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)

ACE inhibitors which till recently were used only in the treatment of cardiovascular diseases are becoming a perspective group of drugs also in the treatment of chronic nephropathies. It was revealed that they are effective in particular in the treatment of proteinuria of different etiology and have also a marked renoprotective effect and are therefore recommended to slow down the progression of renal failure. They reduce intraglomerular hypertension, increase glomerular filtration and the renal blood flow, and it is assumed that they can retard the progression of chronic glomerulonephritis and diabetic nephropathy. It may be excepted that their therapeutic application will in the near future be extended also to clinical nephrology.
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PMID:[ACE inhibitors--a prospective new group of drugs for the treatment of kidney diseases]. 129 14

Points of agreement: (1) In IDDM, hypertension occurs in patients who have already developed nephropathy, probably in the microalbuminuric phase. (2) Hypertension is an important accelerator of the development of diabetic nephropathy. (3) Hypertension, obesity and NIDDM are often associated, and insulin resistance is commonly observed in all three states. (4) Antihypertensive therapy retards the development of diabetic nephropathy in IDDM and reduces proteinuria in NIDDM. (5) The choice of antihypertensive agent in the diabetic patient must be based upon the efficacy of the drug as well as avoidance of side effects including deleterious influence on glucose, insulin and lipid levels and renoprotection. (6) Carefully conducted long-term comparative trials between different classes of antihypertensive drugs in microalbuminuric IDDM and NIDDM patients are essential. Points of major controversy: (1) Detection of IDDM patients prone to the development of diabetic nephropathy can be performed by measuring specific parameters such as erythrocyte Na(+)-Li+ countertransport activity. (2) Insulin resistance is a pathogenic mechanism rather than purely an association with hypertension and obesity. (3) A certain class of antihypertensive agents--ACE inhibitors--confers a specific renoprotective effect in diabetic nephropathy, in addition to its effects upon systemic blood pressure. (4) Reduction of blood pressure should be considered in the normotensive microalbuminuric diabetic patient. (5) Microalbuminuria is a sufficient 'surrogate endpoint' for the progression of renal failure.
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PMID:Meeting report of the International Society of Hypertension Conference on Hypertension and Diabetes. 131 6

We report here the alterations of serum angiotensin-converting enzyme activity (S-ACE) and of active renin plasma concentrations (ARPC) in 41 insulin-dependent diabetes mellitus (IDDM) patients compared with those of 26 control subjects. The IDDM patients had S-ACE activity (54 +/- 16 I.E.) in the upper normal range (controls, 39 +/- 7). When the patients were subclassified according to their diabetic complications, a significant increase of S-ACE within the IDDM group compared to the controls was observed in patients with nephropathy (68 +/- 13, P less than 0.001) with persistent proteinuria and with retinopathy (63 +/- 14, P less than 0.001). A significant correlation was found between proteinuria and S-ACE (r = 0.98, P less than 0.001) and between retinopathy and S-ACE levels (r = 64, P less than 0.001). No correlation between blood pressure and S-ACE or between blood glucose and S-ACE was observed. The ARPC were within the normal range in the IDDM (21 +/- 9 ng/l) and in control (19 +/- 3) groups. No correlations between ARPC and blood pressure or blood glucose or the degree of diabetic complications were registered. These data show that S-ACE activity is elevated in IDDM patients with nephropathy-proteinuria and/or with retinopathy and the circulating renin may not represent the renal renin-angiotensin vascular system.
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PMID:Serum angiotensin-converting enzyme activity and active renin plasma concentrations in insulin-dependent diabetes mellitus. 133 Apr 63

We studied the effects of symptomatic, antiproteinuric treatment with NSAID's (n = 28) and ACE-inhibitors (n = 14) in patients with proteinuria due to idiopathic membranous glomerulopathy (MGP). These two treatment groups were compared with a group of patients who did not receive antiproteinuric medication (n = 14). Urinary protein loss was effectively lowered by NSAID and ACE inhibitor therapy from 9.5 +/- 1.0 to 4.5 +/- 0.5 g/day (mean +/- SEM) and from 9.8 +/- 1.4 to 3.9 +/- 0.7 g/day respectively, whereas the control group showed a slight fall in proteinuria from 6.9 +/- 0.8 to 5.5 +/- 0.8 g/day. As a result of this treatment hypoalbuminaemia and hypercholesterolaemia improved significantly: serum albumin rose in the NSAID group from 25.4 +/- 1.2 to 29.0 +/- 1.0, and in the ACEi group from 29.9 +/- 1.8 to 32.7 +/- 1.2 g/l (control group from 27.4 +/- 1.6 to 27.8 +/- 1.6 g/l, while cholesterol was lowered in the NSAID group from 8.5 +/- 0.5 to 7.5 +/- 0.4 and in the ACEi group from 8.7 +/- 0.5 to 7.6 +/- 0.4 mmol/l (control group from 9.7 +/- 1.1 to 8.5 +/- 1.0 mmol/l). The antiproteinuric effect of both drugs was well maintained during an 18-month follow-up. Progression towards end-stage renal failure was observed especially in patients with impaired renal function at entry. Remission of proteinuria occurred particularly in patients with lower baseline values of proteinuria, irrespective of the treatment modality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antiproteinuric drugs in patients with idiopathic membranous glomerulopathy. 133 89

Measurement of proteinuria, microalbuminuria, and sodium-lithium countertransport in red cells has no practical value. A low-protein diet and ACE inhibitor therapy are currently the best way to retard progression of diabetic renal disease.
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PMID:Proteinuria and microalbuminuria as predictors of nephropathy. 134 41

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.
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PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63

In patients with diabetes mellitus, metabolic control, hypertension and kidney function are important prognostic factors. In this respect ACE inhibitors exhibit, according to previous publications, a potentially beneficial effect on diabetic patients. To further clarify this effect of ACE inhibitors, a meta-analysis of 21 studies of type I and II diabetics under therapy with ACE inhibitors was performed. Altogether 325 cases were analyzed. The duration of diabetes varied between 2.5 and 22 years. Therapy with ACE inhibitors under long-term treatment (up to 12 months) reduced diastolic blood pressure (-25%) and, both for type I and II diabetics, fasting blood sugar (-14%) and HbA1 (-9%). Microalbuminuria/proteinuria was reduced by 33% under short-term treatment with ACE inhibitors (up to 3 months) and by 66% under long-term treatment. Analysis of the subgroups with microalbuminuria (30-300 mg/day, n = 48) or clinical proteinuria (greater than 300-1500 mg/day, n = 9) showed similar results. The outcome of this meta-analysis shows that the treatment of diabetic patients with ACE inhibitors not only effectively reduces high blood pressure but also reduces microalbuminuria/proteinuria and, in addition, exhibits an anti-hyperglycemic effect by improving blood sugar levels.
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PMID:[Improved glucose regulation and microalbuminuria/proteinuria in diabetic patients treated with ACE inhibitors. A meta-analysis of published studies of 1985-1990]. 141 95

The treatment of hypertension in pregnancy is justified by the need to reduce blood pressure in order to avoid the onset of preeclampsia, eclampsia, retarded intrauterine growth and even neonatal, perinatal and maternal death. The value of using drugs to treat slight-moderate hypertension in pregnancy is, however, not clearly defined in the literature. In fact, from an etiopathogenetic point of view, the significance of increased blood pressure in pregnancy has not yet been satisfactorily explained, and above all the positive significance of increased blood pressure not be forgotten since, up to diastolic levels of 90 mmHg, it is accompanied by an increase in birth weight. The aim of the present study was to verify the efficacy of pharmacological treatment in cases of slight-moderate hypertension during pregnancy in a population of 121 pregnant women attending the Obstetrics-Gynecological Clinic of the "Istituto per l'Infanzia" in Trieste during the period from 14-11-1984 to 24-4-1991. Data for this retrospective study were extrapolated from an analysis of medical records and then memorized in a data-base file. The degree of hypertension was classified as slight, moderate and severe according to blood pressure levels measured on hospitalisation. Clinical signs taken into account included: edema, proteinuria and hypoprotidemia. Anti-hypertensive therapy was selected between one or more associated drugs belonging to the following classes: central action and peripheral action anti-adrenergic drugs, beta-blockers, calcium channel blockers, vasodilators, diuretics, ACE-inhibitors and sedatives. Moreover, patients also received non-pharmacological treatment in the form of low sodium diets and bed-rest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Moderate arterial hypertension in pregnancy: therapeutic aspects]. 148 Mar 1

A 65-year-old man presented proteinuria in the nephrotic range that occurs in the setting of high renin hypertension. Proteinuria persisted after normalizing blood pressure by nifedipine. In contrast, treatment with an ACE-inhibitor (enalapril) resulted in the prompt resolution of the proteinuria. Interestingly, proteinuria relapsed after removing the ACE-inhibition. These observations suggest a causal relation between the overactivity of the renin-angiotensin system in this patient and his proteinuria.
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PMID:Nephrotic-range proteinuria in a patient with high renin hypertension: effect of treatment with an ACE-inhibitor. 148 13

Diabetic renal disease is a clinical syndrome in which proteinuria is followed by the development of renal failure, and is commonly associated with the concomitant development of hypertension. In insulin-dependent diabetic (IDDM) patients, hypertension often first appears in the microalbuminuric phase of diabetic nephropathy whereas in non-insulin-dependent diabetic (NIDDM) patients, hypertension often antecedes nephropathy and may precede the diagnosis of diabetes. Antihypertensive regimens including diuretics, vasodilators such as hydralazine, beta-blockers and ACE inhibitors reduce proteinuria and delay the decline in renal function in IDDM patients with established nephropathy. No such data are as yet available for calcium antagonists. In microalbuminuric diabetic patients with hypertension, conventional antihypertensive agents, ACE inhibitors and calcium antagonists have been shown to decrease urinary albumin excretion. In the diabetic patient with normal blood pressure and microalbuminuria, there is much less information. It appears likely that ACE inhibitors reduce or retard the rate of increase in albuminuria in these patients. The effect on ultimately delaying or preventing renal failure remains unknown although the preliminary evidence is encouraging. Data on calcium antagonists remain inconclusive with some reports suggesting an increase in proteinuria with the dihydropyridine calcium antagonists. However, a recent longer term study suggested that nifedipine may prevent the rise in albuminuria which is generally observed in the untreated normotensive microalbuminuric subject.
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PMID:The management of diabetic proteinuria. Which antihypertensive agent? 150 44


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