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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of renal artery stenosis (RAS) in patients with coronary artery disease (CAD) has not been well documented. Over a 9-month period, 196 patients who underwent coronary angiography because of clinically suspected CAD had routine nonselective renal cine or digital subtraction angiography. There were 68 females and 128 males with a mean age of 63 years (range 35-85). Angiographically significant CAD was present in 152 patients (78%). Of the total patient cohort, 29 patients (15%) had mild RAS (< 50%), and 36 patients (18%) had significant RAS (> or = 50%). In patients with normal coronary arteries, only three patients (7%) had RAS. Thirty-three patients (92%) with severe RAS also had CAD. Of these 33 patients, 45% had hypertension, 30% had hyperlipidemia, 24% had diabetes mellitus, 24% had renal insufficiency (creatinine > or = 1.5), and 51% were smokers. In addition, it was noted that 20 of these patients (61%) had two or more of the above-listed clinical parameters. However, univariate analysis using the chi-square test revealed that only CAD (22% P < 0.03) and renal insufficiency (29% P < 0.15) were reliable clinical predictors of RAS. In conclusion, RAS is a frequent finding in patients with CAD, particularly when renal insufficiency is also present.
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PMID:High incidence of renal artery stenosis in patients with coronary artery disease. 803 26

Because of the high rate of spontaneous remission, treatment of membranous nephropathy with prednisolone and chlorambucil is still controversial. The aim of this study was to give this therapy only to those patients at risk of developing renal insufficiency and to test the efficacy of a low-dose therapeutic regimen. Seventeen patients with more than 10 g protein excretion per day (mean 16.9) and/or a deterioration in renal function (mean serum creatinine, 162 mumol/l) were included. Serum total protein, serum lipids, proteinuria, serum creatinine, and blood pressure were measured, along with the diuretic and antihypertensive medication. The observation time before the start of treatment was 27 +/- 27 months. Steroids were given during months 1, 3, and 5 (methylprednisolone 3 x 500 mg intravenously) prednisolone 0.5 mg/kgBW daily per os for 1 week, then tapered by 0.1 mg/kg BW/week for 1 month). Chlorambucil was given during months 2, 4, and 6 at a dose of 0.12 mg/kgBW daily. At the end of treatment proteinuria had significantly decreased (mean of all patients, 7.8 +/- 1.4 g/d) in all patients. Six months after the end of treatment proteinuria was significantly lower than at baseline in 14 of 17 patients. Hypoproteinemia and hyperlipidemia had improved; diuretic and antihypertensive medication were reduced. Elevated serum creatinine decreased in 7 of 9 patients (pretreatment, 227 +/- 39 mumol/l; 6 months, 176 +/- 28 mumol/l). Nonresponders with respect to serum creatinine responded with respect to proteinuria. Regarding adverse effects, two patients complained of dyspepsia while taking steroids; during chlorambucil treatment two patients experienced nausea and lack of appetite, and one developed leukopenia (1600/microliters).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-dose prednisolone/chlorambucil therapy in patients with severe membranous glomerulonephritis. 804 74

Two children with congenital nephrosis of the Finnish type were studied successively at the three stages of the disease: (A) nephrosis, (B) renal insufficiency/peritoneal dialysis and (C) post-transplantation; two additional patients were studied at two stages. Plasma lipoprotein profiles were determined by density gradient ultracentrifugation and lipids by enzymatic methods. Stage A was characterized by hyperchylomicronemia, low high density lipoprotein (HDL) cholesterol and the presence of dense low density lipoprotein (LDL) and HDL particles. Total cholesterol and triglycerides showed great daily variation (5-14 and 5-33 mmol/l, respectively). During stage B, hyperlipidemia weakened. Yet HDL concentration remained low and the concentration of intermediate density lipoproteins (IDL) increased. At stage C, hyperlipidemia had almost subsided, but the presence of IDL persisted. In conclusion, severe hyperlipoproteinemia of congenital nephrosis at the nephrotic stage is attenuated during renal insufficiency and dialysis, and essentially normalizes after kidney transplantation. Yet the presence of IDL implies an increased risk of atherosclerosis.
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PMID:Severe hyperlipoproteinemia in congenital nephrotic syndrome of the Finnish type: effect of dialysis and kidney transplantation. 824 75

Hyperlipidemia has been associated with glomerulosclerosis and a glomerular monocyte infiltrate in models of progressive renal insufficiency. The pathogenesis of hyperlipidemia-induced renal injury remains unknown. We postulated that the effect of hyperlipidemia may be mediated through LDL-induced activation of mesangial cells, which have recently been shown to possess LDL receptors. To test this hypothesis, cultured human mesangial cells were co-incubated with human LDL. Monolayers treated with LDL demonstrated a greater level of tissue culture supernatant fibronectin than control mesangial cells. This correlated with enhanced expression of fibronectin mRNA in LDL-treated mesangial cells. Additionally, LDL conditioning of mesangial cells caused a dose- and time-dependent increase in the expression of monocyte chemoattractant protein-1 mRNA, a monocyte specific chemotactic factor, as well as an increase in the monocyte chemotactic activity of mesangial supernatants. Thus, the deleterious effects of hyperlipidemia on the kidney may be mediated by the mesangial cell through an increase in production of mesangial matrix and recruitment of inflammatory cells to the glomerulus.
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PMID:LDL stimulates mesangial fibronectin production and chemoattractant expression. 843 62

Hyperlipidemia is associated with accelerated glomerular sclerosis in experimental renal insufficiency. To investigate whether the dyslipoproteinemia seen in human renal failure also influences the future course of renal insufficiency, we have correlated plasma levels of lipids and apolipoproteins at start of follow-up with the subsequent change in renal function in 34 adult patients with chronic renal disease. Nineteen patients had primary renal disease, and 15 patients had diabetic nephropathy. Except for antihypertensive therapy no specific treatment to modify the progression of the disease was given during the follow-up. The rate of progression was determined by repeated measurements of the glomerular filtration rate (GFR). The time of follow-up ranged from 12 to 91 months with an average of 39.7 +/- 16.7 months. The mean initial GFR was 34.7 +/- 13.9 ml/min x 1.73 m2 body surface area and the average decline in renal function was -0.27 +/- 0.26 ml/min/month. The entry levels of triglycerides (TG; p = 0.04), very-low-density lipoprotein cholesterol (p = 0.03), apolipoprotein-B (ApoB; p = 0.008) and systolic blood pressure (SBP; p = 0.04) were significantly correlated with the rate of progression. Among lipoprotein variables, ApoB showed the strongest correlation with the decline in GFR. Patients with a progressive course of their disease also tended to have initially higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (NS), whereas the initial plasma concentration of high-density lipoprotein cholesterol did not show an association with the progression of renal insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Apolipoprotein-B-containing lipoproteins and the progression of renal insufficiency. 772 19

Lipoprotein metabolism is altered in the majority of patients with renal insufficiency and renal-failure, but may not necessarily lead to hyperlipidemia. The dyslipoproteinemia of renal disease has characteristic abnormalities of the apolipoprotein (apo) profile and lipoprotein composition. It develops during the asymptomatic stages of renal insufficiency and becomes more pronounced as renal failure advances. The qualitative characteristics of renal dyslipoproteinemia are not modified substantially by dialysis treatment. Patients with chronic renal disease may therefore be exposed to dyslipoproteinemia for long periods of time. The characteristic plasma lipid abnormality is a moderate hypertriglyceridemia. The alterations of lipoprotein metabolism affect both the apoB-containing very low-density and intermediate-density, and low-density lipoproteins and the apoA-containing high-density lipoproteins. The main underlying abnormality of lipoprotein transport is a decreased catabolism of the apoB-containing lipoproteins caused by decreased activity of lipolytic enzymes and altered lipoprotein composition. There is an increase of intact or partially metabolized, triglyceride-rich, apoB-containing lipoproteins with a disproportionate elevation of apoC-III and, to a lesser extent, apoE, resulting in a marked increase of the intermediate-density lipoproteins and an enrichment of triglycerides, apoC-III, and apoE in the low-density lipoproteins. In high-density lipoproteins there are decreases in the concentrations of cholesterol, apolipoproteins A-I and A-II, and the high-density lipoprotein-2 to high-density lipoprotein-3 ratio. These abnormalities result in a characteristic decrease of the apoA-I to apoC-III ratio and anti-atherogenic index apoA-I/apoB. The pathophysiologic links between the renal insufficiency and the abnormalities of lipoprotein transport are still poorly defined. Changes in the action of insulin on lipolytic enzymes, possibly mediated via increased levels of parathyroid hormone, have been suggested to play a contributory role. The clinical consequences of a defective lipoprotein transport may be related to the atherogenic character of lipoprotein abnormalities. Renal dyslipoproteinemia may contribute to the development of atherosclerotic vascular disease and progression of glomerular and tubular lesions with subsequent deterioration of renal function. Dietary and/or pharmacologic intervention may ameliorate the uremic dyslipoproteinemia, but the long-term clinical effects of such treatment have yet to be established.
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PMID:Lipoprotein metabolism and renal failure. 850 11

In children with steroid-resistant nephrotic syndrome (SRNS) hyperlipidaemia may in the long term be associated with progressive renal insufficiency and increased risk of coronary heart disease. We have assessed the efficacy and tolerability of diet prior to and in combination with a hydroxymethylglutaryl CoA reductase inhibitor, simvastatin, in seven children with SRNS with a mean age of 8 years (range 1.8-16.3 years). Dietary advice to maintain adequate energy and protein intakes with reduced saturated fat and cholesterol intake had little impact on lipid levels pre treatment (mean reduction in cholesterol 1 mmol/l, triglyceride 1.1 mmol/l) but was maintained throughout the study duration. The mean cholesterol and triglyceride concentrations pre treatment were 12.1 +/- 2 (SEM) mmol/l and 8 +/- 2.1 (SEM) mmol/l, respectively. On a median simvastatin dose of 10 mg/day (range 5-40 mg) there was a 41% reduction in cholesterol to 6.6 +/- 0.77 (SEM) mmol/l and a 44% reduction in triglyceride to 3.9 +/- 1.38 (SEM) mmol/l at 6 months which was sustained at 12 months in five patients. The drug was well tolerated with no clinical side effects being noted. Over 6 months the mean plasma albumin concentrations increased from 18.2 +/- 1.26 (SEM) g/l to 23 +/- 2.51 (SEM) g/l, accounted for by three patients (1 complete remission, 1 partial remission, 1 end-stage renal failure). Plasma creatinine concentrations remained stable in five patients with two having progressive chronic renal failure. Growth parameters for both weight and height were maintained. Simvastatin has a beneficial effect on abnormal lipid levels in SRNS but the effectiveness of long-term therapy needs to be evaluated.
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PMID:Hyperlipidaemia, diet and simvastatin therapy in steroid-resistant nephrotic syndrome of childhood. 870 4

Renal disease is accompanied by specific alterations of the lipoprotein metabolism. While marked hyperlipidemia is a characteristic finding in the nephrotic syndrome, the dyslipoproteinemia of renal insufficiency is predominantly reflected in an abnormal apolipoprotein pattern but does not necessarily include elevated plasma lipid concentrations. The specific changes in nephrotic syndrome include increased formation primarily of cholesterol-rich and to a varying extent of triglyceride-rich ApoB-containing lipoproteins in the VLDL-LDL density range with little or no change among the ApoA-containing lipoproteins in HDL. The dyslipoproteinemia of renal failure is, on the other hand, mainly characterized by a decreased catabolism of the triglyceride-rich ApoB-containing lipoproteins with increased concentrations of partially metabolized lipoproteins of intermediate and very low density and a decreased concentration of ApoA-containing lipoproteins in HDL. In addition, increased levels of Lp(a) are found both in the nephrotic syndrome and in renal failure. Dialysis treatment appears to have only a modest influence on the renal dyslipoproteinemia. Due to its atherogenic character, the dyslipidemia of renal disease may be related to the accelerated development of cardiovascular disease in these patients.
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PMID:Diagnosis and classification of dyslipidemia in renal disease. 871 66

Patients with renal disease have an increased cardiovascular mortality. Hyperlipidemia, a hallmark of renal disease, is recognized as a principal cause of atherosclerosis. However, it is difficult to prove a pathogenetic role of renal dyslipidemia per se in this increased cardiovascular risk since multiple risk factors are often present in patients with progressive renal insufficiency, e.g. hypertension, diabetes and hypercoagulability. However, evidence is accumulating demonstrating detrimental effects of hyperlipidemia during both initiation and progression of the atherosclerotic process. The present review discusses this evidence in patients with renal disease, and the possible implications for treatment.
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PMID:Mechanisms of cardiovascular injury in renal disease. 871 68

We have analyzed diagnostic efficiencies of the individual "Essential laboratory test" items when these tests were applied to 520 new outpatients in the division of comprehensive medicine in a teaching hospital. The integration of these test results with history-taking and physical examination resulted in 544 primary clinical diagnoses which corresponded to the patient's illness complained and in 361 additional diagnoses unrelated to their chief complaints but found by chance by the addition of the test results. Clinical usefulness of these test items were variable depending on the disease category, demonstrating a superior diagnostic efficiency in infectious or inflammatory diseases, liver and biliary tract diseases, hematological disorders or metabolic diseases such as hyperlipidemia and diabetes mellitus, but a lesser degree of usefulness in gastro-intestinal or neurogenic diseases. Urine urobilinogen could not establish its clinical usefulness because of extremely low diagnostic sensitivity even in liver diseases. The leukocyte differential count provided confirmatory information for infectious or inflammatory diseases and was helpful for the estimation of the etiologic nature of infectious diseases. This study failed to terminate a controversy for the adoption of sialic acid instead of erythrocyte sedimentation rate (ESR) in the "Essential laboratory test" items, since the former test showed lower sensitivity, even though higher specificity, in infectious or inflammatory status than ESR. Low albumin globulin ratio (A/G) revealed equivalent diagnostic sensitivity and specificity to the elevated levels in alpha 1 and/or alpha 2 globulin fractions in infectious or inflammatory status, being helpful for the evaluation of patient's general condition at a glance. Incidental analysis for diagnostic values of cholinesterase and random blood glucose for the detection of fatty liver and diabetes mellitus, respectively, suggested that these two tests may be included in the "Essential laboratory tests". Simultaneous measurement of serum creatinine and blood urea nitrogen levels was recommended for the ambulatory screening of renal insufficiency, rather than the measurement either alone. The results in this study provide scientific bases on the usefulness of the individual test items and should be taken into account in the next version of the "Essential laboratory tests".
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PMID:The results of the "essential laboratory tests" applied to new outpatients--re-evaluation of diagnostic efficiencies of the test items. 875 34


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