Gene/Protein Disease Symptom Drug Enzyme Compound
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Concomitant arterial hypertension and metabolic disorders is a frequent finding raising the risk of micro- and macrovascular complications. While prevalence of stroke and myocardial infarction is going down in hypertensives, end-stage renal disease (ESRD) becomes a bigger problem especially in diabetic hypertensives. The metabolic abnormalities are linked to the hypertension by the sympathoadrenal system mediated by insulin resistance (IR); subjects with hyperinsulinemia and increased sympathetic activity tend to have higher blood pressure, typical dyslipidemia, reduced fibrinolytic activity and other risk factors (RF) called metabolic syndrome of IR. Albuminuria (AUR) is considered as an important RF for the development of nephropathy, ESRD, cardiovascular diseases. AUR is a marker of cardiovascular and total mortality in diabetic and/or non-diabetic hypertensives. AUR reflects the endothelial dysfunction not only in glomerulus but also in the other arteries. Tissue Renin-Angiotensin System plays a significant role in the pathogenesis of hypertension and metabolic disorders; it affects the arterial wall, kidneys and heart longitudinally. Life style is very essential in the treatment of hypertension and metabolic disorders: rational diet with reduced amount of salt and animal proteins, non-smoking and sufficient physical activity. Antihypertensive drugs without any metabolic side effects and with the renal protection are necessary for the patients with hypertension and metabolic disturbances. ACE-inhibitors and/or some of the Ca-antagonists seems to be valuable especially as combined therapy.
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PMID:[New approaches in the treatment of hypertension in metabolic diseases]. 972 74

Several observational studies document a considerably increased risk of advanced renal disease, cardiovascular disease, and early mortality in persons with diabetes. Both epidemiologic and observational studies indicate that progression of cardiovascular disease and renal disease is associated not only with high blood glucose levels, but also with hypertension and dyslipidemia. In persons with type 1 diabetes, hypoglycemic and antihypertensive therapy are important in the prevention of cardiovascular and renal disease. In those with type 2 diabetes, hypoglycemic therapy can help to prevent microvascular disease in the retina and in the kidney, and recent studies show that antihypertensive treatment is important in preventing cardiovascular disease. Thus, a multifactorial intervention program is key to preventing complications of hyperglycemia and, equally important, elevated blood pressure and dyslipidemia.
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PMID:Natural history of cardiovascular and renal disease in patients with type 2 diabetes: effect of therapeutic interventions and risk modification. 982 36

Non-immune mechanisms appear to be important in the majority of patients with lupus nephritis and progressive renal injury. Proteinuria, hypertension and dyslipidemia are associated non-immune risk factors often implicated in the deterioration of kidney function. There is ample animal experimental evidence that they are independent risk factors for progressive renal injury and their treatment results in amelioration of renal function. Proteinuria and hypertension, unlike dyslipidemia, have been shown to be independent risk factors for progressive renal injury in patients with lupus nephritis. Treatment of hypertension and proteinuria in the diabetic and non-diabetic progressive renal disease population results in stabilization of kidney function. Response to treatment should target both blood pressure of 120/80 and significant reductions in protein excretion. If protein excretion rate is unaltered by use of an angiotensin-converting enzyme inhibitor and salt restriction, one might resort to the use of an angiotensin II antagonist. Treatment of the dyslipidemia following good control of proteinuria, blood pressure and dietary change may not alter renal progression but should provide similar protection from accelerated vascular disease to the non-renal dyslipidemia population.
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PMID:Management of chronic renal insufficiency in lupus nephritis: role of proteinuria, hypertension and dyslipidemia in the progression of renal disease. 988 5

The proposal that antioxidants may retard the progression of atherosclerosis is not new. Published studies examining the effect of antioxidants on experimental antioxidants extend back to 1940. The results have all been inconsistent. However, the data regarding the beneficial effects of retarding atherosclerotic progression are strong enough to warrant continued research on the lipoprotein oxidation theory or atherosclerosis. However, caution is needed to avoid embracing a concept without proof. It should be noted that the National Cholesterol Education Program does not recommend the use of antioxidant vitamin supplements to reduce CAD. Atherogenesis is produced by multiple factors. To believe that all such factors are mediated by uncontrolled oxidative events is, to say the least, naive. Finally, should antioxidants prove to be effective in retarding coronary atherosclerosis, their place on the therapeutic ladder of CAD prevention would be low. The overwhelmingly proven evidence favors the following factors that have been proven to lower morbidity and mortality due to atherosclerosis: (a) treatment of hypertension, (b) cessation of tobacco use, (c) treatment of dyslipidemia, (d) achieving a normal weight, (e) regular exercise, (f) treatment of homocystinuria, especially in cases with renal disease, and (g) antioxidants.
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PMID:The use of antioxidants in retarding atherosclerosis: fact or fiction? 1007 4

The pathophysiological events regarding the atherosclerotic processes are present already in early childhood. Various clinical trials confirm tight correlation between dyslipidemia and cardiac and cerebrovascular complications. Over the clinical dyslipidemia genetically determined, various systemic diseases can lead to anomalies of the lipidic metabolism. The determination and analysis of the lipidic pattern is essential during childhood and in particular in patients with renal disease for the increased risk of progressive failure of renal function and for the central role of kidney in lipidic homeostasis. Cardiovascular event is the most important cause of mortality in patients with end-stage renal disease. In children with nephrotic syndrome, renal failure, hemodialysis or after renal transplantation, an increase of the serum values of triglycerides, cholesterol, LDL, VLDL is generally observed. The presence of anomalies in lipidic pattern must be considered during the course of renal disease for preventing the progression of renal damage. Thus, the pharmacological therapy and diet permit to prevent the atherosclerotic events.
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PMID:[Lipid metabolism and atherosclerosis risk in renal diseases in pediatric age]. 1021 Sep 42

Mild hyperhomocysteinemia, a putative risk factor for atherothrombotic cardiovascular disease morbidity and mortality, may contribute to the excess incidence of atherothrombotic outcomes in the dialysis-dependent end-stage renal disease population. Hemodialysis access (fistula or graft) thrombosis is an unfortunately common and costly morbidity in this patient population. In this study, using a prospective design, the potential relationship between baseline nonfasting, predialysis plasma total homocysteine (tHcy) levels and vascular access-related morbidity was examined in a cohort of 84 hemodialysis patients with a fistula or prosthetic graft as their primary hemodialysis access. Vascular access thrombotic episodes were recorded over a subsequent 18-mo follow-up period. Forty-seven patients (56% of the total) had at least one access thrombosis during the 18-mo follow-up period (median follow-up, 13 mo; rate, 0.6 events per patient-year of follow-up). Proportional hazards modeling revealed that each 1 microM/L increase in the tHcy level was associated with a 4.0% increase in the risk of access thrombosis (95% confidence interval, 1.0 to 6.0%, P = 0.008). This association persisted after adjustment for type of access (fistula versus graft), age, gender, time on dialysis, diabetes, smoking, hypertension, nutritional status, urea reduction ratio, dyslipidemia, and the presence of previous vascular disease. Elevated tHcy levels appear to confer a graded, independent increased risk for hemodialysis access thrombosis. A randomized, controlled trial examining the effect of tHcy-lowering intervention on hemodialysis access thrombosis appears to be justified.
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PMID:Plasma total homocysteine and hemodialysis access thrombosis: a prospective study. 1023 97

Renal disease is accompanied by characteristic alterations of lipoprotein metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are primarily reflected in an altered apolipoprotein profile rather than elevated plasma lipid levels. Their full characterization requires identification of discrete lipoprotein particles. While nephrotic syndrome results in increased concentrations of both cholesterol- and triglyceride-rich apoB-containing lipoproteins, renal insufficiency is characterized by an accumulation of intact or partially metabolised triglyceride-rich apoB-containing lipoproteins. The dyslipidemia has been discussed as a contributory factor for the progression of renal insufficiency through development of glomerulosclerosis and tubulointerstitial lesions together with accelerated atherosclerosis. Several experimental studies have shown that hyperlipidemia accelerates renal damage. Lipid-lowering treatment can reduce renal lesions and preserve renal function. The documentation in human nondiabetic progressive renal insufficiency is more limited. We have found that increased concentrations of triglyceride-rich, but not cholesterol-rich, apoB-containing lipoproteins are, associated with a more rapid loss of renal function. The underlying pathophysiological mechanisms for the relation between triglyceride-rich apoB-containing lipoproteins and progression of renal insufficiency are not fully understood. Treatment with hypolipemic drugs may attenuate the renal dyslipidemia, but thus far there have been no reports about controlled clinical trials testing the possible effect of such treatment on the progression of renal insufficiency. In summary, there is evidence to suggest that some specific lipoprotein abnormalities are a risk factor for the progression of renal dysfunction, but the final test of such assumptions still rests on the results of urgently needed controlled intervention studies.
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PMID:Lipoprotein abnormalities as a risk factor for progressive nondiabetic renal disease. 1041 28

Cross-sectional studies suggest that an increased urinary albumin excretion rate is associated with cardiovascular disease, dyslipidemia, and hypertension. The purpose of this study was to analyze prospectively whether the urinary albumin-to -creatinine (A/C) ratio can independently predict ischemic heart disease (IHD) in a population-based cohort. In 1983, urinary albumin and creatinine levels were measured, along with the conventional atherosclerotic risk factors, in 2085 consecutive participants without IHD, renal disease, urinary tract infection, or diabetes mellitus. The participants were followed up until death, emigration, or December 31, 1993. IHD was defined as a hospital discharge diagnosis or cause of death including the diagnoses ICD-8 and 410 to 414. Seventy-nine individuals developed IHD during the 21 130 person-years of follow-up. They were characterized by a preponderance of males and higher age, body mass index, blood pressure, lipoproteins, and proportion of current smokers. Microalbuminuria was defined as an A/C ratio) >90 percentile (>0.65 mg/mmol). When adjusted for other risk factors, the relative risk of IHD associated with microalbuminuria was 2.3 (95% CI, 1.3 to 3.9, P=0.002), and the 10-year disease-free survival decreased from 97% to 91% (P<0.0001) when microalbuminuria was present. An interaction between microalbuminuria and smoking was observed, and the presence of microalbuminuria more than doubled the predictive effect of the conventional atherosclerotic risk factors for development of IHD. It is concluded that microalbuminuria is not only an independent predictor of IHD but also substantially increases the risk associated with other established risk factors.
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PMID:Urinary albumin excretion. An independent predictor of ischemic heart disease. 1044 83

In patients with essential hypertension and in those with diabetes mellitus, the presence of increased amounts of urinary protein or albumin has been shown to be an important and independent risk for an increased incidence of cardiovascular morbidity and mortality. A constellation of cardiovascular risk factors has been described in these individuals, as well as evidence for diffuse endothelial cell dysfunction, which suggests these individuals are particularly susceptible to the development of extensive vascular disease. Recent studies have also suggested that proteinuria is not only a marker for renal disease but it also predicts those patients at greatest risk for the development of chronic and progressive renal insufficiency. This effect of proteinuria was evident in patients in whom urinary protein excretion rates exceeded 1 g/24 hours, but probably is true even in patients with smaller amounts of proteinuria. This effect of proteinuria on progression of renal disease is independent of other risk factors such as level of renal function, blood pressure, and dyslipidemia. Recent clinical studies have demonstrated that modification of proteinuria by the use of angiotensin-converting enzyme (ACE) inhibitors independent of reductions in systemic blood pressure results in slowing of the rate of loss of renal function and even stabilization of renal function over longer periods of treatment. In patients with renal disease, the totality of evidence suggests that multiple pharmacological and dietary modifications will be necessary to achieve the optimal slowing of the progression of renal disease. In addition, strategies will be required to reduce risks involved in the development of cardiovascular disease to ensure optimal patient survival. The similarity of risk factors involved in cardio-renal disease progression should allow us to achieve this goal with our current therapeutic armamentarium.
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PMID:Proteinuria: its clinical importance and role in progressive renal disease. 1076 8

Elevated plasma homocysteine (Hcy), dyslipidemia and hemorheological abnormalities all occur commonly in end-stage renal disease (ESRD) and are recognized risk factors for arteriosclerosis. To study the effect of folate supplementation on these factors we conducted a randomized controlled trial. Thirteen hemodialysis (HD) and 8 continuous ambulatory peritoneal dialysis (CAPD) patients received either 5 mg folic acid daily or placebo for 3 months. After 1 and 3 months, fasting blood samples were taken for Hcy, lipid profile, blood and plasma viscosity, red blood cell (RBC) osmotic fragility, plasma fibrinogen concentration and in vivo platelet aggregability. At baseline, the CAPD patients had a higher mean plasma fibrinogen concentration than the HD patients and they also tended to have higher mean plasma viscosity. Folate-treated patients showed marked increases in RBC folate and an average decrease in plasma Hcy concentration of 33%. Mean total cholesterol, LDL cholesterol and triglyceride concentrations decreased significantly in the CAPD patients who took folate. Folate had no significant effect on hemorheology. In conclusion, folate supplements in ESRD reduce plasma Hcy concentrations and may improve lipid profiles. In our patients, hemorheological abnormalities were more marked in patients on CAPD than in those on HD and were not improved by folate supplementation.
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PMID:A controlled trial of the effect of folate supplements on homocysteine, lipids and hemorheology in end-stage renal disease. 1086 36


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