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)

LCAT activity and mass were assayed simultaneously in 23 members of a new family case, revealing two homozygotes with a markedly low HDL--cholesterol level and ester cholesterol ratio. The LCAT mass in these patients was only 0.8 and 0.9 micrograms/ml, respectively (normal range 4.4-8.1) and their LCAT activity was 4 and 6 nM/ml/h 37 degrees C (normal range 60-120). Apolipoprotein (Apo) A-I and II levels were significantly low; however, apolipoprotein E tended to be high. In two-dimensional electrophoresis, apo A-I isoform visualized the increase of immature apo A-I; that is, A-I2. One subject showed the clinical characteristics of classic LCAT deficiency; however, the other, who was a vegetarian, showed corneal opacities and red cell deformity, but not proteinuria. This suggests that a low fat diet which decreases the level of atherogenic large LDL, may lead to a more favourable prognosis with a reduced risk for renal insufficiency. There were two different types of LCAT abnormality in this family series. Among the 10 examined paternal kindred of the proband who was one of two homozygotes, seven had a low LCAT mass but normal LCAT activity with the exception of one kindred who had a low mass and low activity. In contrast, among his seven maternal kindred examined, two had a low LCAT activity but normal mass.
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PMID:A new case of familial lecithin: cholesterol acyltransferase (LCAT) deficiency--paradoxical findings regarding LCAT mass and activity in 23 members of a family. 263 46

The association of apolipoprotein E (apo E) genetic polymorphism, particularly apo E2, with renal failure (plasma creatinine > or = 1.4 mg/dl, and urinary albumin excretion index > or = 300 mg/g.creatinine and/or persistent proteinuria) was investigated in 57 non-insulin-dependent diabetic (NIDDM) patients. Apo E2 allele frequency was significantly higher in diabetic patients with renal failure (9.6%) than in diabetic patients without renal failure (3.2%) and in the general Japanese population (3.7%). This finding suggests that apo E2 is associated with renal failure in NIDDM. In addition, to elucidate the association of apo E2 with lipid abnormalities, plasma lipid and lipoprotein levels were compared among the apo E2 (E2/2 and E3/2) and E3/3 groups of NIDDM with renal failure (n = 27) and the apo E2 (E3/2) and E3/3 groups of NIDDM with normoalbuminuria (n = 34). In diabetic patients, the apo E2 group with renal failure had significantly higher levels of plasma total cholesterol (T-chol), very-low-density lipoprotein (VLDL)-chol, triglyceride (TG), VLDL-TG and apo E than the apo E3/3 group with renal failure, and had significantly higher levels of plasma T-chol, VLDL-chol, TG and VLDL-TG than the apo E2 and E3/3 groups with normoalbuminuria. Furthermore, the apo E2 group with renal failure had significantly higher ratios of VLDL-(chol/TG) and VLDL-chol/TG (an index of remnants in plasma) than the apo E3/3 group with renal failure and the apo E2 and E3/3 groups with normoalbuminuria. These results suggest that apo E2 leads to the accumulation of TG-rich lipoprotein and remnants in plasma. It is concluded that apo E2 is associated with renal insufficiency in NIDDM and that apo E2 may be a factor that aggravates lipid abnormalities in NIDDM with renal failure.
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PMID:Apolipoprotein E2, renal failure and lipid abnormalities in non-insulin-dependent diabetes mellitus. 798 Jun 94

This report describes a male patient who was found to have proteinuria at age 31. Renal biopsy showed glomerular hypercellularity with enlarged, lipid-filled endocapillary cells. On subsequent lipid analysis there was elevation of cholesterol and triglyceride, with apolipoprotein E genotype E2/E2. The clinical course was complicated by pancreatitis and onset of diabetes. After treatment with gemfibrozil and some improvement of the lipid profile, a second renal biopsy showed marked reduction of the glomerular foam cells, despite an increased level of proteinuria. This case emphasizes the potential role that lipid abnormalities may play in renal dysfunction.
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PMID:Glomerular lipid deposition and proteinuria in a patient with familial dysbetalipoproteinaemia. 886 25

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

Hypercholesterolemia is a major determinant of the decline of renal function in patients with diabetes. Apolipoprotein E polymorphism may influence the metabolism of lipoprotein in diabetic patients. The purpose of this study was to investigate the association between genetic polymorphisms in apolipoprotein E and the progression of diabetic nephropathy in patients with non-insulin-dependent diabetes mellitus over a 10-year period (13 to 37 years; median, 20 years). Subjects with a stable renal function without overt proteinuria had a higher cholesterol level, lower incidences of hypertension and proliferative diabetic retinopathy, and a higher frequency of the E4 allele than subjects with a decline in renal function (end-stage renal failure requiring dialysis treatment). In the diabetic patients, the apolipoprotein E4 carriers had a higher cholesterol level than did the noncarriers. The survival rate from renal disease in the apolipoprotein E4 carriers was higher than in the noncarriers among the diabetic patients. Apolipoprotein E polymorphism and hypertension were identified as independent risk factors for the progression to renal failure. Results indicate that apolipoprotein E polymorphism is associated with the progression of diabetic nephropathy. Presence of the apolipoprotein E4 allele is a protective factor, and other alleles are risk factors.
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PMID:Apolipoprotein E4 reduces risk of diabetic nephropathy in patients with NIDDM. 953 Nov 84

We saw a patient with proteinuria and characteristics of lipoprotein glomerulopathy (LPG). Histologic analysis of renal biopsy showed a thrombus-like substance in the markedly dilated glomerular capillaries, which stained positive with oil red O. Increased concentration of plasma apolipoprotein E (apoE) was also noted. Those findings are consistent with the diagnostic criteria of LPG, as reported by Oikawa et al. In isoelectric focusing gel electrophoresis of apoE, a band (apoE3') between apoE3 and E2 was observed. The patient's DNA sequence exhibited a C to G substitution in exon 3 of the apoE gene at the position of the 25th amino acid, resulting in an amino acid substitution of the arginine residue for cysteine residue. To clarify the pathophysiologic role of this mutation, we investigated the binding and the uptake of apoE3' triglyceride-rich lipoproteins to human umbilical vein endothelial cells (HUVEC). The binding of apoE3'-triglyceride-rich lipoproteins to the cell-surface of HUVEC increased up to 30% to 50%, compared with apoE3-triglyceride-rich lipoproteins. But the uptake of apoE3'-triglyceride-rich lipoproteins into the cells was not different between them. These findings are consistent with the idea that an increase in binding of triglyceride-rich lipoproteins possessing apoE (Arg(25)-->Cys) to endothelial cells may promote deposition of lipid in the glomerular capillaries.
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PMID:Interaction of endothelial cells and triglyceride-rich lipoproteins with apolipoprotein E (Arg-->Cys) from a patient with lipoprotein glomerulopathy. 1183 49

Lipoprotein glomerulopathy (LPG), characterized by glomerular lipoprotein thrombi, presumably composed of abnormal apolipoprotein E (apoE), leads to a progressive decline in renal function and eventually results in end-stage renal failure. A successful treatment for LPG has not yet been established. The authors treated a 36-year-old woman with LPG and exhibiting a nephrotic syndrome using an intensive lipid-lowering therapy consisting of fenofibrate (300 mg), niceritrol (750 mg), ethyl-icosapentate (1,800 mg), and probucol (500 mg). After the start of treatment, a remarkable decrease in urinary protein excretion and improvement in the hyperlipidemia were obtained; proteinuria was no longer detected 11 months after the initiation of treatment. A second biopsy performed 11 months after the initiation of treatment showed the complete disappearance of the lipoprotein thrombi that had been observed in a diffuse and global manner in the first renal biopsy. These findings suggest that typical LPG could be regressed if the abnormal lipoproteinemia is controlled sufficiently.
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PMID:Resolution of typical lipoprotein glomerulopathy by intensive lipid-lowering therapy. 1250 Feb 44

Obesity and hyperhomocysteinaemia are found very frequently after kidney transplantation (Tx). They may independently represent risk factors for development of atherosclerosis and chronic allograft nephropathy. In a prospective metabolic study, we monitored, over a period of 24 months, a total of 118 obese transplant patients [body mass index (BMI) > or =30 kg/m(2)] with hyperhomocysteinaemia. We compared the findings of a new therapeutic regimen at 1 year (start of the study) and 2 years after renal transplantation. Based on a Subjective Global Assessment Scoring Sheet, we started at the end of the first year with an individualized hypoenergic-hypolipidaemic diet (IHHD). Subsequently, after corticoid withdrawal, IHHD was supplemented regularly with orlistat at a dose of up to 3 x 120 mg/day, statins (pravastatin 10-40 mg), folic acid 5 mg/day and vitamin B6 50 mg/day, and followed-up for up to 2 years. All patients were on a regimen of cyclosporin A and mycophenolate mofetil. During the study period, there was a significant decrease in BMI (P < 0.025) and total homocysteine level (P < 0.001). Long-term therapy was associated with a significant decrease in serum leptin (P < 0.001) and lipid metabolism parameters (P < 0.01). The mean values of serum folate and vitamin B6 also increased significantly (P < 0.01); creatinine clearance, mean blood pressure, proteinuria, lipoprotein(a) and apolipoprotein E isoforms did not differ significantly. Based on our results, we assume that obesity and hyperhomocysteinaemia after renal transplantation can be treated effectively by modified immunosuppression (corticosteroid withdrawal), long-term diet (IHHD), folic acid and vitamin B6 supplementation, and drugs suppressing digestion or absorption to reduce atherosclerotic and chronic allograft nephrop-athy processes.
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PMID:Obesity and hyperhomocysteinaemia after kidney transplantation. 1281 77

Nephrotic syndrome is characterized by increased triglycerides resulting from decreased clearance of VLDL and chylomicrons. These triglyceride-rich lipoproteins are structurally altered by interaction with HDL derived from animals with proteinuria and not as a consequence of hypoalbuminemia. HDL isolated from rats with massive proteinuria is depleted in apolipoprotein E (apoE). It is unknown at what threshold of urinary albumin loss HDL structure is altered, and it is unknown what effects proteinuria has on apolipoproteins other than apoE. Two models of albuminuria were used in Sprague-Dawley rats: Adriamycin and passive Heymann nephritis (HN). The adriamycin group was divided into minimal albumin excretion (MAE) and intermediate albumin excretion (MAE, 1 to 40; intermediate albumin excretion, 60 to 210 mg/d per 100 g body wt). Urinary albumin excretion exceeded 300 mg/d per 100 g body wt in the HN rats. HDL apolipoprotein composition was analyzed with SDS-PAGE densitometry and liquid chromatography-time of flight mass spectrometer mass spectrometry. HDL apoA-IV content relative to apoA-I was reduced at all levels of albuminuria (P < 0.0001). ApoE was not reduced in MAE but was significantly reduced in IAE (72%; P < 0.001). By contrast, apoA-II and apoC-III were each significantly increased with increasing UAE. ApoA-IV and apoE were decreased to approximately 10% of control in HDL isolated from rats with HN, whereas apoA-II, apoC-II, and apoC-III were each significantly increased relative to apoA-I. HDL is structurally altered by levels of albuminuria that are insufficient to change serum albumin levels and is progressively altered as albuminuria increases.
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PMID:Graded effects of proteinuria on HDL structure in nephrotic rats. 1578 71

It has not been established firmly whether dyslipidemia contributes independently to the progression of kidney disease. Lipid and lipoprotein parameters, including levels of total, HDL, and LDL cholesterol; triglycerides; lipoprotein(a); apolipoprotein A-IV; and the apolipoprotein E and A-IV polymorphisms, were assessed in 177 patients who had mostly mild to moderate renal insufficiency and were followed prospectively for up to 7 yr. Progression of kidney disease was defined as doubling of baseline serum creatinine and/or terminal renal failure necessitating renal replacement therapy. In univariate analysis, patients who reached a progression end point (n = 65) were significantly older and had higher serum creatinine and proteinuria as well as lower GFR and hemoglobin levels. In addition, baseline apolipoprotein A-IV and triglyceride concentrations were higher and HDL cholesterol levels were lower. Multivariate Cox regression analysis revealed that baseline GFR (hazard ratio 0.714; 95% confidence interval [CI] 0.627 to 0.814 for an increment of 10 ml/min per 1.73 m(2); P < 0.0001) and serum apolipoprotein A-IV concentrations (hazard ratio 1.062; 95% CI 1.018 to 1.108 for an increment of 1 mg/dl; P = 0.006) were significant predictors of disease progression. Patients with apolipoprotein A-IV levels above the median had a significantly faster progression (P < 0.0001), and their mean follow-up time to a progression end point was 53.7 mo (95% CI 47.6 to 59.8) as compared with 70.0 mo (95% CI 64.6 to 75.4) in patients with apolipoprotein A-IV levels below the median. For the apolipoprotein E polymorphism, only the genotype epsilon2/epsilon4 was associated with an increased risk for progression. In summary, this prospective study in patients with nondiabetic primary kidney disease demonstrated that apolipoprotein A-IV concentration is a novel independent predictor of progression.
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PMID:Apolipoprotein A-IV predicts progression of chronic kidney disease: the mild to moderate kidney disease study. 1638 17


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