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)

Seventeen hypertensive patients were treated with captopril, an orally active inhibitor of converting-enzyme. All patients showed a fall in blood pressure (BP), although in some patients only after the addition of diuretics. In 2 patients a skin rash developed. One patient developed proteinuria. A renal biopsy revealed membranous glomerulopathy. Correlations were found between pretreatment plasma renin activity (PRA) and the decrease in BP, and between pretreatment PRA and the decrease in plasma aldosterone concentration (PAC). Filtration fraction (FF) fell, indicating a decrease in renal vascular resistance. Captopril decreased the sensitivity to exogenous angiotensin I (AI), dependent on the captopril dose used. The sensitivity to exogenous bradykinin increased impressively even on the lowest dose of the drug. These observations suggest extrapulmonary conversion of AI to angiotensin II (AII).
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PMID:Treatment of moderate to severe hypertensive patients with an orally active converting-enzyme inhibitor. 23 14

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.
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PMID:SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension. 68 62

To investigate plasma renin and prorenin levels in non-insulin-dependent diabetes mellitus (NIDDM) and their relation with autonomic nervous function and renal impairment, we measured plasma renin and prorenin levels in 39 NIDDM patients. The patients included 21 males and 18 females, aged 56.3 +/- 6.2. Thirty-four normal age-matched subjects served as controls. Autonomic nervous function was evaluated in 23 patients by the performance of cardiovascular reflex tests. The plasma renin concentration was measured by angiotensin I generation after the addition of an exogenous substrate. Plasma prorenin was activated by trypsin. The results showed that the plasma renin concentration was similar between NIDDM patients and normal subjects, while plasma prorenin was higher in NIDDM patients. No correlation existed between the plasma renin or prorenin levels and autonomic nervous function. The patients with abnormally high levels of prorenin also had a similarly high plasma renin level but not a high creatinine clearance (Ccr) or daily proteinuria. The plasma renin level was correlated inversely with daily proteinuria but not with Ccr. These results suggest that the high plasma prorenin levels in some diabetic patients cannot be explained by renal impairment, poor prorenin conversion or autonomic dysfunction. The hyporeninemia in some patients may be related to microvascular involvement of the kidney.
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PMID:Plasma prorenin and renin levels in non-insulin-dependent diabetes mellitus. 136 16

Angiotensin converting enzyme (ACE) inhibitors are known to lower urinary protein excretion in human renal disease. This proteinuria lowering effect of ACE inhibition has been hypothesized to be a result of renal hemodynamic changes due to the inhibition of angiotensin II (Ang II) production. To test this hypothesis we studied the short-term effects of different doses of exogenous Ang II (5%, 10% and 20% of the pressor dose) on renal hemodynamics and urinary protein excretion in comparison with placebo infusion in six non-diabetic normotensive proteinuric patients, both before and after three months treatment with the ACE inhibitor, lisinopril. Lisinopril lowered proteinuria from 7.5 +/- 1.9 to 2.7 +/- 0.6 g/24 hr and induced a fall in blood pressure, renal vascular resistance and filtration fraction, whereas plasma Ang II levels were similar to the pre-treatment values. Ang II infusion induced typical effects which appeared to be similar before and during lisinopril treatment: a dose-related fall in renal plasma flow and rise in systemic blood pressure, renal vascular resistance and filtration fraction, while the glomerular filtration rate remained relatively stable. However, neither before nor during lisinopril therapy did any changes in urinary protein loss occur during the infusions of Ang II, despite the fact that Ang II reversed the long-term systemic and renal hemodynamic changes induced by the ACE inhibitor. We conclude that the long-term antiproteinuric effect of the ACE inhibitor, lisinopril, is neither mediated through changes in circulatory Ang II levels nor influenced by acute changes in systemic and renal hemodynamics, suggesting a non-hemodynamic mechanism of action.
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PMID:Angiotensin II does not acutely reverse the reduction of proteinuria by long-term ACE inhibition. 166 May 50

Albuminuria (UAlbV) can be reduced by converting-enzyme inhibitors (CEI), but the hormonal mechanism responsible for this effect has not previously been defined. Since CEI increase kinin activity as well as reduce angiotensin II (ANG II) activity, experiments were performed to determine the effect of isolated alterations in kinin and ANG II metabolism on UAlbV in rats with passive Heymann pephritis. Phosphoramidon was used to potentiate kinin activity without altering ANG II synthesis. Aprotinin was utilized in combination with the CEI, enalapril, to prevent the increase in kinin activity caused by CEI. UAlbV and the fractional renal clearance of albumin (FCAlb) decreased significantly after either phosphoramidon or enalapril, although only enalapril reduced blood pressure. Glomerular filtration rate (GFR) was not affected by either drug. Phosphoramidon did not affect plasma renin activity (PRA) or the pressor response to angiotensin I (ANG I), indicating that ANG II synthesis was not altered. Aprotinin prevented the reduction in UAlbV and FCAlb produced by CEI but not the hypotension, elevated PRA, or ANG I pressor blockade produced by CEI. Aprotinin alone had no effect on UAlbV, GFR, PRA, or blood pressure. UAlbV can be reduced by increasing kinin activity by a mechanism that is not dependent on suppression of ANG II activity or reduction in GFR or blood pressure. CEI may reduce proteinuria as a result of their action on the kallikrein-kinin system rather than on the renin-angiotensin system.
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PMID:Effects of modulation of renal kallikrein-kinin system in the nephrotic syndrome. 169 47

Angiotensin II has many actions in the kidney, including regulation and distribution of renal circulation and glomerular filtration, as well as effects on mesangial contraction and on the filtration coefficient. The reduction in circulating and intrarenal angiotensin II by angiotensin converting enzyme (ACE) inhibitors in essential hypertension is associated with a significant increase in renal blood flow and a decrease in filtration fraction, without changes in glomerular filtration rate. In addition, administration of ACE inhibitors can reduce proximal sodium reabsorption via changes in peritubular hydrostatic and oncotic forces resulting from the fall in postglomerular capillary resistance. In severe hypertension the state of the renal vasculature does not allow ACE inhibition to induce similar haemodynamic changes and, therefore, it cannot contribute to renal sodium handling that requires the recruitment of alternate mechanisms. In spite of this, ACE inhibitors may exert a protective effect on the renal function of patients with severe hypertension as well as in those with renal impairment, by lowering systemic and, probably, intraglomerular pressure, reducing proteinuria and slowing the progression of renal failure.
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PMID:Effects of ACE inhibition on renal haemodynamics in essential hypertension and hypertension associated with chronic renal failure. 171 68

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

Angiotensin-1 converting enzyme inhibitors (ACEI) have been shown to reduce proteinuria in azotaemic diabetics and in other glomerulopathies, and such treatment has also slowed the development of experimentally-induced glomerulosclerosis in animals. We have treated 13 patients with focal segmental glomerulosclerosis (FSGS) and IgA nephropathy (IgAN) with Captopril 12.5 mg twice daily for six months and assessed their response in terms of 24 hour urinary protein excretion, blood pressure, glomerular filtration rate, effective renal plasma flow and derived values for filtration fraction and renal vascular resistance. A mean fall of 29 per cent in urinary protein excretion was observed over the six months treatment schedule. No significant changes were observed in other parameters of renal haemodynamics measured. We conclude that Captopril therapy in patients with FSGS and IgAN reduces urinary protein excretion consistently over a six month period, and that this may in the longer term retard the progression of their renal failure.
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PMID:Reduction of proteinuria with captopril therapy in patients with focal segmental glomerulosclerosis and IgA nephropathy. 181 Aug 99

This study was designed to contrast the effects of prolonged treatment with a thromboxane (Tx) synthase inhibitor (UK 38485 or SC 41156) and a Tx receptor antagonist (SQ 29548) on the development of angiotensin II (Ang II)-salt-induced hypertension. Ang II infusion (125 ng/min i.p. for 12 days) in rats drinking 0.15 M NaCl resulted in severe hypertension accompanied by proteinuria, reduction of urinary creatinine excretion and augmentation of urinary TxB2 excretion and TxB2 release from aortic rings and renal cortex slices. In saline-drinking rats undergoing Ang II infusion, the concomitant administration by gavage of UK 38485 (100 mg/kg/day) or SC 41156 (25 mg/kg/day) reduced serum and urinary TxB2 and TxB2 release from aortic rings and/or renal cortex slices, but it was without effect on the development of hypertension. In contrast, concomitant infusion of SQ 29548 (4.2 mg/24 hr s.c.) significantly attenuated the increase of blood pressure produced by the infusion of Ang II in saline-drinking rats. This effect of SQ 29548 may be the consequence of blockade of the actions of one or more endogenous eicosanoids that increase blood pressure by a mechanism(s) involving interaction with TxA2 receptors. This implies that pressor eicosanoids play a contributory role in the development of severe Ang II-salt hypertension.
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PMID:Contrasting effect of thromboxane synthase inhibitors and a thromboxane receptor antagonist on the development of angiotensin II-salt-induced hypertension in rats. 213 70


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