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)

A 57-year-old patient presented with periorbital and lower limb edema. The physical examination revealed no signs of cardiac insufficiency or chronic liver disease. Initial laboratory values showed significant hypoproteinemia and hyperlipidemia. Renal function was normal. Urinary protein excretion was 5.5 g/d. Thus, the patient was diagnosed to have nephrotic syndrome. The patient's history, the physical examination and further laboratory work-up suggested a primary glomerulopathy. Percutaneous renal biopsy was performed. The biopsy was diagnostic of minimal change glomerulonephritis. A therapy with steroids was initiated which induced a complete remission of the nephrotic syndrome. The patient has been relapse-free for the entire follow-up period.
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PMID:[Eyelid and ankle edema]. 231 82

The effect of exercise on the progression of experimental renal disease was studied in adriamycin (ADR)-treated rats, a model of sclerosing glomerulonephritis with nephrotic syndrome. Two hours of daily swimming exercise was carried out for 20 weeks in ADR-treated male Lewis rats fed with either an ad libitum intake of regular chow (group 1) or a restricted amount of food (group 3), which was equal to the amount of food freely ingested by ADR-treated rats not undergoing swimming exercise (group 2). Group 3 resulted in a significantly lower serum creatinine, higher inulin clearance and lower glomerular sclerosis index compared to group 2. The progress of renal dysfunction did not differ significantly between group 1 and group 2. Hyperlipidemia, especially, hypertriglyceridemia was significantly lower in the exercise groups than in the sedentary group. Among all the rats, inulin clearance was inversely correlated with either cholesterol (r = 0.560, p less than 0.01) or triglyceride (r = 0.423, p less than 0.05) and the glomerular sclerosis index correlated positively with cholesterol (r = 0.599, p less than 0.005). Systolic blood pressure was 10 mm Hg lower in group 3 than in group 2 and the difference was significant. It is concluded that swimming exercise with a relative restriction of food intake can improve hyperlipidemia and prevent progressive renal dysfunction in ADR-induced nephritic rats.
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PMID:Effect of swimming exercise on the progress of renal dysfunction in rat with focal glomerulosclerosis. 237 Sep 32

A paediatric case of lipoprotein glomerulopathy, a new kidney disease characterized by glomerular lipoprotein thrombi, is reported. The patient had massive proteinuria from the age of 8 years, when the nephrotic syndrome was first detected. This was resistant to conventional treatment for more than 10 years. During the course of the disease, the hyperlipidaemia characteristic of hyper-pre-beta-lipoproteinaemia and elevation of apoprotein E persisted, and renal function gradually deteriorated. The renal histopathological findings from four biopsies were essentially the same, with storage of beta-lipoprotein in dilated, balloon-like glomerular capillary lumina. However, the number of glomeruli showing global sclerosis increased and tubulo-interstitial changes progressed in parallel with the gradual clinical deterioration. As in other cases reported in Japan some familial involvement has been noted.
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PMID:Long-term follow-up of a paediatric case of lipoprotein glomerulopathy. 239 77

Hyperlipidemia is usually present in patients with the nephrotic syndrome. The most common lipid abnormality is hypercholesterolemia, although as the disorder progresses, hypertriglyceridemia may develop. Elevated plasma lipids have two potential vascular consequences, namely, atherosclerosis and progression of renal failure. Neither of these complications has been proven with certainty, but there is growing evidence to indicate that both may be long-term consequences of the nephrotic syndrome. Therefore, effective therapy of hyperlipidemia, particularly elevated cholesterol levels, is needed as a protection against these complications. Since nephrotic hypercholesterolemia frequently is severe, dietary therapy, although a valuable adjunct, will not normalize cholesterol levels in most nephrotic patients. Thus, if effective serum cholesterol lowering is to be achieved, drug therapy will be required. Bile acid-binding resins have been shown to lower cholesterol levels in nephrotic patients, but the decline in cholesterol concentrations is usually insufficient to produce a marked reduction in coronary risk. Nicotinic acid theoretically should be useful for treatment of nephrotic hyperlipidemia, but it has not been adequately tested. The new drugs that inhibit cholesterol synthesis, e.g., lovastatin, appear to be highly promising for treating elevations of both serum cholesterol and triglycerides in the nephrotic syndrome. However, testing of these drugs in this condition has been limited, and the possibility of significant side effects in an appreciable portion of patients has not been ruled out. Of particular concern is the development of severe myopathy that can produce myoglobinuria and acute renal failure. This side effect is relatively rare in patients without the nephrotic syndrome, but its prevalence in the latter condition has not been determined. The fibric acids will lower triglyceride levels in nephrotic patients, but they are not effective in lowering cholesterol levels; consequently, they probably have little role in the treatment of nephrotic hypercholesterolemia. Finally, the drug probucol will lower cholesterol levels in nephrotic patients, although not to desirable levels; still, probucol could prove useful in combination with other cholesterol-lowering drugs.
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PMID:Rationale and management of hyperlipidemia of the nephrotic syndrome. 248 42

The authors described the clinical, biologic and histologic particularities of two cases of congenital nephrotic syndrome, Finnish type. Clinically, the hydropic syndrome was represented by anasarca: biologically by marked proteinuria, hypoproteinemia with dysproteinemia and hyperlipemia with dyslipemia. Histologically both cases presented microcystic dilatation of the proximal tubuli contorti. The evolution was unfavorable and ended in death.
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PMID:[The Finnish-type congenital nephrotic syndrome. Comments on 2 cases]. 250 64

The pathogenesis of avascular necrosis of bone (ANB) was investigated in 111 patients with systemic lupus erythematosus (SLE) (24 with ANB, 87 without ANB); patients' ages, corticosteroid treatment, clinical and laboratory features associated with SLE, and haemostatic profiles were all taken into account. The mean ages of patients with and without ANB at the time of diagnosis of SLE was 24.1 and 31.2 years respectively. The mean maximal daily dose of prednisolone in the group with ANB was 50.8 mg, which was significantly higher than the dose (41.8 mg) in the group without ANB. Disease features of SLE, such as Raynaud's phenomenon, hyperlipidaemia, nephrotic syndrome, hypertension, and disease activity, were not found to be related to ANB. The percentage of patients who had lupus anticoagulant as well as a shorter activated partial thromboplastin time was greater in those with ANB than in those without. Multiple factors may be involved in the pathogenesis of ANB in SLE, and it is suggested that haemostatic abnormalities, which could be influenced by corticosteroids and young ages, play some part in the development of ANB.
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PMID:Avascular necrosis of bone in systemic lupus erythematosus: possible role of haemostatic abnormalities. 250 41

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81

Hyperlipidemia and hypertension, two major risk factors for accelerated atherosclerosis, undoubtedly contribute to the excessive cardiovascular morbidity and mortality experienced by renal transplant recipients. The present survey of posttransplant hyperlipidemia in 500 cyclosporine-treated patients documented a 37.6% incidence of hypercholesterolemia, which occurred within 6 months posttransplant in 82% of patients. An etiologic relation to corticosteroid therapy was suggested by the strong correlation between prednisone doses and cholesterol levels, by the reduced cholesterol levels in patients undergoing steroid withdrawal, and by the reduction in hypercholesterolemia to 13% by 3 years posttransplant when steroid doses were less than 10 mg daily. Hypertriglyceridemia, which was present in 14.7% of the patients, was more severe under CsA-prednisone compared with azathioprine-prednisone therapy. Hypertriglyceridemia, which occurred later in the posttransplant course than hypercholesterolemia, strongly correlated with an excessive percent relative weight and elevated serum creatinine but not with steroid or CsA doses. Increasing age, diabetes mellitus, beta-blockers and nephrotic syndrome contribute to posttransplant hyperlipidemia in the CsA-Pred era as they did in the azathioprine era of immunosuppression.
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PMID:Lipid abnormalities in cyclosporine-prednisone-treated renal transplant recipients. 266 33

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

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


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