Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microalbuminuria in the general population is associated with recognized risk factors for cardiovascular disease such as hypertension, hyperglycemia, hyperinsulinemia, and hyperlipidemia; and it is an independent predictor of subsequent cardiovascular mortality in hypertensive, diabetic, and elderly populations. Although different methods have been used for measuring and expressing urinary albumin excretion and a variety of cutoff levels have been used for defining microalbuminuria, prevalence of microalbuminuria appears to be higher in non-Europeans (8%-28%) than in Europeans (2%-10%). However, because of the large within-individual variability of urinary albumin excretion and the relatively low prevalence of microalbuminuria, large studies are required to detect statistically significant associations between albuminuria and cardiovascular risk factors. Evidence presented here supports the proposition that microalbuminuria represents a marker of cardiovascular disease risk in nondiabetic individuals as well as diabetic individuals. Moreover, because of a high sensitivity of the test and because albuminuria is a concomitant of many forms of renal disease, microalbuminuria also has a role in detecting patients with renal involvement associated with essential hypertension, lupus erythematosus, women with pre-eclampsia, and subjects with unsuspected primary and secondary nephropathies.
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PMID:Epidemiology of microalbuminuria in the general population. 808 51

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.
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PMID:[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus]. 814 30

Autonomic and peripheral nerve function was examined in a group of patients with primary biliary cirrhosis using standard cardiovascular reflex tests and peripheral nerve conduction studies. Sixty-three percent had cardiovascular autonomic dysfunction with predominantly parasympathetic abnormalities. Symptoms of peripheral neuropathy were rarely volunteered spontaneously but occurred frequently when specifically sought; 40.7% had definite peripheral neuropathy, with symptoms and/or signs plus peripheral neurophysiological abnormalities. A close association between autonomic and peripheral nerve function was found with correlation between the heart rate variation on deep breathing and both peroneal nerve conduction velocity (r = 0.67, P < 0.001) and sural nerve conduction velocity (r = 0.52, P < 0.008). Correlations were also noted between other autonomic tests and peripheral nerve function. Both autonomic and peripheral nerve function correlated with serum bilirubin and albumin; no significant association was noted with vitamin E deficiency or hyperlipidaemia. A generalised neuropathy with peripheral and autonomic abnormalities is common in primary biliary cirrhosis and could be related to hepatic damage. Although rarely clinically disabling, the autonomic impairment associated with this neuropathy may be of prognostic significance.
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PMID:Autonomic and peripheral neuropathy in primary biliary cirrhosis. 769 49

The nephrotic syndrome is a consequence of urinary loss of intermediate-sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Pathophysiologic changes are a consequence of the nature of the proteins lost and of the proteins that are increased in plasma to replace them. Plasma oncotic pressure (pi) falls because of the replacement of relatively small plasma proteins by larger ones. Decreased pi increases transudation of fluid into the interstitium and favors edema. This is exacerbated by causing renal insensitivity to atrial natriuretic factor (ANF), primary renal sodium retention, and plasma volume expansion. Many proteins lost in the urine, such as erythropoietin and IgG, are not defended by increased synthesis. Their loss may result in reduced immunity, anemia, and endocrinopathies. Albumin synthesis can be increased by dietary protein augmentation; however, urinary protein losses also increase, offsetting any palliative effect of increased albumin synthesis on albumin stores. The synthesis of many other proteins secreted by the liver is also increased, causing an elevation in plasma levels of several large proteins, including lipoproteins and elements of the coagulation cascade. This results in hyperlipidemia and, in conjunction with the urinary loss of smaller proteins that impede coagulation, a hypercoagulable state. Lipoprotein catabolism is also reduced as a consequence of proteinuria contributing to increased lipid levels.
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PMID:Nonrenal complications of the nephrotic syndrome. 819 77

Considerable experimental evidence indicates that hyperlipidemia can induce glomerular injury. The importance of lipids in the progression of established glomerular disease has not been established and is of clinical relevance because of the frequent association of lipid abnormalities with human renal disease. In the present study, 26-week-old hyperlipidemic obese Zucker rats (OZRs) with established nephropathy were treated for a period of 18 weeks with daily injections of the cholesterol synthesis inhibitor lovastatin (4 mg/kg). Compared with control OZRs treated with vehicle, lovastatin-treated OZRs had significantly (P < 0.05) lower serum cholesterol and triglyceride levels throughout the treatment period. Blood pressure and urine albumin excretion in lovastatin-treated OZRs were reduced over the first 12 weeks of therapy, but increased toward the levels in the control OZRs at the end of the protocol. After 18 weeks of therapy, the incidence of glomerulosclerosis in lovastatin-treated OZRs (23.2% +/- 5.8%) was approximately half of that in vehicle-treated OZRs (44.6% +/- 7.7%) (P < 0.05). The reduction in glomerular injury in lovastatin-treated OZRs was not associated with changes in either glomerular area or glomerular macrophage content. In separate experiments, mesangial cells were cultured from glomeruli isolated from 26-week-old proteinuric OZRs. Lovastatin (5 to 40 mumol/L) caused a significant dose-dependent inhibition of serum-stimulated mesangial cell DNA synthesis. The inhibitory effects of lovastatin were completely prevented in the presence of exogenous mevalonate (100 mumol/L). Thus, lovastatin retarded the progression of established glomerular disease in OZRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lovastatin retards the progression of established glomerular disease in obese Zucker rats. 832 99

Insulin resistance in Type 1 (insulin-dependent) diabetes mellitus may be associated with raised erythrocyte sodium-lithium countertransport activity in patients with hypertension, or nephropathy, or both. However, in these circumstances it is difficult to separate the impact of hypertension, hyperlipidaemia and nephropathy on erythrocyte sodium-lithium countertransport from that of insulin resistance. We have therefore examined the relationship between insulin-mediated glucose disposal and erythrocyte sodium-lithium countertransport in 41 normotensive (mean blood pressure 120/74 mmHg), normoalbuminuric (mean albumin excretion 6.2 micrograms/min), normolipidaemic (mean serum cholesterol 4.3 mmol/l and mean serum triglycerides 1.0 mmol/l) Type 1 diabetic patients. Erythrocyte sodium-lithium countertransport was on average 0.31 mmol Li.h-1.l erythrocytes-1 (range 0.07-0.69). Nine patients had values above 0.40 mmol Li.h-1.l erythrocytes-1 (0.51 +/- 0.10 mmol Li.h-1.l erythrocytes-1). The patients with high erythrocyte sodium-lithium countertransport were matched for age, sex, BMI, HbA1 and duration of diabetes, with nine patients with normal erythrocyte sodium-lithium countertransport. Insulin-mediated glucose disposal was evaluated during the last hour of a euglycaemic clamp (insulin 0.015 U.kg-1.h-1; blood glucose clamped at 7.0 mmol/l). The free insulin levels were comparable between the patients with high and normal erythrocyte sodium-lithium countertransport (37.2 +/- 14.7 mU/l and 34.7 +/- 17.2 mU/l respectively). Insulin-mediated glucose disposal was on average 3.1 +/- 1.5 (range 0.8-6.8) mg.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Erythrocyte sodium-lithium countertransport activity and total body insulin-mediated glucose disposal in normoalbuminuric normotensive type 1 (insulin-dependent) diabetic patients. 843 53

The pathophysiological mechanisms resulting in hyperlipidaemia in albuminuric insulin-dependent diabetic patients are largely unknown. Increased non-specific hepatic protein synthesis as a response to urinary protein loss, has been proposed. However in that case it is unexplained why the plasma concentration of the high density lipoprotein (HDL) subfraction, in contrast to all other lipoprotein subfractions, is normal or even reduced in albuminuric patients. We studied the urinary excretion of HDL-cholesterol in 26 insulin-dependent diabetic patients matched according to sex and age into three groups. I: normal urinary albumin excretion (< 30 mg 24 h-1; n = 8); II: incipient nephropathy (urinary albumin excretion in the range of 30-300 mg 24 h-1; n = 7); and III: clinical nephropathy (urinary albumin excretion > 300 mg 24 h-1; n = 11). Eight normal subjects served as controls. Lipoproteins in urine were separated by ultracentrifugation, and the daily urinary loss of HDL-cholesterol was 1.30 mumol (0.83-2.21) (median and range) in controls, 1.27 mumol (0.56-2.59) in group I, 1.39 mumol (0.55-1.97) in group II and 4.02 mumol (1.33-42.12) in group III (p < 0.01). More than 95% of cholesterol in urine was found in the HDL-fraction. The plasma concentrations of total cholesterol, very low density lipoprotein cholesterol, low density lipoprotein cholesterol and triglyceride were 21-94% higher in patients with clinical nephropathy compared with normal controls and group I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased urinary loss of high density lipoproteins in albuminuric insulin-dependent diabetic patients. 846 18

The objective of this paper is to examine the usefulness of plasmatic fructosamine finding as an indicator of glycemic control in patients with hypocaloric parenteral nutrition with glycerol. Thirty abdominal surgery patients were studied. None displayed malnutrition, diabetes mellitus, hepatopathy, nephropathy or hyperlipemia in the preoperative stage or during the five days of postoperative recovery they were administered hypocaloric parenteral nutrition with glycerol. Their plasma levels of glucose, fructosamine, triglycerides, albumin and total proteins were found in the preoperative stage and on the first and fourth day of postoperative recovery. Following surgery, findings showed an increase in triglycerides and a decrease in the protein compartment, while glycemia levels remained steady. Furthermore there was a positive correlation between the figures for glycemia and later fructosamine figures. The conclusion was that providing hypocaloric nutrition with glycerol does not increase fructosamine levels. This confirmed prior observations on the slightness of its effect on hydrocarbonic metabolisms.
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PMID:[The fructosamine monitoring of the effect on glycemic control of hypocaloric parenteral nutritional support with glycerol]. 847 51

Rats of the Milan normotensive rat strain (MNS) spontaneously develop severe proteinuria and excessive glomerular thromboxane (Tx)A2 production at a young age. These abnormalities are accompanied by podocyte alterations, progressive focal glomerulosclerosis (FGS), and interstitial fibrosis, resembling human FGS. Since it has been shown that pharmacologic Tx-synthase inhibition protects MNS rats from these changes, it was hypothesized that a fish oil (FO) enriched diet, by enhancing TxA3 production instead of TxA2, might afford similar protection, compared with diets enriched in safflower oil (SO) or lard (LD). Rats were pair-fed 11% fat diets from age of 1 to 11 months. Glomerular TxA2 at 11 months was significantly lower in PO-fed rats than in SO- and LD-fed rats (11 +/- 3.0, 69 +/- 3.0, 59 +/- 19.0 nanograms per min/mg, respectively; P < 0.001). At 3 months, urinary albumin excretion was similar among the groups. Over the course of the study, rats fed FO developed significantly less albuminuria than the SO and LD groups (P < 0.001 by analysis of variance for repeated measures), such that the values at 11 months were 25 +/- 5.8, 49 +/- 8.7, and 68 +/- 13.0 mg/24h, respectively. Serum cholesterol and triglycerides were also significantly lower in FO-fed rats than in SO- and LD-fed rats. The extent of FGS was similar in the three groups, but FO-fed rats had less interstitial injury than the other groups. It was observed that a fish-oil diet substantially alleviated albuminuria, normalized nephrotic hyperlipidemia, and reduced interstitial injury, but did not prevent the development of FGS in the MNS model.
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PMID:Fish oil ameliorates renal injury and hyperlipidemia in the Milan normotensive rat model of focal glomerulosclerosis. 858 25

A female, term neonate presented with generalized edema, heavy proteinuria, hypoalbuminemia and hyperlipidemia in the second week of life. The clinical and laboratory features were compatible with the diagnosis of congenital nephrotic syndrome. Treatment included albumin infusion, empirical penicillin, steroid and continuous arterio-venous hemofiltration. Intestinal perforation developed at the 19th day of age and led to a fatal outcome. At autopsy, thrombosis of the superior mesenteric artery and its branches was noted, and histology of the kidney was compatible with congenital nephrotic syndrome of the Finnish type. The risk of thromboembolism, arterial or venous, should be considered in patients with nephrotic syndrome, even in the neonatal period. Preventive measures, including avoiding volume depletion and femoral arterial/venous puncture, are essential in managing these patients. Prophylactic anticoagulation and infusion of fresh frozen plasma may be warranted to avoid such potentially lethal complications of thromboembolism.
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PMID:Mesenteric arterial thrombosis complicating congenital nephrotic syndrome of Finnish type: report of one case. 859 34


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