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)

Hyperlipidemia is common in patients with the nephrotic syndrome. The main cause is probably increased hepatic lipogenesis, a non-specific reaction to falling oncotic pressure secondary to hypoalbuminemia. Cardiovascular morbidity and mortality are increased in patients with the nephrotic syndrome, with the exception of patients with minimal change disease. It is not clear whether this is caused by the hypercholesterolemia or secondary to uremia or medical treatment. Experiments suggest that hypercholesterolemia may cause glomerulosclerosis, a common complication of the nephrotic syndrome. The hypercholesterolemia of the nephrotic syndrome can now be treated effectively with HMG coenzyme A reductase inhibitors.
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PMID:[Hyperlipidemia in nephrotic syndrome]. 194 40

Similarities between atherosclerosis and glomerulosclerosis suggest that hyperlipidaemia may contribute to glomerular injury. Dietary supplementation with 4% cholesterol + 1% cholic acid was administered to rats 4 weeks after 1 1/3 nephrectomy and continued for 7 weeks. There was a significant increase in serum cholesterol (peak = 11.52 +/- 1.09 mmol l-1 vs. 4.73 +/- 0.31 on control diet, P less than 0.001) and triglyceride concentrations (peak = 2.31 +/- 0.27 mmol l-1 vs. 1.41 +/- 0.29, P less than 0.05) and a marked increase in beta-migrating lipoproteins. The severity of hypercholesterolaemia was significantly correlated with proteinuria (control diet: r = 0.600, cholesterol diet: r = 0.672, P less than 0.0001) as was hypertriglyceridaemia (control diet: r = 0.544, cholesterol diet: r = 0.678, P less than 0.0001). The percentage of glomeruli containing lipid deposits was increased from 21% to 60% (P less than 0.05). The kidney total cholesterol content was increased from 29.2 +/- 0.8 to 47.7 +/- 3.3 mumols g-1 dry weight (P less than 0.0001), with esterified cholesterol increasing from 7.5 +/- 0.4% to 14.5 +/- 2.1% of total (P less than 0.01). Serum cholesterol concentration was significantly correlated with both glomerular lipid deposition (rs = 0.7195, P less than 0.0001) and tissue total cholesterol content (rs = 0.6053, P less than 0.001). Lipid vacuolation was prominent in the paramesangium and within mesangial cells. Despite these changes hypertension, uraemia, proteinuria and glomerulosclerosis were not significantly increased on the cholesterol diet. Cholesterol deposition in the glomeruli occurs secondary to hyperlipidaemia in rats following subtotal nephrectomy but over 7 weeks no exacerbation of glomerulosclerosis is detectable.
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PMID:The role of lipids in the pathogenesis of glomerulosclerosis in the rat following subtotal nephrectomy. 210 41

Disordered lipid metabolism is believed to play an important role in accelerating the progression of chronic renal disease toward uremia. We examine this hypothetic role of lipids in a large population of patients on long-term dietary protein restriction. In our experience, there is no conclusive evidence that lipids may accelerate the progression of functional deterioration in patients with reduced renal function. Hyperlipidemia seems to be only one among the many factors affecting the prognosis of primary renal disease. Dietary protein restriction is effective in maintaining normal or only slightly elevated serum lipid levels in patients with early renal failure. Moreover, patients with renal failure maintained on this diet, which provides an elevated ratio of polyunsaturated to saturated fatty acids, have a more favorable lipid composition of erythrocyte membrane (low percentage of saturated fatty acids and high percentage of polyunsaturated fatty acids) when compared with patients on an unrestricted diet.
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PMID:Serum lipids in patients with chronic renal failure on long-term, protein-restricted diets. 248 48

Hyperlipidemia, long recognized as a difficult and common problem following organ transplantation, may be the underlying cause of the accelerated atherosclerosis observed in heart transplant recipients and children with renal transplants. In addition, hyperlipidemia may play a role in late renal graft loss. The cause of post-transplant hyperlipidemia is unclear. In patients treated with azathioprine and prednisone, hypertriglyceridemia is the commonest finding and probably results from an increased consumption of calories from carbohydrate and fat following resolution of uremia, in conjunction with glucose intolerance secondary to steroid administration. In patients treated with cyclosporine, hypercholesterolemia is the most common form of hyperlipidemia. Cyclosporine is a lipophilic drug that is transported in the plasma, largely in association with lipoproteins, and may require the low-density lipoprotein (LDL) receptor for internalization into cells. Hypercholesterolemia may result from interference with the basic cholesterol feedback mechanism via the LDL receptor. In addition, cyclosporine affects bile acid synthesis and worsens glucose tolerance, both factors that may promote hyperlipidemia. The first therapeutic approach to hyperlipidemia in the transplant recipient is dietary calorie-fat restriction and supplementation with soluble fiber. Ongoing clinical trials of the available pharmacologic lipid-lowering agents are addressing the safety and efficacy of these agents in the setting of immunosuppression; until that time, they should be used cautiously and in low doses.
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PMID:Hyperlipidemia after organ transplantation. 248 50

Patients on chronic hemodialysis often present both hyperlipidemia and a high incidence of cardiovascular disease (CVD). Uremic hyperlipidemia has usually been regarded as one of the most important cardiovascular risk factors (CVRF) in these patients. In order to study whether the "uremia-induced" lipid abnormalities are actually associated with evidence of uremic CVD, and consequently may be considered reliable CVRF, 123 patients on chronic dialysis were reviewed for the presence of CVD and, at the same time, examined for their lipoprotein pattern and other clinical and biochemical variables. Lipids and lipoproteins did not prove helpful in our study in identifying patients with CVD. Despite the fact that they had been on dialysis for a shorter time, CVD patients were significantly older and had higher blood pressure than patients without CVD. Our data suggest that the uremia-induced lipid abnormalities are not reliable markers of CVD in dialysis patients, and support the hypothesis that dialysis per se does not accelerate the atherosclerotic process in uremic patients.
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PMID:Are lipid abnormalities reliable cardiovascular risk factors in dialysis patients? 259 65

Abnormalities of Zn metabolism are well documented in patients with chronic renal disease, especially those with nephrotic disease and uremia. The causes of Zn deficiency in kidney disease are not clear. Decreased dietary Zn intake and intestinal absorption, increased endogenous Zn secretion, and increased urinary Zn excretion (as in the nephrotic syndrome and in renal transplant recipients) all may contribute to altered Zn metabolism. Zn depletion may account for decreased taste, sexual and gonadal dysfunction, hyperprolactinemia, glucose intolerance, hyperlipidemia, growth retardation in children, neuropathy, anemia, abnormalities of neutrophil and lymphocyte function, and delayed wound healing. The benefit of pharmacologic doses of Zn, in the treatment of such manifestations, requires further evaluation under controlled conditions. Before use of Zn routinely for therapeutic purposes in uremic subjects, the cause(s) of abnormal Zn metabolism should be identified.
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PMID:Zinc in kidney disease. 267 56

Various endocrine and metabolic disturbances associated with long standing uremia persist after kidney transplantation or arise from the use of immunosuppressive drugs. Hyperlipidemia for long time being implicated as the cause of corticosteroids is also observed in renal transplant recipients treated with cyclosporin A monotherapy. After conversion from cyclosporin to azathioprine serum cholesterol and triglyceride concentration fall, and elevation of LDL-cholesterol may also be reversed. There is a tendency for higher HDL-cholesterol in azathioprine and prednisolone treated transplant patients. Those patients who are at risk for clinically significant cholesterol elevations can be predicted by their pretransplant lipid levels, specifically the LDL-fraction. Risk-benefit ratio of conversion and of treatment with lipid-lowering drugs, especially with lovastatin, should be carefully examined, also in view of glucose intolerance. Higher incidence of diabetes mellitus requiring insulin therapy in cyclosporin treated transplant recipients has been reported. Cyclosporin may cause toxic effects on pancreatic beta-cells resulting in inhibition of insulin secretion. High doses of cyclosporin induce inhibition of glycogen synthesis in rat liver. Glucose intolerance is reversible after reduction of cyclosporin dose or conversion to azathioprine. Therefore glucose metabolism in kidney transplant recipients treated with cyclosporin should be carefully followed. Immunosuppressive therapy may affect reproductive function, arachidonate metabolism and renin-angiotensin-aldosterone system as well as posttransplant calcium and phosphate metabolism. Endocrine and metabolic abnormalities are associated with long standing uremia. After successful kidney transplantation several observations are normalized but further complications arise from the use of immunosuppressive drugs. The present paper reviews various endocrine and metabolic disturbances described following renal transplantation.
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PMID:Endocrine and metabolic abnormalities following kidney transplantation. 268 69

Hyperlipidemia is an identified risk factor for atherosclerosis in patients following renal transplantation that may be related to previous uremia and various drugs including steroids. Recent evidence has suggested that treatment with cyclosporine may be an independent risk factor for development of hyperlipidemia in some patients. Twenty-four Sprague Dawley rats were given CsA at 30 mg/kg by gavage for 28 days in 1 ml of olive oil or fish oil vehicle, and compared with controls receiving just vehicle. Increases of both triglyceride (233.6%) and cholesterol (50.9%) were observed in olive oil/CsA animals (P less than .01), with no significant change noted with either vehicle alone. An increase of triglyceride from baseline was observed with fish oil/CsA (119%) (P less than .01) but was significantly less than the increase with olive oil/CsA animals (P less than .05). No increase in cholesterol was found in CsA-treated rats using the fish oil vehicle. The mechanisms leading to hyperlipidemia with four weeks of CsA administration in these rats are unknown, but may be related to altered hepatic synthesis. CsA levels were lower in fish oil-treated animals, possibly explaining the difference noted in lipid levels--or, alternatively, reduction of plasma lipoproteins may have altered drug kinetics and CsA binding. This work emphasizes a need for further study of lipids in CsA-treated patients, and advises some caution in the use of lipoprotein-reducing agents in patients using CsA without consideration of the possible effect on free drug levels.
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PMID:Effect of cyclosporine on plasma lipids and modification with dietary fish oil. 319 39

Although the importance of the profunda femoris artery in maintenance of lower extremity integrity was recognized in the earliest days of modern vascular surgery, disappointment with the performance of primary profundaplasty has emerged fully only in recent years. During the 10 year period from 1977 to 1987, only 17 patients were subjected to this procedure at Northwestern Memorial Hospital. The nine men and eight women averaged 65.6 years in age and exhibited the usual precursors of arterial insufficiency: a history of smoking in 12 patients (71 percent), clinical coronary artery disease in 8 patients (47 percent), hypertension in 7 patients, diabetes mellitus in 6 patients, hyperlipidemia in 2 patients, and uremia in 1 patient. Four patients exhibited hemodynamic improvement after profundaplasty (ankle-brachial index increase of greater than 0.15). Four required amputation postoperatively, and a fifth exhibited hemodynamic failure 9 months postoperatively and required amputation. Two patients required subsequent femoral-to-peroneal bypass to improve distal arterial perfusion. One patient died after the procedure, for a 5.9 percent mortality rate. Thus, the fact that profundaplasty has proved disappointing in the treatment of severe arterial insufficiency deserves emphasis at this time.
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PMID:The demise of primary profundaplasty. 340 Aug 10

To investigate the effect of long-term acetate administration on uremic and nonuremic rats, the blood lipid level, the incorporation of [14C]acetate into exhaled 14CO2 and into tissue lipids, and morphological changes were studied. Experimental chronic uremia was caused by partial nephrectomy, and sodium acetate of NaC1 was given intraperitoneally for approximately 12 weeks. Controls were sham-operated rats given acetate or NaC1. Hyperlipidemia was found in the uremic rats; it was more severe in the rats given acetate. Incorporation of [14C]acetate into 14CO2 was lower in uremic rats given acetate than in other groups, and incorporation into liver lipids was not different in different groups. Small fat droplets had accumulated diffusely in the hepatocytes of nonuremic and uremic rats, but accumulation was more severe in the former. Large fat droplets were found in rats given acetate, mostly in the periphery of liver lobules. Uremic rats given NaC1 did not have such changes. The results suggested that chronic acetate administration may contribute to hyperlipidemia in uremic rats and to lipid accumulation in hepatocytes in both uremic and nonuremic rats, causing fatty degeneration of the liver.
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PMID:Effect of acetate administration on rats with chronic uremia. 361 95


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