Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nephrotic syndrome may be associated with several complications caused by severe proteinuria. The consequences of severe renal protein loss are disturbances of water and electrolyte metabolism, thromboses and thromboembolic complications, hyperlipidemia with accelerated atherosclerosis and, finally, some other complications due to the decreased oncotic pressure and the renal loss of transport globulins and immunoglobulins. Diagnosis and treatment of these complications are important in the management of patients with nephrotic syndrome. In the present study, the frequency and localization of thromboses and thromboembolic complications in 11 patients with nephrotic syndrome are described. In addition, factors which are known to be responsible for the hypercoagulable state in nephrotic syndrome were evaluated and correlated to the thromboembolic complications in these patients. An important finding was that in all patients with thromboses and thromboembolic complications, the serum albumin concentrations were below 2 g/100 ml, whereas, with one exception, serum albumin levels were above 2 g/100 ml in cases without thromboembolic complications. Our results indicate that serum albumin levels may be used as an indirect parameter to assess the risk of thromboembolic complications in patients with nephrotic syndrome.
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PMID:[Complications of nephrotic syndrome with special reference to thromboembolic accidents]. 37 Sep 77

Hyperlipidemia and premature atherosclerosis are known metabolic complications in patients with the nephrotic syndrome. In this study, we have measured serum levels of cholesterol, triglycerides and serum-cholesterol-binding reserve (SCBR) in 22 patients (14 men, 8 women) with the nephrotic syndrome and in 21 hyperlipidemic men who served as control subjects. Serum cholesterol levels were higher (p less than 0.005) in patients when compared to those of controls while triglyceride levels did not differ significantly between the groups. SCBR levels were lower (p less than 0.001) in the nephrotic subjects. The abnormally low SCBR values may be an important risk factor for atheroclerosis as suggested by previous studies in patients surviving premature myocardial infarction.
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PMID:Serum-cholesterol-binding reserve in patients with the nephrotic syndrome. 49 25

The evaluation of the results of nearly 800 percutaneous renal biopsies, including biopsies in which insufficient renal tissue was obtained or histologic changes were non-specific, indicated that in 85% of the cases a positive diagnosis could be made. The liberal extension of the indication to percutaneous renal biopsy to include oligosymptomatic renal diseases, the nephrotic syndrome and acute renal failure often resulted in therapeutic and prognostic consequences. Renal biopsy does not facilitate the diagnosis of pyelonephritis. Uremia, severe atherosclerosis, small kidneys, advanced age and lack of cooperation are not contraindications to percutaneous renal biopsy nor do they increase its risk. Severe complications are extremely rare and are always secondary to retroperitoneal hemorrhage. Close observation and prompt treatment can always preclude a fatal outcome. Long-term complications are not to be expected. If the technique of percutaneous renal biopsy and its histologic evaluation are efficiently performed, further extension of the indications to biopsy could be medically sanctioned.
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PMID:[Percutaneous kidney biopsy. Evaluation of a diagnostic method]. 71 Oct 98

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
Atherosclerosis 1977 Jan
PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

We report the case of a 5-year-old girl who died two years after onset of the idiopathic nephrotic syndrome, which failed to respond to treatment with corticosteroid and cyclophosphamide. Severe atherosclerotic changes were noted in both coronary arteries. Prolonged hyperlipidemia in patients with long-standing nephrotic syndrome may represent a major risk factor predisposing to premature coronary atherosclerosis in children who are also destined to develop chronic renal failure.
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PMID:Premature coronary atherosclerosis in a 5-year-old with corticosteroid-refractory nephrotic syndrome. 90 86

Over a 16-year period, 205 patients with hypertension were shown to have a renovascular aetiology. Of these, 125 (61 per cent) had Takayasu's arteritis, 58 (28.3 per cent) had fibromuscular dysplasia, 16 (7.8 per cent) had atherosclerosis, five (2.4 per cent) had polyarteritis nodosa and one (0.5 per cent) had renal artery aneurysm. Among patients with Takayasu's arteritis, males were affected as commonly as females. The mean age of these patients at the time of detection was 26.8 +/- 8.6 years (range 5-52 years). Type I arteritis was seen in nine (7.2 per cent), Type II in 40 (32 per cent) and Type III in 76 (60.8 per cent) patients. The abdominal aorta was involved in 117 (93.3 per cent) patients. Takayasu's arteritis was associated with ulcerative colitis in two patients and with renal amyloidosis and focal segmental glomerulosclerosis with a nephrotic syndrome in one patient each. Surgical intervention consisting of bypass procedures, autotransplantation or nephrectomy was performed in 17 (13.6 per cent) and angioplasty in nine (7.2 per cent) patients. Cure and improvement in blood pressure was observed in 82.4 per cent and 77.8 per cent respectively. Adequate control of blood pressure was achieved with drugs only in 22 (22.2 per cent) patients. A definite cause and effect relationship could not be established between any infective or immunological disorder and Takayasu's arteritis. Takayasu's arteritis is a far more common cause of renovascular hypertension in Indian population than fibromuscular dysplasia or atherosclerosis, which are more common in the western population.
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PMID:Renovascular hypertension due to Takayasu's arteritis among Indian patients. 136 62

The development of the nephrotic syndrome is associated with a lipid profile characterized by increased total and low density lipoprotein cholesterol. Although total high density lipoprotein (HDL) values may be in the normal range, there is frequently abnormalities of HDL subclasses, with reduction of the mature HDL2 subfraction. While these lipid changes may be considered a risk for atherosclerosis, they revert to normal with remission of the nephrotic syndrome. However, with chronic nephrotic range proteinuria, these abnormalities persist and may also be associated with increased levels of lipoprotein (a), increased levels of very light density lipoprotein and further reductions in HDL. These factors could all contribute to greater risk for atherosclerosis. Although coronary artery disease is frequently seen in patients with end-stage renal disease, and many uncontrolled studies in patients with chronic nephrotic syndrome have suggested an increased prevalence of cardiovascular disease, no prospective studies to evaluate relationship between lipid abnormalities and cardiac disease have been performed in patients with the nephrotic syndrome. Recent experimental data have also suggested a relationship between hyperlipidemia and progressive renal injury. Unfortunately, human epidemiological data are incomplete in correlating lipid changes with renal disease in patients with chronic nephrotic syndrome. No therapeutic trials have tested whether or not pharmacologic interventions will benefit either the cardiac or renal disease that ensues in patients with chronic persistent nephrotic syndrome. Thus, considerably more data are needed to help clarify this important area.
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PMID:Is the aggressive management of hyperlipidemia in nephrotic syndrome mandatory? 140 64

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia and hypercholesterolemia. Hypercholesterolemia is in some cases a risk factor for atherosclerosis in this group of patients. The lipid plasma spectrum was studied in 45 patients with the nephrotic syndrome. Most pronounced changes of the lipid composition of the plasma were revealed in patients with systemic lupus erythematosus and a special form of mesangio-proliferative glomerulonephritis which is characterized by a torpid course and rapid development of chronic renal failure. Plasma atherogenicity was calculated according to the index of plasma atherogenicity. A high atherogenicity index was revealed in patients with an association of the nephrotic syndrome and arterial hypertension. Plasma atherogenicity is determined mainly by the level of high-density-lipoprotein cholesterol.
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PMID:[Lipidemia in the nephrotic syndrome and the atherogenicity of the plasma]. 145 41

The nephrotic syndrome is often accompanied by hyperlipidemia associated with an increased risk of accelerated atherosclerosis. The present study was undertaken to evaluate the effects of pravastatin, a novel competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the serum lipids and apolipoproteins in patients with this syndrome and marked hyperlipidemia. Eleven adult patients received 10 mg of pravastatin twice daily for 4 to 8 weeks. The total serum cholesterol decreased from 426 +/- 44 to 309 +/- 18 mg/dl (-27.4%, mean +/- S.E.; p less than 0.01) following administration of pravastatin. The serum triglyceride decreased from 332 +/- 122 to 229 +/- 50 mg/dl (-30.9%), although this change was not significant. Despite the fact that the HDL cholesterol level was barely changed (51 +/- 7 to 51 +/- 6 mg/dl), the LDL cholesterol fell from 313 +/- 30 to 211 +/- 16 mg/dl (-32.5%; p less than 0.005), and the LDL to HDL cholesterol ratio fell from 7.57 +/- 1.59 to 4.94 +/- 0.88 (-34.8%; p less than 0.05). These changes caused the atherogenic index to decline from 9.6 +/- 2.4 to 6.1 +/- 1.2 (-36.5%; p less than 0.05). No significant alterations could be found among apolipoproteins A-1, A-2, B, C-2, C-3, and E. During the present study period, pravastatin was well tolerated and did not affect the serum protein, albumin, serum urea nitrogen, creatinine levels, or urine protein excretion. Also, there were no serious adverse effects. Pravastatin appears to be effective for treating patients with hyperlipidemia of the nephrotic syndrome.
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PMID:Effects of pravastatin on serum lipids and apolipoproteins in hyperlipidemia of the nephrotic syndrome. 163 84

The abnormalities of lipid metabolism in nephrotic syndrome consist in an increase in total and low-density lipoprotein (LDL) cholesterol, apolipoproteins B (ApoB), C-II and C-III, associated in patients with heavier or marked hypoalbuminemia with an increase in triglycerides and very low-density lipoprotein (VLDL) cholesterol, while the high-density lipoproteins (HDL) are distributed abnormally (increased HDL3 fraction and decreased HDL2 fraction) and the Apo A-I to Apo B ratio is reduced. Both increased hepatic lipoprotein synthesis and reduced removal capacity contribute to this hyperlipidemia. Proteinuria may lead to the lipoprotein abnormalities through stimulation of VLDL synthesis by the liver induced by hypoalbuminemia, although it has been more recently suggested that urinary protein loss is associated with the urinary loss of some important cofactor for the regulation of lipid synthesis or catabolism. Treatment of lipid abnormalities in patients with long-lasting heavy proteinuria is mandatory, because they may cause or contribute to accelerated atherosclerosis, but also because they appear to accelerate progression of renal disease by favouring mesangial sclerosis. Four groups of lipid-lowering drugs have been tested: 1) bile acid-binding resins; 2) fibric acid; 3) probucol; 4) inhibitors of HMG CoA reductase. The drugs of the last group appear to be effective and safe in short-term experiments, but long-term studies are necessary to confirm their validity. A dietary approach, consisting in a strictly vegetarian soy diet, very rich in poly- and monounsaturates fatty acids, has been recently tested by the author, with very promising results.
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PMID:Lipid changes in the nephrotic syndrome: new insights into pathomechanisms and treatment. 175 84


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