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)

Severe renal failure associated with proteinuria occurred in a 21-year patient, who had massive rheumatic aortic regurgitation. There was no sign of congestive heart failure or extra-cellular dehydration. Subacute bacterial endocarditis was ruled out by appropriate laboratory investigations. Prosthetic aortic valve replacement resulted in normalization of the renal function and marked reduction of proteinuria. Renal histology showed severe sclerotic endarteritis involving predominantly the large arteries, and membrano-proliferative-like glomerulopathy without immune deposits. The role of the massive aortic regurgitation in the production of renal failure and histologic alterations is suggested.
J Cardiovasc Surg (Torino)
PMID:Reversible renal failure secondary to severe compensated aortic regurgitation. 65 89

Roughly 40% of all diabetics, whether insulin dependent or not, develop persistent albuminuria, a decline in their glomerular filtration rate, and elevated blood pressure, i.e., diabetic nephropathy. Diabetic nephropathy is the single most important cause of end-stage renal disease in the Western world, accounting for over one-quarter of all end-stage renal disease. Systemic/glomerular hypertension plays a role in the initiation and progression of diabetic glomerulopathy. Angiotensin-converting enzyme (ACE) inhibitors are superior to conventional antihypertensive drugs in preventing the development of glomerular lesions in insulin-treated streptozotocin diabetic rats. Lowering of glomerular hypertension may be the crucial factor involved. Human studies suggest that ACE inhibitors postpone the progression to clinical overt diabetic nephropathy in normotensive diabetic patients with persistent microalbuminuria. ACE inhibitors combined with a diuretic reduce albuminuria and postpone renal insufficiency in hypertensive diabetics with overt nephropathy. No treatment modality other than antihypertensive treatment has yet been proven to be effective in protecting renal function in diabetic nephropathy. All previous reports dealing with the natural history of diabetic nephropathy have demonstrated a cumulative death rate between 50 and 77% 10 years after the onset of proteinuria. Effective antihypertensive treatment has reduced the cumulative death rate to 15-20% 10 years after the onset of nephropathy.
J Cardiovasc Pharmacol 1992
PMID:Renoprotective action of angiotensin-converting enzyme inhibition in diabetes mellitus. 138 60

The mechanism of the antiproteinuric effect of angiotensin-converting enzyme (ACE) inhibitors in diabetic and nondiabetic renal disease is as yet unknown. A meta-analysis of studies on the effects of ACE inhibitors and other antihypertensive drugs on proteinuria, blood pressure, and renal hemodynamics in nondiabetic renal disease revealed that ACE inhibitors lower proteinuria more than other antihypertensives. Moreover, a close correlation (p less than 0.01) between changes in urinary protein loss and in filtration fraction was found, whereas such a correlation could not be detected between changes in proteinuria and in blood pressure. This suggests that, at least in nondiabetic renal disease, the fall in proteinuria during ACE inhibition is the consequence of the intrarenal effect of the drug more than the systemic effect. Data on the mechanism of action of ACE inhibitors in diabetic microalbuminuria and in diabetic overt proteinuria are less consistent. A fall in proteinuria on antihypertensive drugs in these patients can be observed also without a significant fall in blood pressure, and without any change in filtration fraction. We therefore conclude that one should be cautious in extrapolating the data from studies in diabetic renal disease to patients with nondiabetic nephropathies. Moreover, we argue also that nonhemodynamic effects of ACE inhibitors also could be involved in the antiproteinuric effect of these drugs.
J Cardiovasc Pharmacol 1992
PMID:The antiproteinuric effects of blood pressure-lowering agents: differences between nondiabetics and diabetics. 138 62

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.
J Cardiovasc Pharmacol 1992
PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63

Enalapril is an effective agent in the treatment of mild to severe hypertension. It is equally effective in elderly and young adult patients but appears to be more effective in white than in black hypertensive patients. Following treatment with enalapril, an assessment of maximum exercise performance found a decrease in total peripheral resistance without significant changes in cardiac output, heart rate, or stroke volume compared with pretreatment values. In addition, there have been reports of reversal of left ventricular hypertrophy in enalapril-treated hypertensive patients. Enalapril is also effective and well tolerated in hypertensive patients with renal impairment of varying etiology. The most common adverse experiences reported in controlled clinical trials were headache (5.2%), dizziness (4.3%), and fatigue (3.0%). In high-risk hypertensive patients, no enalapril-treated neutropenia, proteinuria, dysgeusia, or ageusia were reported. It may be concluded that the benefit-to-risk ratio of enalapril is among the best of the antihypertensive therapies currently available.
J Cardiovasc Pharmacol 1990
PMID:Enalapril: benefit-to-risk ratio in hypertensive patients. 169 15

In 11 hypertensive patients with chronic renal failure we studied the short-term effects of the calcium antagonist nitrendipine, the angiotensin-converting enzyme inhibitor cilazapril, and the combination of both drugs on blood pressure, renal hemodynamics, and proteinuria in a randomized, double-blind, placebo-controlled way. After one week of treatment, blood pressure at 2-5 h after drug administration amounted to 159 +/- 5/101 +/- 3 mm Hg (means +/- SEM) during placebo. Nitrendipine, cilazapril, and the combination lowered mean arterial pressure by 1.4 +/- 1.6 (NS), 6.0 +/- 1.7 (p less than 0.10), and 10.3 +/- 2.1% (p less than 0.01), respectively. Glomerular filtration rate did not change. As compared to placebo, renal blood flow increased and renal vascular resistance decreased significantly during the combination. Filtration fraction amounted to 22.7 +/- 1.2% during placebo and was 22.0 +/- 1.4 (NS), 20.4 +/- 1.2 (p less than 0.01), and 20.5 +/- 1.4% (p less than 0.05) during nitrendipine, cilazapril, and the combination, respectively. During nitrendipine, albuminuria was slightly higher than during placebo: 0.86 +/- 0.39 vs. 0.58 +/- 0.25 mg/min (NS). During cilazapril alone and during the combination of both drugs, albuminuria was lower as compared to nitrendipine: 0.38 +/- 0.14 mg/min (p less than 0.01) and 0.44 +/- 0.18 mg/min (p less than 0.01), respectively. The data suggest that the combination of nitrendipine and cilazapril is an effective treatment in renal hypertension. In addition, cilazapril alone as well as the combination with nitrendipine reduced albuminuria, possibly by decreasing filtration fraction and/or reduction of blood pressure.
J Cardiovasc Pharmacol 1990 Dec
PMID:Effects of nitrendipine and cilazapril on renal hemodynamics and albuminuria in hypertensive patients with chronic renal failure. 170 85

A better understanding of the hemodynamic abnormalities in gestational hypertension together with the use of effective antihypertensive agents have resulted in more rational therapeutic approaches and a substantial improvement in maternal and fetal welfare. In normal pregnancy, there is reduced vascular reactivity with peripheral pooling and decreased circulatory responses to pressor agents. These are prostacyclin-dependent processes. In gestational hypertension, the normal increase in plasma volume and cardiac output with pregnancy is attenuated and prostacyclin-dependent processes are impaired, resulting in persistent vasoconstriction, enhanced responses to pressor agonists, and failure to develop adequate uteroplacental interchange. Among the modern antihypertensive agents, alpha- and beta-adrenergic antagonists and calcium ion entry blockers have permitted safe and effective long-term blood pressure control with sustained fetal growth. The development of proteinuria that can occur in chronic hypertension or in previously normotensive women (toxemia of pregnancy) can be prevented by the use of beta-adrenergic blocking agents and possibly by low-dose aspirin (75 mg/day). Maternal prostacyclin-thromboxane imbalance, important in the pathogenesis of gestational hypertension, is corrected by low-dose aspirin treatment. With the prevention of pre-eclampsia, the adverse maternal and fetal prognosis in gestational hypertension has been improved.
J Cardiovasc Pharmacol 1990
PMID:Treatment of hypertension in pregnancy. 170 7

Many lipoprotein abnormalities are seen in the untreated, hyperglycemic diabetic patient. The non-insulin-dependent diabetic (NIDDM) patient with mild fasting hyperglycemia commonly has mild hypertriglyceridemia due to overproduction of TG-rich lipoproteins in the liver, associated with decreased high-density lipoprotein (HDL) cholesterol levels. The more hyperglycemic untreated NIDDM and insulin-dependent diabetic (IDDM) patient have mild to moderate hypertriglyceridemia due to decreased adipose tissue and muscle lipoprotein lipase, (LPL) activity. These patients also have decreased HDL cholesterol levels associated with defective LPL catabolism of TG-rich lipoproteins. Treatment of diabetes with oral sulfonylureas or insulin corrects most of the hypertriglyceridemia and some of the decrease in HDL cholesterol. The abnormality in adipose tissue LPL activity corrects slowly over several months of therapy. The treated IDDM patient often has normal lipoprotein levels. The treated NIDDM patient may continue to have mild hypertriglyceridemia, increased intermediate-density lipoprotein levels, small dense low-density lipoproteins (LDL) with increased apoprotein B, and decreased HDL cholesterol levels. The central, abdominal distribution of adipose tissue in IDDM is associated with insulin resistance, hypertension, and the above lipoprotein abnormalities. Improvement in glucose control, in the absence of weight gain, leads to lower triglyceride and higher HDL cholesterol levels. In addition, the diabetic patient is prone to develop other defects that, in themselves, lead to hyperlipidemia, such as proteinuria, hypothyroidism, and hypertension, treated with thiazide diuretics and beta-adrenergic-blocking agents. When a diabetic patient independently inherits a common familial form of hypertriglyceridemia, he might develop the severe hypertriglyceridemia of the chylomicronemia syndrome.
J Cardiovasc Pharmacol 1990
PMID:Pathophysiology of hyperlipidemia in diabetes mellitus. 171 Jul 39

In 15 randomized, double-blind studies with blood pressure measured at the end of the dosing interval, diltiazem sustained-release or conventional tablets were found to be equal in efficacy to hydrochlorothiazide, beta-blockers, angiotensin-converting enzyme inhibitors, and other calcium-channel antagonists. The total number of patients with adverse effects and those who drop out due to adverse effects are similar for diltiazem and the other drugs. Combination therapy with diltiazem and captopril showed additive effects, and combination of diltiazem with hydrochlorothiazide or atenolol showed additional, but perhaps less than additive, effects. Six studies in older and younger patients have shown no overall effect of age on the antihypertensive effect of diltiazem. Two studies showed no difference in mean antihypertensive response between black and non-black patients. In contrast to diuretics and beta-blockers, diltiazem does not have adverse metabolic effects on electrolytes, carbohydrate metabolism, and lipid metabolism. Diltiazem is an excellent antianginal agent. It has been shown in one study to decrease proteinuria as effectively as lisinopril, and it may have renal protective effects. The antihypertensive efficacy of diltiazem as monotherapy is equal to that of all other antihypertensive classes, and it is tolerated as well or better than most other antihypertensive drugs. Diltiazem is particularly indicated in patients with hypertension and concurrent angina pectoris, diabetes, hyperlipidemias, and, perhaps, chronic renal disease.
J Cardiovasc Pharmacol 1991
PMID:Diltiazem: its place in the antihypertensive armamentarium. 172 39

Based on studies in the rat remnant kidney model, it has been proposed that glomerular hypertension is responsible for the progressive nature of chronic renal disease. In that model, therapy with angiotensin converting enzyme (ACE) inhibitors reduced glomerular pressures. As a result, glomerular injury was reduced and the rate of progression of renal disease was slowed. Thus, alterations in hemodynamics may play an important role in glomerular injury. However, it is now evident that a variety of metabolic and other factors affect the progression of renal disease. Moreover, recent studies suggest that ACE inhibitors may also have beneficial effects that are independent of alterations in glomerular pressure. In humans, the glomerular hemodynamic response to renal disease cannot be measured, and it is not known whether or under which conditions glomerular capillary pressure might be elevated. Treatment with ACE inhibitors safely lowers blood pressure without adversely affecting renal function in most patients with nondiabetic chronic renal failure. Although proteinuria and the rate of progression of renal disease may decrease in some patients, these effects are inconsistently seen. Identification of the factors that modulate this variability in response to ACE inhibition may provide new insight into the pathogenesis and treatment of progressive renal disease in humans.
Cardiovasc Drugs Ther 1990 Feb
PMID:Renal effects of angiotensin converting enzyme inhibitors: nondiabetic chronic renal disease. 228 14


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