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)

An examination of the principal physiological actions of angiotensin II should make it clear why in vivo attempts to inhibit the rate of angiotensin II generation have been an attractive avenue in pursuing control of high blood pressure. The major physiological effect of angiotensin II relates to its direct pressor effect, but there are supplementary blood pressure regulating actions. Therefore, if we limit the rate of angiotensin II generation by inhibiting the angiotensin converting enzyme (ACE) we should expect to control high blood pressure in a number of clinical syndromes. This paper reviews the future of ACE inhibitors in the treatment of conditions such as hypertension associated with unilateral renal artery stenosis, essential hypertension and severe and previously unresponsive hypertension, with respect not only to efficacy but also to the side-effect profile and ancillary properties. Side effects seen with this class of drug are cough, rashes (both morbilliform and urticarial) and, rarely, angio-oedema. Proteinuria, nephrotic syndrome, leukopenia and taste disturbance were previously reported with captopril but only taste disturbance, and that less frequently, is apparent at the lower doses now employed. Several studies have examined the 'quality-of-life' aspects of ACE therapy and have usually but not always reported favourably. There are features of the ACE inhibitors which make them attractive drugs, and while we should be cautious because of limited experience, we should critically and creatively examine their properties over the next years.
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PMID:Angiotensin converting enzyme inhibition in hypertension. 331 25

We have previously reported on a high prevalence of high renin essential hypertension in psoriasis. Since angiotensin-converting enzyme (ACE) was also reported to be increased in some psoriatics, we found it rational to treat 10 patients with hypertension and diffuse psoriasis with captopril at a dose of 25 mg t.i.d. Five patients had high PRA levels and in 1 of them serum ACE was also increased. Serum creatinine, BUN and urinalysis were normal in all of them. SPB fell from 163 +/- 3 to 138 +/- 3 and DBP from 107 +/- 3 to 86 +/- 2 mm Hg after 1 month of captopril treatment. A surprising clinical improvement of the cutaneous lesions occurred in 3 patients previously resistant to every local or systemic treatment. Unfortunately, however, 3 patients developed heavy proteinuria (greater than 2 g/day) which disappeared after captopril discontinuation. The unexpected incidence of reversible proteinuria induced by low doses of captopril in our patients recommends a careful monitoring of the renal function every time this drug is employed in the treatment of hypertension in a psoriatic.
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PMID:Captopril-induced proteinuria in hypertensive psoriatic patients. 354 Jun 94

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.
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PMID:Proteinuria in hypertension. 368 33

For the purpose of clinical management, any woman with an acute rise in blood pressure in the latter half of pregnancy must be regarded as having preeclampsia with the possibility of progression to eclampsia. Unfortunately, such diagnoses have been accepted uncritically in the selection of cases for clinical and laboratory studies of preeclampsia, with inevitably erroneous and contradictory conclusions about the disorder. The diagnosis of mild preeclampsia may be correct in roughly one-half of cases, but others may be latent or frank essential hypertension or any of a variety of renal diseases. In selecting cases for research, the diagnostic errors can be greatly reduced by the exclusion of all multiparas and all primigravidas without abundant proteinuria. The primigravidas should have a reliable history of normality or follow-up studies proving it, be aged 25 or less, and have hyperuricemia. The selection of cases for the study of preeclampsia demands far more rigid criteria for diagnosis than does the diagnosis for clinical management.
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PMID:Diagnosis of preeclampsia. 388 67

Cadmium, a toxic heavy metal, has been incriminated in the etiology of essential hypertension. Zinc, an essential micronutrient necessary for growth, competes with cadmium for binding sites in biochemical processes; zinc deficiency states (i.e. pregnancy and low protein diet) might expose an individual to increased risk of cadmium toxicity. The increased sensitivity to cadmium during pregnancy could also be related to the effect of progesterone on zinc and cadmium metabolism through the actions of metallothionein (MT). MT is a low molecular weight protein believed to function in cadmium detoxification. Several studies in lab animals have documented a late gestation drop of maternal MT levels. This was thought to be due to rising progesterone levels. If there is also a late gestation drop in human maternal MT, then the propensity toward maternal cadmium toxicity would be enhanced. Therefore, we propose that when a zinc deficient woman becomes pregnant and is exposed to both the nutritional demands of the fetus and to the influence of progesterone, she will be likely to develop the manifestations of cadmium toxicity (i.e. hypertension, proteinuria, edema, etc.).
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PMID:Zinc, cadmium, metallothionein, and progesterone: do they participate in the etiology of pregnancy induced hypertension? 390 Jun 51

The aim of the present study was to evaluate changes in urinary micro-albumin and in serum and urinary beta 2-microglobulin during treatment with captopril at low doses in a group of hypertensive outpatients without any sign of renal impairment. Thirty-four patients with essential hypertension entered the study, all having been treated for at least one year with beta-blockers and diuretics. None had proteinuria (by Albustix) and creatinine clearance was normal. The patients were randomly allocated to two groups: the first group was maintained on the previous regimen (group BD) and the second received captopril 50 mg twice daily instead of the beta-blocker (group CD). During the year of observation blood pressure values and serum and urinary beta 2-microglobulin were not significantly different between the two groups. There was, however, a significant reduction in albumin excretion rate (AER) in the CD group at both 3 and 6 months. Since arterial measures did not differ between the two groups, it is proposed that the reduction of AER was due to a diminution of the transcapillary hydraulic pressure due to the inhibition of the intrarenal angiotensin II induced by captopril.
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PMID:Long-term captopril therapy at low doses reduces albumin excretion in patients with essential hypertension and no sign of renal impairment. 391 Jul 71

The relationships between blood pressure and renal function were investigated in 78 hypertensive patients with diabetes mellitus type I or II. Renal function was assessed by determining the glomerular filtration rate and the para-aminohippurate clearance in 32 and serum creatinine in 46 subjects. In the latter, the reciprocal serum creatinine, corrected for age and changing creatinine/insulin clearance ratio, was used as an estimate of glomerular filtration rate. In the 54 patients with serial determinations, the duration of follow-up averaged 10.5 years. In older patients with type II diabetes without clinical proteinuria, hypertension developed either before or after the onset of diabetes. When it appeared, renal function was only slightly reduced. During follow-up, the decline in reciprocal serum creatinine averaged 2.7% per year, a figure very similar to that found in nondiabetic patients with benign essential hypertension. It did not correlate with the blood pressure. In patients with a proteinuria greater than 2.5 g per day and histologic and/or clinical evidence of diabetic glomerulosclerosis, the severity of hypertension correlated inversely with the level of renal function. The rate of decline in function averaged 11% per year but varied widely. It was not significantly related to the blood pressure. These data suggest that different types of hypertension (essential, diabetic, and nephrogenic) may be associated with diabetes mellitus. The rate of decline in renal function is closely related to the presence or absence of clinical proteinuria but not to the level of blood pressure.
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PMID:Hypertension as related to renal function in diabetes mellitus. 407 37

This paper describes enzyme studies in normal and abnormal pregnancy. Urinary leucine aminopeptidase (L.A.P.) excretion remained relatively low throughout normal single pregnancy. Urinary L.A.P. excretion was, however, raised towards term in four out of five cases of multiple pregnancy, but in one patient the predelivery urinary L.A.P. was not raised, and the second twin in this case died shortly after delivery with gross congenital abnormalities. Urinary L.A.P. was also investigated in ;high-risk' patients. One such patient had excessive loss of this enzyme throughout pregnancy, and in the discussion it is suggested that this could be due to excessive loss of oxytocinase in the urine. Patients with toxaemia were assessed on the basis of foetal survival and the maximum 24-hour pre-delivery urinary levels of leucine aminopeptidase. This urinary value could not be used to predict foetal outcome, but rose to over 120 mg. beta-naphthylamine per 24 hours in the presence of frank proteinuria. If intrauterine death occurred, the urinary L.A.P. value fell gradually. Urinary L.A.P. was also elevated in essential hypertension towards term, but in these patients there was no gross proteinuria.
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PMID:Urinary excretion of leucine aminopeptidase in pregnancy. 560 84

The combination of prazosin (3-21 mg/day) and oxprenolol (60-360 mg/day) was used to treat 25 pregnant women with severe essential hypertension and 19 women with the hypertension-oedema-proteinuria syndrome. In the group with essential hypertension control of blood pressure was sufficient to avoid addition of hydralazine infusions in all but one patient. No patient developed late proteinuria and exacerbation of hypertension once control was established using this regimen. The birthweights of 58 percent of infants were above the 50th percentile of birthweights for the same ages of gestation in normal pregnancies; two intrauterine deaths occurred. In the hypertension-oedema-proteinuria group, blood pressure control was more difficult to sustain, necessitating additional hydralazine infusions in 11 patients. Pregnancy had to be terminated urgently because of progression of the disorder in 13 patients. There were three intrauterine deaths in this series and one infant was lost eight hours after delivery at 27 weeks following five weeks of antihypertensive therapy.
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PMID:Combined alpha- and beta-adrenoceptor antagonism with prazosin and oxprenolol in control of severe hypertension in pregnancy. 611 42

Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin. Captopril therefore reduces blood pressure in a variety of animal models of hypertension. In 96 studies on 1570 patients, captopril has been shown to be superior to placebo and equivalent to either propranolol or a diuretic in the treatment of essential hypertension. In the management of severe treatment-resistant hypertension, the response to captopril (alone or in combination with a diuretic and/or propranolol) was better than the response to standard triple therapy. Captopril, with digitalis and a diuretic, also improved the haemodynamic and clinical status of patients with refractory congestive heart failure. Side-effects include skin rashes (15%), proteinuria (1,1%, or 0,4% of patients with no prior renal disease) and the nephrotic syndrome (0,9%, or 0,3% of patients with no prior renal disease). Nearly all patients with the nephrotic syndrome in whom renal biopsies were performed were found to have membranous glomerulopathy. Neutropenia (total white cell count less than 1,000/microliter) was found in 33 of over 6,000 patients (0,4%), but in all cases there were other possible causes for this. Captopril is the first of an important group of antihypertensive and afterload-reducing drugs; its major indications are likely to be in the treatment of refractory severe hypertension or congestive heart failure.
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PMID:Captopril--an overview. 621 58


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