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 connection between lipids and the rate of progression of chronic renal disease was retrospectively examined in 70 patients who were divided into 2 groups according to their baseline creatinine clearance (CCr): Group 1 (Gp1) contained 30 patients with CCr 60-40 mL/min followed for 40.0 +/- 13.3 months; Group 2 (G2) contained 40 patients with CCr 39-15 mL/min followed for 39.0 +/- 18.2 months. The following parameters were considered: basal and final CCr proteinuria per unit of CCr (UProt/CCr); the difference between final and basal UProt/CCr (delta UProt/CCr); the change in CCr/month (delta CCr); baseline triglycerides (TG), total (TC), HDL (HDLC) and LDL (LDLC) cholesterol, Apo AI, Apo B, Lp(a). Besides in basal CCr the 2 groups significantly differed in the final CCr, final UProt/CCr, delta UProt/CCr, delta CCr. No differences were observed concerning lipid parameters except for Lp(a) (G1 14.8 +/- 13.6, G2 28.7 +/- 27.4 mg/dL; p < 0.05). Baseline TG (G1 184.1 +/- 61.3, G2 187.5 +/- 72.1 mg/dL) and Apo B (only G2 1.05 +/- 0.32 g/L) were significantly higher than normal subjects and the Apo AI/Apo B ratio (G1 1.42 +/- 0.43, G2 1.33 +/- 0.45) were significantly lower than in normal subjects. delta CCr, while inversely correlated in both groups with delta UProt/CCr (p < 0.01), only in G2 did it correlate directly with the Apo AI/Apo B ratio (p < 0.05) and inversely with Apo B and LDLC (p < 0.05). Although a correlation between Lp(a) and delta CCr was not found, 20/22 patients (3/5 G1, 17/17 G2) with a level > 30 mg% ran a progressive course. A natural progression of CRI, heralded by an increasing UProt, is highly frequent when baseline CCr is < 40 mL/min; only then lipids seem to add a burden to the renal damage.
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PMID:Role of dyslipidemia in the progression of chronic renal disease. 957 67

The highly atherogenic lipoprotein(a) [Lp(a)] is significantly elevated in patients with renal disease. It is discussed controversially whether Lp(a) concentrations decrease after renal transplantation and whether the mode of immunosuppressive therapy influences the Lp(a) concentrations. In a prospective study the Lp(a) concentrations before and on average 48 months after renal transplantation were measured in 145 patients. The determinants of the relative changes of Lp(a) concentrations were investigated in a multivariate analysis. Patients treated by CAPD showed a larger decrease of Lp(a) than hemodialysis patients, reflecting their markedly higher Lp(a) levels before transplantation. The relative decrease of Lp(a) was higher with increasing Lp(a) concentrations before transplantation in combination with an increasing molecular weight of apolipoprotein(a) [apo(a)]. That means that the relative decrease of Lp(a) is related to the Lp(a) concentration and the apo(a) size polymorphism. With increasing proteinuria and decreasing glomerular filtration rate, the relative decrease of Lp(a) became less pronounced. Neither prednisolone nor cyclosporine (CsA) had a significant impact on the Lp(a) concentration changes. Azathioprine (Aza) was the only immunosuppressive drug which had a dose-dependent influence on the relative decrease of Lp(a) levels. These data clearly demonstrate a decrease of Lp(a) following renal transplantation which is caused by the restoration of kidney function. The relative decrease is influenced by Aza but not by CsA or prednisolone.
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PMID:Lipoprotein(a) plasma concentrations after renal transplantation: a prospective evaluation after 4 years of follow-up. 1040 99

High lipoprotein(a) (Lp(a)) serum concentrations and the underlying apolipoprotein(a) (apo(a)) phenotypes are risk factors for cardiovascular disease in the general population as well as in patients with renal disease. Lp(a) concentrations are markedly elevated in patients with end-stage renal disease. However, nothing is known about the changes of Lp(a) depending on apo(a) size polymorphism in the earliest stages of renal impairment. In this study, GFR was measured by iohexol technique in 227 non-nephrotic patients with different degrees of renal impairment and was then correlated with Lp(a) serum concentrations stratified according to low (LMW) and high (HMW) molecular weight apo(a) phenotypes. Lp(a) increased significantly with decreasing GFR. Such an increase was dependent on apo(a) phenotype. Only renal patients with HMW apo(a) phenotypes expressed higher median Lp(a) concentrations, i.e., 6.2 mg/dl at GFR >90 ml/min per 1.73 m2, 14.2 at GFR 45 to 90 ml/min per 1.73 m2, and 18.0 mg/dl at GFR <45 ml/min per 1.73 m2. These values were markedly different when compared with apo(a) phenotype-matched control subjects who had a median level of 4.4 mg/dl (ANOVA, linear relationship, P < 0.001). In contrast, no significant differences were observed at different stages of renal function in patients with LMW apo(a) phenotypes when compared with phenotype-matched control subjects. The elevation of Lp(a) was independent of the type of primary renal disease and was not related to the concentration of C-reactive protein. Multiple linear regression analysis found that the apo(a) phenotype and GFR were significantly associated with Lp(a) levels. Non-nephrotic-range proteinuria modified the association between GFR and Lp(a) levels. In summary, an increase of Lp(a) concentrations, compared with apo(a) phenotype-matched control subjects, is seen in non-nephrotic patients with primary renal disease even in the earliest stage when GFR is not yet subnormal. This change is found only in subjects with HMW apo(a) phenotypes, however.
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PMID:Lipoprotein(a) serum concentrations and apolipoprotein(a) phenotypes in mild and moderate renal failure. 1061 46

Obesity is very frequently found after renal transplantation (Tx). It may represent risk factor for development of atherosclerosis and chronic allograft nephropathy. In a prospective randomized metabolic study we monitored for a period of 12 months a total of 427 patients (pts) (M 228/F 199) aged 20-70 yrs after Tx. All patients were treated with cyclosporin A and prednisone at standard doses. We compared the findings of 118 pts with a body mass index (BMI) > or = 30 (kg/m2, Group I) with data obtained from 309 pts with BMI < 30 (Group II) one year after Tx. The mean values of the analysed parameters were as follows (Gr I vs Gr II): total cholesterol (TC): 7.2 +/- 2.4 vs 6.1 +/- 2.0, triglycerides (TG) 3.8 +/- 1.6 vs 2.6 +/- 0.6; LDL-cholesterol 4.1 +/- 1.2 vs 3.0 +/- 0.7; fasting glycemia 8.0 +/- 3.2 vs 5.2 +/- 2.0 (all mmol/L, all p < 0.01); HDL-cholesterol/TG 0.28 +/- 0.07 vs 0.38 + 0.06, p < 0.025). The mean values of corrected Ccr, cyclosporine level, Lp(a) and proteinuria did not differ significantly. There were also no statistical differences in apo E isoforms. In conclusion, our data suggest hyperlipidemia-associated obesity should be treated effectively as a high-risk factor after Tx.
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PMID:Hyperlipidemia and obesity after renal transplantation. 1180 13

In 1989, we encountered a 68-year-old male patient with marked hyperlipoprotein(a)emia (hyperLp(a)emia), who was being treated for hypertension and arteriosclerotic obliterans (ASO) at an outpatient clinic of our hospital. He began to develop leg edema in 2002 and was referred to the Department of Internal Medicine. It was determined that he had severe hyperlipidemia (total cholesterol, 362 mg/dl), proteinuria, and hypoalbuminemia, suggesting the presence of nephrotic syndrome. On lipoprotein analysis, he was found to have very high levels of Lp(a) in the plasma (329 mg/dl). Severe atherosclerosis was also found: that is, abdominal aortic aneurysm (AAA) and coronary artery disease (CAD) were detected, in addition to ASO. After remission of the nephrotic syndrome, the plasma Lp(a) level decreased to 204 mg/dl and the total cholesterol concentration decreased to 179 mg/dl, while very high levels of Lp(a) persisted. We estimate that the markedly elevated Lp(a) plasma levels in this patient may have played some role in the progression of atherosclerosis.
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PMID:A case of marked hyperlipoprotein(a)emia associated with nephrotic syndrome and advanced atherosclerosis. 1614 4

Silent myocardial ischemia (SMI) and silent coronary stenoses (CS) are two to seven times more frequent in diabetic patients than in non-diabetic patients. In addition to this, they have a higher predictive value for cardiovascular events than the classical cardiovascular risk factors, either taken alone or combined. Coronary arterial disease is the leading cause of mortality and morbidity in the diabetic population. Altogether, these data suggest that screening for SMI and silent CS is an important issue. We assume that detecting SMI and silent CS improves patient management, and leads to optimised follow-up, action taken on nutrition, exercise and lifestyle, management of the cardiovascular risk factors, and revascularisation procedures whenever possible. However, screening for SMI and silent CS is expensive and may induce morbidity. Selecting the patients with a high a priori risk of SMI and silent CS is therefore of major concern. Carotid or lower limb peripheral arterial disease, proteinuria, male gender, an age greater than 60 years, and two or more cardiovascular risk factors among smoking, microalbuminuria, dyslipidemia, hypertension, a family history of premature cardiac disease, and cardiac autonomic neuropathy have been demonstrated to be the best current predictors of SMI and silent CS. New markers, such as adhesion molecules, Lp(a), inflammation parameters or homocysteine, and endothelium function assessment might be of further help in the future.
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PMID:Markers for silent myocardial ischemia in diabetes. Are they helpful? 1595 27

Familial LCAT deficiency (FLD) is a rare genetic disorder associated with corneal opacities, anaemia and proteinuria with renal failure. Here we report detailed analyses on plasma lipids, lipoproteins, and the molecular defect in two siblings from a Polish family presenting classical symptoms of FLD and their family members with newly discovered Val309Met mutation in exon 6 of LCAT gene. Both patients displayed low total (2.19 and 2.94 mmol/l) and HDL-cholesterol concentrations (0.52 and 0.48 mmol/l), low percentage of cholesteryl esters (CE) (11.1 and 12%), and decreased apo AI and apo AII serum levels. Low LDL-cholesterol, apo B and Lp(a) levels, and increased oleate/linoleate ratios in CE could be of importance in the development of atherosclerosis in these patients with low HDL-cholesterol. LCAT activity was 10% of normal, alpha-LCAT activity was 0, and LCAT concentration was undetectable by immunoassay. Plasma CETP activity was at lower limits of normal. PCR and sequence analysis of DNA from the proband and affected brother revealed a novel G-->A mutation in exon 6 of LCAT gene, which resulted in an amino acid substitution of valine for methionine (Val309Met). The proband and affected brother were both homozygous carriers, while the mother, siblings and children of patients were heterozygous carriers of a newly discovered mutation. This is the first LCAT mutation described in the Slavic population.
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PMID:Familial lecithin-cholesterol acyltransferase deficiency: biochemical characteristics and molecular analysis of a new LCAT mutation in a Polish family. 1605 Dec 54

Hyperlipidemia (HLP), a common complication, is very prevalent in children with primary nephrotic syndrome (PNS). HLP not only significantly increases the cardiovascular risk in adulthood, but also accelerates the progression of renal disease. Proteinuria as the most important pathophysiological change can reduce serum colloid osmotic pressure, which leads to an increase in the synthesis of serum proteins including lipoproteins in the liver for export to the serum. Thus, the severity of lipid abnormalities may correlate with the degree of proteinuria. A total of 378 children with PNS were divided into three groups according to their urinary protein excretion (UPE), group A (50 mg/kg/d < or = proteinuria <100 mg/kg/d, 125 cases), group B (100 mg/kg/d < or = proteinuria <200 mg/kg/d, 132 cases) and group C (proteinuria > or =200 mg/kg/d, 121 cases). In addition, 200 healthy volunteers with neither allergic nor renal disease between 3 and 14 years of age were recruited as the control group. Fasting serum levels of lipoprotein (a) [Lp(a)], total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (apoA1), apoB, and albumin (Alb) were measured. Serum low density lipoprotein cholesterol (LDL-C) was calculated by the Friedewald formula. As expected, when all patients were compared with healthy children in this study, UPE and the serum concentrations of Lp(a), TC, TG, HDL-C, LDL-C, and apoB were higher in the PNS than in the control group (p<0.01), whereas for apoA1/B ratio the opposite was observed (p<0.01). Furthermore, patients in group C exhibited significantly higher Lp(a), TC, TG, LDL-C, and apoB concentrations than those in group A or B (p<0.01), whereas for apoA1/B ratio the opposite was found (p<0.01). The increase in serum lipids was accompanied by a significant augmented UPE in all patients (p<0.05). More specifically, positive correlations were observed between serum levels of TC (r=+0.80, p<0.01), HDL (r=+0.49, p<0.01), LDL (r=+0.79, p<0.01), ApoB (r=+0.62, p<0.01) and log proteinuria in group B; additionally, a negative correlation was observed between apoA1/B ratio and log proteinuria in group B (r=-0.38, p<0.01). However, no correlation of serum lipid profiles with UPE was determined in group A and C, respectively (p>0.05). Serum Alb was negatively correlated with Lp(a) (r=-0.96, p<0.01), TC (r=-0.78, p<0.01), TG (r=-0.78, p<0.01), LDL-C (r=-0.88, p<0.01), apoA1 (r=-0.26, p<0.01), and apoB (r=-0.71, p<0.01), while positively correlated with apoA1/B (r=+0.27, p<0.01) in all nephrotic children. Furthermore, no correlation existed between serum lipid profiles and Alb in group A, B and C, respectively (p>0.05). In Conclusion, secondary dyslipidemia in children with PNS is in parallel with the degree of UPE. There are diverse characteristics of lipid metabolism under different UPE. As for the patients with medium-UPE, positive correlation between serum lipids and proteinuria is presented.
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PMID:Characteristics of lipid metabolism under different urinary protein excretion in children with primary nephrotic syndrome. 1946 31

Niacin has profound and unique effects on lipid metabolism. In addition to increasing high-density lipoprotein cholesterol, it is also known to decrease total cholesterol, low-density lipoprotein cholesterol, and triglyceride. Interestingly, the plasma concentration of lipoprotein(a) [Lp(a)], which has been suggested to play a role as an independent risk factor for coronary heart disease, is also decreased by niacin. Therefore, it is not surprising that in the literature it was given unique description as broad-spectrum lipid drug. Its impact is referred to as desirable normalization of a range of cardiovascular risk factors. However, its clinical use is limited due to harmless but unpleasant unique side effect of cutaneous flushing. Interestingly, recent experimental and clinical studies suggest the potential benefit of niacin as a treatment of dyslipidemia and high plasma phosphate associated with chronic kidney disease (CKD). Both dyslipidemia and high serum phosphate levels are shown to be associated with higher cardiovascular mortality. Furthermore, niacin administration improves renal tissue lipid metabolism, renal function and structure, hypertension, proteinuria, and histological tubulointerstitial injury. Further studies are required before the use of niacin for the treatment of both dyslipidemia and hyperphosphatemia with CKD advocated.
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PMID:Niacin as potential treatment for dyslipidemia and hyperphosphatemia associated with chronic renal failure: the need for clinical trials. 2048 51

Lipoprotein(a) is one of the strongest genetically determined risk factors for cardiovascular disease, and patients with chronic kidney disease have major disturbances in lipoprotein(a) metabolism. Concentrations are increased and are influenced by glomerular filtration rate (GFR) and the amount of proteinuria. The reason for this elevation can be increased synthesis, as is the case for patients with nephrotic syndrome or those treated by peritoneal dialysis. In hemodialysis patients, a catabolic block is the reason for this elevation. The elevated concentrations might contribute to the tremendous cardiovascular risk in this particular population. In particular, the genetically determined small apolipoprotein(a) isoforms are associated with an increased risk for cardiovascular events and total mortality.
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PMID:Causes and consequences of lipoprotein(a) abnormalities in kidney disease. 2412 57


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