Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of dihydralazine, propranolol, clonidine, furosemide and reserpine on the clearance of I125 hippurate in rats in alcohol intoxication was investigated. It was found that both in acute and subacute ethanol intoxication the renal blood flow was impeded. Reserpine and propranolol did not significantly change the half time of I125 hippurate in blood both in animals treated and not treated with alcohol. Furosemide prolonged the clearance of hippurate and increased kidney ischemia in alcohol intoxication. Dihydralazine and clonidine increased the effective renal blood flow in normal animals but not in acute and subacute ethanol intoxication.
Pol J Pharmacol Pharm
PMID:Effects of some hypotensive drugs on the clearance of I125 hippurate in rats after acute and subacute ethanol intoxication. 668 71

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.
Pol Merkur Lekarski 1998 Nov
PMID:[Screening for renovascular hypertension in own material (1986-1998)]. 1010 95

We report three cases in which arterial hypertension occurred after percutaneous renal biopsy due to perirenal hematoma. Perirenal hematoma is common complication of renal biopsy. The mechanism of hypertension depends on renal ischemia. Compressive ischemia decrease the renal blood flow, increase mechanism RAA, the amount of urine is decreased, with low sodium concentration and finally the arterial hypertension appears.
Pol Arch Med Wewn 1998 Nov
PMID:[Arterial hypertension due to perirenal hematoma after renal percutaneous biopsy]. 1041 May 81

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
Pol Arch Med Wewn 2000 Sep
PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62

Acute kidney injury evokes renal tubular cholesterol synthesis. However, the factors during acute kidney injury that regulate HMG CoA reductase (HMGCR) activity, the rate-limiting step in cholesterol synthesis, have not been defined. To investigate these factors, mice were subjected to 30 minutes of either unilateral renal ischemia or sham surgery. After 3 days, bilateral nephrectomy was performed and cortical tissue extracts were prepared. The recruitment of RNA polymerase II (Pol II), transcription factors (SREBP-1, SREBP-2, NF-kappaB, c-Fos, and c-Jun), and heat shock proteins (HSP-70 and heme oxygenase-1) to the HMGCR promoter and transcription region (start/end exons) were assessed by Matrix ChIP assay. HMGCR mRNA, protein, and cholesterol levels were determined. Finally, histone modifications at HMGCR were assessed. Ischemia/reperfusion (I/R) induced marked cholesterol loading, which corresponded with elevated Pol II recruitment to HMGCR and increased expression levels of both HMGCR protein and mRNA. I/R also induced the binding of multiple transcription factors (SREBP-1, SREBP-2, c-Fos, c-Jun, NF-kappaB) and heat shock proteins to the HMGCR promoter and transcription regions. Significant histone modifications (increased H3K4m3, H3K19Ac, and H2A.Z variant) at these loci were also observed but were not identified at either the 5' and 3' HMGCR flanking regions (+/-5000 bps) or at negative control genes (beta-actin and beta-globin). In conclusion, I/R activates the HMGCR gene via multiple stress-activated transcriptional and epigenetic pathways, contributing to renal cholesterol loading.
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PMID:Renal ischemia-induced cholesterol loading: transcription factor recruitment and chromatin remodeling along the HMG CoA reductase gene. 1909 62

Acute kidney injury stimulates renal production of inflammatory mediators, including TNF-alpha and monocyte chemoattractant protein 1 (MCP-1). These responses reflect, in part, injury-induced transcription of proinflammatory genes by proximal tubule cells. Because of the compact structure of chromatin, a series of events at specified loci remodel chromatin to provide access for transcription factors and RNA polymerase II (Pol II). Here, we examined the role of Brahma-related gene-1 (BRG1), a chromatin remodeling enzyme, in the transcription of TNF-alpha and MCP-1 in response to renal ischemia. Two hours after renal ischemic injury in mice, renal TNF-alpha and MCP-1 mRNA increased and remained elevated for at least 1 wk. Matrix chromatin immunoprecipitation assays revealed sustained increases in Pol II at these genes, suggesting that the elevated mRNA levels were, at least in part, transcriptionally mediated. The profile of BGR1 binding to the genes encoding TNF-alpha and MCP-1 resembled Pol II recruitment. Knockdown of BRG1 by small interfering RNA blocked an ATP depletion-induced increase in TNF-alpha and MCP-1 transcription in a human proximal tubule cell line; this effect was associated with decreased recruitment of BRG1 and Pol II to these genes. In conclusion, BRG1 promotes increased transcription of TNF-alpha and MCP-1 by the proximal tubule in response to renal ischemia.
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PMID:BRG1 increases transcription of proinflammatory genes in renal ischemia. 1955 65

Inflammatory cytokines are evoked by acute kidney injury (AKI) and may contribute to evolving renal disease. However, the impact of AKI-induced uremia on proinflammatory (e.g., TNF-alpha, MCP-1, TGF-beta1) and anti-inflammatory (e.g., IL-10) cytokine gene expression remains unknown. This study was undertaken to gain some initial insights into this issue. CD-1 mice were subjected to left renal ischemia-reperfusion (I/R) in the absence or presence of uremia (+/- right ureteral transection). TNF-alpha, MCP-1, TGF-beta1, and IL-10 mRNAs, cytokine protein levels, and RNA polymerase II (Pol II) recruitment to these genes were assessed. Renal cytokine mRNA levels were also contrasted with unilateral vs. bilateral renal parenchymal damage (I/R or ureteral obstruction). Potential effects of uremia on cytokine mRNAs in the absence of parenchymal renal damage [bilateral ureteral transection (BUTx)] were sought. Finally, the impact of simulated in vitro uremia (HK-2 tubular cells exposed to peritoneal dialysate from uremic vs. normal mice) on cytokine mRNA and microRNA profiles was assessed. Uremia blunted TNF-alpha, MCP-1, and TGF-beta1 mRNA increases in all three in vivo parenchymal acute renal failure models. These results were paralleled by reductions in cytokine protein levels and Pol II recruitment to their respective genes. Conversely, uremia increased IL-10 mRNA, both in the presence and absence (BUTx) of parenchymal renal damage. The uremic milieu also suppressed HK-2 cell proinflammatory cytokine mRNA levels and altered the expression of least 69 microRNAs (P < 0.0001). We conclude that both pro- and anti-inflammatory cytokine gene expressions are influenced by uremia, with a potential predilection toward an anti-inflammatory state. Changes in gene transcription (as reflected by Pol II recruitment), and possible posttranscriptional modifications (known to be induced by microRNAs), are likely involved.
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PMID:Uremia impacts renal inflammatory cytokine gene expression in the setting of experimental acute kidney injury. 1965 11

Endothelial cells lining the inner blood vessel walls play a key role in the response to hypoxia, which is frequently encountered in clinical conditions such as myocardial infarction, renal ischemia and cerebral ischemia. In the present study we investigated the effects of hypoxia and hypoxia/reoxygenation on gelatinases (matrix metalloproteinase-2 and -9), their inhibitor (TIMP-2) and activator (MT1-MMP), in human umbilical vein endothelial (HUVE) cells. HUVE cells were subjected to 4 h of hypoxia or hypoxia followed by 4 and 24 h of reoxygenation. The pro- and active forms of MMP-2 and MMP-9 were analyzed by gelatin zymography; TIMP-2 protein level was assayed using ELISA, while MT1-MMP activity was measured using an activity assay. The secretion of MMP-2 proform increased significantly in cells subjected to 4 h of hypoxia followed by 4 or 24 h of reoxygenation, compared with the normoxic group. TIMP-2 protein level also increased significantly in the hypoxia/reoxygenation groups, compared with the normoxic group. There were no statistically significant differences in the levels of active MT1-MMP in all groups. This study indicates that MMP-2 and TIMP-2 could be regarded as important components of a mechanism in the pathophysiology of ischemic injury following reperfusion.
Acta Biochim Pol 2010
PMID:In vitro reoxygenation following hypoxia increases MMP-2 and TIMP-2 secretion by human umbilical vein endothelial cells. 2021 78