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For about three decades glomerular diseases have been the most intensively investigated research area in nephrology. The increasing proportion of patients with end-stage renal disease (ESRD) secondary to hypertension has now revived interest in hypertension. Prospective studies have firmly established that high blood pressure is associated with an increased risk of renal failure independent of other risk factors. Hypertension-related renal injury might be interpreted in a general context taking into account genes, intrauterine growth and environmental factors. Disturbed intrauterine growth (due to malnutrition or other factors) has a negative influence on the development of the cardiovascular system and favours the occurrence of hypertension, insulin resistance, hypercholesterolaemia and hyperuricaemia in adult life (Barker's hypothesis). Altered intrauterine growth has also been associated with a reduced number of nephrons at birth. Damage attributable to glomerular hyperperfusion in kidneys with a reduced number of nephrons is aggravated by vascular lesions in middle and small arterial vessels (secondary to hypertension, hyperlipidaemia and environmental risk factors such as smoking). The observation that subjects homozygous for the D allele of the ACE gene are predisposed to both cardiovascular complications and nephrosclerosis, suggests that genetic factors may interact with altered intrauterine growth in determining the risk of cardiovascular and renal diseases.
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PMID:[Nephropathy associated with arterial hypertension: genes and Barker's hypothesis]. 1243 39

With the increased attention being given to cardiovascular risk factor reduction, the opportunity exists to substantially decrease the largest cause of mortality in diabetic patients. The concept that type 2 diabetes and CVD are linked via a common etiologic pathway (metabolic syndrome) has substantial ramifications for the care of individual patients. Many of the metabolic abnormalities that contribute to both glycemic disorders and CVD are interrelated. For example, hyperinsulinemia and insulin resistance coupled with abdominal obesity further worsens HTN and hyperlipidemia. Likewise, the procoagulant state and endothelial dysfunction increase with worsening glycemic control. Specific interventions include tobacco cessation, a food management and physical activity plan, choice of antidiabetic agent (such as metformin), and use of ACE inhibitors for hypertension and microalbuminuria (Table 5). Programs to enhance cardiovascular risk factor reduction as part of the comprehensive evaluation and management of diabetic patients have been described [95,99]. One community-based program provided free screening to diabetic patients with randomization to either annotated result reports provided to the patient and their physician or results provided by a project nurse (either face-to-face or over the phone). Greater improvements in mean glycohemoglobin, cholesterol, and blood pressure were noted with verbal presentation of results [99]. Recent data from the Centers for Disease Control and Prevention Diabetes Cost-effectiveness Group support the idea that interventions to decrease CVD in diabetics are economically beneficial. Intensive management of hypertension, glycemic control, and hyperlipidemia each improved health outcomes. Hypertension control reduced costs. Although intensive treatment of glucose and hyperlipidemia increased costs, the increase was comparable to that of other frequently used health care interventions [100]. Further directions include further exploration of the implications and management of metabolic syndrome as it relates to CVD prevention. Interventions such as exercise, which can impact on all outcomes, require special attention. Efforts by physicians, health systems, and society are necessary to increase physical activity for individuals of all ages. It makes clinical sense that the recommendations for prevention of CVD in diabetics described in this article may also benefit patients with prediabetes (fasting glucose 110-125 mg/dl), but this remains to be definitively shown.
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PMID:Preventing cardiovascular disease in diabetes and glucose intolerance: evidence and implications for care. 1469 2

Systemic embolism is a frequent cause of stroke. At the beginning of the last decade by introduction of transesophageal echocardiography and other imaging techniques atheromatosis of the aortic arch has been recognized as an important source of embolism. Formerly in the pre-TEE era, this entity was included into cryptogenic strokes. Aortic atheromas are found in about one quarter of patients presenting with embolic events. The severity of atherosclerosis graded by TEE correlates with the risk for future embolism, especially if mobile lesions or superimposed thrombi are present. Independent of plaque extension, patients with unstable plaques characterized by echo-lucency, inhomogenity, lacking of calcifications, ulceration, mobile parts and concomitant spontaneous echo contrast within the aorta have a higher risk for embolic events. However, the diagnosis of aortic atheromatosis is mostly established if an embolic event has already occurred. Therefore, it is important to identify patients at risk, especially before they undergo interventions with manipulation at the aorta like coronary bypass surgery. Risk factors are age above 70, diabetes mellitus, hyperlipidemia, arterial hypertension, aortic calcifications on standard chest X-ray, elevated serum levels of C-reactive protein, other inflammatory markers, and an activated coagulation. Randomized studies for treatment of patients with severe aortic atheromatosis are not yet existing. Warfarin has been shown to prevent stroke in patients with mobile atheromas and superimposed thrombi, but there are case reports about aggravation of cholesterol embolism under warfarin treatment. It is concluded from other atherosclerotic manifestations that plaque stabilizing treatment with statins and ACE inhibitors is also beneficial.
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PMID:Atheromatous disease of the thoracic aorta and systemic embolism. Clinical picture and therapeutic challenge. 1474 Feb 36

In the last decade the number of patients with congestive heart failure has increased noticeably and today heart failure is one of the major problems in civilized countries. While in earlier decades arterial hypertension was the main reason for developing heart failure, today coronary artery disease has become the focus of attention. However, arterial hypertension, diabetes and hyperlipidemia are also main risk factors for developing coronary artery disease. In addition to non-pharmacological management with reduced fluid intake and periodical exercise training particularly in stable heart failure, in the last decade some special drug compounds have demonstrated a significant reduction in mortality in great double blind randomized trials. ACE-inhibitors and betablockers are essential components in treating congestive heart failure. Angiotensin-II-receptorblockers are indicated if ACE inhibitors and/or beta-blockers are not tolerated. The combined use of all three compounds was shown to result in a further reduction of mortality in the recently presented CHARM study. In progressive heart failure the use of diuretics is necessary and effective especially when fluid overload exists. Not treating heart failure is followed by high mortality, as we know, and so adequate and uncompromising treatment of hypertension is the most important approach to prevent the further development of heart failure.
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PMID:[Therapeutical strategies in hypertensive patients presenting heart failure symptoms]. 1500 83

Vascular reactivity to nitric oxide (NO) is mediated by NO-sensitive soluble guanylyl cyclase (sGC). Since a diminished activity of vascular sGC has been reported in an animal model of type 2 diabetes, the sGC activity was assayed in vitro in internal mammary artery specimens obtained during bypass surgery from patients with and without type 2 diabetes. The sensitivity of sGC to NO, which is dependent on Fe(2+)-containing heme, was measured in vitro using stimulation with diethylamine NONOate (DEA/NO). In addition, the novel cyclic guanosine monophosphate-elevating compound HMR-1766 was used to test the stimulation of the oxidized heme-Fe(3+)-containing form of sGC. Basal activity of sGC and its sensitivity to stimulation by DEA/NO and HMR-1766 were not different between control and type 2 diabetic patients: maximum stimulation by DEA/NO amounted to 475 +/- 67 and 418 +/- 59 pmol. mg(-1). min(-1) in control and type 2 diabetic patients, respectively. The maximum effects of HMR-1766 were 95 +/- 18 (control subjects) and 83 +/- 11 pmol. mg(-1). min(-1) (type 2 diabetic patients). Hypertension, hyperlipidemia, drug treatment with statins, ACE inhibitors, or nitrates had no effect on sGC activity. In conclusion, the present findings do not support the hypothesis that desensitization of sGC contributes to the pathogenesis of diabetic vascular dysfunction in humans.
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PMID:Nitric oxide-sensitive soluble guanylyl cyclase activity is preserved in internal mammary artery of type 2 diabetic patients. 1544 95

When kidney disease of any aetiology results in substantial loss of nephrons, a common clinical syndrome, characterised by hypertension, proteinuria and a progressive decline in renal function, ensues. This observation suggests that common mechanisms may contribute to progressive renal injury and that therapeutic interventions that inhibit these common pathways may afford renal protection. Research to date has identified several mechanisms that may contribute to progressive renal injury including glomerular haemodynamic changes, multiple effects of angiotensin II and detrimental effects of excessive filtration of plasma proteins by injured glomeruli. Clinical trials over the past decade have identified several interventions that are effective in slowing the rate of progression of chronic kidney disease (CKD). The use of ACE inhibitors, angiotensin receptor antagonists or a combination of the two should be regarded as fundamental to any therapy for slowing the rate of CKD progression. Hypertension should be treated aggressively to achieve a blood pressure target of < 130/80 mm Hg. Reduction of proteinuria to < 0.5 g/day should be regarded as an independent therapeutic goal. Although inconclusive, there is some evidence to support moderate dietary protein restriction to 0.6 g/kg/day in appropriate patients. Hyperlipidaemia may contribute to CKD progression and should be treated to reduce cardiovascular risk and potentially improve renal protection. Smoking cessation should be encouraged and, where necessary, assisted. Among diabetic patients tight glycaemic control should be achieved (glycosylated haemoglobin < 7%). These interventions are simple and relatively inexpensive. If applied to all patients with CKD they will result in substantial slowing of renal function decline in many patients and thereby reduce the number who progress to end-stage renal disease and require renal replacement therapy.
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PMID:Slowing the progression of adult chronic kidney disease: therapeutic advances. 1545 27

Hyperglycemia is associated with excess mortality in AMI and should be treated aggressively in the intensive care setting. The exact goal of therapy is unclear because different blood glucose targets were used in earlier studies (eg, 215 mg/dL in DIGAMI versus 110 mg/dL in the Belgian study of critically-ill patients). In the setting of AMI, it is prudent to avoid excessive hypoglycemia and, thus, more modest goals for blood glucose may be considered until more definitive data are present. Aggressive therapy with continuous infusion of insulin seems to improve a host of metabolic and physiologic effects that are associated with acute hyperglycemia and improves mortality in the acute setting. Aggressive glycemic control should be coupled with appropriate use of reperfusion therapies, glycoprotein IIb/IIa inhibitors, aspirin, 1-blockers, ACE inhibitors, and antithrombotic agents. The role of intensive chronic glucose control in reducing CV events is less clear but earlier studies were not well-powered; did not achieve aggressive, durable glycemic control; and did not use insulin-sensitizing agents routinely. Given the results of the DIGAMI trial, the goal of therapy postdischarge should include strict glycemic control while future studies help to delineate the role of insulin-sensitizing agents versus insulin-providing agents in reducing recurrent macrovascular events. Careful attention also should be paid to aggressive lifestyle modifications and treatment of hypertension, hyperlipidemia, and left ventricular dysfunction, as well as appropriate use of anti-platelet and antithrombotic agents.
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PMID:The role of intensive glycemic control in the management of patients who have acute myocardial infarction. 1569 41

Effect of dietary supplementation of two types of rice bran fraction on blood pressure (BP), lipid profile, and glucose metabolism in stroke-prone spontaneously hypertensive rats was studied. Male 4-week-old rats were divided into one group fed the AIN-93M-based control (C) diet and two groups fed diet supplemented with 60 g/kg of Driselase and ethanol fractions (DF and EF, respectively) of rice bran. After 8 weeks feeding, the BP decreased in the DF and EF groups in comparison with the C group (p < 0.01). Plasma ACE inhibitory activity, BUN, BUN/creatinine ratio, albumin, triglyceride, and glucose levels were lower in the DF and EF groups than in the C group (p < 0.01). Plasma nitric oxide and urinary 8-hydroxy-2'-deoxyguanosine levels were lower in the DF and EF groups than in the C group (p < 0.01). Rice bran fractions appear to have a beneficial dietary component that improves hypertension, hyperlipidemia, and hyperglycemia.
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PMID:Rice bran fractions improve blood pressure, lipid profile, and glucose metabolism in stroke-prone spontaneously hypertensive rats. 1650 53

We aimed to investigate prognostic factors for a composite end-point of end-stage renal disease (ESRD) and the progression of renal disease in Japanese patients with chronic renal disease. Using a composite end-point comprising a doubling of serum creatinine (sCr), an increase in sCr level to 6.0 mg/dL, or initiation of dialysis and renal transplantation caused by ESRD, we examined data obtained in a prospective cohort study. The present study consisted of 641 patients who were 20 years of age or older with chronic renal disease caused by diabetic nephropathy, glomerulonephritis, or nephrosclerosis, and who had baseline sCr levels of 5.0 mg/dL or less. The following criteria were examined as prognostic factors: sex; age; elapsed time from initial diagnosis; disease underlying the nephropathy (diabetic or non-diabetic); complications with hypertension, hyperlipidemia, or anemia; baseline sCr level; therapeutic regimen, including use of ACE inhibitors or Ca2+ -channel blockers; and diet. A log-rank test was used for univariate analysis, and Cox regression analysis was used for multivariate analysis. Underlying disease (diabetic or non-diabetic), baseline sCr level, and Ca2+ -channel blocker therapy were significantly related to event incidence. In the present study, we identified underlying disease and baseline sCr level as important prognostic factors for a composite end-point in a predialysis patient population in both the early and middle stages of renal disease. These factors should be considered as balancing variables for randomization in future clinical studies.
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PMID:Prognostic factors for a composite end-point of renal outcomes in patients with chronic kidney disease. 1655 40

New-onset diabetes mellitus in a previously non-diabetic transplant recipient is a serious adverse event that confers significant morbidity and mortality. The most significant consequences of post-transplant diabetes mellitus (PTDM) in solid organ transplant recipients include decreased patient and graft survival, an increased risk of infectious complications, and morbid cardiovascular events. The development of PTDM in the elderly is of particular concern because this group is already at increased risk of progression of cardiovascular disease. Because the elderly, especially those aged >65 years, are the fastest-growing segment of the renal transplant population, attention needs to be given to PTDM risk reduction and post-transplant management. PTDM develops as a consequence of both impaired insulin production and enhanced peripheral insulin resistance. A number of non-modifiable factors such as age, race, family history, hepatitis C, polycystic kidney disease and emerging genetic causes have been identified as risk factors for PTDM. However, a number of modifiable factors can be targets for intervention in high-risk patients, including bodyweight (through dietary restriction and exercise), hypertension, hyperlipidaemia and the effects of certain immunosuppressive agents. The two agents most responsible for PTDM are tacrolimus and corticosteroids, especially when used in combination. Attempts to modify doses and regimens designed to eliminate or avoid these drugs should be considered. Use of HMG-CoA reductase inhibitors ('statins') and ACE inhibitors is particularly helpful in controlling hypertension and hyperlipidaemia in the elderly because these agents confer protection against future adverse cardiovascular events. Bisphosphonates are also advantageous in controlling the progression of osteoporosis and possible increased risk of bone fractures. Future trials in the elderly should focus on such endpoints as PTDM, post-transplant neoplasia, cardiovascular events and bone fracture events in order to identify the safest regimens that provide the optimal control of rejection while limiting the morbidity from these secondary events.
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PMID:Post-transplant diabetes mellitus: risk reduction strategies in the elderly. 1706 82


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