Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thus I would like to conclude by saying that an idiopathic form of obliterative renal arteriopathy account for the rare presentation of severe hypertension and progressive renal failure with or without overt hemolytic anemia and thrombocytopenia in children. It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. This, essentially intimal changes, is seen in diverse conditions and appears to result from primary endothelial injury followed by intimal exudation, thrombosis, and repair by fibrosis. Persistent or recurrence of this process form the basis of progressive obliterative arteriopathy. The result is renal ischemia and renin-angiotensin mediated hypertension. Establishment of a vicious circle would further accelerate HT and lead to end stage renal failure. Early recognition and prompt therapeutic intervention might prove beneficial.
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PMID:Thrombotic microangiopathy with hypertension and acute renal failure in children (a typical hemolytic uremic syndrome). 869 75

We describe a 17-year-old hypertensive man with a left abdominal mass on the computed tomographic scan. Radiologic studies revealed a large tumor near the left renal hilus, resulting in renal compression and displacement toward the posterolateral abdominal cavity. Aortography excluded stenosis of the renal arterial vessels. Plasma and urinary catecholamines were normal and plasma renin activity (PRA) was high. The left renal vein renin was 2.1-fold higher than the right one. After resecting the tumor including the left kidney and adrenal, high blood pressure and elevated PRA returned to normal. Histologically, the tumor was a paraganglioma, and the affected kidney showed hyperplasia of the juxtaglomerular apparatus. Thus, the hypertension in our patient was probably due to renal ischemia extrinsically compressed by a non-functioning retroperitoneal paraganglioma (Page kidney).
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PMID:Hypertension and unilateral renal ischemia (Page kidney) due to compression of a retroperitoneal paraganglioma. 891 22

In human essential hypertension, and in all forms of experimental hypertension studied thus far, volume regulation and the relationship between blood pressure (BP) and sodium excretion (pressure natriuresis) are abnormal. Considerable evidence indicates that resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as a consequence of increased BP. In patients with essential hypertension, resetting of pressure natriuresis is characterized either by a parallel shift to higher BPs and salt-insensitive hypertension, or by a decreased slope of pressure natriuresis and salt-sensitive hypertension. This clearly indicates that essential hypertension cannot be ascribed to a single abnormality of kidney function. Multiple physiological studies have shown that salt-sensitive hypertension can be elicited by renal abnormalities that cause either loss of functional kidney mass or an inability to modulate the renin-angiotensin-aldosterone (RAA) system appropriately; these abnormalities include loss of functional nephrons, decreased glomerular capillary filtration coefficient, patchy renal ischemia, and increased distal and collecting tubular reabsorption. Renal abnormalities that cause salt-insensitive hypertension are characterized by normal functional kidney mass, and the ability to appropriately modulate the renin-angiotensin system during changes in sodium intake; important causes of salt-insensitive hypertension include widespread increases in preglomerular resistance and increased reabsorption in the proximal tubules and loops of Henle. By comparing the characteristics of pressure natriuresis in essential hypertensive subjects with those found in experimental hypertension of known origin, we can gain considerable insight into the etiology of human hypertension.
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PMID:Central role of the kidney and abnormal fluid volume control in hypertension. 900 86

Contralateral uninephrectomy attenuates unilateral ischemic injury. The present work was performed to elucidate whether the beneficial effect of uninephrectomy was associated with the modification of ischemia-induced changes in plasma or renal renin activity. A 60-min left renal artery occlusion was conducted in right nephrectomized (Nx) and sham-nephrectomized (Sham-Nx) rats. The decline in inulin clearance 48 h after ischemia was significantly less in Nx rats than in Sham-Nx animals (0.50 +/- 0.10 vs. 0.052 +/- 0.029 ml/min/kidney, p < 0.05). Following ischemia, plasma renin activity (PRA) significantly increased in Sham-Nx (from 5.4 +/- 0.9 to 15.5 +/- 1.4 ng AI/ml/min, p < 0.01) but not in Nx (from 3.5 +/- 0.5 to 5.0 +/- 1.0 ng AI/ml/ min) animals. PRA and renal cortical renin content (2,200 +/- 225 vs. 1,257 +/- 187 ng AI/h/mg protein, p < 0.05) were significantly less in Nx rats than in Sham-Nx animals 48 h after renal ischemia. The decrease in body weight was greater in Nx rats than in Sham-Nx animals. Plasma atrial natriuretic peptide (ANP) (195 +/- 30 vs. 302 +/- 40 pg/ml, p < 0.05) and renal dopamine (DA) content (3.2 +/- 0.5 vs. 13.7 +/- 1.3 ng/g tissue, p < 0.01) were rather lower in the Nx group when compared with the Sham-Nx group. No significant difference was found in the intrarenal content of norepinephrine (NE) between two ischemic groups. These findings suggested that uninephrectomy prevents the ischemia-induced increase in renin activity. The prevention of the increase in renin activity in Nx rats is not be mediated through the modulation of ischemia-induced changes in sodium balance, plasma ANP level and/or intrarenal contents of NE and DA.
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PMID:Uninephrectomy prevents the ischemia-induced increase in renin activity. 903 Dec 73

Little attention has been paid to nephropathies and proteinuria in renovascular hypertension (RVH). Recently there has been a growing interest in the conditions induced by RVH. 10 cases of RVH were diagnosed by angiography and renin sampling from renal veins in the last 6 years in our hospital. The patients were all male and mean age was 64 +/- 8 (SD) years. Data were as follow: protein excretion was 3.8 +/- 2.2 g/day (> or = 3.5 g/day in 8 patients), sBP 202 +/- 24 mmHg, dBP 113 +/- 17 mmHg, serum renin concentration 64 +/- 45 pg/ml, and ipsilateral/contralateral renal vein renin ratio 3.3 +/- 1.0. RVH was treated by nephrectomy in 3 patients, percutaneous transluminal renal angioplasty (PTA) in 2, and angiotensin converting enzyme inhibitors (ACE-I) administration in 8. Biopsies were performed on contralateral kidney in 4 patients. Focal segmental glomerulosclerosis (FGS) was found in 3 patients, and nephrosclerosis in 1, whereas only nephrosclerosis was found in nephrectomized kidneys in all 3 patients. After nephrectomy, PTA and the treatment by ACE-I, not only blood pressure but also proteinuria was markedly reduced. These findings suggest that severe stenosis of the renal artery led to renal ischemia, which activated renin excretion, to cause glomerular hyperfiltration through vasoconstriction of the efferent arterioles in the contralateral kidney. FGS-like lesion thus induced appeared to have caused massive proteinuria.
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PMID:Renovascular hypertension may cause nephrotic range proteinuria and focal glomerulosclerosis in contralateral kidney. 935 55

The renin-angiotensin system plays an important role in renal growth and development: exposure of the fetus or neonate to angiotensin-converting enzyme (ACE) inhibitors increases mortality and results in growth retardation and abnormal renal development. This study was designed to investigate the effects of ACE inhibition in the neonatal rat on the expression of genes known to modulate renal cellular proliferation, cell interactions, and extracellular matrix. Newborn rat pups were treated with enalapril (30 mg/kg/d) or vehicle for 14 d, and kidneys were removed for Northern analysis of mRNA for transforming growth factor-beta1 (TGF-beta1), prepro epidermal growth factor (EGF), clusterin, and renin. Distribution of TGF-beta1, EGF, and clusterin was also determined by immunohistochemistry. Enalapril treatment resulted in 40% mortality by d 14, reduced body and kidney weight, decreased glomerular area, and caused tubular dilatation (p < 0.05 versus vehicle group). Enalapril decreased renal TGF-beta1 and EGF mRNA expression, and increased renal clusterin and renin expression (p < 0.05). Renal tubular immunoreactive EGF was decreased, and clusterin was increased by enalapril treatment. These results indicate that ACE inhibition in the developing kidney reduces the renal expression of critical growth factors, which may account for renal growth impairment. Clusterin expression may increase either due to blockade of tonic angiotensin-mediated inhibition, or as an adaptive response to renal ischemia.
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PMID:Angiotensin-converting enzyme inhibition decreases growth factor expression in the neonatal rat kidney. 935 28

The aim of the present study was to provide an overview of the role of circulating gonadal steroids on the adaptive changes of the renin-angiotensin system to chronic hypobaric hypoxia (CHH: 4400 m simulated altitude in an hypobaric chamber) and the development of experimental hypertension by bilateral renal ischemia. In order to fulfill this goal, blood pressure (BP), plasma renin activity (PRA) and plasma angiotensinogen concentration (PAoC) as well as haematocrit (Htc) and body weight (BW) of intact and post-puberal castrated normotensive (Nt) and hypertensive (Ht) rats of both sexes were studied following an experimental design similar to that of previous works. Post-puberal castration decreased BP of Nt and Ht rats subjected to CHH. Sexual dimorphism in BP, PRA and PAoC was maintained while that in haematocrit disappeared after castration. Results suggest that circulating sexual steroid hormones are involved in the response of the renin-angiotensin system to the experimental conditions of environmental reduced O2 partial pressure.
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PMID:Effect of castration on renin-angiotensin system of hypertensive rats submitted to chronic hypobaric hypoxia (simulated altitude: 4400 m). 943 79

The present studies determined the effect of renal ischemia/reperfusion on components of the intrarenal renin-angiotensin system in rats and evaluated the effect of AT1 angiotensin (ANG) II receptor blockade on functional recovery. After bilateral renal pedicle occlusion for 60 min, serum creatinine increased, peaking at 72 h, and returned to sham levels after 120 h. ANG II levels in ischemic kidneys were significantly increased 24 h after reperfusion but did not differ from levels in sham kidneys after 120 h. Both renal cortical angiotensinogen mRNA and proximal tubular AT1 receptor mRNA were significantly reduced early after reperfusion, returning to sham levels by 120 and 72 h, respectively. AT2 ANG II receptor mRNA was undetectable in proximal tubules from sham rats but was consistently present in ischemic rats at 120 h. By histoautoradiography, we found that binding of 125I-labeled ANG II was preserved in glomeruli but was decreased in whole cortex and outer medulla early after reperfusion and was completely blocked by the AT1 antagonist losartan. Treatment of rats with losartan (25 mg/kg s.c. daily), starting at the time of reperfusion, had no effect on expression of proliferating cell nuclear antigen in cortical tubules but caused a significant decrease in serum creatinine at 72 h (ischemia: 334 +/- 69 microM vs. ischemia + losartan: 135 +/- 28 microM; P < 0.025, n = 6). These data indicate that renal ischemic injury causes an early increase in intrarenal ANG II levels, associated with reduction of mRNA for angiotensinogen and proximal tubular AT1 receptors, and maintenance of glomerular ANG II binding. Losartan accelerates recovery of renal function, suggesting that activation of AT1 receptors impairs glomerular filtration in the postischemic kidney.
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PMID:Role of AT1 angiotensin II receptors in renal ischemic injury. 945 26

In 370 patients (pts) with hypertension(HT) in years 1986-1998 (168F + 202M, mean age 46 yrs) screening value of the following tests was evaluated: standard initial angioscintigraphy DTPA 99mTc(SA) in all pts(1-st screening group), significance of clinical suspicion on renovascular hypertension (RVHT) in the group of 74 pts (II-nd screening group). Captopril tests: renin captopril test(RCT) and isotopic captopril test (ICT) were performed in all 370 pts. Classical renal angiography as a reference test for renal artery stenosis (RAS) was performed in all pts suspected for RVHT on the basis of clinical anamnesis and or positive results of captopril tests. Results were as follows. Initial SA being abnormal in the whole group, appeared to be more significant for RAS only in the case of profound one side renal ischemia (GFR lower than 30% of total GFR). Resistance to three antihypertensive drugs, diastolic blood pressure > 120 mmHg and sudden onset of Ht, found in all 74 pts from the II-nd group, were the most significant clinical symptoms of RVHT, because critical RAS was found in 41, that is 55% of pts from the II-nd group. At least one positive CT was found in 37 from 42 pts with critical RAS in angiography with RTC being more sensitive and ICT more specific for hemodynamically significant RAS. The following screening protocol for RVHT was presented and discussed: precise clinical anamnesis followed by angiography or captopril tests according to the severity of clinical symptoms, aim of the study as well as accessibility and laboratory reproducibility of the captopril tests.
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PMID:[Screening for renovascular hypertension in own material (1986-1998)]. 1010 95

Renal artery stenosis or occlusion causing the hyponatremic-hypertensive syndrome has been rarely reported. Our impression, however, was that the disorder is not uncommon. Case records from patients in one city (population 350 000) presenting between 1980 and 1997 with hypertension, hyponatremia, and evidence of renal ischemia were scrutinized. Thirty-two patients fulfilling inclusion criteria were identified. Admission supine arterial pressures were high (mean 228/124 mm Hg), but there was a vigorous fall in pressure on standing (26/12.7 mm Hg recorded in 27 patients). Mean plasma concentrations of sodium (129.7 mmol/L) and potassium (2.7 mmol/L) were low, and 24-hour urine protein excretion was elevated in 19 of 26 patients. Twenty-two of the 32 patients were female, the majority were asthenic, and all but 5 were smokers. Symptoms precipitating hospitalization were headache, clouding of consciousness, confusion, weakness, weight loss, thirst, and polyuria. Plasma renin levels, measured in 20 patients, were elevated in most cases and correlated inversely (r=-0.63, P<0.01) with the plasma sodium concentration. The hyponatremic-hypertensive syndrome in patients with renal ischemia is not rare: Rather, it is underreported. It tends to affect elderly asthenic women who smoke heavily. Stimulation of renin release from the ischemic kidney is probably central to the pathophysiology. The syndrome deserves better recognition to ensure appropriate investigations and management.
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PMID:Hyponatremic-hypertensive syndrome with renal ischemia: an underrecognized disorder. 1020 41


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