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

Alterations in lipid metabolism occur in patients with chronic renal disease and in patients with the nephrotic syndrome and may have a role in the progression of renal disease in such patients. Evidence accumulated over the last few years indicates that increased ingestion of cholesterol accelerates the development of glomerulosclerosis in guinea pigs, rats and rabbits, and in rats with endogenous hyperlipidemia due to the nephrotic syndrome. Lowering the levels of serum lipids ameliorates the progression of renal disease in obese rats, rats with a remnant kidney and rats with the nephrotic syndrome produced by the aminonucleoside of puromycin. Changes in dietary fatty acids also influence the progression of renal disease. Several eicosanoids influence the progression of renal disease in experimental animals. Maneuvers that decrease the production of thromboxane A2 ameliorate renal disease in rats with a remnant kidney and in mice with lupus nephritis. Increasing the production of vasodilatory prostaglandins (PGE2, prostacyclin) seems to have a beneficial role in the progression of renal disease. The mechanisms by which dietary lipids and/or renal eicosanoids affect the progression of renal disease remain to be defined.
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PMID:Role of dietary lipids and renal eicosanoids on the progression of renal disease. 269 98

The available data indicate that in chronic renal failure (CRF) loss of renal function usually progresses at a constant rate toward end-stage renal disease. Although immunological events might be responsible for initiating most glomerular diseases, certain clinical and experimental observations suggest that the rate of progression of these diseases is influenced by several non immunological factors. These factors include systemic hypertension, proteinuria, hyperlipidemia, high protein intake, and probably conditions leading to glomerular hypertrophy. Interventions designed to minimize the potential contribution of these factors to the progression of renal insufficiency may halt or slow the loss of function at early and late stages of CRF.
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PMID:[Mechanisms of progression of glomerular sclerosis in chronic renal diseases in man]. 270 30

Hyperlipidemia may contribute to the pathogenesis of glomerular sclerosis. We therefore studied binding and uptake of low density lipoprotein (LDL) by cultured rat mesangial cells. In addition effects of LDL on PGE2 synthesis and cell proliferation were determined. At 4 degrees C mesangial cells bound [125I] LDL in a time- and concentration-dependent manner with half-maximal binding observed at 5 micrograms/ml of LDL protein. Binding was blocked by excess unlabeled LDL and by heparin. Uptake (binding plus internalization) of LDL at 37 degrees C markedly exceeded binding at 4 degrees C, continued to increase even with longer periods of incubation, and showed no saturability, consistent with uptake of LDL by mesangial cells. Further evidence for LDL uptake by mesangial cells was obtained by use of the fluorescent probe 1,1'-dioactadecyl-3,3,3', 3'-tetramethylindocarbocyanine perchlorate-labeled LDL (Dil-LDL). Incubation of mesangial cells with Dil-LDL at 37 degrees C showed positive fluorescence for all mesangial cells, indicating uptake of the Dil-LDL. LDL had a biphasic effect on mesangial cell proliferation as determined by [3H] thymidine incorporation. LDL at 10 micrograms/ml enhanced [3H] thymidine uptake modestly, but significantly, whereas a progressive and marked inhibition occurred at LDL concentration from 100 to 500 micrograms/ml. While LDL at 10 and 100 micrograms/ml significantly stimulated PGE2 production, inhibition of PGE2 by meclofenamate did not influence the effects of LDL on [3H] thymidine incorporation. We conclude that mesangial cells show specific binding and uptake of LDL and that high concentrations of LDL markedly decrease mesangial cell proliferation. These findings may pertain to the pathogenesis of glomerular lesions in hyperlipidemia of renal disease.
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PMID:Interactions of low density lipoprotein with rat mesangial cells. 277 Jan 1

Doxycycline and minocycline are second-generation tetracyclines. They are readily absorbed, distributed throughout the organism as a function of their lipophilicity and eliminated in both the urine and the faeces. The influence of age, renal disease, malnutrition and hyperlipidaemia is reviewed, together with the main pharmacokinetic interactions.
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PMID:Clinical pharmacokinetics of doxycycline and minocycline. 307 40

The awareness of hypertension as one of the major risk factors for mortality and morbidity in NIDDM has increased greatly in the past few years. It is now accepted practice to measure BP at least yearly in all such patients. Unfortunately, one cannot yet be sure to what extent diabetics benefit from anti-hypertensive therapy, and the simple assumption that treatment of the increased risk reduces that risk must be constantly questioned. No specific data are yet available for NIDDM, though it would be remarkable if the benefits of decreased cerebrovascular mortality and probable reduced total mortality (Sleight, 1987) did not apply to the higher-risk diabetic subject, at least at the higher levels of diastolic pressure (greater than 105 mm Hg). There is, though, no evidence that mortality or morbidity of coronary artery disease, the major killer in NIDDM, is reduced even in non-diabetics and the present author does not consider there to be any evidence suggesting that thresholds for treatment of hypertension in uncomplicated patients with NIDDM should be lower than those for non-diabetics, unless progressive nephropathy is present. Current advice in the non-diabetic is that levels of blood pressure in adults consistently above 95 mm Hg warrant therapy, aiming to reduce it below 90 mm Hg (World Health Organization, 1986). While the importance of hypertension should not be underestimated, it should not deflect attention from the other risk factors. Cessation of smoking, and by implication its reduction, will, for all smoking patients but the most hypertensive, produce a greater reduction in cardiovascular and total mortality risk than will anti-hypertensive therapy. There are also early signs that effective dietary and/or drug treatment of significant hyperlipidaemia lowers cardiovascular mortality. Choice of anti-hypertensive therapy is especially important, not only for efficacy but also for quality of life, in patients who already suffer major restrictions on diet, freedom and life expectancy. While controlled trials in the subject are of immense importance in determining optimum therapy, there is currently no evidence to favour any particular group of drugs, and an individual patient's therapy should be decided on the basis of their own circumstances.
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PMID:Hypertension. 307 98

Genetic markers would be useful to study the transmission of type 2 diabetes and to identify patients with enhanced risk of development of late diabetic complications. The aim of this study was to evaluate the influence of selected possible genetic markers on the development of diabetic complications. One hundred and eighty patients with type 2 diabetes (79 males, 101 females) were therefore studied with respect to ABO and Rh blood grouping and chlorpropamide alcohol flush (CPAF) and acetylator phenotype status, in addition to life style (smoking, dietary, alcohol and drug taking habits) and metabolic indexes (HbA1, M-value, serum cholesterol, serum triglycerides), with regard to late complications coronary heart disease (CHD), arterial hypertension (AH), peripheral vascular disorders (PVD), retinopathy and nephropathy. None of the genetic markers considered appeared to be associated with diabetic complications. Multiple logistic analysis identified different risk-factors for each complication: AH and age for CHD; hyperlipidaemia for AH; age of patients for PVD; duration of diabetes for retinopathy; AH for nephropathy. It is concluded that the possible genetic markers evaluated in this study do not identify a higher or lower risk for late complications. On the contrary, most of the risk factors identified support previous studies. Active correction of these risk-factors might improve the overall prognosis of patients with type 2 diabetes.
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PMID:Risk factors for micro- and macroangiopathic complications in type 2 diabetes: lack of association with acetylator phenotype, chlorpropamide alcohol flush and ABO and Rh blood groups. 311 87

We started a special follow-up system for women who had a history of severe toxemic pregnancy in our department since 1975. All medical records from 1956 to 1975 were reviewed and 468 deliveries with such disease were registered at that time. One hundred and ninety five deliveries (186 women) also were added from the prospective point of view until 1985. Among 654 patients, 374 women were available to address. I. The latter 186 women were divided into 7 groups: A1, A2, A3, A4, B1; and B2. The definitions of each group were as follows. A1: primipara with severe toxemia; A2: multipara that had a severe toxemia at the first time and then normal pregnancy (ies); A3: multipara that had a severe toxemia in the first pregnancy and then mild one(s); A4: multipara that repeated severe diseases; A5: multipara that had a severe toxemia and then unclassified type(s) of the disease; B1: multipara that had a normal pregnancy at the first time and then severe toxemia(s); B2: multipara that had a mild toxemia in the first pregnancy and then severe one(s). The percent of each group was 25, 24, 13, 15, 4, 6, and 12% respectively. Those women who had severe toxemia(s) were found to have hypertension, high levels of blood urea nitrogen, hyperhematocritemia, and hyperlipemia from the results of clinical and laboratory data. Consequently, they are a high risk group of atherosclerosis, because hypertension and hyperlipemia are main risk factors of that disease. II. Eighty percent of 374 women who had a history of severe toxemia from 1956 to 1985 was able to be followed up by us until 1987. Those women also were divided into the same groups as described above except A5, and checked up as to hypertension, hyperlipemia, body weight, and so on. The characteristic features were that the group A2 is in a well condition, and that many of group A4 are suffering from various diseases with regard to the remote prognosis. In conclusions, it was suggested that there may be four etiologic causes as to toxemia of pregnancy. The first is a disadaptation during pregnancy, and this seems to consist mainly of pregnancy induced hypertension. The second has various underlying diseases, such as chronic hypertension or renal disease, etc.. The third has a hypertensive trait which is manifested as the pregnancy advances. The fourth is considered to be related to biologic ageing.
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PMID:[Follow-up study on women suffered from severe toxemia of pregnancy]. 325 67

Focal glomerulosclerosis (FGS) is commonly seen in human and in experimental models of chronic renal disease. Although considerable experimental data suggest that hypertension is important in progressive nephron damage, recent studies also have indicated that abnormal lipid metabolism may be an independent risk factor in the pathogenesis of FGS. Indeed, the synergistic impact of hypertension and hyperlipidemia in the pathogenesis of FGS may be analogous to the role of these factors in the pathogenesis of atherosclerosis. This review focuses on some of the recent and pertinent data that support a role of lipid-mediated glomerular injury in the pathogenesis of progressive renal disease.
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PMID:Hyperlipidemia and the progression of renal disease. 327 33

The diversity of its causes, the unpredictability of its clinical course, and our expanding knowledge of the conditions that may exacerbate or retard its progression suggest that glomerular sclerosis cannot be attributed to a single aberration in glomerular physiology. Nonetheless, the welter of clinical and experimental observations is beginning to yield a pattern. Agents or conditions injurious to glomerular epithelium tend to cause glomerular sclerosis. Agents or conditions that induce short-term or long-term activation of mesangial cells may lead to glomerular sclerosis. Indeed, one contribution of the healthy epithelium may be to serve as a tonic inhibitor of the intraglomerular processes arising from mesangial-cell activation. Long-term activation of the mesangium is associated with the proliferation and infiltration of cells and with the expansion of the mesangial matrix--the antecedents of sclerosis. We anticipate that different diseases associated with glomerular sclerosis will be found to depend to varying extents on these two potential mechanisms of sclerosis. Beyond a certain threshold of glomerular injury, glomerular diseases share an additional factor: the capacity of both intrinsic cells and infiltrating cells to alter the microenvironment of the glomerulus so that sclerosis progresses inexorably long after the disappearance of the initiating insult. Several potential risk factors may contribute to the progression of chronic renal disease. These factors include systemic hypertension, proteinuria, hyperlipidemia, high protein intake, and probably conditions that lead to glomerular hypertrophy. Interventions designed to minimize the potential contribution of these factors to the progression of renal insufficiency may halt or slow the loss of function of the kidney. Clinical trials designed to examine the effects of these factors on the progressive course of renal insufficiency will help to establish their role and relative importance in humans.
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PMID:The progression of renal disease. 328 63

The National High Blood Pressure Education Program has released three Joint National Committee reports and a task force report on the detection, evaluation, and treatment of high blood pressure. Like its predecessors, the 1988 Joint National Committee report was developed using the consensus process; it is based on the latest scientific research and reflects the state of the art regarding hypertension management. This report updates findings of previous reports in several respects: it broadens the step-care approach to provide more flexibility for clinicians; encourages greater patient involvement in the treatment program; emphasizes a consideration of the quality of life in the management of patients; and addresses the cost of care. It also provides more emphasis on control of other risk factors for cardiovascular disease; includes a discussion of the new cholesterol guidelines; recommends a reduction in alcohol consumption; and discusses the use of calcium and fish oil supplementation. This document expands earlier reports on special populations, including blacks and other racial and ethnic minority groups, young and elderly patients, pregnant patients, surgical candidates, and hypertensive patients with cerebrovascular disease, coronary artery disease, left ventricular hypertrophy, congestive heart failure, peripheral vascular disease, renal disease, chronic obstructive pulmonary disease or bronchial asthma, gout, diabetes mellitus, and hyperlipidemia. The report also updates previous drug tables to include new drugs, revised recommended doses of some drugs, and drug interactions. Consideration of step-down therapy after blood pressure has been controlled is suggested. This report is intended as a guide for practicing physicians and other health professionals in their care of hypertensive patients and as a reference for those participating in the many community high blood pressure control programs throughout the country.
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PMID:The 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. 256


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