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)

Patients with renal functional impairment are prone to develop hypertension and hyperlipidemia, and both abnormalities tend to occur already at an early stage of kidney disease. In 18 patients with mild renal disease (glomerular filtration rate 65 +/- 5 ml/min) and hypertension (mean blood pressure 126 +/- 4 mm Hg), the effect of six weeks of treatment with the loop-diuretic muzolimine on serum lipoproteins was assessed. Compared to placebo values, the diuretic significantly increased serum low-density lipoprotein cholesterol (LDL-C) and apoprotein B (+ 18 and 11%, respectively, P less than 0.005) in 13 men or postmenopausal women, but not in 5 premenopausal women. Serum high-density lipoprotein cholesterol (HDL-C), and total triglycerides or lipoprotein triglyceride fractions were not consistently changed in both subgroups. Thus, the ratio LDL-C/HDL-C was increased from 3.2 +/- 0.3 to 3.9 +/- 0.3 (P less than 0.05) in the men or postmenopausal women, while no such tendency occurred in the premenopausal women (4.1 +/- 0.6 to 3.7 +/- 0.6). Changes in serum LDL-C were not associated with hemoconcentration or alterations in carbohydrate metabolism and were not related to variations in serum potassium or blood pressure. Increased serum levels of the atherogenic LDL-C fraction during diuretic treatment in men or postmenopausal women with renal disease may represent a potentially undesirable effect, particularly since such patients may tend to have hyperlipidemia in the untreated state.
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PMID:Serum lipoproteins in patients with mild renal disease treated with the diuretic muzolimine. 715 18

Patients with analgesic nephropathy are reported to have a higher risk of atherosclerosis. One possible reason for this is a high incidence of hyperlipaemia in patients with analgesic nephropathy. In a retrospective study, serum cholesterol and serum triglyceride concentrations of patients with analgesic nephropathy and moderately restricted renal function were significantly higher compared to a control group with other renal diseases of similar age and degree of renal insufficiency. Hyperlipaemia in analgesic nephropathy is not explained by end-stage renal failure on one side or protein loss as in nephrotic syndrome on the other side. Some possible mechanisms for hyperlipaemia in analgesic nephropathy are discussed.
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PMID:Hypercholesterolaemia and hypertriglyceridaemia in patients with analgesic nephropathy. 741 66

It has been suggested that hyperlipidemia may contribute to the progression of renal disease via the deleterious effects of oxidized low-density lipoprotein (LDL) on the glomerular mesangium. Because estrogens possess potent antioxidant activity, we sought to determine whether sex hormones influence the oxidation of LDL by mesangial cells. Rat mesangial cells were incubated with LDL (200 micrograms/ml), and the extent of lipid oxidation was assessed by the generation of thiobarbituric acid reactive substances (TBARS), by increased electrophoretic mobility, and by enhanced uptake of mesangial cell-modified LDL by macrophages. A progressive rise in TBARS and an increase in electrophoretic mobility was observed on incubation of LDL with mesangial cells. Coincubation with estradiol (10 mumol/L) reduced TBARS generation by 46% at 36 hours (p < 0.01) and reversed the increase in relative electrophoretic mobility (1.25 +/- 0.07 vs 1.01 +/- 0.03, p < 0.05). LDL that had been oxidized by mesangial cells in the presence of estradiol (10 mumol/L) showed reduced uptake by macrophages when compared with LDL that had been oxidized by mesangial cells in the absence of estradiol (14 +/- 2 pmol/10(6) cells per hour vs 22 +/- 3 pmol/10(6) cells per hour, p < 0.05). In contrast, neither testosterone nor estrone had any effect on these parameters. We conclude that estradiol, by virtue of its antioxidant properties, inhibits mesangial cell-mediated oxidation of LDL and reduces the uptake of mesangial cell-modified LDL by macrophages.
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PMID:Estradiol inhibits mesangial cell-mediated oxidation of low-density lipoprotein. 756 48

We studied the effects of 6-week treatment with nifedipine (35 mg/kg/day orally, p.o.) on streptozotocin (STZ)-induced diabetic rats. Injection of STZ [45 mg/kg intravenously, (i.v.) single dose] produced a significant increase in blood pressure (BP), bradycardia, hyperglycemia, hypoinsulinemia, hyperlipidemia, hypothyroidism, depression in left ventricular developed pressure (LVDP), cardiomyopathy, and nephropathy. Treatment of diabetic rats with nifedipine normalized the BP and prevented bradycardia. Insulin levels were decreased after nifedipine treatment in diabetic as well as nondiabetic rats. However, serum glucose levels were also partially decreased in diabetic animals by nifedipine treatment. In control animals as well, glucose levels were in the normal range despite lower insulin levels observed after nifedipine treatment. Nifedipine treatment significantly prevented STZ-induced increase in cholesterol and triglyceride levels. Nifedipine treatment significantly prevented STZ-induced hypothyroidism and also prevented STZ-induced cardiac depression and cardiomyopathy. Our data indicate that nifedipine increases insulin sensitivity and has some beneficial effects on cardiovascular parameters. It may therefore be considered a preferred drug in the treatment of hypertension associated with diabetes mellitus.
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PMID:Effects of chronic nifedipine treatment on streptozotocin-induced diabetic rats. 756 66

This review describes categories of renal function (normal, renal insufficiency, end-stage renal failure), types of treatment modalities (renal insufficiency management, dialysis, transplantation), and corresponding dietary parameters (protein, energy, fiber, sodium, fluid, potassium, phosphorus, calcium, vitamins, minerals). The focus is directed toward general and nonrenal specialty practitioners, who are encountering a growing number of geriatric patients and patients who have undergone renal transplantation or are in early renal failure. The findings indicate that early intervention may delay or prevent rapid progression of renal disease in some patients, that treatment modalities continue to need individualized dietary support to maintain nutritional status, and that transplant goals should include control of obesity and hyperlipidemia to reduce cardiovascular mortality.
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PMID:Which diet for which renal failure: making sense of the options. 861 54

We have investigated the activity and kinetics of sodium-lithium countertransport (SLC) in patients with IgA nephropathy and their relationship to plasma lipids. Standard SLC activity, the Michaelis constant (Km) and maximum velocity (Vmax) were measured in patients who had IgA nephropathy with either normal serum creatinine (IgA-NRF), or raised serum creatinine (IgA-IRF), and normal subjects (NC). The standard SLC activity was raised in hypertensive patients with IgA-NRF due to a raised Vmax in association with hyperlipidaemia. The Km was significantly lower and Vmax also tended to be lower in IgA-IRF. Km and Vmax were not different in IgA-NRF compared with the NC. There was no difference in the mean standard SLC activity between all three groups. The low Km and low Vmax resulted in a normal standard SLC activity being observed in IgA-IRF which is similar to the situation we have observed in a proportion of diabetic patients with nephropathy. The low Km in patients with IgA nephropathy may be due to inheritance associated with familial essential hypertension or to an acquired change of the kinetics related to a change in the environment of the plasma membrane during the development of renal impairment.
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PMID:Sodium-lithium countertransport kinetics in IgA nephropathy: relation to plasma lipids and renal impairment. 777 2

A number of fine bands which occur in positions between the beta- and pre-beta-lipoproteins in polyacrylamide gell electrophresis are called mid-bands (MB). In this study, the relationship between the occurrence of these MB and metabolic abnormalities or vascular complications was evaluated in 181 patients with non-insulin-dependent diabetes mellitus (NIDDM). The incidence of MB in diabetic patients was significantly higher than that in 149 healthy control subjects (35 vs. 20%, p < 0.01). Analysis according to the type of MB revealed that the incidence of the central type in diabetic patients was significantly higher than that in healthy control subject (11 vs. 5%, p < 0.05). When the values of HbAlc were elevated, the incidence of MB and its central type slightly increased. The occurrence of the lower type of MB showed no relationship with the levels of HbAlc. The incidence of MB and its central type were significantly higher in patients with type IIb hyperlipidemia (86 and 41%, respectively) and with type IV hyperlipidemia (63 and 25%) than in those with normolipidemia (21 and 5%) (p < 0.01 of all). The incidence of the lower type of MB was significantly higher in patients with type IIa hyperlipidemia (25%) and with type IIb hyperlipidemia (36%) than in those with normolipidemia (11%) (p < 0.05, p < 0.01, respectively). There was no significant difference in the occurrences of MB and of the central and lower types of MB between the normolipidemic patients and healthy control subjects. The incidence of MB and its central type were significantly higher in patients with nephropathy (54 and 23%, respectively) than in those without nephropathy (32 and 9%) (p < 0.05 of all). There was no significant difference in the incidence of lower type of MB between patients with and without nephropathy. These results indicate that the incidence of central type of MB may be high in NIDDM, and that the occurrence of central type may be associated with abnormal metabolism of glucose or lipid and with diabetic nephropathy.
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PMID:Three types of "mid-band" lipoproteins in non-insulin-dependent diabetes mellitus: relation to metabolic abnormalities and vascular complications. 781 88

In addition to factors such as protein intake or hyperlipidemia, hypertension contributes to the progressive deterioration of renal function in experimental animal models of renal disease, and has a prominent role in the imbalance of intrarenal hemodynamics. Reduction of arterial pressure was shown to alter the course of human chronic renal disease. In patients with diabetic as well as nondiabetic nephropathy, the lowering of proteinuria by angiotensin-converting enzyme inhibitors is greater than that observed with other antihypertensive drugs and appears to be independent of blood pressure control alone, whereas albuminuria may be unaffected or worsened during nifedipine treatment. Angiotensin-converting enzyme inhibitors may afford better protection than conventional treatment at various stages of diabetic nephropathy and prevent the evolution from incipient to overt nephropathy. In patients with nondiabetic renal disease, no unequivocal evidence exists for such a protective effect. In renal transplant recipients receiving cyclosporine, converting enzyme inhibitors and calcium antagonists are equally effective in the control of hypertension and both leave unaltered the glomerular filtration rate. It remains to be demonstrated, using adequate study designs, whether a particular class of agent is superior to another in patients with chronic renal disease.
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PMID:Angiotensin-converting enzyme inhibitors versus calcium antagonists in the progression of renal diseases. 781 39

Patients with diabetes mellitus are more frequently hypertensive than age-matched non-diabetic subjects. They are confronted with a markedly increased risk of coronary vascular disease, of progressive nephropathy and renal end-stage diseases. The most common type of hypertension in type I and type II diabetics is essential hypertension, probably as a consequence of insulin resistance and hyperinsulinemia. Hyperglycemia and hypertension are both significantly involved in the progression of diabetic nephropathy. Hence, the modern therapeutic concept consists of optimal blood glucose control and strict blood pressure control. Progression of the nephropathy may be halted in most of the cases by adhering to set limits in mean arterial blood pressure, glycated hemoglobin and urinary albumin excretion rate. Furthermore, a significant decrease in cardiovascular mortality may be achieved. In case the blood pressure targets cannot be met by non-drug therapies and life-style modifications, antihypertensive drug therapy has to be initiated. The selection of antihypertensives should be based on the concomitant diabetes mellitus with its additional cardiovascular risk factors hyperlipidemia and hyperinsulinemia. In general, preference should be given to so-called metabolic neutral substances such as ACE inhibitors or calcium antagonists or to alpha-blockers which may have positive metabolic effects. Meanwhile, data from several prospective studies claim that ACE inhibitors and calcium antagonists exert nephroprotective effects beyond their beneficial blood pressure lowering effects, thereby preventing the progression of diabetic nephropathy. However, these drugs should not be uncritically used and we should be aware of their potential adverse effects. The differential therapy of hypertension in diabetes mellitus requires mature consideration before initiation of therapy, an individualized concept of therapy, and careful monitoring during treatment.
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PMID:[Hypertension, microalbuminuria and insulin resistance in diabetes mellitus]. 784 97

The discovery and production of HMGCoA reductase inhibitor and the fundamental research work of the LDL receptor unraveled a receptor-mediated cholesterol homeostasis. HMGCoA reductase inhibitors are the most commonly prescribed class of lipid-lowering drugs in many countries. The decrease of the intracellular cholesterol caused by the inhibitor induces the compensatory increase of LDL receptor protein at liver plasma membrane. The increased receptor promotes LDL catabolism and results in decrease of plasma LDL. Serious side effects involving the liver or muscle are rare. But the risk of myopathy is increased when the drug is used with other hypolipidemic agents. A principle of the treatment of hyperlipidemia, including secondary one associated with diabetes mellitus and renal disease, by HMGCoA reductase is discussed in this review.
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PMID:[HMG-CoA reductase inhibitor for therapy of patients with hyperlipoproteinemia ]. 785 22


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