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)

Plasma lipoprotein distribution and apolipoprotein concentrations, as well as kidney function and histopathology of heart, aorta, liver and kidney were investigated in 1-year-old Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR). The NAR, particularly the females, were found to be severely hyperlipidemic. Plasma total cholesterol in non-fasted animals was 6.1 +/- 0.3 mM in the female NAR vs. 2.5 +/- 0.2 mM in the female SDR (P less than 0.01). Most of the cholesterol was located in the LDL (1.019-1.063 g/ml) and HDL2 (1.063-1.125 g/ml) density range. Plasma triglycerides were 6.1 +/- 0.6 mM in the female NAR vs. 1.3 +/- 0.3 mM (P less than 0.01) in the female SDR. Plasma phospholipids were raised up to 5.4 +/- 0.3 mM vs. 2.4 +/- 0.1 mM (P less than 0.01). NAR have increased concentrations of plasma apolipoproteins A-I (about 3-4-fold) and B (about 2-fold), but the levels of apolipoproteins A-IV and E are not increased. There was less proteinuria in the male NAR than in the male SDR (P less than 0.01). Relevant histopathological findings in the NAR included hepatocytic lipofuscinosis and hemosiderosis in Kupffer cells. Tubular lesions were more common in kidneys from NAR than from SDR, and included protein casts, cortical lipofuscinosis, proximal tubular hyperplasia and proliferative interstitial nephritis. Glomerular changes were similar in both strains. Calcinosis of the aortic media and the corticomedullary region of the kidney was characteristically present in the female SDR but absent in the female NAR. Atherosclerotic lesions were not observed. In summary, 1-year-old NAR maintained on standard rat chow, are hyperlipoproteinemic. The increased levels of plasma LDL and HDL cholesterol are not associated with an increase in the incidence or severity of atherosclerotic or glomerular lesions.
Atherosclerosis 1991 May
PMID:Hyperlipoproteinemia in one-year-old analbuminemic rats. 187 8

Diabetics have an increased risk of cardiovascular morbidity and mortality. Compelling evidence suggests that there is cause-effect relationship between alterations of serum lipids and lipoproteins, and atherosclerosis and coronary heart disease in non diabetic-population. Among insulin dependent diabetics, the prevalence of macrovascular disease is particularly increased in those with established clinical nephropathy and it has been partly attributed to concomitant hypertension and serum lipoprotein abnormalities. However, the effect of diabetic nephropathy and factors associated with it on Coronary Artery Disease (CAD) appears to be conditional. Many Patients in many studies did not have CAD despite a long duration of persistent proteinuria and renal failure There is the possibility that CAD is an outcome of a multistage process, and diabetes related conditions may accelerate progression through certain stage only. In that case, the pattern of appearance of CAD would be determined by the natural history of atherosclerosis rather than by duration of diabetes. The purpose of our study is to analyze retrospectively the incidence of CAD and its association with blood pressure, serum total cholesterol, HDL cholesterol, duration of diabetes, serum triglycerides and HbAlc in a cohort of insulin dependent diabetic patients without nephropathy.
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PMID:"Cardiovascular risk factors in insulin dependent diabetes". 192 85

It has been recently suggested that focal glomerulosclerosis (FGS) is analogous to atherosclerosis. Obese Zucker (OZ) rats spontaneously develop hyperlipidemia, proteinuria and FGS. To evaluate the role of the monocyte (MO) and its derivatives in the pathogenesis of the lesion, 30 OZ rats and 15 lean littermates (LZ) were followed for up to 240 days of age. At 75, 120 and 240 days of age, groups of 10 OZ and 5 LZ were assessed with respect to serum total and free cholesterol (TC and FC), triglyceride, lipoprotein electrophoresis, renal histology, histochemistry and immunohistochemistry. All serum lipids were raised at 75 days in OZ rats and increased progressively at 120 and 240 days. The early lesions of FGS were first demonstrated in OZ at 120 days with more advanced lesions at 240 days. FGS was seen in LZ only at 240 days when their serum lipids were raised. Intraglomerular MO infiltration was significantly higher in OZ than in LZ at all time periods (p less than 0.01) and greater in glomeruli with FGS lesions than in those without (p less than 0.01 and 120 days and p less than 0.05 at 240 days). Staining for ED1 and Ia antigens with monoclonal antibodies demonstrated increasing numbers of intraglomerular ED1+ and Ia+ cells with increasing age and extent of FGS. The findings suggest a role for intraglomerular macrophages in the pathogenesis of FGS in OZ.
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PMID:Monocytes and macrophages in focal glomerulosclerosis in Zucker rats. 194 26

Patients with insulin-dependent diabetes mellitus (IDDM) have a significantly increased risk of macrovascular disease, particularly if they have persistent proteinuria. To determine whether altered levels of apolipoprotein(a) [apo(a)], the plasminogenlike glycoprotein of the potentially atherogenic lipoprotein(a); contribute to the increased risk of atherosclerosis, apo(a) levels were measured in 107 patients with IDDM and compared with nondiabetic control subjects and male elective coronary artery graft patients. Apo(a) levels were increased in diabetic patients with microalbuminuria (geometric mean 245 U/L, 95% confidence interval [CI] 142-427, n = 30) and albuminuria (mean 196 U/L, 95% CI 97-397, n = 18) with levels comparable to patients with coronary artery disease (mean 193 U/L, 95% CI 126-298, n = 40), which were higher than in the control group (mean 107 U/L, 95% CI 85-134, n = 140; P = 0.016). Apo(a) levels in diabetic patients without microalbuminuria (mean 86 U/L, 95% CI 63-116, n = 59) were comparable with the control population and less than in those with microalbuminuria (P less than 0.001) and albuminuria (P = 0.014). The elevated apo(a) levels found in patients with IDDM and increased urinary albumin loss may contribute to their heightened risk of macrovascular disease.
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PMID:Increased plasma apolipoprotein(a) levels in IDDM patients with microalbuminuria. 204 Mar 96

The nephrotic syndrome comprises proteinuria, oedema, albuminuria, hypoalbuminaemia, and hyperlipidaemia. Some of its manifestations are present throughout the course of progressive renal disease. Hyperlipidaemia is one of the most dramatic of the clinical manifestations of the syndrome, but has not been seen as relevant to the progression of renal disease. Recently, however, increasing interest has been shown in the lipid abnormalities of patients with persistent proteinuria, largely as a result of experimental data which have emphasised the connection between progressive disease and hyperlipidaemia in animal models. This review considers some aspects of the metabolic background against which the pathological changes in animal models of nephrotic syndrome take place. Attention is drawn to analogies between glomerular disease and atherosclerosis. Lack of information on the value of long-term lipid lowering therapy in patients with proteinuria, hyperlipidaemia, and progressive renal disease emphasises the need for long-term studies of lipid-lowering therapy in these individuals. A conceptual framework for understanding the role of lipids is discussed in relation to the underlying disease processes and possible therapeutic approaches in man.
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PMID:Lipids and progressive kidney disease. 204 69

A single i.v. injection of daunomycin (10 mg/kg) into rats produced severe proteinuria and hypercholesterolemia without atherosclerosis on the 20th and 40th days after the treatment. However, these changes were not observed on the 5th day. No change in systolic blood pressure was seen through the 40-day experimental period. Relaxation to acetylcholine, A23187 and nitroprusside was examined in aortic rings precontracted with phenylephrine (3 x 10(-6) M). Acetylcholine-induced relaxation was significantly attenuated in the nephrotic rats on the 20th and 40th days, in comparison to the control animals. In aortic rings taken from control and nephrotic rats on the 40th day, removal of the endothelium or treatment with methylene blue (10(-5) M) completely abolished the relaxation induced by acetylcholine (10(-5) M). In addition, acetylcholine (10(-5) M) induced a transient increase in the aortic cyclic GMP and this increase was completely abolished by removal of the endothelium. In the preparations of nephrotic rats on the 20th and 40th days, the cyclic GMP levels stimulated by acetylcholine (10(-5) M) were decreased to about 50% in comparison to their respective control. A23187 also evoked diminished relaxation in nephrotic rats on the 20th and 40th days. However, on the 40th day after the treatment, the effects of nitroprusside in relaxing the aorta and in elevating the cyclic GMP level in the aorta were not altered by nephrosis. In addition, the nitroprusside-induced relaxation and cyclic GMP accumulation were not affected by removal of the endothelium. These results indicate that endothelium-dependent relaxation is attenuated with the development of nephrosis.
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PMID:Impaired endothelium-dependent relaxation in isolated thoracic aorta of rats with daunomycin-induced nephrosis. 207 10

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Similarities between atherosclerosis and glomerulosclerosis suggest that hyperlipidaemia may contribute to glomerular injury. Dietary supplementation with 4% cholesterol + 1% cholic acid was administered to rats 4 weeks after 1 1/3 nephrectomy and continued for 7 weeks. There was a significant increase in serum cholesterol (peak = 11.52 +/- 1.09 mmol l-1 vs. 4.73 +/- 0.31 on control diet, P less than 0.001) and triglyceride concentrations (peak = 2.31 +/- 0.27 mmol l-1 vs. 1.41 +/- 0.29, P less than 0.05) and a marked increase in beta-migrating lipoproteins. The severity of hypercholesterolaemia was significantly correlated with proteinuria (control diet: r = 0.600, cholesterol diet: r = 0.672, P less than 0.0001) as was hypertriglyceridaemia (control diet: r = 0.544, cholesterol diet: r = 0.678, P less than 0.0001). The percentage of glomeruli containing lipid deposits was increased from 21% to 60% (P less than 0.05). The kidney total cholesterol content was increased from 29.2 +/- 0.8 to 47.7 +/- 3.3 mumols g-1 dry weight (P less than 0.0001), with esterified cholesterol increasing from 7.5 +/- 0.4% to 14.5 +/- 2.1% of total (P less than 0.01). Serum cholesterol concentration was significantly correlated with both glomerular lipid deposition (rs = 0.7195, P less than 0.0001) and tissue total cholesterol content (rs = 0.6053, P less than 0.001). Lipid vacuolation was prominent in the paramesangium and within mesangial cells. Despite these changes hypertension, uraemia, proteinuria and glomerulosclerosis were not significantly increased on the cholesterol diet. Cholesterol deposition in the glomeruli occurs secondary to hyperlipidaemia in rats following subtotal nephrectomy but over 7 weeks no exacerbation of glomerulosclerosis is detectable.
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PMID:The role of lipids in the pathogenesis of glomerulosclerosis in the rat following subtotal nephrectomy. 210 41

The incidence of some risk factors of ischaemic heart disease (IHD) was investigated in a group of 91 type 2 diabetics. A group of 57 patients who had a myocardial infarction was compared with a control group of 34 diabetics without clinical and electrocardiographic signs of IHD. In the group of diabetics with IHD there was a significantly higher proportion of hypertonic patients (70%), as compared with the control group (47%). The diabetics with an infraction in the case-history had a significantly higher mean age and a longer mean duration of diabetes. There was not a significant difference between the two groups as regards mean values of cholesterol, triacylglycerols, blood sugar, urea, creatinine, proteinuria and cerebrovascular attacks. As to metabolic factors, there were significantly higher mean uric acid values in the whole group with a myocardial infarction in the case-history, whereby this increase was more marked in men with IHD. Regression analysis did not reveal a significant correlation between uric acid values and the serum cholesterol or triacylglycerol levels or the incidence of hypertension. A significant biserial correlation between the presence of myocardial infarction and uric acid serum levels persisted also after elimination of the effect of age and creatinine serum levels. Based on these results and analyses of data in the literature, the authors favour the view that uric acid is rather a marker than true risk factor of atherosclerosis in type 2 diabetics.
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PMID:[Uric acid--a risk factor or atherosclerosis marker in type 2 diabetes?]. 213 61

From 1974 to 1989, 18 patients underwent surgical treatment for isolated dissection of the renal artery causing high grade stenosis, including 2 patients with bilateral renal involvement. The causes of renal artery dissection were blunt trauma (1 patient), unsuccessful percutaneous transluminal angioplasty (5) and atherosclerosis (5) or intimal fibroplasia (7) of the renal artery. The most common presenting signs or symptoms of a dissection were hypertension (94%), an abdominal bruit (44%), headache (44%), minimal proteinuria (44%), microscopic hematuria (38%) and flank pain (38%). Renal artery dissection led to segmental or total renal infarction in 8 of 20 involved kidneys (40%). Seventeen patients underwent unilateral surgical revascularization with amelioration of hypertension and preservation of renal function. Three kidneys were lost due to irreversible ischemic damage from an occlusive dissection. Isolated renal artery dissection is an uncommon lesion that can cause hypertension and threaten renal function.
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PMID:Surgical treatment for isolated dissection of the renal artery. 214 39


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