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)

Antihypertensive treatment can slow down the decline in glomerular filtration rate (GFR) with time. In patients with diabetic nephropathy, angiotensin converting enzyme (ACE) inhibition has been shown to be more effective in this regard than conventional antihypertensive therapy. Whether this applies to the much larger population of patients with essential hypertension is not yet known. In the present study, the effects of two different antihypertensive therapies on the loss of GFR with time, determined with Cr51-EDTA clearance after 6, 12 and 24 months of treatment, were assessed in a prospective, randomised, double-blind trial in 257 patients with essential hypertension. All had normal renal function and none had diabetes mellitus or glucosuria. Proteinuria (dipstick positive or trace) was detected in 7 patients initially. The two therapeutic modalities were the ACE inhibitor cilazapril and the beta-adrenoceptor blocking agent atenolol. Both therapies were equally effective in lowering systolic blood pressure (e.g. from 168 mmHg to 152 mmHg with cilazapril and from 170 mmHg to 155 mmHg with atenolol after 6 months, p < 0.001 for both). However, atenolol was slightly but significantly more effective in lowering the diastolic blood pressure at 6, 12 and 24 months. The decline in GFR with time was significantly smaller with cilazapril than with atenolol. After 6 months the reduction in GFR was 1.0 vs. 4.0 ml/min x 1.73 m2, p = 0.008 (cilazapril vs. atenolol) and after 12 months the corresponding changes were 2.0 vs. 4.5 ml/min x 1.73 m2, p = 0.04 and after 24 months 3.0 vs. 4.0 ml/min x 1.73 m2, respectively (n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ACE inhibition preserves renal function better than beta-blockade in the treatment of essential hypertension. 759 59

The kidney can be considered as both culprit and victim in the hypertensive process. Deranged renal function contributes to the development of arterial hypertension and of secondary vascular damage at the glomerular and arteriolar level and accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans from the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by hyperuricaemia and increased urinary excretion of enzymes such as N-acetyl-beta-glucosaminidase and proteins such as albumin and beta 2-microglobulin. Later, a progressive fall in glomerular filtration rate, sometimes accompanied by proteinuria, can be observed if high blood pressure persists.
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PMID:Renal damage in hypertension. 760 39

A growing interest in the study of microalbuminuria (Mi) in essential hypertension (EH) has recently emerged. While clinical proteinuria is found with a low frequence (between 4 and 16%) in patients with EH, a variable but generally higher prevalence (10-40%) of Mi has been reported, even in the absence of diabetes and nephropathy. Mi is defined as an abnormal urinary excretion of albumin (20-200 micrograms/min), undetectable by conventional tests. Variations in the prevalence of Mi in different studies may be attributed to different selection criteria, techniques for detection of albuminuria, the severity of hypertension, age, race, coexistence of renal disease as well as the number of patients studied and the presence or absence of antihypertensive treatment. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and target organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis. Mi has been associated with higher blood pressure levels, a worse lipid profile as well as the presence of target organ damage, namely peripheral artery disease and left ventricular hypertrophy in patients with EH. Several studies have shown a correlation between Mi and/or proteinuria and cardiovascular diseases independently of other risk factors and cardiovascular mortality to be ten times higher in patients with Mi than in normoalbuminuric patients. Long-term prospective studies are needed in order to clarify the exact prevalence of Mi, its predictive value for the development of clinical proteinuria and renal function deterioration as well as the effect of different antihypertensive drugs.
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PMID:[Microalbuminuria, hypertension, and cardiovascular risk]. 763 60

Time course of 187 pregnancies was followed up in 103 females with chronic renal diseases (CRD), 76 females with essential hypertension (EH) and 14 posteclampsia females. Three variants of arterial pressure (AP) and 5 types of proteinuria changes were recognized in CRD and EH patients. The pattern of these changes was compared to that in posteclampsia patients, the eclampsia being an absolute criterium of late toxicosis. It is shown that neither elevated AP and proteinuria nor their absolute values can serve reliable signs of late gestosis in CRD and EH patients. Only the trend in these parameters is significant. CRD and EH females with late gestosis exhibit rapidly growing proteinuria in line with the onset or exacerbation of EH. Retrospective analysis of the pregnancies has confirmed association of late gestosis in 15% of EH and 7% of chronic glomerulonephritis patients. These estimates are lower than commonly accepted. Early diagnosis of late gestosis in pregnant females with CRD and EH requires not only regular AP registration, but also dynamic, in some cases hourly, evaluation of proteinuria.
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PMID:[The dynamic importance of proteinuria and arterial pressure for detecting late toxicosis in pregnant women with chronic kidney diseases and hypertension]. 763 70

An endogenous sodium pump inhibitor, or digitalis-like factor (DLF), has been postulated to mediate essential hypertension. It may also play a role in preeclampsia. However, studies of this factor in hypertensive pregnancy have not provided consistent findings. Part of this may be due to the absence of subclassification of pregnant women with pregnancy-induced hypertension (PIH) when assessing these parameters. In this study we explored serum DLF and digoxin-like immunoreactive factor (DLIF) in insulin-dependent diabetic (IDDM) women with normotensive pregnancies or PIH, comparing them to each other and to nondiabetic pregnant women. Our results demonstrated that nondiabetic women with preeclampsia (PE, PIH with proteinuria) had significantly increased serum DLF and DLIF compared to normotensive pregnant women (NL BP). Women with transient hypertension of pregnancy (THP, PIH without proteinuria) had intermediate values (DLF. NL BP: 3.3 +/- 0.6, THP: 4.8 +/- 1.1, PE: 7.6 +/- 1.3% inhibition [Na,K]-ATPase, P < .05 ANOVA; DLIF. NL BP: 0.22 +/- 0.02, THP: 0.28 +/- 0.03, PE: 0.35 +/- 0.02 ng digoxin equivalents/mL, P < .05 ANOVA). Pregnant normotensive IDDM women had significantly higher serum DLF and DLIF activity than their nondiabetic counterparts (DLF. non-IDDM NL BP: 3.3 +/- 0.6 v IDDM NL BP: 8.8 +/- 1.2% inhibition [Na,K]-ATPase, P = .0008; DLIF. non-IDDM NL BP: 0.22 +/- 0.02 v IDDM NL BP: 0.31 +/- 0.02 ng digoxin equivalents/mL, P = .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Digitalis-like factor and digoxin-like immunoreactive factor in diabetic women with preeclampsia, transient hypertension of pregnancy, and normotensive pregnancy. 873 86

ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower proteinuria. These effects can be due to a decrease in angiotensin II (AII) levels as well as an increase in bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by angiotensin II and those exerted by bradykinin. We investigated the effects of losartan in 9 patients with essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous inulin-and PAH-clearance (GFR and RPF) after stopping antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with losartan (50 mg/die) followed by a therapy with an ACE-inhibitor (ramipril 5mg/die). Additionally, urine albumin excretion (UAE) was measured. Treatment of patients with essential hypertension with losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under losartan; * = p < 0.05). MAP after four weeks of losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither losartan nor the ACE-inhibitor. Urine albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that losartan induced a significant reduction in MAP in patients with essential arterial hypertension with only moderate effects on renal hemodynamics.
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PMID:Renal hemodynamics in essential hypertensives treated with losartan. 778 Dec 6

Porteinuria was quantitatively measured in twenty-five controls and eighty-one newly detected patients of essential hypertension without renal insufficiency. Hypertension was treated with enalapril, enalapril and nifedepine and nifedepine alone. Mean proteinuria was more in patients of hypertension as compared to controls (P < .001). Proteinuria decreased significantly (P < .001) after six weeks of control of hypertension. Patients treated with enalapril alone had maximum reduction in proteinuria than those with enalapril and nifedepine, and nifedepine alone.
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PMID:Proteinuria in essential hypertension. 782 37

The Joint National Committee Reports IV (1988) and V (1992) have emphasized individualization of drug therapy for patients with hypertension-a departure from the "stepped" care approach of initiating therapy with diuretics as advocated by the JNC I-III in the 1970's and 1980's. This review highlights individualization or "patient profiling" using calcium channel blockers as first-line treatment strategy for patients with primary hypertension--especially in the patient who has attendant risk factors and sequelae. The calcium channel antagonists, especially effective in elderly and Black patients, have proven efficacy in reducing left ventricular hypertrophy and improving diastolic function in patients with hypertensive heart disease. The heart rate limiting calcium antagonist, verapamil, has been found effective in outcome trials of reducing death and reinfarction rates post myocardial infarction and is an alternative therapy for the beta blocker intolerant hypertensive post myocardial infarction. More vascular specific dihydropyridines (felodipine, isradipine, and amlodipine) may be preferable to rate limiting agents in hypertensives with sinus node or AV conduction disorders and in those with impaired left ventricular systolic function. Verapamil and diltiazem have been effective in preliminary trials in reducing proteinuria and preserving renal function in both diabetic and non diabetic hypertensives. Calcium channel antagonists appear to prevent the progress of atherosclerosis independent of their antihypertensive properties. Further, they have theoretic value in improving endothelial mediated vasodilation.
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PMID:Individualization of therapy for hypertension in the 1990's: the role of calcium antagonists. 785 64

We investigated endothelin-1 mRNA expression in peripheral blood monocytes from 40 patients with IgA nephropathy, 40 with other glomerulonephritides and 10 with essential hypertension without renal diseases, and from 30 healthy age-matched controls. 95% of patients with IgA nephropathy had increased endothelin-1 mRNA expression in monocytes but little was detected from the other groups. Endothelin-1 mRNA was positively correlated with urinary protein excretion (95% CI 0.835-0.952) and histopathological findings (0.796-0.939). In 15 patients with IgA nephropathy endothelin-1 mRNA values and proteinuria decreased gradually after treatment. Endothelin-1 mRNA-expressing activated monocytes may be associated with the progression of IgA nephropathy.
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PMID:Endothelin-1 mRNA expression by peripheral blood monocytes in IgA nephropathy. 790 78

Proteinuria (protein excretion > 300 mg/d) is an independent risk factor for the development of cardiovascular disease and renal failure. The finding of persistent proteinuria in otherwise asymptomatic patients often precedes the development of arterial hypertension and renal failure. When proteinuria is accompanied by arterial hypertension, blood pressure control can decrease the quantity of protein excretion but not the incidence of proteinuria. In this sense, converting enzyme inhibitors seem to possess a higher capacity to reduce proteinuria. Nevertheless, the effects of reducing proteinuria on renal function and cardiovascular risk remain to be elucidated. Microalbuminuria (urine albumin excretion oscillating between 30 and 300 mg/d) seems to be a predictor of cardiovascular disease in diabetic and nondiabetic subjects and has been established as a predictor for the development of diabetic nephropathy. Blood pressure levels and urinary albumin excretion correlate positively, and antihypertensive therapy of any kind decreases the quantity of albumin present in the urine. The role of increased albumin excretion in essential hypertension and in renal failure remains to be elucidated.
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PMID:Clinical relevance of proteinuria and microalbuminuria. 792 40


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