Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal vascular damage caused by arterial hypertension participates in alterations of the systemic vascular function and structure. Nephrosclerosis seems to run in parallel with the systemic atherosclerosis that accounts for the increased cardiovascular morbidity and mortality seen in hypertensive patients. Parameters indicating the existence of an alteration in renal function (increased serum creatinine, proteinuria and microalbuminuria) are independent predictors for an increased cardiovascular morbidity and mortality. Hence, parameters of renal function must be considered in any stratification of cardiovascular risk in hypertensive patients.
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PMID:Renal implications of arterial hypertension. 914 77

In the present paper, longitudinal studies in non-insulin-dependent diabetes mellitus (NIDDM) dealing with risk factors, especially microalbuminuria, blood pressure, and glycemic control, and the course of the kidney function are addressed. The definition of microalbuminuria, limits for abnormal albuminuria, and possible causes of microalbuminuria in NIDDM are discussed. Microalbuminuria is a major independent risk marker for early mortality, and new studies indicate that even "high normoalbuminuria" carries a risk. Furthermore, risk markers agreed on among various studies include apart from abnormal albuminuria, age and preexisting cardiovascular disease, whereas there is some inconsistency concerning glycemic control, lipoproteins, and even hypertension. People with microalbuminuria, NIDDM patients as well as nondiabetics, share an increased prevalence of atherosclerosis and its risk factors as well as an increased TER(alb). Albuminuria in NIDDM may thus have two different causes: general vascular disease and diabetic glomerulopathy. The clinical course of renal function is with large interindividual variation in both patients with or without overt proteinuria. Systolic blood pressure, glycemic control, and level of albuminuria appear to determine the deterioration in kidney function and progression of albuminuria, and to influence the overall prognosis, thus being obvious items for intervention. Long-term intervention studies demonstrating improved survival are, however, still awaited.
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PMID:Microalbuminuria, blood pressure, metabolic control, and renal involvement: longitudinal studies in white non-insulin-dependent diabetic patients. 932 21

Insulin resistance (IR) and secondary hyperinsulinaemia are major risk factors of atherosclerosis and probably also of related glomerulosclerosis. Angiotensin converting enzyme inhibitors (ACEI), while improving IR in essential hypertension, do not improve it in patients with chronic renal disease. Thus, the combination of ACEI and low protein diet was evaluated. Thirty-eight patients with various kidney diseases and mild to moderate impairment of kidney function were included in the study. Thirteen of them suffered from IR. Their dietary protein intake was decreased from > or = 1.0 g/kg/d to 0.6-0.7 g/kg/d. Moreover, they were treated by ACEI enalapril at dosages of 2-10 mg/d depending on the absence/presence and severity of hypertension. The patients were followed for 8 months. No clinically relevant kidney disease progression (KDP) was found. IR patients improved remarkably. IR was examined by the oral glucose tolerance test and glucose, insulin and C-peptide determinations. Their increased plasma triglyceride, VLDL concentrations and proteinuria decreased, HDL concentration increased. Acid-base balance and anaemia did not change. It is concluded that protein restriction in combination with ACEI treatment improve IR and the associated dyslipoproteinaemia and proteinuria.
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PMID:Dietary protein restriction in combination with angiotensin converting enzyme inhibitor improves insulin resistance in patients with chronic renal disease. 940 10

Plasma lipoproteins (LP) may be identified on the basis of density properties or apolipoprotein (apo) composition. ApoB-containing LP occur in VLDL, IDL and LDL. There are several types of apoB-containing LP characterized by specific composition of minor apolipoproteins (apoC, apoE etc.) and lipid constituents (triglycerides and cholesterol), metabolic properties and relative atherogenicity. The alterations of lipoprotein metabolism in renal disease resulting in elevated levels of apoB-containing LP may be reflected in hyperlipidemia. Whereas nephrotic syndrome and heavy proteinuria are associated with increased formation of cholesterol-rich apoB-containing LP in LDL and VLDL, the characteristic feature in renal failure is the accumulation of intact or partially metabolised triglyceride-rich LP in IDL and VLDL. The potentially atherogenic apoB-containing LP have been linked to the pathogenic processes that result in progressive glomerular and interstitial lesions and ultimate loss of renal function. The mechanisms of injury are not fully understood. Receptor- and non-receptor mediated uptake of LP by mesangial cells may induce or accelerate proliferative and sclerotic processes in the glomerular mesangium that are analogous to atherosclerosis in the arterial wall. Changes in glomerular permeability can result in increased filtration of LP that may be internalized by tubular cells and elicit corresponding lesions in the interstitial tissues. The negative impact of proteinuria on the prognosis of renal disease could be mediated in part through an increased filtration of lipoproteins. Induction of hyperlipidemia accelerates glomerular and interstitial damage in experimental renal failure. This can be attenuated by treatment with hypolipemic agents. In patients, increased concentrations of apoB-containing LP are associated with more rapid progression of renal insufficiency in both primary renal disease and diabetic nephropathy. It is, however, presently not known to what extent treatment of the renal dyslipidemia can modify the progression of chronic renal failure. Experimental and clinical evidence suggest that apoB-containing LP may play a pathogenetic role in the progression of renal disease.
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PMID:Progression of renal failure: role of apolipoprotein B-containing lipoproteins. 940 33

Renal vascular damage caused by arterial hypertension participates in the alterations to systemic vascular function and structure. Nephrosclerosis seems to run in parallel with systemic atherosclerosis, which accounts for the increased cardiovascular morbidity and mortality seen in hypertensive patients. Parameters indicating the existence of an alteration in renal function (increased serum creatinine, proteinuria and microalbuminuria) are independent predictors for an increased cardiovascular morbidity and mortality. Hence, parameters of renal function have to be considered in any stratification of cardiovascular risk in hypertensive patients.
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PMID:Prevalence of renal disease in elderly hypertensive patients with cardiovascular problems. 943 74

Hyperfibrinogenemia is a common feature of the nephrotic syndrome, and contributes to increased tendency for thrombosis and atherosclerosis. Its genesis is not certain, but the increase in liver fibrinogen mRNA in nephrotic rats indicates increased synthesis. Data in humans are scarce. We presently compared synthesis rates of fibrinogen and albumin in nephrotic adults (N = 7; plasma albumin 22.3 +/- 0.7 g/liter, proteinuria 12 g/day) and healthy control subjects (N = 8) using a primed/continuous infusion of the stable isotope L-[1-13C]valine for six hours. Absolute synthesis rate (ASR) of fibrinogen was 31 +/- 3 mg/kg/day in nephrotic subjects and 21 +/- 1 mg/kg/day in control subjects (P < 0.05), and positively correlated with plasma fibrinogen (P = 0.0317). The plasma fibrinogen pool was disproportionately increased in the nephrotic patients (271 +/- 30 mg/kg) compared to the controls (126 +/- 8 mg/kg), suggesting decreased fractional catabolic rate as well. The ASR of albumin was increased from 71 +/- 4 mg/kg/day in the controls to 160 +/- 19 mg/kg/day in the patients (P < 0.0001), and strongly correlated with the ASR of fibrinogen (P = 0.0046). Plasma alpha 2-macroglobulin was also elevated and correlated with the albumin synthesis rate, whereas plasma serum amyloid A and C-reactive protein were not elevated. These data suggest that in nephrotic patients the increased albumin synthesis is associated with an increase in synthesis of a specific and coordinated group of proteins, among which is fibrinogen.
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PMID:Proportionate increase of fibrinogen and albumin synthesis in nephrotic patients: measurements with stable isotopes. 945 16

Renal vascular damage caused by arterial hypertension brings about changes in the systemic vascular function and structure. Nephrosclerosis appears to run in parallel with systemic atherosclerosis, accounting for the increased cardiovascular morbidity and mortality in hypertensive patients. Parameters indicating a change in renal function (increased serum creatinine concentration, proteinuria, and microalbuminuria) are independent predictors of increased cardiovascular morbidity and mortality and must therefore be considered in the classification of cardiovascular risk in hypertensive patients.
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PMID:The kidney as part of the cardiovascular system. 1002 47

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.
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PMID:[Antihypertensive therapy in diabetes mellitus]. 1006 31

The administration of L-arginine to normal animals leads to an increase in renal plasma flow and glomerular filtration rate (GFR). Administration on a chronic basis of N-nitro-L-arginine methylester (L-NAME), an antagonist of L-arginine, increases blood pressure and reduces the ultrafiltration coefficient. In rats with ureteral obstruction, the administration of L-arginine increases GFR and renal blood flow in the postobstructive kidney. Administration of L-arginine decreased the macrophage infiltration of the renal parenchyma that occurs in this model. L-arginine administration also blunted the increases in interstitial volume, collagen deposition, and expression of alpha-smooth muscle actin in the obstructed kidney. L-arginine administration to rats with subtotal nephrectomy reduced proteinuria and the number of abnormal glomeruli. Some of these effects may be mediated by nitric oxide (NO). In rats with diabetes, administration of L-arginine decreased hyperfiltration and proteinuria. The role of arginine and NO in glomerular diseases is controversial. In general most of the evidence indicates a beneficial change in the renal pathology and function in animals with glomerulonephritis receiving L-arginine. Most of the evidence indicates that the L-arginine-NO pathway has an important role in ameliorating hypertension, renal disease, inflammation and atherosclerosis.
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PMID:Can L-arginine manipulation reduce renal disease? 1022 37

Lipid abnormalities are associated with various disorders ranging from generalized atherosclerosis to renal diseases, including lipoprotein glomerulopathy that is characterized by glomerular lipoprotein thrombi and causes type III hyperlipoproteinemia, proteinuria, and renal failure. This study examines lipoprotein glomerulopathy, which recurred in a transplanted kidney. Molecular biologic analysis of the patient's apolipoprotein (apo) E gene demonstrated E2/E5 type variants. Immunohistochemical analysis of the diseased kidney demonstrated various lipid peroxidation-specific protein adducts, suggesting a potential role of oxidative stress in this disorder. Recurrence in the transplanted kidney suggested a pathogenic role of extraglomerular humoral component(s) resulting from abnormal lipoprotein metabolism, presumably linked to apo E and other genetic or acquired factor(s). Furthermore, the finding that the patient showed pathologic abnormalities in the transplanted kidney with no clinical signs or symptoms of renal disease indicated that lipoprotein glomerular damage progresses early before any clinical manifestations.
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PMID:Apolipoprotein E2/E5 variants in lipoprotein glomerulopathy recurred in transplanted kidney. 1040 16


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