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 clinical diagnosis of preeclampsia is often erroneous, for it may be confused with latent hypertension, acute or chronic renal disease, or frank essential hypertension that had abated during much of pregnancy. Eclampsia and "true" preeclampsia run in families with a frequency suggesting that a single recessive gene may be responsible. Eclampsia and "true" preeclampsia do not cause chronic hypertension, whatever their durations. Gestational hypertension is merely hypertension without proteinuria or abnormal edema. It often has been the basis for the diagnosis of mild preeclampsia, although renal biopsy samples almost never show the characteristic lesion in the absence of proteinuria. Gestational hypertension is often a sign of latent hypertension unmasked by pregnancy. Women with gestational hypertension ultimately have a high prevalence of chronic hypertension, whereas all those whose pregnancies are normotensive ultimately have a low prevalence.
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PMID:Hypertension in pregnancy: definitions, familial factor, and remote prognosis. 700 1

The antihypertensive effects of the oral converting enzyme inhibitor captopril and of propranolol were evaluated in a single-blind trial of 12 weeks in 19 ambulatory men with moderated essential hypertension (supine diastolic blood pressure [DPB], 100 to 120 mm Hg after receiving placebo for two weeks) whose sodium intake was unrestricted. The captopril group included 12 patients and the propranolol group seven. After the initial dose-finding period of four weeks, supine DBP was significantly reduced in eight patients receiving captopril and in four of the patients receiving propranolol. In these patients DBP decreased throughout the following eight weeks. In the remaining patients from each group, DBP was not reduced by either drug given alone at maximum allowable dosages during dose-finding periods, nor by combined administration in following weeks. No adverse side effects attributable to captopril were noted, except in one patient in whom proteinuria developed after seven weeks. Captopril has potential value in the treatment of moderate essential hypertension.
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PMID:Comparison of antihypertensive effects of captopril and propranolol in essential hypertension. 700 74

The glomerular filtration rate (creatinine clearance), glomerular permeability (qualitative and quantitative proteinuria), tubular reabsorption (k-lambda chains of immunoglobulins and lysozyme) and indexes of tubular cell lysis (alpha-glucosidase and gamma-glutamyltranspeptidase) were measured in the urine of 10 patients with moderate, uncomplicated essential hypertension during placebo therapy and after captopril given at increasing doses of 25, 50, 100 and 200 mg twice daily, the first three doses being given for 3 days and the last one for 4 weeks in all patients and for an additional 6 months in 5 patients. During placebo therapy, proteinuria was absent in eight patients and detectable (glomerular and selective) in two; selective proteinuria appeared in two and a decrease in selectivity was observed in two patients with previous proteinuria after 4 weeks of captopril therapy. No proteinuria was detectable in the five patients followed up to 6 months, not even in the one in whom a decrease in glomerular selectivity had occurred after 4 weeks. The glomerular filtration rate was unchanged as were lysozyme and gamma-glutamyltranspeptidase values, while light chains were always undetectable. Alpha-glucosidase showed some increase; however, increments were transient and always much lower than those observed with known tubular toxic drugs. These data show that under our experimental conditions captopril caused no evident changes in glomerular and tubular function.
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PMID:Effect of captopril on renal function in patients with essential hypertension. 704 2

1 Eighty-five women with severe hypertension complicating pregnancy were treated with oral labetalol (Trandate). Six of these had a twin pregnancy and 54 had proteinuria. 2 Effective control of the blood pressure was achieved in all but six patients. The maximum dose of labetalol prescribed was 1200 mg daily. There were no significant maternal or foetal side-effects. 3 Foeto-placental function was carefully monitored in all patients. Twenty-four of the 89 infants born alive showed evidence of intra-uterine growth retardation, the highest incidence occurring in the group of patients with essential hypertension complicated by pregnancy induced hypertension. 4 The low perinatal mortality of 4.4% was a reflection of the meticulous control of the blood pressure. 5 There were no congenital malformations or evidence of oculotoxicity in any of the infants delivered. 6 The efficient hypotensive action of orally administered labetalol together with the absence of maternal and foetal side effects and consequent improved perinatal mortality confirms that it is an eminently suitable drug for the treatment of hypertension complicating pregnancy.
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PMID:The evaluation of labetalol in the treatment of hypertension complicating pregnancy. 709 96

The platelet count in 550 patients with gestational hypertension was significantly lower and the mean platelet volume significantly higher than in normal pregnant women. Both the platelet count and volume became increasingly abnormal when hypertension was accompanied by oedema, proteinuria or both, and women with severe pre-eclampsia or eclampsia had the lowest platelet counts and the highest mean platelet volume. The proportion of patients with thrombocytopenia and/or macrothrombocytosis also varied with the severity of the clinical presentation. Fibrinogen degradation products were found mainly in fully developed pre-eclampsia. These findings confirm the concept of a rapid platelet turnover caused by low-grade disseminated intravascular coagulation in gestational hypertension. The platelet pattern in essential hypertension is similar to that seen in normal pregnancy.
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PMID:Thrombocytopenia and macrothrombocytosis in gestational hypertension. 729 1

In an attempt to determine the effects of antihypertensive treatment on proteinuria and renal function, these factors were studied in 155 patients with essential hypertension, before and during antihypertensive therapy. Slight renal impairment tended to increase with the progress of hypertension, as evidenced by a slight but significant increase in the levels of blood urea nitrogen (BUN) and serum creatinine, and by a progressive decrease in creatinine clearance. A decrease in proteinuria appeared as early as one month after initiation of treatment and continued for at least two years during treatment. Apparently the proteinuria was caused by increased glomerular pressure and by vascular damage in the glomerular vessels. In 7 patients, normalization of blood pressure resulted in an elevation of BUN and creatinine concentrations, although initial renal function did not differ significantly from that in other groups who did not show such derangement during treatment. Thus, a reduction of proteinuria seems to be a good criterion for predicting beneficial results from antihypertensive treatment.
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PMID:Proteinuria and renal function during antihypertensive treatment for essential hypertension. 735 3

The triad of severe pre-eclampsia is often described as a combination of hypertension, oedema and proteinuria. Hypertension alone arising in the second half of pregnancy however is not associated with any greater perinatal mortality or low birthweight than normotensive primigravidae and it is probable that this hypertension may be either physiological or a manifestation of essential hypertension or, in some cases, a mild form of pre-eclampsia. Oedema also does not necessarily signify abnormality. High weight gain, fluid retention or oedema is associated with a lower incidence of small babies, but with a higher incidence of pre-eclampsia. Considerable amounts of water retention can occur in normal pregnancy, either measured as an increase during pregnancy, or as a fall after delivery. The diuretics cyclopenthiazide, spironolactone and clopamide given prophylactically to high weight gain primigravidae did not prevent the onset of proteinuric pre-eclampsia, but caused the babies to be lighter in weight than those of controls. Sodium potassium and water content of leucocytes from primigravidae with proteinuric pre-eclampsia is the same as in mild pre-eclampsia and normal pregnancy. Although salt and water retention are common features of pre-eclampsia, they do not cause the condition and are not an essential part of it.
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PMID:The relevance of hypertension and oedema in pregnancy. 742 67

The characterization and cloning of constitutive and inducible nitric oxide (NO)-synthesizing enzymes and the development of specific inhibitors of the L-arginine NO pathway have provided powerful tools to define the role of NO in renal physiology and pathophysiology. There is increasing evidence that endothelium-derived NO is tonically synthesized within the kidney and that NO plays a crucial role in the regulation of renal hemodynamics and excretory function. Bradykinin and acetylcholine induce renal vasodilation by increasing NO synthesis, which in turn leads to enhancement of diuresis and natriuresis. The blockade of basal NO synthesis has been shown to result in decreases of renal blood flow and sodium excretion. These effects are partly mediated by an interaction between NO and the renin angiotensin system. Intrarenal inhibition of NO synthesis leads to reduction of sodium excretory responses to changes in renal arterial pressure without an effect on renal autoregulation, suggesting that NO exerts a permissive or a mediatory role in pressure natriuresis. Nitric oxide released from the macula densa may modulate tubuloglomerular feedback response by affecting afferent arteriolar constriction. Nitric oxide produced in the proximal tubule possibly mediates the effects of angiotensin on tubular reabsorption. In the collecting duct, an NO-dependent inhibition of solute transport is suggested. The L-arginine NO pathway is also active in the glomerulus. Under pathologic conditions such as glomerulonephritis, NO generation is markedly enhanced due to the induction of NO synthase, which is mainly derived from infiltrating macrophages. An implication of NO in the mechanism of proteinuria, thrombosis mesangial proliferation, and leukocyte infiltration is considered. In summary, the data presented on NO and renal function have an obvious clinical implication. A role for NO in glomerular pathology has been established. Nitric oxide is the only vasodilator that closely corresponds to the characteristics of essential hypertension. Using chronic NO blockade, models of systemic hypertension will provide new insights into mechanisms of the development of high blood pressure.
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PMID:Nitric oxide in the kidney: synthesis, localization, and function. 751 25

One hundred nine patients with essential hypertension and without either diabetes mellitus or clinical proteinuria were examined to investigate possible racial differences in urinary albumin excretion rates. The black hypertensive patients were found to have significantly higher urinary albumin excretion rates compared with the white patients; in addition, a significantly greater proportion of the black patients than the white patients (32% v 14%) had microalbuminuria, defined as a urinary albumin excretion rate greater than 30 micrograms/min. These differences could not be explained by age, blood pressure, body mass index, glycosylated hemoglobin, serum creatinine, duration of hypertension, or type of hypertension treatment. Hypertensive renal failure occurs six to 18 times more frequently in blacks than in whites; to our knowledge, these data are the first to indicate that microalbuminuria may be more prevalent during the course of hypertension in black patients and thus may be an early marker for end-organ damage susceptibility among hypertensive patients.
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PMID:Racial differences in the prevalence of microalbuminuria in hypertension. 757 9

The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). The incidence of cerebral hemorrhage was significantly higher (p < 0.05) in the patients with APA when compared to the EHT group. On the other hand, the incidence of myocardial infarction and/or congestive heart failure in the APA group was lower, although this difference did not reach statistical significance. Diastolic blood pressure in the APA group was significantly higher (p < 0.001) in the EHT group. However, a significant difference in diastolic blood pressure was not detected between the APA groups with and without vascular complications, whereas in the EHT group diastolic blood pressure was significantly higher (p < 0.001) in cases with vascular complications as compared to those without complications. As a possible factor contributing to the higher incidence of cerebral hemorrhage in the APA group, proteinuria was suggested. It was recommended that patients with primary aldosteronism should undergo operation when localization of the APA is established.
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PMID:Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. The Research Committee of Disorders of Adrenal Hormones in Japan. 759 26


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