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)

Lipoprotein abnormalities are common in patients with chronic renal failure (CRF) on either dialysis or conservative therapy. In order to investigate the changes in lipid and apolipoprotein pattern from early CRF to dialysis treatment, plasma lipids with apoproteins AI, B, E, CII, CIII, CII/CIII ratio, E/CIII ratio, parathyroid hormone (PTH) and insulin levels were examined in 72 patients with different degrees of CRF and 31 patients on hemodialysis (HD), and compared the values of 28 controls. A significant decrease in the Apo CII/CIII ratio was the earliest lipoprotein abnormality to occur in CRF. Hypertriglyceridemia (HTG) with reduced high-density lipoprotein cholesterol levels, increased Apo CIII and decreased Apo E/Apo CIII ratio only occurred in more advanced renal failure (creatinine clearance < 31 ml/min). HD patients showed a general worsening of the lipoprotein profile with elevated Apo E levels and indirect evidence of remnant accumulation. While PTH did not have any significant influence on lipoprotein pattern, increased insulin levels during HD might partly account for the HTG of these patients. Our results point to elevated Apo CIII, reduced Apo CII/Apo CIII and Apo E/ Apo CIII ratios as typical features of uremic hyperlipidemia and show that a defective triglyceride removal is the major pathogenetic mechanism of uremic HTG. HD treatment seems generally to worsen the lipid and apolipoprotein pattern observed in the predialytic stage of CRF.
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PMID:Lipoprotein abnormalities in chronic renal failure and dialysis patients. 873 41

Diabetic nephropathy can be regarded mainly as a type of microangiopathy, but is a disease that may also include aspects of macroangiopathy. This is especially true of renal disease in non-insulin dependent diabetes mellitus (NIDDM), which is characterized not only by diabetic glomerulosclerosis, but also by atherosclerosis. We performed morphological studies on the kidney, using computed tomography (CT), focusing on such points as: (1) abdominal aortic calcifications at the level of kidney, (2) calcifications in the renal artery, and (3) wedge-shaped defects on the renal surface. We noted that these findings became more prominent in NIDDM patients during end-stage renal failure than during normal renal function, and were significantly more common in those two NIDDM groups than in age-matched nondiabetic patients without hypertension, hyperlipidemia or gout. NIDDM patients exhibited these features more frequently than IDDM patients.
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PMID:[Computed tomographical evaluation of diabetic nephropathy]. 875 67

Important observations have continued to expand our understanding of gout. The increased risk of gout in black Americans has been linked more closely with the development of hypertension, and an increasing prevalence in African blacks and in England may have a similar association, possibly through the use of diuretics. The association of gout and insulin resistance appears to be related to fat distribution, and the link with hyperlipidemia may be related to genetic factors. The relationship between gout and renal disease and the frequency of gout in patients with renal failure continue to be areas of controversy. The mechanism and a possible therapeutic approach to the hyperuricemia associated with cyclosporine therapy are better understood. The potential for antibodies against urate crystals to potentiate further crystallization may explain some of the uncertainties about gouty attacks. Unusual manifestations of gout, including more cases of spinal involvement, were reported. The role of formalin in dissolving urate crystals in pathologic specimens was further clarified, and the use of atomic force microscopy to detect crystals was reported. Corticosteroids are increasingly accepted in treating acute gout, and the role of colchicine in acute and intercritical gout has come under increasing scrutiny. Urate-lowering drugs appear to be cost effective in patients with more than one or two attacks per year.
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PMID:Gouty arthritis and uric acid metabolism. 879 84

Hypertension is one of the most important cardiovascular risk factors. Without therapy hypertension leads to stroke, coronary heart disease with angina pectoris and myocardial infarction, kidney failure and/or peripheral vascular disease. The association between blood pressure and these cardiovascular complications can be demonstrated over the entire blood pressure range. The risk of stroke, myocardial infarction, renal failure or peripheral vascular disease increases with increasing blood pressure. Additional cardiovascular risk factors such as hyperlipidemia, smoking and diabetes involve a further increase in risk. Today hypertension can be effectively treated. To that end, diuretics, betablockers, ACE-inhibitors or calcium antagonists can be used. Alpha receptor antagonists and angiotensin AT1 receptor antagonists are also of value. The antihypertensive effectiveness of these drugs is comparable but may vary in individual patients. During antihypertensive therapy, a reduction in cerebrovascular and cardiac complications has been demonstrated for alpha methyldopa, diuretics and betablockers. In these studies, fatal and non-fatal strokes were reduced by 42%, while the reduction in cardiac events was less pronounced (14%). The reasons for this greater efficacy of antihypertensive therapy in the cerebral circulation are not clear. Other risk factors may be particularly important in the pathogenesis of coronary artery disease (e.g. genetic factors, hyperlipidemia and others) or hypertensive vascular changes in the coronary circulation may not be as reversible as they are in the cerebral circulation. The well documented correlation between stroke, myocardial infarction and hypertension, as well as the proven efficacy of antihypertensive therapy in preventing cardiovascular events, underscores the importance of effective and sustained blood pressure control in these patients.
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PMID:[Heart, brain and hypertension]. 884 9

Hyperlipidemia in patients of secondary glomerulopathies, a well established entity with very little knowledge of its management modifies its prognosis by predisposing these patients to develop atherosclerosis, coronary artery disease, hypertension cerebro-vascular accidents and also thromboembolic phenomenon leading to renal vein thrombosis and renal failure. Guggulsterone was administered orally in these patients in a daily divided dose of 75 mg for a period of 8 weeks together with supportive measures like high protein diet, diuretics and hematinics. Total serum lipid, total serum cholesterol, triglycerides, phospholipids, HDL, LDL, and VLDL were analysed at 4 and 8 weeks of therapy. Significant reduction was observed in the values of total serum lipid and total serum cholesterol. Other parameters of lipid profile showed downward trend except rise of HDL with insignificant difference. There was no significant side effect throughout the study.
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PMID:A study of effect of guggulsterone on hyperlipidemia of secondary glomerulopathy. 895 Jan 39

The purpose of the present study was to perform an electron microscopic investigation of patients with chronic glomerulonephritis and to find correlations between the type of glomerular disorder and the features of the clinical course of the disease. 26 patients--16 female and 10 male aged 17-62 years (mean age, 34.5 years) were investigated. All patients were clinically diagnosed as having chronic glomerulonephritis with a disease duration ranging from 3 months to 2 years. The main clinical and laboratory parameters studied were presence of edemas, hypertension, proteinuria, hyperlipidemia, haematuria and renal failure confirmed by the creatinine clearance. A puncture renal biopsy was performed by classical methods under ultrasound guidance using a Vim-Silverman needle. An electron microscope Philips CM-12 was used in the study. We found in all patients a significant correlation between the degree of proteinuria and the marked deformation and edema of the podocyte pedicles. In making the integral histological diagnosis of chronic glomerulonephritis it is necessary to determine more precisely the mesangial involvement and the changes in the membrane by means of an electron microscopic study. This will be conducive to a reduction in the number of mistakes in diagnosing some primary chronic glomerulonephrites.
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PMID:Clinical electron microscopic correlations in patients with glomerulonephritis. 900 60

Lupus nephritis is a prototype of immune complex-mediated glomerulonephritis. A broad range of clinical presentations and histological changes (proliferative, membranous, or both) are observed. Patients are at risk for progressive renal function deterioration as a result of the interaction of various active immunologic and chronic sclerosing mechanisms of kidney injury. Hypertension and hyperlipidemia contribute to morbidity and mortality. Monitoring serological parameters, urinary protein excretion rate and, especially, the urinary sediment facilitate the prompt recognition and treatment of this disorder. Kidney biopsy evaluation often clarifies the type, severity, and potential reversibility of the underlying renal lesions. Although contemporary immunosuppressive regimens for proliferative lupus nephritis have reduced the risk of end-stage renal failure, they are potentially toxic and not universally effective. Decisions regarding the intensity and duration of these treatments are difficult and are based on the severity of the disease, the initial response to therapy, and the risk for drug-induced toxicities. Studies are in progress to evaluate alternative regimens for proliferative lupus nephritis and membranous lupus nephropathy.
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PMID:Treatment of lupus nephritis. 912 97

Recently, the hypothesis that all renal diseases are inherently progressive and self-perpetuating has focused attention on adaptive changes in renal structure and function that occur whenever renal function is reduced. These glomerular adaptations to renal disease include increases in filtration rate, capillary pressure and size, and are referred to as glomerular hyperfiltration, glomerular hypertension and glomerular hypertrophy, respectively. Extrarenal changes, such as dietary phosphate excess, systemic hypertension, hyperlipidaemia, acidosis and hyperparathyroidism occur in animals with renal disease and may be contributors to progression of renal disease. Emphasis in the management of companion animals with renal disease has shifted to identifying, understanding and controlling those processes that play a role in the progression from early to end-stage renal failure. Advances made by veterinary nephrologists in the past 15 years permit resolution of old controversies, formulation of new hypotheses and discussion of unresolved issues about the nature of progressive renal disease in dogs and cats.
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PMID:Pathophysiology and management of progressive renal disease. 930 97

We report the case of a 60-year-old man with recent onset of poorly controlled diabetes mellitus, frequent anginal chest pains, paroxysmal hypertension, hyperlipidemia, and mild renal insufficiency. The patient was found to have pheochromocytoma of the left adrenal gland, resection of which resulted in total resolution of diabetes, hypertension, chest pain, hyperlipidemia and renal failure.
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PMID:Insulin-requiring diabetes mellitus, hyperlipidemia, and anginal chest pains as prominent features of pheochromocytoma. 938 71

Chylomicrons are formed in the intestine and transport dietary triglyceride to peripheral tissues and cholesterol to the liver. The enzyme lipoprotein lipase, with apolipoprotein (apo)C-II as a co-factor, hydrolyzes chylomicron triglyceride allowing the delivery of free fatty acids to muscle and adipose tissue. As a result, a new particle called a chylomicron remnant is formed. This particle is enriched in cholesteryl ester and fat-soluble vitamins and contains apoB-48 and apoE. It is rapidly removed from the circulation by the liver. ApoE is the moiety required for rapid hepatic removal. Its activity is inhibited by C apolipoproteins, especially apoC-I. Hepatic removal appears to be accomplished by several overlapping mechanisms. The particle must first achieve a size that allows it to be "sieved" through the endothelial fenestre allowing entrance into the space of Disse. Here, it may 1) be removed directly by LDL receptors; 2) acquire additional apoE that is secreted free into the space, and then be removed directly by the LDL receptor-related protein (LRP); or 3) it may be sequestered in the space. Sequestration occurs by binding of apoE to heparan sulfate proteoglycans and/or binding of apoB to hepatic lipase. Sequestered particles may be further metabolized allowing apoE, and lysophospholipid enrichment, followed by transfer to one of the above receptors for hepatic uptake. The above formulation is based upon animal studies. In humans, delayed removal of chylomicron remnants has been documented in diabetes, renal failure, and familial combined hyperlipemia and is the abnormality resulting in type III hyperlipidemia. Case control studies have identified delayed remnant removal as an independent risk factor for atherosclerotic cardiovascular disease. Thus, understanding the further details of the processes, and how it can be regulated in humans, is an important challenge for the future.
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PMID:Hepatic uptake of chylomicron remnants. 939 16


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