Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrotic syndrome causes hypercholesterolemia. Chronic renal failure results in hypertriglyceridemia, low HDL cholesterol and, more often, apolipoprotein abnormalities. This dyslipidemia is not corrected by hemodialysis. Transplantation corrects it but leads to other kinds of lipid abnormalities. Whether the treatment of these potentially atherogenetic abnormalities is beneficial of not remains unproved. There is some evidence of lipid contribution to the constitution of glomerulosclerosis in animals but it remains hypothetical in man.
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PMID:[Kidneys and lipids]. 160 59

It has been proposed that fish oil dietary supplementation in the chronic rat 5/6 renal ablation model may be either protective or toxic. These conflicting hypotheses were tested in rats who underwent renal ablation or sham surgery. Twenty rats received sham surgery, and 40 received 5/6 renal ablation. All rats were fed a regular laboratory diet up to 1 week postsurgery. At that time, one half of the renal ablation group was provided with an isocaloric diet supplemented with 24% MaxEPA (fish oil), 1% safflower oil, and antioxidants. The renal ablation rats developed hypertension, albuminuria, gammaglobulinuria, and a decline in glomerular filtration rate, which was less in the fish oil group compared with that in the regular laboratory diet group at 10 and 20 wk postsurgery. The fish oil renal ablation rats had significantly less glomerulosclerosis than did the regular laboratory diet renal ablation animals, and no more glomerular fibrin deposition than did the sham controls. The renal ablation regular laboratory diet rats had a significant dyslipidemia at 20 wk which was prevented in the fish oil renal ablation cohort. The fish oil renal ablation rats also demonstrated a significant decline in renal tissue arachidonic acid incorporation and a concomitant increase in eicosapentaenoic acid and docosahexaenoic acid incorporation. The mortality of the renal ablation group was greater than that of the sham controls but not significantly different for the fish oil or the regular laboratory diet groups. These results support the hypothesis that the fish oil diet containing specific antioxidant, vitamin E, and essential fatty acid supplementation is protective in the rat remnant nephron model and prevents the evolution of glomerulosclerosis with associated renal functional impairment, while preserving glomerular filtration.
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PMID:Chronic effects of omega-3 fatty acids (fish oil) in a rat 5/6 renal ablation model. 191 96

Normotensive rats of the Milan strain (MNS) spontaneously develop focal glomerulosclerosis. In order to explore the contribution of glomerular thromboxane (TX) A2 synthesis to the development of the disease, we have characterized the time course of renal functional and biochemical changes, and their modification by long-term treatment with a TX-synthase inhibitor. Oral administration (150 mg.kg-1 from 1 to 14 months of age) of FCE 22178 suppressed enhanced glomerular TXB2 production at all experimental times (mean inhibition 80%) and proteinuria (varying between 27.1 and 73.0%) while preserving renal blood flow and glomerular filtration rate. These effects of TX-synthase inhibition were seen in the absence of any statistically significant changes in systemic blood pressure. Moreover, FCE 22178 had no antihypertensive effects in hypertensive rats of the Milan strain (MHS) nor in spontaneously hypertensive rats (SHR). Treatment also prevented the age-related hypoalbuminemia and hyperlipidemia observed in control MNS and significantly (P less than 0.01) reduced glomerular histologic damage, as demonstrated by light microscopy studies and measurement of sclerotic area. We conclude that: 1) MNS rats provide an animal model of long-lasting proteinuria characterized by an age-related increase in glomerular TXB2 production paralleled by progressive loss of renal structural integrity and function and by a secondary dyslipidemia; 2) pharmacological inhibition of glomerular TX-synthase attenuates the structural as well as the functional expression of kidney disease, without a primary effect on systemic blood pressure. These data are suggestive of an important modulating role of TXA2 in the progression of MNS renal disease.
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PMID:Role of enhanced glomerular synthesis of thromboxane A2 in progressive kidney disease. 223 87

Dyslipidemia is a common feature of renal failure. It is primarily caused by delayed catabolism of lipoprotein particles. This is due to decreased activity of the key enzymes of delipidation of lipoprotein particles (LPL, HTGL) and of HDL remodeling (LCAT). In epidemiological studies no correlation has been found in dialysis patients between total lipids and atherosclerotic endpoints and a modest relation, at best, between more sophisticated apolipoprotein indices and vascular disease. Such lack of correlations are presumably explained by malnutrition as a confounding factor. Fascinating new observations in animal studies document that in various models of renal damage, development of glomerulosclerosis is accelerated by hyperlipoproteinemia, either endogenous hyperlipoproteinemia or hyperlipoproteinemia induced by feeding of fat. Conversely, correction of hyperlipoproteinemia mitigates development of glomerulosclerosis. Currently there is no firm evidence that the same is true in humans.
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PMID:[Dyslipoproteinemia: its importance in nephrology]. 814 62

Dietary protein restriction and fish oil supplementation (MaxEPA) have been reported to have favourable effects on the remnant nephron model. In the present study female Munich-Wistar rats underwent 5/6 renal ablation (60 rats) or sham surgery (20 rats). The renal ablation rats were randomized one week post-surgery to receive a diet that contained either regular laboratory diet (RLD), 6% low protein diet (LPD) or 24% fish oil diet (FOD) supplementation. Mortality rates at 10 and 20 weeks post-surgery were not different amongst the RLD, LPD or FOD renal ablation cohorts. However the G.F.R. was significantly preserved in the FOD and LPD versus the RLD renal ablation rat groups. Both the LPD and FOD decreased albuminuria and gammaglobulinuria but LPD was more effective. Both dietary interventions prevented glomerulosclerosis but only LPD significantly reduced mesangial expansion. The FOD diet prevented intraglomerular fibrin formation and the LPD had no effect. The dyslipidemia noted at 20 weeks in the renal ablation group was significantly abrogated by both FOD and LPD, although only LPD prevented the heavy proteinuria. The LPD rats gained significantly less weight than the FOD and RLD cohorts. FOD exerted a significantly greater effect on blood pressure reduction than the LPD and also produced significant changes in the renal tissue phospholipids. These results indicate that protein restriction and fish oil supplementation preserve renal structure and function in the remnant nephron model but have different effects on mechanisms known to be co-factors in the progressive renal injury.
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PMID:Dietary protein restriction versus fish oil supplementation in the chronic remnant nephron model. 833 56

Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.
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PMID:Atypical hyperlipidemia and nephropathy associated with apolipoprotein E homozygosity. 858 83

Platelets (PLT) play an important role in hemostasis, modulation of immunological and inflammatory processes. There is also evidence that PLT takes part in the development of atherosclerosis and glomerulosclerosis. The aim of presented study was to determine morphological and functional changes of platelets and their relation to the lipid, protein and coagulation factors disturbances in patients with chronic glomerulonephritis (CGN). The studies were carried out in 60 patients with CGN diagnosed by renal biopsy: 30 patients without nephrotic syndrome (NS)-CGN and 30 patients with NS-CGN+NS. Protein and lipid disturbances, coagulation factors were estimated using routine laboratory methods. Platelet count (PLT), mean platelet volume (MPV) and modal platelet volume (PLT-Mode) were measured using Technicon H1 hematological autoanalyser. Platelet function was assessed by aggregometry using turbidimetric method (inductors: ADP 1-3 microM, collagen 50g/ml, epinephrine 0.25-5 microM). Spontaneous platelet aggregation (SPA) was measured in platelet rich plasma (PRP) without inductors for 15 min, in 1-2 hours after venesection. SPA was observed in 9 of 30 patients with CGN and in 19 of 30 patients with CGN+NS. MPV and PLT Mode were significantly higher in patient showing SPA compared with those without. Significant correlations between SPA and the concentration of plasma albumin (r = -0,70; p < 0.02) TG and CH-LDL (r = 0,61; p < 0.05) were found in CGN+NS patients. APTT was significantly shorter in patients showing SPA compared with those without and negative significant correlation between SPA and APTT was found. Platelet aggregation to inductors in CGN and CGN+NS patients was diminished compared with control group. Lack of second phase aggregation in response to aggregation inducers was observed in patients with SPA. Conclusions. 1. Platelet hyperaggregation play an important role in hypercoagulation state in CGN patients. 2. SPA in vitro was observed in majority of CGN+NS patients and in some without NS. 3. Pathomechanism of SPA is probably multifactorial (hypoalbuminemia, dyslipidemia, changes in concentration of coagulation parameters).
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PMID:[Evaluation of factors influencing platelet aggregation in patients with chronic glomerulonephritis (CGN)]. 875 9

During the last decade, our understanding of the role of nitric oxide for central renal functions has greatly been enhanced. We know now that nitric oxide is produced in renal arteries, macula densa, glomeruli, and tubules by different NO-synthases. Nitric oxide contributes to physiological regulation of renal blood flow, renal autoregulation, tubuloglomerular feedback, renin release, pressure natriuresis, and tubular function. The physiological role of nitric oxide can be modulated by a variety of pathophysiological influences, such as dyslipidemia, diabetes mellitus, hypertension, specific drugs, or radiocontrast agents. In this article, the possible interactions between nitric oxide and atherogenic lipoproteins with regard to important renal functions and development of glomerulosclerosis have been stressed. Atherogenic lipoproteins impair endothelium-dependent, nitric oxide-mediated dilations of renal arteries. The underlying mechanism involves formation of reactive oxygen species which inactivate nitric oxide. Lipoproteins induce formation of oxygen radicals not only in arteries, but also in glomeruli and juxtaglomerular cells, causing, e.g., stimulation of renin release. Although interactions between lipoprotein and nitric oxide take place at different levels, they finally may contribute to renovascular hypertension. Future studies will have to prove that treating hyperlipidemia has a positive influence on nitric oxide-mediated renal functions.
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PMID:Impact of nitric oxide on renal hemodynamics and glomerular function: modulation by atherogenic lipoproteins? 881 12

Renal disease is accompanied by characteristic alterations of lipoprotein metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are primarily reflected in an altered apolipoprotein profile rather than elevated plasma lipid levels. Their full characterization requires identification of discrete lipoprotein particles. While nephrotic syndrome results in increased concentrations of both cholesterol- and triglyceride-rich apoB-containing lipoproteins, renal insufficiency is characterized by an accumulation of intact or partially metabolised triglyceride-rich apoB-containing lipoproteins. The dyslipidemia has been discussed as a contributory factor for the progression of renal insufficiency through development of glomerulosclerosis and tubulointerstitial lesions together with accelerated atherosclerosis. Several experimental studies have shown that hyperlipidemia accelerates renal damage. Lipid-lowering treatment can reduce renal lesions and preserve renal function. The documentation in human nondiabetic progressive renal insufficiency is more limited. We have found that increased concentrations of triglyceride-rich, but not cholesterol-rich, apoB-containing lipoproteins are, associated with a more rapid loss of renal function. The underlying pathophysiological mechanisms for the relation between triglyceride-rich apoB-containing lipoproteins and progression of renal insufficiency are not fully understood. Treatment with hypolipemic drugs may attenuate the renal dyslipidemia, but thus far there have been no reports about controlled clinical trials testing the possible effect of such treatment on the progression of renal insufficiency. In summary, there is evidence to suggest that some specific lipoprotein abnormalities are a risk factor for the progression of renal dysfunction, but the final test of such assumptions still rests on the results of urgently needed controlled intervention studies.
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PMID:Lipoprotein abnormalities as a risk factor for progressive nondiabetic renal disease. 1041 28

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease marked by immune-complex mediated lesions in small blood vessels of various organs, especially the kidneys, although other factors may also be implicated in the pathogenesis of the disease. This article focuses on the role of lipids in the progression of glomerular, vascular and tubulo-interstitial lesions in two patients with lupus nephritis associated with pronounced hyper- and dyslipidemia. The pathogenesis of progressive glomerulosclerosis in both patients appears to be multifactorial. In addition to immune complex mediated lupus glomerulonephritis, progressively active in the first patient, severe nephrotic-range persistent proteinuria, arterial hypertension associated with hyperfiltration and hyperperfusion injuries and, to a minor extent, hyper- and dyslipidemia were observed. Immunological and non-immunological factors were shown to contribute to the development of tubulo-interstitial lesions. In both patients, in addition to local immune deposits, prominent tubulo-interstitial lipid deposits were probably causally related to both hyperlipidemia and the increased permeability of the glomerular filtration barrier. Tubular lesions were highlighted by intracytoplasmic lipid droplets as well as small cleft-like spaces found to be impacted in the tubular lumina. They were seen to penetrate tubular epithelial cells and eventually lodge in the interstitium, surrounded by mononuclear cell infiltrates and foam cells. In both patients, hypertensive angiopathy and extraglomerular vascular immune deposits were demonstrated. In addition, in the second patient, arteriolar and small arterial hyaline was found at the age of 28 years to be full of lipids and calcium precipitates, suggesting a peripheral atherosclerosis-like process which never occurs as a natural age-related condition. In conclusion, all parts of the nephron may be involved in the pathogenetic process causally related or influenced by hyper- or dyslipidemia. Associated either with endothelial cell injury and consequent insudation of lipids in the vascular walls, glomerular filtration barrier injury with hyperfiltration, or tubulo-interstitial lipid deposition, the mechanism of tissue damage by lipids in all parts of the nephron shares similarities with the pathogenesis of systemic atherosclerosis.
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PMID:Role of lipids in the progression of renal disease in systemic lupus erythematosus patients. 1102 Sep 63


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