Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between serum lipids, apolipoprotein levels including apolipoprotein (a) to albumin excretion rate (AER) in 52 (17 male, 35 female) type 2 diabetic patients was studied. Patients were classified in groups as follows: (1) patients with normal AER (< 30 mg/24 h); (2) patients with microalbuminuria (AER 30-300 mg/24 h), and (3) patients with macroalbuminuria (AER > 300 mg/24 h). Apolipoprotein B levels were significantly (p < 0.05) elevated in the patients with macroalbuminuria compared to the normoalbuminuric group. Further, we observed a significant correlation between total cholesterol, low-density lipoprotein cholesterol, as well as apolipoprotein B levels to the degree of AER. No correlation between apolipoprotein (a) levels and AER, which is in contrast to recently published data for type 1 diabetic patients, was found. Systolic blood pressure was significantly higher (p < 0.002) in the patients with micro- and macroalbuminuria compared to the group with normal albumin excretion, whereas no relationship between diastolic blood pressure and albuminuria was found. We conclude that elevated increased atherogenic lipid fractions in addition to systolic hypertension may contribute to an increased cardiovascular risk in type 2 diabetic patients with proteinuria.
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PMID:Apolipoprotein (a) levels and atherogenic lipid fractions in relation to the degree of urinary albumin excretion in type 2 diabetes mellitus. 819 Jan 78

In a prospective follow-up of 30 patients with type 1 diabetes and nephropathy, serum cholesterol, triglycerides, apolipoprotein Al and B, and lipoprotein(a) were determined to study their relationship to the rate of decline in glomerular filtration rate. The patients had proteinuria and advanced nephropathy with a mean +/- SD glomerular filtration rate of 39 mL/min/1.73 m2. The decline in glomerular filtration rate was determined during 2.5 +/- 0.5 years. High serum cholesterol, triglycerides, and apolipoprotein B were correlated to a more rapid deterioration in kidney function. The rate of decline in glomerular filtration rate was 1.0 +/- 2.5 mL/min/yr in the 10 patients with the lowest cholesterol level, compared with 4.5 +/- 3.2 mL/min/yr in the patients with the highest serum cholesterol (P = 0.015). The combined effect of the measured lipids, blood pressure, type of antihypertensive treatment, protein intake, proteinuria, and hemoglobin A1C on the rate of decline in glomerular filtration rate was assessed by multiple regression analysis. The measured factors together had a high explanatory power for the rate of decline in glomerular filtration rate. In this model, 73% of the variation in decline in glomerular filtration rate was explained by the measured variables (multiple r2 = 0.73). Low cholesterol and treatment with an angiotensin-converting enzyme inhibitor were the strongest predictors of a favorable renal prognosis. This suggests that hypercholesterolemia is an important risk factor for diabetic nephropathy.
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PMID:Cholesterol: a renal risk factor in diabetic nephropathy? 832 83

Lecithin:cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP) are key factors in the esterification of free cholesterol, and the distribution of cholesteryl ester among lipoproteins in plasma. Alterations in these processes may play a role in the lipoprotein abnormalities associated with glomerular proteinuria. The activities of LCAT and CETP were measured using excess exogenous substrate assays in nine patients with nephrotic-range proteinuria and in 18 matched controls. The proteinuria-lowering effect of four weeks of angiotensin converting enzyme (ACE) inhibition with enalapril was also studied. Plasma very low lipoprotein and low density lipoprotein (VLDL and LDL) cholesterol, triacylglycerol and apolipoprotein B levels were significantly elevated in the patients compared with controls. High density lipoprotein (HDL) total cholesterol, free cholesterol, cholesteryl ester and the free cholesterol/cholesteryl ester ratio in HDL were lower. Total plasma apolipoprotein A1 was normal. Plasma LCAT and CETP activities were elevated in the patients by 30% (P < 0.01) and by 39% (P < 0.01), respectively, and were both inversely related to serum albumin. VLDL and LDL cholesterol levels were positively related to LCAT and CETP activities, whereas the HDL free cholesterol content was inversely related to LCAT activity. ACE inhibition resulted in a 40% reduction of proteinuria, a partial normalization of LCAT activity, and a decrease in VLDL and LDL cholesterol. In conclusion, elevated activities of LCAT and CETP may provide a mechanism that contributes to the low proportion of cholesterol in HDL relative to that in VLDL and LDL, as well as to the compositional changes of HDL seen in glomerular proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of elevated lecithin: cholesterol acyltransferase and cholesteryl ester transfer protein activities in abnormal lipoproteins from proteinuric patients. 835 71

The hypothesis that increased cholesterol synthesis provides a mechanism that contributes to nephrotic syndrome-associated hyperlipidemia is mainly based on experimental evidence. The serum level of the cholesterol precursor, lathosterol (expressed per millimole cholesterol), is a reliable marker of whole-body cholesterol synthesis in normocholesterolemia and primary hypercholesterolemia. Serum lathosterol and lipoprotein levels were measured in 11 moderately hyperlipidemic patients with nephrotic-range proteinuria and 22 matched controls. The proteinuric patients were evaluated before and during three antiproteinuric treatment periods with angiotensin-converting enzyme (ACE) inhibition therapy (n = 6) or a low-protein diet (n = 5) alone, in combination, and again as a single treatment. In untreated patients, serum total cholesterol, very-low-density (VLDL) and low-density (LDL) lipoprotein cholesterol, apolipoprotein B (apo B), and lipoprotein (a) [Lp(a)] levels were higher than in controls (P < .01 to P < .001), but the lathosterol to cholesterol ratio tended to be lower in patients (0.99 +/- 0.43 micromol/mmol) as compared with controls (1.29 +/- 0.41 micromol/mmol, P < .10). During combined antiproteinuric treatment, total and VLDL + LDL cholesterol, apo B, and Lp(a) decreased (P < .02 to P < .01), but remained higher than levels in controls. Yet the serum lathosterol to cholesterol ratio changed little and was even lower (P < .05) in treated patients than in controls. Serum total cholesterol (r = -.82, P < .01) and apo B (r = -.84, P < .01) were inversely correlated with serum albumin in untreated patients, whereas the serum lathosterol to cholesterol ratio was not (r = -.01, NS). In the patient group, multiple regression analysis showed that changes in the lathosterol to cholesterol ratio during the study were only related to changes in the dietary polyunsaturated to saturated fatty acids ratio (P:S) coinciding with the low-protein diet (P < .01). In contrast, the decrease of VLDL + LDL cholesterol, apo B, and Lp(a) was independently related to reduction of proteinuria (P < .02 to P < .001), but not to changes in the lathosterol to cholesterol ratio. In conclusion, the present data, based on the serum lathosterol to cholesterol ratio, do not support the concept that increased cholesterol synthesis plays an important role in the maintenance of human nephrotic syndrome-associated hypercholesterolemia. Moreover, it appears unlikely that the decrease of apo B-containing lipoproteins with antiproteinuric treatment is attributable to inhibition of cholesterogenesis. These findings warrant further documentation of cholesterol synthesis in human nephrotic syndrome by direct methods.
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PMID:The serum lathosterol to cholesterol ratio, an index of cholesterol synthesis, is not elevated in patients with glomerular proteinuria and is not associated with improvement of hyperlipidemia in response to antiproteinuric treatment. 863 47

Proteinuria in passive Heymann nephritis is primarily caused by reactive oxygen species that are produced by glomerular cells. Reactive oxygen species apparently exert their damaging effects on the glomerular filter by lipid peroxidation and subsequent adduct formation on matrix proteins of glomerular basement membranes. This raised the question as to the source of polyunsaturated fatty acids required as substrates for lipid peroxidation. Here we have localized by immunocytochemistry rat apolipoprotein E and apolipoprotein B within subepithelial immune deposits. Moreover, apolipoprotein B extracted from isolated glomeruli of proteinuric passive Heymann nephritis rats shows degradation and lipid peroxidation adduct formation, similar to apoproteins of oxidized lipoproteins in atherosclerotic lesions. These data provide evidence that lipoproteins accumulate within immune deposits and suggest that their lipids generate lipid-peroxidation-derived reactive compounds.
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PMID:Lipoproteins accumulate in immune deposits and are modified by lipid peroxidation in passive Heymann nephritis. 886 78

To study the relationship of the concentration of serum lipoprotein (a) [Lp(a)] with diabetic complications in non-insulin dependent diabetes mellitus (NIDDM), 100 non-diabetics with 150 patients with NIDDM were compared. There was no difference in Lp(a) concentration (P > 0.5) between the two groups. Lp(a) concentration was not significantly correlated with the levels of total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein A-I, apolipoprotein B in both groups. In NIDDM group, patients with hypertension, macro- and microangiopathy had higher levels of Lp(a) than those without these complications (P < 0.001 and P = 0.002 respectively). Lp(a) level was positively related to presence of macroangiopathy (r = 0.185, P = 0.024) and proteinuria (r = 0.316, P < 0.001) in NIDDM.
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PMID:[Lipoprotein (a) and non-insulin dependent diabetes mellitus]. 938 40

Overt nephrotic syndrome is characterized by albumin and fibrinogen hyperproduction and reduced very low density lipoprotein apolipoprotein B-100 (VLDL apoB-100) clearance. Whether similar changes also occur in low-grade proteinuria is not known. Thus we measured albumin, fibrinogen, and VLDL apoB-100 kinetics in six patients with modest proteinuria and normal creatinine clearance (P) and in ten control subjects (C) by leucine tracer infusion and precursor-product relationships. In P, plasma albumin concentration was decreased (P < 0.003), whereas concentrations of fibrinogen and VLDL apoB-100 were increased (P < 0.001). In P, albumin fractional secretion rate (FSR) was increased (P < 0.01), fibrinogen FSR was normal, and VLDL apoB-100 FSR was decreased (P < 0.03). As a result, in P, absolute secretion rates (ASR) of albumin and fibrinogen were increased (P < 0.03), whereas VLDL apoB-100 ASR was normal. Albumin FSR was inversely correlated to oncotic pressure in P but not in C. These findings suggest that low-grade nephrotic proteinuria is characterized by simultaneous multiple alterations in turnover rates of albumin, fibrinogen, and VLDL apoB-100. Their pathogenesis, however, appears to be multifactorial.
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PMID:Plasma protein synthesis in patients with low-grade nephrotic proteinuria. 1125 66

Hyperlipidemia, an important characteristic of idiopathic nephrotic syndrome in children (NS), is usually observed during the active phase of the disease and disappears with the resolution of the proteinuria. However, persisting lipid anomalies during remission have been reported in a few studies and raise the question of the later development of atherosclerosis. Plasma lipid profiles in 25 children with NS at remission, with or without active prednisone treatment, were compared with those of an age-matched population. The results indicate that plasma total and LDL-cholesterol levels were above the 95(th) percentile for age and sex in 12 of the 25 patients (48%) with 7 of them having apolipoprotein B and triglyceride concentrations above the 95(th) percentile. Moreover, frequently relapsing children were more likely to have abnormal lipid profile during the remission. We conclude that close monitoring of lipid levels during the remission of the NS especially in those with frequent relapses, is necessary to select the high-risk patients.
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PMID:Hyperlipidemic profiles during remission in childhood idiopathic nephrotic syndrome. 1456 52

Nonenzymatic glycation of apolipoprotein B in the low-density lipoprotein (LDL) complex has been considered a proatherogenic modification contributory to the increased susceptibility of patients with diabetes to atherosclerosis. We postulated that glycated LDL concentrations might be associated with other markers of cardiovascular disease. To explore this hypothesis, we measured glycated LDL concentrations by a monospecific immunoassay in 50 patients with type 1 and 100 patients with type 2 diabetes and examined relationships with the amount of albumin excretion and the serum cholesterol and triglyercide concentrations. Plasma glycated LDL showed a significant positive correlation (r = 0.325; P < 0.001) with urinary albumin excretion that was higher in type 1 (r = 0.463) than in type 2 (r = 0.245) patients. The mean glycated LDL concentration progressively increased with increasing albumin excretion when patients were subcategorized into groups of normoalbuminuria, low (</=100 microg/mg of creatinine), and high (101-300 microg/mg) microalbuminuria, and proteinuria. Glycated LDL also correlated positively and significantly with cholesterol (r = 0.578) and triglyceride (r = 0.350) concentrations. The significant correlations in this cross-sectional analysis between glycated LDL and urinary albumin excretion, an index of cardiovascular mortality, and cholesterol and triglyceride concentrations, traditional markers of risk for cardiovascular disease, support the hypothesis that an elevated level of glycated LDL represents an atherogenic risk factor in patients with diabetes.
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PMID:Increased plasma glycated low-density lipoprotein concentrations in diabetes: a marker of atherogenic risk. 1519 38

Literature data point to the relationship between leptin concentration and certain markers of the metabolic syndrome, including cholesterol, triglycerides and apolipoproteins. A substantial lipid metabolism disturbance occurs in children with idiopathic nephrotic syndrome (NS). The aim of the study was to find out whether in NS children, serum and urine leptin levels change proportionally to lipid metabolism disturbances. The study was performed on two groups: (I) 30 children with NS (A) before, (B) during, prednisone therapy after proteinuria regression; (II) 25 healthy children. Serum and urine leptin levels were determined by the immunoenzymatic ELISA method. Serum leptin level in NS children before and after treatment was similar to that in the control group (p>0.05). Leptin urinary excretion in group A was approximately 60 times and in group B 24 times higher than in the controls (p<0.01). Before treatment, children with NS had increased concentrations of TC, TG, LDL, beta-lipoprotein, apolipoprotein B (apo B) (p<0.01) and reduced HDL and apolipoprotein A (apo A) (p<0.01). The conclusions were that: (1) in NS children leptin urinary excretion increases but its level is unchanged in serum; (2) serum leptin level is correlated with lipid parameters.
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PMID:Serum and urine leptin concentration in children with nephrotic syndrome. 1578 10


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