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)

Plasma triglycerides are increased in the majority of patients with advanced renal failure but cholesterol is not. HDL cholesterol is reduced while LDL IDL and VLDL cholesterol is increased. Lecithin:cholesterol acyltransferase (LCAT), an enzyme necessary for HDL maturation, is reduced in chronic renal failure (CRF). As a consequence, while all subtypes of HDL are reduced, the small HDL3 subtype is relatively enriched at the expense of the larger, more functional HDL2 subtype. Triglycerides are increased in all lipoprotein fractions. HDL-associated apolipoproteins, apo A-I and A-II are decreased, while apo B is increased. Lipoprotein catabolic rate is reduced, but the cause of hyperlipidemia is multifactorial; reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance. Hyperlipidemia is not corrected by dialysis. Lipid levels are somewhat higher in CAPD patients, possibly as a consequence of increased glucose absorption or as a consequence of transperitoneal HDL losses. Triglycerides decrease and cholesterol increases following transplantation. Oxidized lipids are increased in plasma of patients with CRF. Plasma polyunsaturated fatty acids are decreased and saturated fatty acids increased. The same changes occur in the lipid bilayers composing leukocytes and red blood cell membranes. These changes result in altered membrane fluidity, and are corrected by dialysis. While atherosclerotic disease is a leading cause of death in dialysis patients, it is not certain that the specific lipid disorders of CRF are responsible for this morbidity, nor is it recommended at this time that qualitative abnormalities be treated pharmacologically in the absence of increased lipid levels.
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PMID:Hyperlipidemia of chronic renal failure. 798 78

Several factors promote the progression of renal disease, including glomerular hypertension and hypertrophy, molecular factors such as cytokines and growth hormones, proteinuria, acidosis, and hyperlipidemia. Regardless of the underlying etiology, many patients with chronic renal insufficiency will ultimately require kidney replacement therapy. Your goal is to delay the progression of renal failure, mainly through aggressive control of blood pressure. Other possible interventions include protein restriction, bicarbonate therapy, and lipid-lowering drugs.
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PMID:Chronic renal disease: new therapies to delay kidney replacement. 803 27

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

Low-density lipoprotein apheresis (LDL-A) was performed for nine episodes of steroid-resistant nephrotic syndrome in eight patients. The clinical and immunohistological findings were analysed retrospectively. Six of the patients had focal glomerular sclerosis (FGS), one had minimal-change nephrotic syndrome (MCNS), and one had membranous nephropathy (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.33 +/- 4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5 +/- 5.1 days) and combined with steroid pulse therapy and the administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 patients) more than 50% reduction of proteinuria occurred (less than 3.5 g/day) (response-group). A significant elevation of serum albumin (more than 3.0 g/dl) was obtained in five of these episodes. The other three patients were resistant (resistant-group). The number of and intervals between LDL-A treatments in the response group (5 +/- 2.8 times and 5.8 +/- 4.1 days) were significantly less than those in the resistant-group (12.0 +/- 0.8 times and 13.2 +/- 1.8 days) (P < 0.05). After LDL-A, significant reductions were observed in the serum total cholesterol (T-CHO), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-lipoprotein (beta-lipo) (P < 0.05). HDL-cholesterol (HDL-C) increased somewhat after LDL-A. Further, Ccr was elevated in all nephrotic episodes, except in one patient who manifested renal failure after 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does LDL-apheresis in steroid-resistant nephrotic syndrome affect prognosis? 805 31

Lipid metabolism was studied in 161 patients with renal diseases, 62 of them had nephrotic syndrome (NS). The measurements were made of cholesterol, triglycerides, dienic conjugates, B2-microglobulins in urine and blood, functional and morphological parameters, red cell resistance to peroxide hemolysis. It was found that NS patients, especially those with additional renal failure, displayed high-intensity lipoperoxidation (LPO). LPO intensity proved unrelated to NS etiology. NS-associated hyperlipidemia gives rise to multifunctional biomembrane instability responsible for antioxidant disorders.
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PMID:[Lipid metabolic disorders and lipid peroxidation in patients with the nephrotic syndrome]. 807 11

Hyperlipidaemia is an invariable complication of the nephrotic syndrome. The quantitative and qualitative changes in lipoproteins which occur may accelerate atherosclerosis. The pathogenetic mechanisms of the hyperlipidaemia are complex and poorly understood. Increases in lipoprotein production are compounded by reduced lipolysis of very low density lipoprotein and impaired catabolism of low density lipoprotein. Both proteinuria and hypoalbuminaemia have been implicated in the genesis of these abnormalities. The optimum treatment of the hyperlipidaemia has not been determined. 3-Hydroxy-3-methyl-glutaryl co-enzyme A reductase inhibitors appear to be the most effective lipid-lowering drugs, although their ability to reduce ischaemic events or prevent/delay renal failure remains to be proven.
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PMID:Pathogenesis of lipid abnormalities in patients with nephrotic syndrome/proteinuria: clinical implications. 823 98

A 61-year-old woman with hyperlipidemia was treated with gemfibrozil. She also had insulin-treated diabetes mellitus and chronic renal failure and was admitted because of severe chest pain. The ST segment was depressed and creatine kinase levels were elevated. The original diagnosis was acute myocardial infarction. In the presence of increasing chest pain, the onset of limb muscle tenderness, and increasing levels of creatine kinase, the diagnosis of myopathy secondary to gemfibrozil therapy was made and the drug was discontinued. All symptoms then subsided and creatine kinase levels returned to normal. Myopathy is a well-known complication of blood lipid-lowering drugs, especially in patients with renal failure.
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PMID:[Gemfibrozil-induced myopathy]. 825 19

The hyperlipidemia associated with the nephrotic syndrome is well characterized. There is, however, a paucity of data in humans on the risk factors for atherosclerotic heart disease and the role of hyperlipidemia on the risk of progression of renal disease in this population. In our study, we retrospectively evaluated a large uniform population of patients (mean creatinine, 1.78 mg/dL; mean 24-hour proteinuria, 7.1 g) with idiopathic nephrotic syndrome for the presence of risk factors for coronary artery disease. One hundred patients with either focal segmental glomerulosclerosis (n = 56) or membranous nephropathy (n = 44) were assessed for the following cardiovascular risk factors: male sex or postmenopausal female, hyperlipidemia, hypertension, smoking history, and left ventricular hypertrophy. Sixty-six percent of the patients were either male or postmenopausal females; 35% were smokers. Hypertension and left ventricular hypertrophy were present in 53% and 13% of patients, respectively. Eighty-seven percent, 53%, and 25% of patients had a total cholesterol of more than 200 mg/dL, more than 300 mg/dL, and more than 400 mg/dL, respectively. Low-density lipoprotein cholesterol was greater than 130 mg/dL and greater than 160 mg/dL in 77.2% and 64.9% of patients, respectively. Virtually all patients (99%) had at least one risk factor for cardiovascular disease; over two thirds (68%) had two risk factors and over one quarter (26%) had three risk factors. In comparing the group that progressed to renal failure with the groups that did not, the initial mean serum cholesterol was lower in the group that progressed (292 mg/dL v 388 mg/dL, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The nephrotic syndrome, lipids, and risk factors for cardiovascular disease. 832 76

To clearly determine whether hyperuricemia participates directly in atherosclerotic disease or not, the prognosis and associated factors were studied, based on data from 104 patients whose serum uric acid had been completely maintained at normal levels with prolonged medication. The mean age at death was 65.8 +/- 10.5 years. The causes of death were as follows: cardiovascular disease (26.9%), cerebral disease (26.2%), malignant neoplasms (26.0%), uremia (7.6%), and miscellaneous disease (18.3%). Serum lipids especially triglycerides, body weight and influenced on the prognosis of the patients FBS. Most common complications were in the cardiovascular disease group; hypertension and hyperlipidemia. These data suggested that the apparent increased incidence of cardiovascular disease in gout rather than renal failure bore a relationship to such complications as hypertension or hypertriglycemia. Hyperuricemia alone may not be an atherosclerotic risk factors. There was no correlation between treatment with allopurinol and probenecid and cardiovascular complications.
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PMID:[Hyperuricemia and atherosclerosis]. 841 89

Hyperlipidemia is associated with accelerated glomerular sclerosis in experimental renal insufficiency. To investigate whether the dyslipoproteinemia seen in human renal failure also influences the future course of renal insufficiency, we have correlated plasma levels of lipids and apolipoproteins at start of follow-up with the subsequent change in renal function in 34 adult patients with chronic renal disease. Nineteen patients had primary renal disease, and 15 patients had diabetic nephropathy. Except for antihypertensive therapy no specific treatment to modify the progression of the disease was given during the follow-up. The rate of progression was determined by repeated measurements of the glomerular filtration rate (GFR). The time of follow-up ranged from 12 to 91 months with an average of 39.7 +/- 16.7 months. The mean initial GFR was 34.7 +/- 13.9 ml/min x 1.73 m2 body surface area and the average decline in renal function was -0.27 +/- 0.26 ml/min/month. The entry levels of triglycerides (TG; p = 0.04), very-low-density lipoprotein cholesterol (p = 0.03), apolipoprotein-B (ApoB; p = 0.008) and systolic blood pressure (SBP; p = 0.04) were significantly correlated with the rate of progression. Among lipoprotein variables, ApoB showed the strongest correlation with the decline in GFR. Patients with a progressive course of their disease also tended to have initially higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (NS), whereas the initial plasma concentration of high-density lipoprotein cholesterol did not show an association with the progression of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein-B-containing lipoproteins and the progression of renal insufficiency. 772 19


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