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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated urinary calcium and phosphate excretion have been observed in children with insulin-dependent diabetes mellitus (IDDM). This may be related to a defect in tubular reabsorption. It is well known that converting enzyme inhibition decreases microalbuminuria and may prevent or retard diabetic nephropathy. We investigated whether enalapril also improves the defect in calcium and phosphate reabsorption. We studied 16 children and young adults (age 12-21 years) with IDDM and persistent microalbuminuria before and during 12 weeks of enalapril treatment. Before treatment microalbuminuria, urinary calcium excretion, and fractional tubular phosphorus reabsorption (TPR) were 153+/-53 microg/min, 5.5+/-0.9 mg/kg per day, and 71.4+/-3.6%, respectively. At the end of the 12th week, microalbuminuria had decreased to 20.3+/-7.9 microg/min and calcium excretion to 3.3+/-0.4 mg/kg per day (P<0.01), while the TPR increased to 80.1+/-3.8% (NS). The renal threshold phosphate concentration increased from 1.8+/-0.15 to 2.92+/-0.23 mg/dl (P<0.01). The fasting serum glucose and hemoglobin Alc levels did not change significantly during the study. Systolic and diastolic blood pressures were 120.4+/-2.2 / 79.3+/-1.4 mm Hg and 110.5+/-1.8 / 71.3+/-0.9 mm Hg before and after 12 weeks, respectively. We conclude that enalapril treatment improves not only microalbuminuria but also abnormal calcium and phosphate excretion in microalbuminuric children with IDDM.
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PMID:Effect of enalapril on proteinuria, phosphaturia, and calciuria in insulin-dependent diabetes. 981 87

There is a clear relationship between hypertension and the microvascular complications of diabetes. Genetic predisposition to hypertension has been correlated to the risk of diabetic nephropathy in type I diabetes, and hypertension is a well known risk factor for developing nephropathy in patients with type II diabetes. Multiple studies have emphasized the importance of hypertension on renal disease progression, and blood pressure control with conventional antihypertensive drugs slows the rate of renal function loss in diabetic nephropathy. Furthermore, evidence of the role of renin-angiotensin system (RAS) on progression of renal damage has focused much interest on the therapeutic action of the RAS blockade. In patients with type I diabetes, blocking the RAS with angiotensin converting enzyme (ACE) inhibitors prevents progression from microalbuminuria to overt nephropathy, and in overt nephropathy decreases the gradual loss of renal function beyond its blood pressure lowering effect. Less clinical information is available in type II diabetic nephropathy, but our experience and some recent studies suggest that ACE inhibitors also have a renoprotective action in type II diabetes. The role of calcium channel blockers in diabetic nephropathy is not clear. Several short-term studies with the first generation dihydropyridine calcium antagonists showed a lower effect on urinary albumin excretion and a more rapid progression to renal failure than with ACE inhibitors. However, other calcium channel blockers, particularly of the non-dihydropyridine type, have been shown to have a beneficial effect on diabetic nephropathy, decreasing proteinuria and slowing progression.
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PMID:Effects of antihypertensive therapy on progression of diabetic nephropathy. 983 94

We tested the hypothesis that microalbuminuria screening in a general practice setting would identify high-risk nondiabetic hypertensive patients, and we measured microalbuminuria response to drug treatment. General practitioners were enrolled who had collected medical histories and performed physical examinations and routine laboratory tests in more than 11,000 untreated hypertensive, nondiabetic patients. Microalbuminuria was measured with an albumin-sensitive immunoassay test strip. The patients' mean age was 57 years, 51% were men, and mean duration of hypertension was 69 months. Twenty-five percent of patients had coronary artery disease (CAD), 17% had left ventricular hypertrophy (LVH), 5% had had a stroke, and 6% had peripheral vascular disease (PVD). Microalbuminuria was present in 32% of men and 28% of women. In patients with microalbuminuria, 31% had CAD, 24% had LVH, 6% had had a stroke, and 7% had PVD. In patients without microalbuminuria, all of these rates were significantly lower: 22%, 14%, 4%, and 5%, respectively (p < 0.001). Furthermore, in patients with CAD, LVH, stroke, or PVD, microalbuminuria was significantly greater than in patients who did not have these complications (p < 0.001). A multiple stepwise regression analysis with microalbuminuria as the dependent variable showed microalbuminuria depended on the following factors, in order of importance: systolic blood pressure, retinopathy, CAD, diastolic blood pressure, and LVH (all p < 0.0001). A multiple stepwise regression analysis with each of the concomitant diseases as the dependent variable showed that microalbuminuria was an independent and significant variable for each of the conditions. The patients were assigned to monotherapy with either angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, calcium antagonists, or diuretics. All of the drugs reduced microalbuminuria, although the beta-blocker carvedilol was superior (p < 0.05). We concluded microalbuminuria is an important risk factor that can be influenced by treatment.
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PMID:Microalbuminuria as a predictive factor for cardiovascular events. 1002 48

Present study analyses nephroprotective effect of various therapeutic interventions at different stages of kidney involvement in diabetes mellitus. A MEDLINE search of past 10 years data on various experimental studies, controlled clinical trials, meta-analysis and editorials pertaining to nephroprotection in diabetes mellitus was made. Effect of various therapeutic interventions such as metabolic glycaemic control, restricted protein diet and antihypertensive drugs (especially ACE inhibitors) has been analysed on the progression of different stages of kidney involvement in diabetes mellitus such as normoalbuminuria, microalbuminuria, diabetic nephropathy and end stage renal disease (ESRD). An attempt has been made to analyse differential long-term impact of various therapeutic interventions in relation to type of diabetes mellitus (i.e., IDDM and NIDDM) and associated hypertension. Progression of IDDM patients having microalbuminuria or diabetic nephropathy with or without hypertension has improved during the past decade largely because of adequate glycaemic control and effective antihypertensive treatment with conventional drugs e.g. beta-blockers and calcium antagonists, and more so due to the use of ACE inhibitors e.g. captopril, enalapril etc. Superiority of ACE inhibitor tends to decline from normotensive stage to the degree of rise in systemic blood pressure. However, data in NIDDM patients suffering from diabetic nephropathy is incomplete and inconclusive.
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PMID:Nephroprotection in diabetes mellitus. 1005 45

Regardless of the specific antihypertensive agent used, the most important aspect of the management of the patient with coexistent hypertension and renal disease is adequate control of the blood pressure. The current JNC VI recommendation is for a reduction to a target blood pressure of 130/85 mm Hg, or to a lower value of 125/75 in patients with greater than 1 g proteinuria per day. Impaired renal sodium excretion leading to extracellular fluid volume (ECFV) expansion is the most clinically important mechanism leading to renal parenchymal hypertension. Sodium restriction and loop diuretics constitute the cornerstone of effective antihypertensive therapy. Control of blood pressure in patients with chronic renal disease may be difficult without measures that address ECFV. JNC VI recommends the use of angiotensin converting enzyme (ACE) inhibitors in patients with hypertension and chronic renal disease to control hypertension and to slow progressive renal failure. ACE inhibitors have been found by clinical trials to be useful agents in the settings of established insulin-dependent diabetes mellitus (IDDM) nephropathy, non-insulin-dependent diabetes mellitus (NIDDM) nephropathy, IDDM patients with normal blood pressures and microalbuminuria, NIDDM patients with microalbuminuria and normal renal function, and a variety of nondiabetic renal diseases, especially in the setting of significant proteinuria. Calcium antagonists are effective for treating hypertensive patients with chronic renal impairment but have not been studied as intensively as ACE inhibitors with regard to their ability to slow the progression of renal insufficiency independently of their blood-pressure-lowering effects. The initial results for calcium antagonists and for combination calcium antagonist-ACE inhibitor therapy have been promising. The angiotensin II antagonists have theoretical advantages for use in renal impairment, and seem to have similar renal hemodynamic and antiproteinuric effects to ACE inhibitors, but further clinical study is needed.
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PMID:Renoprotective effects of antihypertensive drugs. 1007 16

Renal parenchymal hypertension is defined as hypertension caused by disease of the kidneys. Impaired renal sodium excretion leading to extracellular fluid volume (ECFV) expansion is the most clinically important mechanism leading to hypertension in patients with kidney disease. Most patients with renal parenchymal hypertension have sodium-sensitive hypertension, and, consequently, sodium restriction and loop diuretics constitute the initial steps in effective antihypertensive therapy in patients with renal disease. The loop diuretics (furosemide, ethacrynic acid, bumetanide, torasemide) are used for the management of ECFV and hypertension in patients with renal disease because thiazide diuretics are generally not effective in patients with serum creatinine values above 2.0 mg/dL or creatinine clearances below 30 mL/min. The Joint National Committee VI recommends the use of angiotensin-converting enzyme (ACE) inhibitors in patients with hypertension and chronic renal disease to control hypertension and to slow progressive renal failure. Antihypertensive treatment with ACE inhibitors may favorably alter renal hemodynamics, thereby slowing the progression of renal dysfunction. ACE inhibitors have been found to be useful agents in preventing the progression of renal disease in the settings of established insulin-dependent diabetes mellitus (IDDM) nephropathy, non-insulin-dependent diabetes mellitus (NIDDM) nephropathy, IDDM patients with normal blood pressures and microalbuminuria, NIDDM patients with microalbuminuria and normal renal function, and a variety of non-diabetic renal diseases, especially in the setting of significant proteinuria. Calcium antagonists are effective for treating hypertensive patients with chronic renal impairment, and the initial results for calcium antagonists and for combination calcium antagonist-ACE inhibitor therapy have been encouraging. Although promising, the calcium antagonists and the new angiotensin II antagonists have not been studied as intensively as ACE inhibitors in regard to their ability to slow the progression of renal insufficiency.
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PMID:University of Miami Division of Clinical Pharmacology Therapeutic Rounds: managing hypertension in patients with kidney disease-implications for preservation of renal function. 1009 77

Disturbances in bone marrow vascularisation can be one of the causes of diabetic osteopathy. The aim of the study was to answers the question if microalbuminuria as a results of capillary injury can be a sign of bone mineralisation disorders in IDDM renal sufficient patients. We examined 60 IDDM patients (30 women without menstruation disturbances; 30 men; age 25-36 years old). All the observed subjects were divided into groups: I-30 normoalbuminuric patients (0-29 mg/24 h); II-30 microabuminuric patients (30-295 mg/24 h). Bone mineral density (BMD) of femoral neck, lumbar spine (L2-L4) and total body was measured by dual energy X-ray absorptiometry (DEXA, Lunar). The biochemical parameters of bone turnover were measured both in serum and urine as follows: osteocalcine, total hydroxyproline (HPR, HPR/Cr), total alkaline phosphatase (AP) with bone fraction, total calcium (Ca, Ca/Cr) and inorganic phosphor (P). Microalbuminuric patients presented more severe bone turnover disturbances, shown by differences in: BMD and Z-score for femoral neck (p < 0.05), serum HPR (p < 0.05), AP (p < 0.05), AP (p < 0.01) and its bone fraction (p < 0.05). We proved the presence of statistically significant correlation coefficients for albuminuria and some densytometric and biochemical bone parameeters. Our results suggest that microalbuminuria can indirectly indicate the dynamic of bone turnover derangement in IDDM course. They are present mostly in the femoral neck, which because of the vascularisation type is particularly susceptible to subalimentation in the diabetic microangiopathy course.
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PMID:[Microalbuminuria as a risk factor for diabetic osteopathy in patients with IDDM and renal sufficiency]. 1010 25

Alterations in calcium metabolism can be demonstrated in the course of insulin-dependent diabetes mellitus. In order to clarify if the presence of persistent microalbuminuria (MA) can affect the main parameters of calcium metabolism, we studied 22 diabetic adolescents and young adults with persistent MA and compared them with 24 patients without MA and 24 healthy controls. Mean values of serum calcium, phosphorus and magnesium were similar in diabetic children and young adults without persistent MA and in controls. In addition, the mean values of PTH and 25-OHD, 1,25 (OH)2D3 and OC did not differ between these diabetics and controls. Diabetics with persistent MA showed no significant difference from the values of either controls or the group of diabetics without persistent MA for the mean values of serum calcium, phosphorus and magnesium and PTH. In contrast, diabetics with persistent MA had significantly (p<0.01) lower 25-OHD (26.5+/-5.2 ng/ml) and 1,25 (OH)2D3 (24.7+/-5.6 pg/ml) as well as OC levels (9.8+/-2.5 ng/ml; p<0.001) than controls (38.1+/-4.9 ng/ml, 40.7+/-6.4 pg/ml and 16.5+/-5.8 ng/ml, respectively) and subjects with normoalbuminuria (36.0+/-4.5 ng/ml, 38.8+/-8.9 pg/ml and 14.5+/-3.2 ng/ml). In conclusion, our study suggests that abnormalities in 25-OHD, 1,25(OH)2D3 and OC can be present in diabetic adolescents and young adults with incipient nephropathy.
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PMID:Calcium metabolism in adolescents and young adults with type 1 diabetes mellitus without and with persistent microalbuminuria. 1021 87

Type 2 (noninsulin-dependent) diabetes mellitus (DM) affects about 3% of the UK population. Diabetes often coexists with a cluster of other potent cardiovascular risk factors, including hypertension, dyslipidaemia and increased tendency for thrombosis, and increases the risk of early death from cardiovascular causes by about threefold. Microalbuminuria or proteinuria also may be present, further increasing the risk of cardiovascular mortality. Cardiovascular risk factors must be treated aggressively in patients with Type 2 diabetes and control of blood pressure at 140/85 mm Hg or lower is a priority. The management of hypertension in patients from some ethnic groups demands special consideration because they have a high incidence of diabetes and hypertensive complications. Patients must be urged to adopt appropriate lifestyle changes in the first instance but additional drug treatment for hypertension is usually required. All the major classes of antihypertensive agents lower blood pressure in Type 2 diabetic patients but have different effects on metabolic risk factors in different ways. Low-dose thiazide diuretics, beta-blockers, calcium channel blockers and angiotensin converting enzyme (ACE) inhibitors have been shown to reduce cardiovascular risk. Individually, the effects of low-dose thiazide diuretics and beta-blockers on glucose and lipid metabolism is clinically insignificant, though in combination much larger metabolic effects are seen. ACE inhibitors and calcium channel blockers have no, or small, beneficial effects on glucose and lipid metabolism, while the greater beneficial effects of alpha1-blockers on lipid profiles may render them especially useful in the Type 2 diabetic patient. Long-acting calcium-channel blockers and ACE inhibitors protect renal function and are suitable as first line therapy in patients with microalbuminuria or proteinuria. Until results from the current batch of randomized, placebo-controlled trials comparing different classes of antihypertensive agents are available, the choice of antihypertensive agent is difficult. Addressing overall cardiovascular risk factors, rather than hypertension alone, is essential in the management of the hypertensive Type 2 diabetic patient.
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PMID:Blood pressure control, microalbuminuria and cardiovascular risk in Type 2 diabetes mellitus. 1034 35

Hypertension is a significant and prevalent risk factor for the development of cardiovascular disease and target organ damage. The urgency of treatment of high blood pressure depends on the level of blood pressure elevation and the presence of coexistent risk factors for cardiovascular disease. Likewise, the level to which blood pressure is reduced is not restricted to the definition of high blood pressure but instead depends on the underlying disease. Diabetes and renal insufficiency, for example, require blood pressure goals below those that are traditionally defined. In the absence of contraindications, beta-blockers and diuretics are still recommended as first-line agents for treatment of uncomplicated hypertension. Calcium channel antagonists also may reduce mortality. In patients with diabetes, ACE inhibitors are effective first-line agents in type 1 and type 2 diabetic patients who are hypertensive or have microalbuminuria. ACE inhibitors may be beneficial in patients with nondiabetic renal insufficiency as well. Calcium channel antagonists may have some effect in retarding progression of diabetic nephropathy although a recent trial found a higher incidence of death as a secondary endpoint in hypertensive diabetic patients who were treated with calcium channel antagonists. Beta-blockers seem to be safe and well tolerated in patients with mild to moderate intermittent claudication, although patients with rest pain or limb ischemia have not been studied. Beta-blockers should not be used in patients with asthma. Dihydropyridine calcium channel antagonists are the preferred treatment of hypertension in patients with Raynaud's but should be avoided in patients with severe gastroesophageal reflux disease. NSAIDs, particularly piroxicam and indomethacin, raise mean blood pressure by approximately 5 mm Hg, enough to consider a change of either NSAID or antihypertensive to one that is not as affected by NSAIDs. Cyclosporine A can induce hypertension by its vasoconstrictive effects, particularly on the kidney. Calcium channel antagonists may antagonize this vasoconstriction while allowing the clinician to reduce the dose of cyclosporine A required to achieve its immunosuppressive effect.
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PMID:Evaluation and treatment of hypertension. 1046 27


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