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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study on doxorubicin-induced cardiotoxicity in LOU/M/Wsl rats, severe nephropathy has been observed; therefore, the question was raised whether nephropathy adds to or even might be responsible for doxorubicin-induced cardiomyopathy in rats. For elucidation of this question, the temporal relationship between the onset of doxorubicin-induced cardiomyopathy and nephropathy was studied. In addition, examination was made of whether modifications of the treatment schedule could circumvent nephrotoxicity. Because preliminary studies had shown that female LOU/M/Wsl rats developed less doxorubicin-induced albuminuria, both male and female LOU/M/Wsl rats were treated with an iv dose of 1 mg doxorubicin/kg (body wt)/rat on five consecutive days and then weekly. Saline-treated animals served as controls. Albuminuria, serum albumin, and serum creatine levels were assessed weekly. For histologic examination, 5 male and 5 female rats were killed weekly. At day 14 and thereafter, doxorubicin-treated male rats showed albuminuria greater than or equal to 10 g/liter. Albuminuria of greater than or equal to 10 g/liter was not avoided by modifications of the treatment schedule. Female rats had on day 14 a urinary albumin level of 1.0-3.0 g/liter, yet reaching the level of greater than or equal to 10 g/liter at day 49. In male rats serum albumin levels decreased to levels below 10 g/liter (p less than .001 vs. finding for day 0); in contrast female rats maintained constant serum albumin levels till day 49. Serum creatine levels showed a tendency to rise, the values of male rats not being measured after day 28 due to hyperlipidemia; the levels of female rats increased from 37.8 +/- 3.0 mumol/liter to 53.7 +/- 2.5 mumol/liter on day 49 (P less than .001). At day 10 in male and female rats a grade 1-1.5 cardiomyopathy score, assessed according to the modified Billingham scoring system, was found, gradually increasing to grade 2.5-3 cardiomyopathy, both in males and females, on day 49. In male LOU/M rats the nephropathy developed steadily from day 14 and thereafter, whereas in females the rate of development of kidney damage was slower and at the end point of the study the severity of kidney lesions was less in comparison to that of the males. The onset of cardiomyopathy and nephropathy was simultaneous. It was concluded that cardiomyopathy observed in LOU/M rats is a phenomenon independent of nephropathy.
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PMID:Time-course study on doxorubicin-induced nephropathy and cardiomyopathy in male and female LOU/M/Wsl rats: lack of evidence for a causal relationship. 345 68

There is much evidence that altered lipid metabolism contributes to the development of coronary artery disease (CAD). It is generally accepted that there is a direct association between the extent of CAD and total plasma cholesterol, as well as an inverse association between the extent of CAD and plasma HDL-cholesterol. No general agreement exists about the atherogenetic potential of plasma triglycerides and of triglyceride-rich lipoproteins. Since lipoprotein lipase (LPL) is the key-enzyme in the catabolism of triglyceride-rich lipoproteins (chylomicrons and very low-density lipoproteins), we examine the relationship between triglyceride-rich lipoproteins and LPL in vitro and in vivo. The concentrations of the main lipoprotein density classes, namely very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), high-density lipoproteins2 (HDL2) and HDL3, are measured by rate zonal ultracentrifugation. The preparation of VLDL, IDL, LDL, HDL2, and HDL3 is performed by sequential ultracentrifugation. The activity of LPL is measured radioenzymatically in a glycerol-based triolein emulsion. It can be demonstrated in vitro that VLDL, IDL, and HDL2 from normal plasma are able to increase LPL-activity in contrast to VLDL, IDL, and HDL2 from hyperlipemic plasma. This difference seems to be caused by an altered composition of apolipoproteins in hyperlipemic lipoproteins. An artificial acidosis in three healthy subjects shows in contrast to alkalotic and neutral blood-pH a significant decrease of LPL-activity. This result seems to be of some interest, since diseases associated with acidotic blood-pH, such as chronic renal disease, diabetes mellitus or chronic alcoholism, show secondary hyperlipemias caused by a deficit of LPL-activity. It can be shown in 15 male patients who produce a secondary type-V hyperlipemia during severe abuse of alcohol, that LPL-activity is decreased significantly as compared to 15 healthy controls. During sober phases, this alcohol-induced hyperlipemia and the impairment of LPL-activity disappears completely. In an other group of 8 male patients, who are not producing severe secondary hyperlipemia during approximately the identical alcohol intake, LPL-activity is also significantly decreased, but the activity of hepatic lipase is significantly increased. This increase of the activity of hepatic lipase seems to protect these patients from the development of secondary type-V hyperlipemia. In 89 male patients with angiographically assessed CAD a very strong inverse association between the activity of LPL and the extent of CAD is found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathologic decrease in lipoprotein lipase activity in relation to the development of hyperlipemias and their significance for coronary heart disease]. 345 43

The diagnosis of analgesic-associated nephropathy (AAN) may be missed because of the patients denial or regular analgesic intake. We therefore performed a cross-sectional study of the 144 patients of our hemodialysis center to investigate differences between the 48 patients with AAN (33%) and patients with other kidney diseases who served as controls. The aim was to find other attributes of analgesic users relating to social history, habits and morbidity. Dialysis patients with AAN were significantly older (60 +/- 10 versus 52 +/- 15 years) and more frequently women (65% versus 37%) compared with controls; they often had a family history of analgesic abuse. Comparison with an age-matched control group of hemodialysis patients with other kidney diseases showed that AAN patients smoked, used hypnotics and laxatives, and required prescriptions significantly more frequently; they were less frequently willing to undergo renal transplantation. With regard to accompanying diseases, they suffered significantly more often than the age-matched controls from anemia, renal osteodystrophy, peptic ulcer disease, diverticulosis, hemorrhoids, atrial fibrillation, coronary heart disease, hyperlipidemia, carpal tunnel syndrome, and urinary tract infections. The characteristic pattern of habits, social history and accompanying diseases may facilitate the diagnosis of AAN even in cases where analgesic consumption is denied.
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PMID:[Characteristics of terminal analgesics-induced nephropathy]. 387 49

In 48 patients with early stage renal disease and mild to moderate hypertension, control of high blood pressure and metabolic alterations during long-term diuretic treatment (mean duration, 71 months) were assessed. Compared to the untreated state, administration of thiazide-potassium sparing diuretics, a single table per day, supplemented by dietary sodium restriction, led to normalization of high blood pressure. Renal function was preserved. Gross abnormalities in electrolyte metabolism did not occur. Deterioration of glucose tolerance was noted in 3 patients. Preexisting hyperlipidemia was aggravated by the diuretics in men and postmenopausal women, but premenopausal women were protected. Long-term diuretic treatment was well tolerated, and caused remarkably few significant untoward reactions. The unfavorable metabolic response to diuretic treatment may, however, cancel part of the potential benefit of blood pressure control in certain patients. During long-term diuretic treatment of renal patients, attention should be given to monitoring of metabolic parameters and the introduction of specific dietary treatment may become the cornerstone of patient management.
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PMID:Clinical efficacy and safety of long-term diuretic treatment in renal parenchymal hypertension. 407 9

A qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome is presented. The following lipids were identified in the urine of patients with the nephrotic syndrome: free cholesterol, cholesterol esters, triglycerides, free fatty acids, and phospholipids. Glass paper chromatography identified the cholesterol esters as palmitate, oleate, linoleate, and arachidonate, and identified the phospholipids as phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine. Urinary lipid excretion was much greater in patients with the nephrotic syndrome than in patients with chronic renal disease and minimal proteinuria, or in patients with hyperlipidemia from other causes. Urinary lipid excretion varied widely among the 13 patients with the nephrotic syndrome studied, and no quantitative correlation with serum lipid levels was observed. However, qualitatively at least, the proportion of cholesterol esters excreted in the urine was similar to the proportion of these esters in plasma. A good correlation was found between lipid excretion and glomerular permeability. Furthermore, during steroid therapy urinary lipid excretion decreased concomitant with a decrease in proteinuria. All these observations support the idea that lipiduria in the nephrotic syndrome is related to protein loss and that most of the lipid in the urine enters the glomerular filtrate in the form of lipoproteins.
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PMID:Qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome. 603 40

To elucidate the pathogenesis of hyperlipidemia in chronic renal disease in children and adolescents, we have measured serum triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C) and activities of postheparin plasma lipoprotein lipase and hepatic triglyceride lipase (EC 3.1.1.3) in nine patients with transplants, and nine hemodialyzed and 18 conservatively treated patients with chronic renal failure. In 29 of 36 patients, serum insulin levels both in fasting and in response to oral glucose load were measured. The lipase activities were measured separately, utilizing antiserum against hepatic triglyceride lipase. All groups of patients had hypertriglyceridemia. The patients with endogenous creatinine clearance less than 20 ml/min/m2 had a low HDL-C level. The HDL-C level was correlated inversely with serum triglyceride level and positively with glomerular filtration rate. The lipoprotein lipase activities were low in patients with endogenous creatinine clearance less than 20 ml/min/m2. Although hepatic triglyceride lipase activities were not significantly low in any groups of patients, they were correlated with glomerular filtration rates in the conservatively treated patients with chronic renal failure. A defective triglyceride removal due to low lipase activities may contribute to uremic hypertriglyceridemia in these patients. On the other hand, patients with transplants had almost normal lipase activities and exhibited hyperinsulinemia; overproduction of triglyceride due to hyperinsulinemia may contribute to their hypertriglyceridemia.
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PMID:Lipid profiles and lipase activities in children and adolescents with chronic renal failure treated conservatively or with hemodialysis or transplantation. 638 39

Usually, ketoacidosis presents few if any diagnostic or therapeutic problems; in this article, we report a case where ketoacidosis was clinically occult and biochemically obscure. The patient presented with acute pancreatitis associated with a modest antecedent alcohol intake. Metabolic acidosis with a normal anion gap (10 meq/L) was observed together with moderate hyperglycemia and a 2 + (but not 4 +) test for serum ketones. None of the usual causes of metabolic acidosis with a normal anion gap was identified nor was there an obvious explanation for a reduction in unmeasured anion gap (e.g., hypoalbuminemia, dysproteinemia, or the presence of abnormal halides). Despite the initial normal anion gap, ketoacidosis was suspected clinically and this was confirmed by the elevated serum B-hydroxybutyrate of 8 mmol/L. We deduced that the serum unmeasured anions, which should have been increased by at least 8 meq/L, were being underestimated because of the effect of hypertriglyceridemia on the serum chloride determination. When the serum chloride was reestimated by a method not influenced by hyperlipidemia, the value was 102 mmol/L not 112 mmol/L and, when reevaluated, the anion gap was indeed appropriately elevated. In addition, the urine anion gap (Na + K - Cl) was 103 meq/L in the absence of renal disease. This indicated that the expected large quantity of urinary ammonium must have been masked by an even greater quantity of unmeasured anion; in this case proven by direct measurement to be B-hydroxybutyrate. Finally, metabolism of the alcohol ingested, which yields hepatic NADH, could explain, in part, the modest hyperglycemia and the absence of a 4 + test for serum ketones.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The urine anion gap: the critical clue to resolve a diagnostic dilemma in a patient with ketoacidosis. 643 76

Oral contrceptives (OCs), usd by over 30% of reproductive aged women in Belgium, are by far the most widely used contraceptive in that country. The various types of OCs include monophasic, biphasic, and triphasic combinations of an estrogen and a progestin, sequentials containing estrogen only for 7-14 days followed by a progestin through the 21st day; macrodose or microdose progestin only formulations, 3-month injectable progestins, and the morning after pill. Side effects of OCs are mainly due to metabolic effects on coagulation factors, the renin-angiotensin system, glucose tolerance, or the lipid profile. Users of OCs face increased risks of cholelithiases, thrombophlebitis, thromboembolism, cerebrovascular accidents, myocardial infarcts (among smokers over 35 years of age), and hepatic adenomas. The most troubling secondary effect is the excess cardiovascular morbidity and mortality show by contraceptive users, not just those who are obese, hypertensive, or who have histories of vascular pathology, but also those over 40 years of age and smokers. Lenght of use of OCs does not increase vascular risks. Epidemiologic studies demonstrate that vascular risks are reduced in lower dose formulations. Absolute contraindications to OC use include serious cardiovascular problems, severe hepatic pathology, estrogen-dependent tumors, pregnancy and undiagnosed gynecologic problems, and significant hyperlipidemia. Relative contraindications include severe headaches, cholelithiase, previous cholestasis of pregnancy, severe renal disease, fibromyomas, benign breast disease, age over 40 years, smoking, surgery anticipated within 4 weeks, infectious mononucleosis, falciform anemia, and immediate postpartum and lactation. Epilepsy, diabetes, depression, and varicose veins are not strictly speaking contraindications but require additonal surveillance. Lower dose formulations should be prescribed if possible. OC users should be followed up every 6-12 months. Among other steroidal contraceptive methods, sequential OCs and high dose progestin-only formulations are used for short-term treatment of specific conditions. Progestin-only minipills are used when an OC is desired but estrogens are contraindicated. Injectable progestins should be reserved for patients who for cultural or medical reasons can use no other type of contraceptive. Morning-after pills should not be considered a regular form of contraception. If OCs are used in adolescents, a low dose pill is indicated. Low dose OCs may be indicated for diabetics because of the danger of infection with IUDs and the lesser efficacy of barrier methods. If OCs are used in epileptics, they should be regular dosed because of the danger of drug interactions. Only low-dose formulations and progestin-only minipills should be used by women over 40.
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PMID:[The choice of oral contraception in 1984: general indications and specific cases]. 672 93

Hyperlipidemia is common in patients with renal disease. This fact may be of great clinical relevance in view of the overwhelming evidence associating disturbed lipid metabolism and atherogenesis. Thus, hyperlipidemia may predispose to vascular disease in patients with chronic renal disorders and premature atherosclerosis could be an important risk in renal disease and a major factor limiting survival of patients on long-term maintenance hemodialysis. The aim of the present review is to present a brief but clinically relevant description of lipoprotein physiology and then to survey the now considerable literature concerned with lipoprotein and thus lipid abnormalities in patients with renal disease. A particular emphasis is placed on the role of the plasma lipoproteins in forming an integrated and controlled pathway for lipid metabolism, and how altered regulatory control within the pathway may be associated with pathogenic mechanisms. Finally, the evidence for accelerated development of vascular disease associated with these lipid abnormalities is briefly considered.
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PMID:Plasma lipid alterations in patients with chronic renal disease. 674 32

Cardiotoxicity of doxorubicin, 2 mg/kg i.p. twice weekly in rats, was assessed by serial electrocardiography and electron microscopy. The toxic effects were markedly inhibited by ICRF-159, 50 mg/kg p.o. given 1 h before doxorubicin. The development of nephropathy characterized by proteinuria, hyperlipidemia and glomerular and tubular changes was significantly retarded, and the degenerative changes of peripheral nerves were markedly reduced. On the other hand, ICRF-159 enhanced the depressant effects of doxorubicin on bone marrow function. Doxorubicin reduced body weight gain, caused ascites, decrease in heart and thymus weight, and increase in liver and kidney weight. These changes were also inhibited or attenuated by ICRF-159 pretreatment.
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PMID:Inhibition of cardiotoxic, nephrotoxic and neurotoxic effects of doxorubicin by ICRF-159. 684 96


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