Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The EDTA (calcium disodium edetate) lead mobilization test revealed lead as the probable cause of renal disease in industrial lead workers and in patients with gout or essential hypertension. The data reviewed here demonstrate persistence of lead nephropathy in the contemporary scene despite the introduction of modern industrial and environmental exposure standards. Renal function and biopsy studies showed that lead nephropathy is a chronic tubulointerstitial renal disease with modest proteinuria which frequently presents with hyperuricemia, gout and hypertension. Only evaluation of body lead stores by either the EDTA lead mobilization test or by x-ray fluorescence is helpful in diagnosing lead nephropathy. While chelation therapy is safe and helpful in reversing early lead nephropathy, the best treatment is prevention. These studies further raise the possibility that chronic environmental lead poisoning and associated renal disease and hypertension may be a more widespread problem than suspected. Assessment of the true extent of chronic lead poisoning requires large scale epidemiological studies.
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PMID:Lead nephropathy, gout, and hypertension. 847 50

The pathogenesis of hypertension associated with diabetes mellitus (DM) involves an interplay of hereditary and acquired mechanisms. A familial trait for essential hypertension appears to be a risk factor for the development of both hypertension and nephropathy in type I DM and coexists commonly with impaired insulin sensitivity, relative hyperinsulinemia, and dyslipidemia, which can already be detected before the appearance of hypertension, obesity, or upper abdominal redistribution of body fat. The latter finding helps explain the frequent development of hypertension as well as dyslipidemia and/or type II DM in given individuals. Obesity is an important factor promoting these complications. Type I or II DM but not uncomplicated essential hypertension is characteristically accompanied by excess body Na+. This abnormality complements a tendency toward vascular hyperreactivity and a presumably morphologic and functional vasculopathy, thereby promoting the pathogenesis of hypertension in diabetic patients. For the treatment of hypertension in diabetic patients, nonpharmacologic measures are indispensable. If drugs are needed, angiotensin-converting enzyme (ACE) inhibitors and some but not all calcium antagonists are the preferred agents. Monotherapy or a combination of these drug types allows effective blood pressure control in most diabetic patients without further metabolic impairment; ACE inhibitors even tend to improve glucose control. Ketanserin may be a potential alternative, and if a diuretic is also needed, the metabolically neutral indapamide is a reasonable choice. If these agents do not allow satisfactory blood pressure highly selective beta 1-blockers or alpha 1-blockers may be introduced as a second choice. In diabetic patients with nephropathy, effective antihypertensive therapy can reduce proteinuria and slow the progression of the nephropathy; ACE inhibitors may improve diabetic proteinuria even at unchanged systemic blood pressure levels. Unless diuretics are needed for reasons other than hypertension, the treatment of diabetic patients with thiazides or loop diuretics in conventional dosage should probably be avoided until clarification of their influence on prognosis. Nevertheless, whether and to what extent other agents and nonpharmacologic measures can modify the prognosis in diabetic patients is also unclear, and the approach to antihypertensive therapy is therefore still largely empiric.
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PMID:Pathogenesis and treatment of hypertension associated with diabetes mellitus. 848 Jun 21

Pregnancy-induced hypertension (PIH) is a heterogeneous disorder which complicates 5-7% of all pregnancies and remains a leading cause of maternal, fetal and neonatal morbidity and mortality. Severe preeclampsia is the most distinctive and life-threatening form; a multi-system disorder more common in first pregnancies, it is characterized by high blood pressure and proteinuria. In a series of Caucasian women with pregnancy-induced hypertension, we have observed a significant association of preeclampsia with a molecular variant of angiotensinogen, T235, found previously to be associated with essential hypertension. This finding is corroborated in a sample ascertained in Japan. Together, these observations support a new pathophysiological interpretation of preeclampsia and of its relation to some forms of essential hypertension.
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PMID:A molecular variant of angiotensinogen associated with preeclampsia. 851 28

Calcium antagonists exert several characteristic effects on the kidney that potentiate their antihypertensive effect. The objective of the present study was to investigate the effectiveness of nitrendipine in the presence of different degrees of renal impairment. Two groups of hypertensive patients were included in the study. Group 1:10 patients with arterial hypertension secondary to chronic renal parenchymatous disease and adequately controlled with a diuretic and/or a beta-blocker who were switched to nitrendipine. These patients were then followed monthly for 1 year. Group 2:24 patients diagnosed as having essential hypertension who presented values of urinary albumin excretion above 30 mg/day after a minimum of 3 years of adequate blood pressure control with a diuretic and/or a beta-blocker. Patients were randomly assigned to continue with the same therapy or to switch to nitrendipine for 1 year. In both groups nitrendipine was as efficacious as standard therapy for controlling blood pressure and did not induce changes in renal hemodynamics. Nitrendipine did not modify the level of proteinuria in group 1, nor the urinary excretion of albumin in group 2. These results seem to indicate that nitrendipine can be safely used in patients with arterial hypertension and different degrees of renal function impairment.
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PMID:Antihypertensive effect of nitrendipine in the hypertensive patient with renal impairment. 851 91

The allele 235T (a threonine in place of a methionine at position 235) of angiotensinogen has been found to be associated with a predisposition to essential hypertension. We investigated whether this allele also confers increased susceptibility to nephropathy in patients with insulin-dependent diabetes mellitus (IDDM). A group of 380 patients who had had IDDM for 15 to 20 years were genotyped at the angiotensinogen 235 locus. Included were 75 patients with normoalbuminuria (albumin excretion rate < 30 micrograms/min), two series of patients with microalbuminuria (n = 30 and n = 136), and two series with overt proteinuria (n = 41 and n = 98). Allele 235T frequency was higher among cases with microalbuminuria (0.41 in the two series combined) or overt proteinuria (0.40) than in the normoalbuminuria group (0.36). However, this difference was not statistically significant with this sample size (chi 2 = 1.2, P = NS with 2 df). Under a recessive model, allele 235T homozygotes had a 1.6-fold risk of developing nephropathy relative to carriers of other genotypes, but this value was not significantly different from 1(95% CI = 0.8 to 3.5). The strength of the association did not improve after stratification by degree of glycemic control. With respect to the hypertension in these IDDM patients, no association with allele 235T was found. Allele 235T frequencies in normotensive and hypertensive individuals were 0.363 and 0.353, respectively, among normoalbuminuric IDDM individuals (chi 2 = 0.01, P = NS) and 0.411 and 0.414 among microalbuminuric IDDM subjects (chi 2 = 0.0, P = NS). We conclude that the angiotensinogen polymorphism M235T might influence susceptibility to nephropathy in insulin-dependent diabetes, but its effect, if any, is rather small and independent of hypertension.
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PMID:Angiotensinogen polymorphism M235T, hypertension, and nephropathy in insulin-dependent diabetes. 862 Dec 7

It is now well-established in experimental models in rodents that increased glomerular pressure results in the development of focal and segmental glomerulosclerosis, proteinuria and progressive renal functional deterioration. In humans, direct measurement of glomerular capillary pressure is impossible. However, it is widely accepted that glomerular hypertension is present in different clinical situations, like diabetic nephropathy, chronic renal failure associated with glomerulonephritides, some forms of essential hypertension and cadaveric kidney transplantation. Many studies were performed on the effects of protein-restricted died and/or angiotensin converting enzyme inhibition on the rate of progression of renal failure in these renal diseases. Although controversial, the overall results suggest that these therapeutic strategies may reduce the rate of progression, particularly in diabetic nephropathy.
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PMID:[Intraglomerular hypertension. Physiopathology and therapeutic implications]. 868 50

The kidneys play an important role in the development of cardiovascular risk factors. It is well known that heavy proteinuria can induce hyperlipidemia, the uric acid is elevated in some renal deficiencies and that hypertension develops in most end stage renal diseases. In prehypertensive states, specially in subjects with a family history of hypertension, some hemodynamic changes take place, characterized by an increase in renal vasoconstriction with a reduction in renal plasma flow and an elevation of sodium reabsorption. The mechanisms for these alterations are not well understood, but an increase in intracytosolic calcium in vascular smooth muscle cells, a reduction in vasodilatory substances such as nitric oxide and an increased sympathetic nervous activity have been proposed. In normotensive subjects with two hypertensive parents a reduction in sodium diet, an increase in protein intake or in arginine diet could prevent established essential hypertension from developing. In borderline hypertension an early therapy with low doses of calcium antagonists, ACE inhibition or diuretics could be indicated.
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PMID:Can the kidney prevent cardiovascular diseases? 874 38

Angiotensin I-converting enzyme (ACE) plays a pivotal role in cardiovascular homeostasis and by activating angiotensin I into angiotensin II and inactivating bradykinin. These two peptides play antagonistic roles on the cardiovascular system by regulating vascular tone and vascular smooth muscle cell proliferation. Identification of the ACE gene as a genetic marker for various forms of cardiovascular disease is a recent result of the progress made in molecular biology and genetics. The insertion/deletion (ID) polymorphism of the ACE gene defined by the presence or absence of the 287 base pair Alu sequence situated in intron 16 has been investigated as a possible genetic marker for a variety of cardiovascular disease including myocardial infarction, essential hypertension, cardiomyopathy, and diabetic vascular complications. This paper reviews prior reports and briefly describes our recent study on the association of the ACE I/D polymorphism and antiproteinuric effect of ACE inhibitors in patients with proteinuria.
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PMID:Angiotensin I-converting enzyme insertion/deletion polymorphism: potential significance in nephrology. 874 24

A study was made of diagnostic significance (sensitivity and specificity) of early (precritical) signs of late gestosis (LG). A total of 179 females (187 pregnancies) with essential hypertension (EH) and chronic renal diseases (CRD) were examined. EH women are at high risk of LG when they have proteinuria above 0.3 g/s, of relative prognostic importance are severe hypertension and marked hyperuricemia. Severe hypertension, fetal growth inhibition, positive roll-over test may indicate LG in CRD. Primiparas with EH or CRD are especially at risk of LG. As all the above LG signs in its precritical stage are not specific and indicate only probability, they can be used primarily for screening of patients with high risk of LG onset. The diagnosis of LG in EH and CRD should be based on follow-up changes in the clinical and laboratory indices.
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PMID:[The diagnostic characteristics of late toxicosis in pregnant women with hypertension and chronic kidney diseases]. 877 12

In patients with essential hypertension, correlations have been reported between the albumin excretion rate (AER) and ambulatory and casual blood pressure. Microalbuminuria has been indicated as a possible predictor of cardiovascular morbidity and mortality. The objective of this trial was to evaluate the effect of quinapril, an angiotensin converting enzyme inhibitor with high tissue affinity for the enzyme, on the AER in patients with mild to moderate essential hypertension and no evidence of diabetes mellitus. In this 12 week, 24 center study, quinapril was administered to 213 patients and titrated to 10, 20, or 40 mg/day alone or 20 mg/day plus 12.5 mg/day hydrochlorothiazide. Overall, blood pressure was reduced from 155.2 +/- 18.1/101.8 +/- 6.7 mm HG (mean +/- SD) to 144.4 +/- 17.8/92.3 +/- 8.9 mm HG (P = .0001) and AER decreased from 20.6 +/- 24.3 mg/24 h to 14.5 +/- 15.4 mg/24 h (P = .0001). The BP reductions were significant in all age groups. AER at endpoint was reduced 37.5% in elderly, 29.8% in middle-aged, and 11.8% in young patients from 32.5 +/- 45.0 mg/24 h, 19.1 +/- 20.9 mg/24 h, and 16.1 +/- 16.9 mg/24 h, respectively. The AER decreased in 60% of patients who had normal AER (0 to 30 mg/24 h), in 79% of those who had microalbuminuria (30 to 300 mg/24 h), and in 90% of those who had proteinuria (> 300 mg/24 h) at baseline. Baseline log-AER correlated with SBP (P = .0126, R = 0.19) and creatinine clearance (P = .026, R = 0.17), while endpoint log-AER correlated with SBP (P = .0015, R = 0.25) and DBP (P = .03, R = 0.17). In summary, we showed, in a large group of patients with mild to moderate essential hypertension and no evidence of diabetes mellitus, that quinapril not only lowers BP significantly but also reduces microalbuminuria.
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PMID:Effect of quinapril on the albumin excretion rate in patients with mild to moderate essential hypertension. Multicenter Study Group. 878 79


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