UMLS:C0033687 - FACTA Search

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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of the angiotensin converting enzyme inhibitor captopril on blood pressure, proteinuria, creatinine clearance and metabolic control in diabetic nephropathy have been evaluated. Captopril 144 mg per day was given to 8 longstanding, insulin-dependent, diabetic females with nephropathy. The blood pressure was significantly reduced (systolic 45.4, diastolic pressure 30.6 and mean arterial pressure 33.8 mm Hg after 24 weeks of treatment). Plasma renin activity rose significantly from a basal value of 1.60 to 6.71 ng.ml-1.h-1, and so did serum potassium (from 4.57 to 4.83 mEq.1-1). Serum aldosterone fell from 161 to 70.9 pgm.ml-1 and from 27.3 to 15.3 micrograms.24 h-1 in plasma and urine, respectively, after 6 months on captopril therapy. Urinary protein excretion was decreased by about 48% and creatinine clearance remained unchanged throughout the study. Plasma triglycerides and cholesterol also remained unchanged, and glycosylated haemoglobin was significantly reduced from 13.8 to 10.2% after captopril. The results suggest that captopril is a useful drug to treat hypertension in patients suffering from diabetic nephropathy, as the decline in kidney function can be reduced without impairing glucose tolerance or the lipid profile.
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PMID:Effects of captopril on diabetic nephropathy in hypertensive women. 176 Oct 66

A 66-year-old male patient of renovascular hypertension with nephrotic syndrome was described. Besides, focal segmental glomerulosclerosis like lesion was accompanied in the contralateral kidney. On admission, his blood-pressure amounted to 220/140 mmHg. Laboratory investigation included; urinary protein 10.5 g/day, serum creatinine 1.8 mg/dl, creatinine clearance 71.4/day, plasma renin activity 10.0 ng/ml/hr, angiotensin I 890 pg/ml and angiotensin II 40.0 pg/ml. Renogram and renal scintigram showed non-functioning pattern of left kidney. Arteriography disclosed approximately more than 95% stenosis of left main artery. Administration was discontinued because of poor control both in blood pressure and in proteinuria. After the left nephrectomy, the former normalized and the latter decreased. Microscopic examination of the right kidney revealed focal segmental glomerulosclerosis like lesion. So far as we know, this report is the first designed to elucidate renovascular hypertension with nephrotic syndrome accompanied by focal segmental glomerulosclerosis like lesion. The relationship between renovascular hypertension and nephrotic syndrome, and microscopic findings has been briefly discussed. It is suggested that the etiology of focal segmental glomerulosclerosis like lesion may be based on compensatory glomerular hyperfiltration caused by renovascular hypertension.
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PMID:[A case of renovascular hypertension with nephrotic syndrome, accompanied by focal segmental glomerulosclerosis-like lesion in the contralateral kidney]. 177 Jun 22

We described a transient low or non-selective proteinuria after forced lordosis as a characteristic of orthostatic proteinuria and the heteroporous theory and sieving function theory which might explain the mechanism of orthostatic proteinuria. The angiogenic action of the renin-angiotensin system played an important part in these theories. Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Since the purpose of this study is to investigate the influence of the renin-angiotensin system on the mechanism of orthostatic proteinuria, proteins and electrolytes in the urine were examined before and after lordosis in 9 healthy children (Group A) and in 6 children with orthostatic proteinuria (Group B). The urinary ratio of protein/creatinine (P/cre) in Group B was already significantly higher than that in Group A before lordosis and significantly increased after lordosis, while P/cre in group A did not increase after lordosis. The urinary Na/K ratio (Na/K) in Group B was already significantly lower than that in Group A before lordosis, and after forced lordosis, Na/K in Group A decrease with no difference between both groups observed. It is suggested that a significant increase on P/cre after lordosis was obtained only in Group A, whereas in both groups the renal vein may be compressed by forced lordosis and as a result angiotensin II may be stimulated. There might be a difference of the responsibility to angiotensin II in glomerular mesangium contraction between both groups.
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PMID:[A study of urinary immunoglobulins and electrolyte excretion after lordosis]. 180 55

Plasma values of atrial natriuretic factor (ANF) were evaluated in 31 women with pregnancy-induced hypertension (PIH) and 31 normal pregnant women at the same age of gestation. In 27 women with PIH and 27 normal pregnant women forearm venous tone (FVT) was evaluated by Strain Gauge Plethysmography. Forearm vascular resistance (FVR) was measured as the ratio of mean blood pressure (MBP) to forearm blood flow. In addition Cardiac Index (CI) by means of transthoracic electrical bioimpedance and total peripheral vascular resistance (TPR) (with the Frank Equation) were also measured. In comparison with the normal pregnant women, the women with PIH had similar values of hematocrit (as an index of plasma volume) and significantly higher levels of FVR and TPR, while ANF plasma values did not differ significantly. Subdividing the women with PIH in relation to the presence of proteinuria (greater than or equal to 0.3 g/l), those with proteinuria, in addition to significantly higher levels of FVR and TPR, had significantly higher levels of FVT than normal pregnant women, while ANF plasma values were higher even though the difference was only near the level of significance. Hypertensive women with proteinuria also had higher values of FVT than hypertensive women without proteinuria. By means of multiple regression ANF did not show any significant correlations with hematocrit or sodium excretion. Hypertension with proteinuria seems to represent a more severe form of the disease in which, in addition to the probable influence of other factors such as the renin-angiotensin and prostaglandin systems, a greater increase in peripheral sympathetic tone than in hypertension alone appears to be present, causing a reduction in venous compliance in addition to the elevation in FVR and TPR, with increase in central blood volume and atrial stretch. This may explain the higher ANF plasma levels in these patients in comparison with normal pregnant women, even though the absence of a significant correlation of ANF with hematocrit and the fact that ANF increase was only near the level of significance may suggest a change in the relation between ANF secretion and atrial volume receptors in pregnancy either normal or complicated by hypertension. ANF does not seem to play an important role in water and sodium excretion in PIH probably because of the presence of very high plasma levels of hormones such as aldosterone, progesterone and oestriol which, together with renal prostaglandins, seem to be involved in diuresis and natriuresis in pregnancy.
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PMID:Plasma concentrations of atrial natriuretic factor and hemodynamics in pregnancy-induced hypertension. 183 84

Pregnancy-induced hypertension (PIH) is characterized by a relative decrease in plasma volume and renin and aldosterone concentrations as well as increased capillary permeability compared with normal pregnancy. As many of these features could be explained by the actions of atrial natriuretic peptide (ANP), we examined the relationship between plasma volume and plasma ANP in women with PIH and in normal third trimester pregnant women, and whether ANP responses to alterations in posture were intact in women with PIH. Basal plasma ANP measured after 20 min lateral recumbency in women with PIH was 24.0 (13.9, 33.1) pmol/L (median [25th, 75th percentile]), which was significantly greater than in normal pregnant women (9.9 [6.3, 16.0]), (P less than .05). Plasma ANP did not differ between those with and without proteinuria in the PIH group. Plasma volume was decreased in women with PIH (20.1 [19.0, 23.2] mL/cm) v 23.5 [21.4, 25.3], P less than .05). Plasma renin concentration but not plasma aldosterone concentration was also decreased significantly in women with PIH compared with normal pregnant women (P less than .001) and both were correlated negatively with plasma ANP. Following prolonged lateral recumbency, plasma ANP rose to 26.9 [19.1, 44.1] pmol/L in women with PIH (P less than .05), which was still significantly greater than in normal pregnant women (15.5 [6.7, 21.9] pmol/L) (P less than .05). In a subgroup of these subjects, 30 min head-up tilt decreased plasma ANP by 5.2 [0.9, 22.3] pmol/L in women with PIH and by 6.1 [2.2, 10.3] pmol/L in normal pregnant women, a nonsignificant difference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide and plasma volume in pregnancy-induced hypertension. 183 91

Chronic renal allograft rejection (CR) is the major cause of graft loss after 1 year following transplantation. Hypertension (HTN) and proteinuria (Up) are the hallmarks of this immunologic allograft response. Over 1 year, 23 patients posttransplantation and with HTN (diastolic greater than 95 mm Hg) were examined. Serial serum creatinine (Scr), Up, urine creatinine (Ucr), and resting and enalapril challenged (EC) plasma renin activity (PRA) were all determined. Renal artery stenosis was excluded by noninvasive imaging. Of the 23 patients, eight eventually lost their renal allografts, while 15 maintained satisfactory renal function (Scr less than 2.5). Results of this study show that: 1) worsening renal function (RF) increases EC reactivity; 2) the presence of proteinuria is not itself related to increase in EC activity; 3) renin before and after EC was higher (P = .06) in the allograft loss group. In this study, patients with high PRA represent the highest EC responses. Therefore, they display not macrovascular lesions, but microvascular intrarenal disease; this defect is most likely secondary to chronic immunologic insult.
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PMID:Plasma renin activity in renal transplant patients with hypertension. 187 18

Exercise-induced proteinuria is of the mixed glomerular-tubular type and has been thought to be due to increased glomerular permeability to macromolecular proteins in response to activation of the renin-angiotensin system and catecholamines and a reduction in renal hemodynamics. The excretion of the tubular type of proteins, however, can't be explained by the above mechanism. Two groups, consisting of subjects with the highest (H-alb, n = 20) and the lowest (L-alb, n = 20) excretion of albumin 30 min after exhaustive exercise were selected from a total of 69 normal male participants. No differences in VO2max, maxHR, changes in plasma angiotensin II, catecholamines, urine volume, or Ccr following exercise were observed between the two groups. The increase in blood lactate concentration immediately after exercise, increases in urinary excretion of lactate, pyruvate, alpha 1 M, beta 2 M, albumin and decrease in Cl- excretion 30 min after exercise in the H-alb group were significantly greater than in the L-alb group. The greater the urinary excretion of lactate and pyruvate, the greater the excretion of albumin, alpha 1M and beta 2M, and the less the urinary excretion of Cl-. The coefficient of correlation between the urinary excretion of lactate and beta 2M was 0.757, and between urinary excretion of albumin and beta 2M, 0.756 (p less than 0.001). These results suggest that exercise-induced organic acids and/or decrease in renal circulatory pH caused by organic acids may alter renal glomerular permeability and inhibit renal tubular reabsorption of low molecular weight proteins (alpha 1M, beta 2M). The permeability of the glomerular basement membrane (GBM) to macromolecular proteins may be altered by a reduction in the charge barrier of the GBM, which may be caused by the over-production of organic acids and a lower pH.
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PMID:[The mechanisms of exercise-induced proteinuria--relationship between urinary excretion of proteins and lactate after exhaustive exercise]. 187 55

A number of studies based on animal models of both diabetes and renal insufficiency have shown that adequately reducing blood pressure attenuates the progression of glomerulosclerosis and decreases urinary protein excretion. Furthermore, compared with conventional antihypertensive therapy, angiotensin converting enzyme (ACE) inhibitors show a greater benefit in reducing these parameters. Nineteen published animal studies have investigated the effects of calcium antagonists on renal hemodynamics and glomerulosclerosis, but only three of them have evaluated the use of calcium antagonists with models of diabetes. Of six micropuncture studies based on a 1 5/6 nephrectomy model of renal insufficiency, five demonstrated reduced efferent arteriolar resistance, two showed reduced glomerular capillary pressure (PGC), and two showed significantly reduced proteinuria and glomerulosclerosis. Studies using nifedipine with both the unilaterally nephrectomized DOCA salt rat model and the 1 5/6 nephrectomy model demonstrated reduced proteinuria and glomerulosclerosis that was independent of reduced PGC. Two separate micropuncture studies of the spontaneously hypertensive rat model also found reduced efferent arteriolar resistance and PGC as well as proteinuria. Finally, studies of Dahl "salt-sensitive" rats showed an early decrease in glomerulosclerosis without a significant change in either proteinuria or glomerulosclerosis after five weeks. The results of eleven clinical studies of diabetic patients have been published; they showed divergent effects of calcium antagonists on renal function and urinary protein excretion. In the various animal models, the divergent renal hemodynamic and histologic effects reported for calcium antagonists may be largely due to the equality of blood pressure reduction, the varied baseline hemodynamic profiles, and the divergent status of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of calcium antagonists in diabetes mellitus. An overview of studies in animal models and in humans. 191 Jun 42

The diagnosis of renovascular hypertension depends heavily on laboratory tests. There is no universally applicable screening test, and it should be actively sought only in patients with clinical clues suggested by the history, physical examination, and routine laboratory testing. Hyperreninemia is a characteristic finding, and acute blockade of the renin system forms the basis of diagnostic tests such as the oral captopril test and captopril renography. Other abnormal laboratory findings include hypokalemia, proteinuria, and azotemia exacerbated by angiotensin-converting enzyme inhibitors.
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PMID:The role of laboratory testing in the diagnosis of renovascular hypertension. 191 98

Strenuous physical exercise causes transient proteinuria and renal hemodynamic changes: decrease of renal blood flow and to a lesser extent of the glomerular filtration rate, and an increase of the filtration fraction. However, the mechanisms of these modifications are still poorly understood. In order to elucidate them we performed maximal exercise tests on 8 untrained healthy volunteers after inhibition of the renin-angiotensin system (RAS) by captopril, the sympathetic nervous system by a beta-blocking drug (acebutolol) or an alpha-blocking drug (prazosin) and the prostaglandin system by indomethacin. Urinary albumin excretion was measured in every subject first at rest (AB) and then after exercise (AA) performed successively without and with blockade by each of theses drugs. AA-AB difference in the captopril test (12.04 +/- 6.11 micrograms/min) compared to that in the control test (68.91 +/- 25.18 micrograms/min) was significantly reduced (p less than 0.02). This difference remained unchanged after acebutolol (59.87 +/- 21.91 micrograms/min, p = 0.62), prazosin (35.23 +/- 27.80 micrograms/min, p = 0.21) and indomethacin (55.21 +/- 28.43 micrograms/min, p = 0.35). There was a negative correlation between the lowering of AA elevation and the rise in plasma renin activity in the captopril test (r = 0.64; p less than 0.03). Only acebutolol decreased systolic blood pressure significantly. These results suggest that the RAS plays a major role in postexercise proteinuria. We hypothesize that stimulation of this system induces an increase of efferent glomerular artery constriction and consequently of glomerular transcapillary pressure and the filtration fraction. Captopril seems able to prevent these hemodynamic changes.
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PMID:Captopril but not acebutolol, prazosin or indomethacin decreases postexercise proteinuria. 192 9

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