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)

Atherosclerosis and coronary artery disease (CAD) are now the commonest sequelae of hypertension and all clinical manifestations of CAD occur in excess in persons with elevated blood pressure. Risk increases in relation to the extent of blood pressure elevation whether this is in the systolic or diastolic component, at any age and in either sex. Even isolated systolic hypertension increases cardiovascular risk. Elevated pressures are often accompanied by lipid abnormalities, hyperglycemia, elevated fibrinogen, obesity, and ECG abnormalities, all of which augment the risk. These risk factors associated with hypertension influence the coronary risk potential more than the nature of the blood pressure elevation. Although blood pressure makes an independent contribution to CAD, the risk at any level of pressure is markedly influenced by the cardiovascular risk profile. In mild to moderate hypertension in particular, the risk of CHD is concentrated in those who have impaired glucose tolerance, increased total/HDL ratio, ECG abnormalities, and smoke cigarettes. One or more of these associated risk factors also predisposes to other cardiovascular sequelae of hypertension, including stroke, peripheral vascular disease, and cardiac failure. The presence of organ involvement indicated by proteinuria, evidence of impaired ventricular function, or left ventricular hypertrophy greatly escalates the risk and usually indicates a compromised coronary circulation. Most myocardial infarctions and sudden deaths occur prior to the appearance of such evidence. Hypertensive risk assessment requires consideration of the multivariate risk profile because of the interdependence of the risk factors. The nature and urgency of treatment is better determined from such a risk profile than from the blood pressure parameters alone. Optimal preventive management of hypertension requires more than normalization of the blood pressure if coronary sequelae are to be avoided.
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PMID:Influence of multiple risk factors on the hazard of hypertension. 1152 37

Supplement with keto acids/amino acids (KA) and erythropoietin can independently improve the metabolic sequels of chronic renal insufficiency. Our study was designed to establish whether a supplementation with keto acids/amino acids (KA) exerts additional beneficial metabolic effects in patients with chronic renal insufficiency (CRF) treated with a low-protein diet (LPD) and recombinant human erythropoietin (EPO). In a prospective randomized controlled trial over a period of 12 months, we evaluated a total of 38 patients (20 M/18 F) aged 32-68 years with a creatinine clearance (CCr) of 20-36 ml/min. All patients were receiving EPO (40 U/kg twice a week s.c.) and a low-protein diet (0.6 g protein/kg/day and 145 kJ/kg/day). The diet of 20 patients (Group I) was supplemented with KA at a dosage of 100 mg/kg/day while 18 patients (Group II) received no supplementation. During the study period, the glomerular filtration rate slightly decreased (CCr from 28.2 +/- 3.4 to 26.4 +/- 4.1 ml/min and 29.6 +/- 4.8 to 23.4 +/- 4.4 ml/min in groups I and II, respectively and Cin); this however was more marked in Group II (Group I vs. Group II, p < 0.01). The serum levels of urea also declined (p < 0.01), more pronouncedly in Group I (p < 0.025). In Group I, there was a significant rise in the levels of leucine (p < 0.01), isoleucine (p < 0.01), valine (p < 0.02) and albumin (p < 0.01) and a decrease in protein-uria (p < 0.01). Analysis of the lipid spectrum revealed a mild yet significant decrease in total cholesterol and LDL-cholesterol (p < 0.02), more pronounced in Group I. In Group I, there was a decrease in plasma triglycerides (from 4.2 +/- 0.8 down to values a low as 2.2 +/- 0.6 mmol/L; p < 0.01) whereas HDL-cholesterol levels increased (from 0.9 +/- 0.1 to 1.2 +/- 0.1 mmol/L, p < 0.01). A further remarkable finding was a reduction in the serum concentration of free radicals (p < 0.01). We conclude that a KA supplementation in patients with CRF receiving LPD and EPO potentiates the beneficial effects on metabolism of proteins, amino acids and surprisingly, also lipids. Long-term co-administration of KA, EPO and LPD was also associated with a delay in progression of renal insufficiency and a reduction in proteinuria. Thus, concomitant administration of KA and EPO during a low-protein diet presents an effective treatment modality in the conservative management of CRF.
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PMID:Metabolic effects of keto acid--amino acid supplementation in patients with chronic renal insufficiency receiving a low-protein diet and recombinant human erythropoietin--a randomized controlled trial. 1160

Ketoacids (KA) and recombinant human erythropoietin (rHuEPO) may each, on their own, influence the metabolic status of patients with chronic renal failure (CRF). A long-term prospective randomized study was designed to monitor the metabolic and nutritional status and progression of CRF using three therapeutic protocols: (A) low-protein diet (LPD) with 0.6 g of protein and 35 kcal/kg/day, with recombinant human erythropoietin (rHuEPO) at a dose of 40 U kg/week and keto acids (KA) 100 mg/kg/day, (Group I), (B) LPD and rHuEPO (Group II), and (C) LPD only (Group III). A total of 105 patients (50M/55F), aged 26-78 years, CCr 22-36 ml/min, were monitored at the beginning, and at every 6 months for 3 years in the above three study groups. Group I comprised 35 patients, Group II 38 patients and Group III 32 patients. During follow-up, a significantly smaller decrease in GFR (CCr, Cin) and in I/SCr, and an increase in serum albumin, transferrin, leucine, body mass, index and HDL-cholesterol were found in Group I (all p < 0.01). In addition, significant decreases were also seen in proteinuria, renal fractional leucine excretion and serum triglycerides level (p < 0.01). Co-administration of LPD, rHuEPO and KA thus constitutes an effective alternative to conservative management of CRF, delaying in follow-up period progression of renal failure and correction of metabolic parameters.
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PMID:Effects of low-protein diet supplemented with ketoacids and erythropoietin in chronic renal failure: a long-term metabolic study. 1180 7

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

Apples may have selective effects on abnormalities associated with the plurimetabolic syndrome. Therefore, the effects of 20% lyophilized apple supplementation on plasma and tissue lipids and on protection against susceptibility to oxidative stress and renal dysfunction were investigated in Zucker lean (Fa/-) or obese (fa/fa) rats. The experimental diets were equilibrated for sugar supply, contained 0.25 g/100 g cholesterol and provided only one third of the vitamin E requirement. Obese Zucker rats were hypercholesterolemic with cholesterol accumulation in LDL and HDL fractions. The apple diet lowered plasma and LDL cholesterol (-22 and -70%, respectively, P < 0.01) in obese Zucker rats and, in parallel, reduced triglyceride accumulation in heart and liver. Zucker rats fed the apple diet also had a larger intestinal pool and greater fecal excretion of bile acids. The heart concentration and urinary excretion of malondialdehyde were reduced by apple consumption in obese Zucker rats, suggesting better protection against peroxidation. Glucosuria and proteinuria in obese Zucker rats were also suppressed by the apple diet. In conclusion, despite their moderate fiber content, apples improve substantially the lipid status and peroxidative parameters in obese Zucker rats, suggesting that other plant constituents such as polyphenols are involved in these effects.
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PMID:Lyophilized apple counteracts the development of hypercholesterolemia, oxidative stress, and renal dysfunction in obese Zucker rats. 1209 78

This review covers lipids, apolipoproteins, and receptors involved in the dyslipidemia of the nephrotic syndrome in humans and in rat or mouse models of the syndrome. It emphasizes research published during the last decade, though earlier work is cited. The focus is on the biosynthesis and catabolism of the plasma lipoprotein density classes and the role of receptors and enzymes in regulating lipoprotein metabolism in nephrosis. Although the factors responsible for the initiation of the hepatic and peripheral cellular responses to proteinuria and hypoalbuminemia remain elusive, recent work highlights the increased risk of atherosclerosis and the progression of renal disease associated with nephrotic dyslipidemia. Understanding of the role of the kidney in the catabolism of apolipoproteins entering the glomerular filtrate has been enhanced by the discovery of the receptor-mediated uptake of apolipoprotein A-I, the main apoprotein of HDL. The following aspects of lipid and lipoprotein metabolism in relation to nephrosis are discussed, with attention paid to differences between experimental nephrosis and the human nephrotic syndrome:(1) Albumin metabolism (2) Lipoprotein metabolism (3) Receptors (4) LCAT and CETP (5) Hepatic and Lipoprotein Lipase (6) Lipid metabolism (7) Lipiduria (8) Hypotheses and Questions (9) Summary.
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PMID:Lipoprotein metabolism in the nephrotic syndrome. 1213 20

Renal reserve is believed to be diagnostic dynamic method for accessing both early renal failure and renal vascular reactivity. The aim of our study was to follow renal reserve during 12 month therapy with omega-3 polyunsaturated fatty acids. Omega-3 was given orally of a: 540 mg of eicosapentaenic acid and 810 mg of docosaheksenic acid daily. Before and after 12 month of therapy renal reserve (expressed as % change of basal creatinine clearance) was estimated during i.v. dopamine infusion in dose 2 ug/min/b.w. Twelve month therapy was associated with increase of renal reserve (respectively 14.86 +/- 16.35 vs 30.25 +/- 14.27%), HDL cholesterol (respectively 47.55 +/- 11.49 vs 58.05 +/- 7.89 mg/dl) and decrease 24 hrs proteinuria (respectively 3.31 +/- 2.01 vs 1.31 +/- 1.37 g/24 h), total cholesterol TCH (respectively 251.15 +/- 50.91 vs 214.15 +/- 24.09 mg/dl), LDL cholesterol (respectively 170.0 +/- 47.22 vs 124.15 +/- 17.93 mg/dl), serum uric acid (respectively 7.53 +/- 1.01 vs 5.59 +/- 0.88 mg/dl), fasting insulinemia (respectively 11.27 +/- 5.28 vs 9.20 +/- 4.80 U/ml) for p < 0.05. The statistically significant correlation coefficient were found only between following parameters: % renal reserve vs insulin (r = -0.55, p < 0.05), delta 24 h proteinuria vs delta TCH (r = 0.69, p < 0.05), delta 24 h proteinuria vs delta LDL (r = 0.51, p < 0.05). Our study suggest that omega-3 therapy improves renal reserve and its effect is to some extend related to improvement of some metabolic disturbances. Also this therapy ameliorate proteinuria which is linked with lipid lowering effect of omega-3.
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PMID:[The effect of therapy with small doses of mega-3 polyunsaturated fatty acid on renal reserve and metabolic disturbances in patients with primary IGA glomerulopathy]. 1247 95

Information about lipid abnormalities and the effect of lipid lowering therapy in the early stage of renal disease is limited, while preventive treatment in this stage might be much more beneficial. Lipid profiles and risk factors were assessed in 150 consecutive, non-diabetic patients. Preventive therapy consisted of cholesterol-reduced diet and atorvastatin 10 mg daily. Patients were considered at risk for cardiovascular disease if LDL-cholesterol was >2.6 mmol/l in the case of manifest cardiovascular disease (n=28) or when they had manifest cardiovascular risk factors (n=105) or if LDL was >3.5 mmol/l (n=17). A total of 128 patients (85%) had increased LDL. In men <60 years and women <40 years, total cholesterol was higher than in the general population. Linear regression analysis showed a decreased creatinine clearance to be significantly associated with the lipid profile. For a 10 ml/min decrease of creatinine clearance, a 0.085 increase of the total cholesterol to HDL ratio was observed (P=0.005). In similar analyses, proteinuria was strongly associated with cholesterol and triglycerides. An increase of 0.28 of the total cholesterol/HDL ratio was observed for each gram per 24 h proteinuria (P<0.001). On atorvastatin 10 mg daily, 30 of 60 treated patients had achieved their target LDL value. On average, LDL-cholesterol was reduced by 39% and triglycerides by 18%. No patient had to interrupt their treatment because of adverse side-effects. In conclusion, the majority of patients had an elevated LDL and other lipid abnormalities. Short-term therapy with atorvastatin and a cholesterol lowering diet appears to be safe and effective. It is probably useful to determine the lipid profile in patients with renal failure already in an early phase and to start lipid lowering treatment as soon as abnormalities are found.
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PMID:Atorvastatin and the dyslipidemia of early renal failure. 1248 66

Ramipril is safe and effective in the treatment of hypertension and heart failure, but this is not reviewed here. Ramipril is a lipophilic angiotensin-converting enzyme inhibitor suitable for once-daily administration. In addition to decreasing angiotensin II and increasing bradykinin levels, ramipril increases the levels of vasodilatory renal medullary neutral lipids and inhibits platelet-derived growth factor-induced proliferation of glomerulus cells. Ramipril also decreases transforming growth factor-beta in the kidney. Changes in kidney structure and proteinuria are characteristics of the streptozotocin (STZ) rat model of diabetes, and these are prevented by ramipril. In STZ diabetes, doses of ramipril that have no effect on blood pressure reverse vascular hypertrophy. In animal models of kidney failure (subtotal nephrectomy, stroke-prone spontaneously hypertensive rats), ramipril is renoprotective and some of this renoprotective effect is independent of blood pressure lowering. In humans, clinical doses of ramipril probably do not modify glucose metabolism but do reduce the levels of LDL- and HDL-cholesterol. In clinical trials of renal effects, ramipril has been shown to increase cortical nephron flow in hypertension and to reduce proteinuria in patients with and without diabetes and/or hypertension. Some of the smaller clinical trials showed beneficial effects on kidney function with low doses of ramipril that do not lower blood pressure. A large clinical trial in nondiabetic proteinuria, the Ramipril Efficacy in Nephropathy (REIN) trial, has shown that ramipril 1.25 mg/day, which does not lower blood pressure, arrested the decline in glomerular filtration rate and prolonged the time to end-stage renal failure. In diabetic patients who have had a previous cardiovascular event or having one other cardiovascular risk factor, the MICRO-HOPE clinical trial showed that ramipril lowers the combined risk of myocardial infarction, stroke and cardiovascular death by 25%. In conclusion, ramipril has proven beneficial effects in kidney disease alone or in association with diabetes and in diabetes without kidney disease, and is the pril for diabetes and kidney disease. (c) 2001 Prous Science. All rights reserved.
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PMID:Is Ramipril the pril for diabetes and kidney disease? 1276 20

There appear to be ethnic disparities in frequencies of diabetic complications in type 2 diabetic patients and such data from Asian countries are relatively few and limited. Thai type 2 diabetic patients who attended the diabetic clinic at Prince of Songkla University hospital during January-December 1997 and had no history of coronary heart disease (CHD) and stroke were studied to determine cause of death and to establish the incidence of and risk factors for cardiovascular disease (CVD). All patients were followed to death or to the end of year 2001. End-points included death from any cause, fatal and nonfatal CHD, fatal and nonfatal stroke and lower-extremity amputation. There were 229 patients who were followed for 4.2+/0.7 (S.D.) years (range: 0.6-5.0) with total follow-up period 958.2 patient-years. Twenty-nine patients died during follow-up; the total mortality rate was 30.3 (95%CI 20.2-43.4)/1000 patient-years. Of these, 9(9.4/1000 patient-years; 95%CI 4.3-17.8) died from sepsis, 7(7.3/1000 patient-years; 95%CI 2.9-15.0) from CVD, 5(5.2/1000 patient-years; 95%CI 2.7-12.2) from end-stage renal disease, 3(3.1/1000 patient-years; 95%CI 0.6-9.2) from malignancy and 1(1.0/1000 patient-years; 95%CI 0.03-5.8) from peripheral vascular disease. The incidences of fatal and nonfatal CHD as well as fatal and nonfatal stroke were 21.4(95%CI 13.0-33.0)/1000 and 12.8(95%CI 6.6-22.4)/1000 patient-years, respectively whereas the incidence of lower-extremity amputation was 4.3(95%CI 1.2-10.9)/1000 patient-years. Age, the presence of proteinuria and serum HDL-C < or = 0.9 mmol/l were independent risk factors of CHD with the respective Hazard ratios 1.09(95%CI: 1.02-1.17; P=0.016), 4.41(95%CI: 1.18-16.45; P=0.027) and 3.91(95%CI: 1.20-12.80; P=0.024). In conclusion, sepsis and CVD were the major causes of death accounting for approximately 50% of total mortality in Thai type 2 diabetic patients. Age, the presence of proteinuria and low HDL-C were independent risk factors for the development of CHD. The mortality from and the incidence of CHD in Thai type 2 diabetic patients are lower than those reported from Caucasian populations but the incidence of stroke appears to be higher. These findings need to be confirmed by a large-scale population-based study.
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PMID:Causes of death, incidence and risk factors of cardiovascular diseases in Thai type 2 diabetic patients: a 5 year follow-up study. 1282 63


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