrome patients. All component of lipids and beta-lipoprotein fractions (LDL) showed an increase in all uncomplicated patients. The increase in serum lipids were inversely proportional to the albumen level in these patients. In 3 patients, lipids and beta-lipoprotein fractions returned to near normal after treatment, the proteinuria diminished and serum albumen became normal. Most of these patients did not need any treatment for hyperlipidemia.
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PMID:The causal role of hypoalbuminemia in human nephrotic hyperlipidemia. 19 Sep 98

The induction of nephrotoxic nephritis in rats with rabbit antibodies preparation results in proteinuria, hypoproteinemia and hyperlipidemia with little glomerular lesions. A study of some hydrolases in cortex and medulla on one hand and glomerular and tubules on the other, showed changes in the activities of following enzymes. 1) A 20-30 % decrease in Na+, K+ dependent ATP-ase in whole kidney. 2) A 20 % decrease in beta-galactosidase activity in glomerular and medulla. 3) A 20 % increase of arylsulphatase A activity in tubules. These results are discussed in the light of the present knowledge of sulphatide metabolism in kidney.
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PMID:[Experimental nephrotic syndrome in the rat. Biologic parameters and study of several hydrolases in different purified kidney fractions]. 20 50

The character of hyperlipidemia was studied in rats with chronic uremia induced by subtotal nephrectomy--5/6 of the renal tissue was removed. 13 to 30 weeks after this operation the blood serum cholesterol and phospholipid concentration almost doubled. Hyperlipidemia was more pronounced in rats with high azotemia (blood urea nitrogen--BUN). No elevation of serum tryglycerides occurred. Total serum beta- and pre-beta-lipoproteins determined nephelometrically increased significantly only with the BUN level of over 80 mg%. Lipoprotein disc electrophoresis of the serum in rats with uremia demonstrated a distinct rise of alpha-lipoproteins and a slight--of beta-lipoproteins; postheparin lipolytic activity of the plasma was normal. Experimental rats displayed massive proteinuria, but hypoproteinuria was insignificant.
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PMID:[Hyperlipidemia in rats with chronic renal failure]. 20 85

The nephrotic syndrome may be associated with several complications caused by severe proteinuria. The consequences of severe renal protein loss are disturbances of water and electrolyte metabolism, thromboses and thromboembolic complications, hyperlipidemia with accelerated atherosclerosis and, finally, some other complications due to the decreased oncotic pressure and the renal loss of transport globulins and immunoglobulins. Diagnosis and treatment of these complications are important in the management of patients with nephrotic syndrome. In the present study, the frequency and localization of thromboses and thromboembolic complications in 11 patients with nephrotic syndrome are described. In addition, factors which are known to be responsible for the hypercoagulable state in nephrotic syndrome were evaluated and correlated to the thromboembolic complications in these patients. An important finding was that in all patients with thromboses and thromboembolic complications, the serum albumin concentrations were below 2 g/100 ml, whereas, with one exception, serum albumin levels were above 2 g/100 ml in cases without thromboembolic complications. Our results indicate that serum albumin levels may be used as an indirect parameter to assess the risk of thromboembolic complications in patients with nephrotic syndrome.
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PMID:[Complications of nephrotic syndrome with special reference to thromboembolic accidents]. 37 Sep 77

The nephrotic syndrome is characterized by gross proteinuria, hypoproteinemia, hyperlipemia, and edema. The authors review the diagnostic features and management protocol of this syndrome in children.
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PMID:Nephrotic syndrome in childhood: diagnosis and management. 41 35

This paper reports the association of diabetes mellitus and hyperlipidemia type III and the relation between the dose of insulin and the serum level of triglycerides and cholesterol. The coexistence of hiperglobulinemia, Bence Jones proteinuria and a positive rheumatoid factor is also reported.
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PMID:[Type III hyperlipoproteinemia--diabetes mellitus and dysglobulinemia]. 70 30

Three hyperlipemic models in rats were compared regarding serum lipid levels and known anti-hyperlipemic agents were tested for their effects on the hyperlipemia. In rats fed a cholesterol diet (group A), only serum cholesterol level resulted in a marked increase as compared with normal level. In animals given a large dose (0.7 ml/100 g body weight, i.v.) of anti-kidney serum (group B), extremely high elevations of serum total lipid, phospholipid, triglyceride and cholesterol levels were observed. In animals given a small dose (0.3 ml/100 g body weight, i.v.) of anti-kidney serum and fed the cholesterol diet (group C), elevations of these serum lipids except for triglyceride were not only greater than in group B, but also synergistic. On the contrary, serum triglyceride level and proteinuria were less in group C than in group B. Furazabol, clofibrate the beta-sitosterol given orally for 7 days at doses of 1,100 and 500 mg/kg/day, respectively were clearly effective on the hyperlipemia of group C, without affecting the proteinuria. Furthermore, this model was more sensitive to these anti-hyperlipemic agents than groups A and B. From the above results, group C would seem to be an adequate and effective experimental hyperlipemic model.
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PMID:Pharmacological studies on experimental nephritic rats. (4) Improvement of hyperlipemic models in rats utilizing anti-rat kidney rabbit serum and effects of anti-hyperlipemic agents on serum lipid levels. 72 1

Serum lipids in 58 renal transplant recipients were related to duration of follow-up, relative body weight, steroid medication, proteinuria and graft performance. Hyperlipidemia was observed between the 4th month and the end of the first year after transplantation in 83% of the patients. Thereafter, the frequency of hyperlipidaemia appeared to decrease: at 4 to 7 years only 61% of the subjects continued to exhibit abnormal high serum lipids. Three mechanisms leading to hyperlipidaemia were identified: 1) overweight, 2) steroid mediation, 3) proteinuria. A forth apparent mechanism was impaired transplant function.
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PMID:Hyperlipidemias in patients with kidney transplants. 78 55

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27


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