Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
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PMID:Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride. 13 13

Thirteen consecutive twin pregnancies affected by the "stuck twin" phenomenon were reviewed to determine the potential benefit of serial amniocenteses. The fetal survival rate for the eight pregnancies that underwent serial amniocenteses was 69% (11 of 16 fetuses). This is significantly improved compared with a fetal survival rate of 20% among the five preceding pregnancies managed without serial amniocenteses at the same institution (p = 0.01). It is also markedly improved compared with a combined fetal survival rate of 16% among 48 previously reported pregnancies with the stuck twin phenomenon managed without serial amniocenteses (p less than 0.0001). Survival correlated with the absence of concomitant pregnancy complications (i.e., maternal hypertension or intractable labor) and with the absence of severe fetal structural abnormalities. Procedural complications occurred in three of eight pregnancies (37.5%) managed with serial amniocenteses and was attributed as a cause of fetal death in one case. Two of 11 survivors (18%) had complications after serial amniocenteses including brain infarction and renal tubular necrosis. Serial amniocenteses may significantly improve the survival rate of twin gestations affected by the stuck twin phenomenon but may be associated with complications among survivors.
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PMID:The "stuck twin" phenomenon: ultrasonographic findings, pregnancy outcome, and management with serial amniocenteses. 224 99

Ten black patients (eight men) with renal shutdown from accelerated hypertension were treated with hemodialysis. Renal function improved, and dialysis was discontinued after 6 +/- 2 months. Five patients (Group I) have maintained good renal function at 25 +/- 3 months of follow-up, whereas the other five (Group II) had deterioration again to advanced azotemia over 16 +/- 6 months. On admission, Group I patients had lower levels of serum creatinine (9 +/- 1.2 mg/dl [mean +/- SE] versus 13.6 +/- 1.7 mg/dl, p = 0.04) and urinary protein (0.98 +/- 0.78 g per day versus 2.17 +/- 1.5 g per day) and were more oliguric (451 +/- 145 ml per day versus 1,122 +/- 494 ml per day) than Group II. In Group I, renal shutdown was faster (8 +/- 4 days versus 38 +/- 28 days), recovery earlier (4 +/- 1.5 months versus 8 +/- 4 months) and greater (lowest serum creatinine level 1.9 +/- 0.3 mg/dl versus 5.7 +/- 1.7 mg/dl, p less than 0.05), and compliance better than in Group II. Two patients in the former group but none in the latter had peripheral schistocytes. It is concluded that the sustained recovery in Group I resulted from the resolution not only of the acute vascular lesions but also of tubular necrosis and microangiopathy, and the postrecovery deterioration in Group II is attributed to the more severe renal damage initially, the progression of the chronic vascular lesions in uncompliant patients, and possibly hyperfiltration damage in the remaining nephrons.
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PMID:Transient and sustained recovery from renal shutdown in accelerated hypertension. 394 32

The appearance of renal failure during episodes of macroscopic hematuria (EMH) in IgA nephropathy (IgAN) has been described as very unusual. The results of a prospective investigation on the effect of EMH on renal function in IgAN are presented. During a 3-year period, 29 episodes of EMH occurring in 21 patients with IgAN have been studied. A derangement of renal function (increase of serum creatinine by more than 0.5 mg/dl) was observed in 11 episodes (37.9%) with peak creatinine values ranging from 1.2 to 6.7 mg/dl. The worsening of renal function was accompanied by a longer duration of EMH (4.8 +/- 1.3 vs. 3.5 +/- 1.5 days; P less than 0.05) but not by arterial hypertension or edema. A complete recovery of renal function was observed in every patient 1 to 2 months after the start of EMH. The histological survey disclosed that the decrease of renal function correlated closely with the presence of red blood cell casts in as much as 50% of the tubular lumen and with findings of tubular necrosis. We conclude that a worsening of renal function can be observed frequently during the EMH. Tubular damage and obstruction by red blood cell casts may play a significant role in the pathogenesis of this complication.
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PMID:Acute worsening of renal function during episodes of macroscopic hematuria in IgA nephropathy. 404 27

162 children with infantile spasms were treated with ACTH at the Children's Hospital, Helsinki, and at the Aurora Hospital, Helsinki, during 1960--76. In a large proportion (37%) of the children the treatment caused pronounced side effects, and the mortality was 4.9%. The most common complications were infections: septic infections, pneumonias, and urinary and gastrointestinal infections. Other side effects were arterial hypertension (11), osteoporosis (2), hypokalaemic alkalosis (2), and other marked electrolyte disturbances (10). In children necropsy showed fresh intracerebral haemorrhages. Four children developed oliguria and hyperkalaemia during and after withdrawal of ACTH. One of them had tubular necrosis confirmed by renal biopsy. Infections were significantly more common with large doses (120 units) of ACTH than with small ones (40 units). It is concluded that side effects, even severe ones, are more common during treatment than had been assumed. Careful watch is important before and after treatment. The benefit of very high dosages should also be reconsidered.
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PMID:ACTH therapy in infantile spasms: side effects. 625 50

Angiotensin II was infused into conscious rabbits at various doses from 0.001 to 0.5 microgram . kg-1 . min-1 for 24 h, and caused multifocal myocardial necrosis, renal tubular necrosis and acute renal failure. The myocardial necroses were found principally in the left ventricle; only at the highest doses of angiotensin II were right ventricular lesions present. The endocardium was not involved and no arterial or arteriolar lesions were seen. Mean arterial plasma angiotensin II concentration during angiotensin infusion was closely correlated with the increase in arterial pressure, the height of the plasma urea at the end of the infusion and the severity of the induced myocardial lesions. The myocardial necroses could be a consequence of the induced hypertension, or a direct effect of angiotensin II, or a combination of effects, although their predominance in the left ventricle suggests high systemic arterial pressure is an important factor. Cardiac lesions were observed with plasma angiotensin II concentrations only some 2 to 3 fold normal values; it is therefore possible that similar myocardial abnormalities might occur as a result of rises in endogenous renin, for example, in experimental or clinical renovascular hypertension.
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PMID:Angiotensin-induced myocardial necrosis and renal failure in the rabbit: distribution of lesions and severity in relation to plasma angiotensin II concentration and arterial pressure. 726 Sep 74

Tubular necrosis is the most frequent hospital-acquired cause of acute renal failure from renal origin. The two main factors leading to tubular necrosis are hemodynamic perturbations and use of nephrotoxic agents. There is recently a growing number of reports on tubular necrosis associated with a non traumatic rhabdomyolysis. In 60-70% of the cases, more than one contributing factor can be identified. In the majority of the patients who developed a transient postoperative acute renal failure, co-morbid factors such as diabetes, hypertension or major cardiovascular problems, are present. Acute renal failure increases the mortality by factors from 2-7. Therefore prevention and (or) early correction of the factors leading to tubular necrosis are of great importance.
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PMID:[Acute kidney failure in tubular necrosis]. 756 91

A prospective study over two and a half years analysed 48 children of acute renal failure requiring dialysis therapy. The mean age was 3 years 9 months and M:F ratio was 1.8:1. Renal causes predominated, accounting for 65%, with prerenal and postrenal causes responsible for 19% and 16%. Acute glomerulonephritis was seen in 13 cases, hypovolemia secondary to gastroenteritis in 9, tubular necrosis in 6, and hemolytic uremic syndrome in 5. A delay in seeking medical attention was present in as many as 48%, and was especially common with female children. All had oligo-anuria, with fluid overload present in 18.7%, hypertension in 23%, hypotension in 16.6%, neuropsychiatric manifestations in 20%, and infections in 47%. Peritoneal dialysis was carried out in 95%, and hemodialysis in 6.2%. Urine output and renal function returned to normal within 1.5 to 16 days (mean 5.9) in the survivors. Of the 28 who survived, 19 were followed up regularly for a mean of 4.25 months and all except one had normal renal function. Factors associated with a poor prognosis included female sex, age < 1 year, neurological manifestations, and hypotension, though these were not statistically significant. Mortality in our series was 41.5%. While etiological factors have shown changing trends, mortality still remains high inspite of dialysis.
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PMID:Acute renal failure in children requiring dialysis therapy. 789 66

Consomic rats (SS.BN13), in which chromosome 13 from normotensive inbred Brown Norway rats from a colony maintained at the Medical College of Wisconsin (BN/Mcw) was introgressed into the background of Dahl salt-sensitive (SS/Mcw) rats, also maintained in a colony at the Medical College of Wisconsin, were bred. The present studies determined the mean arterial pressure (MAP) responses to salt and renal and peripheral vascular responses to norepinephrine and angiotensin II; 24-hour protein excretion and histological analyses were used to assess renal pathology in rats that received a high salt (4% NaCl) diet for 4 weeks. MAP of rats measured daily during the fourth week averaged 170+/-3.3 mm Hg in SS/Mcw rats, 119+/-2.1 mm Hg in SS.BN13 rats, and 103+/-1.3 mm Hg in BN/Mcw rats. After salt depletion, MAP fell an average of 27+/-4.5 mm Hg in SS/Mcw rats, 9+/-2.6 mm Hg in SS.BN13 rats, and 11+/-3.0 mm Hg in BN/Mcw rats. Protein excretion of SS/Mcw rats on a high salt diet averaged 189+/-30 mg/24 h, 63+/-18 mg/24 h in SS.BN13 rats, and 40+/-6.4 mg/24 h in BN/Mcw rats. Compared with SS.BN13 and BN/Mcw rats, SS/Mcw rats exhibited significantly greater increases of renal vascular resistance in response to intravenous norepinephrine and angiotensin II. Severe medullary interstitial fibrosis and tubular necrosis after a high salt diet were found consistently in SS/Mcw rat kidneys but were largely absent in the SS.BN13 and BN/Mcw rat kidneys. A similar degree of glomerular sclerosis was found in both SS/Mcw and SS.BN13 rats. In rats fed a 0.4% salt diet, the glomerular filtration rate of SS/Mcw rats was significantly less than that of BN/Mcw and SS.BN13 rats. These results reveal a powerful gene, or set of genes, within chromosome 13 of BN/Mcw rats that confers protection from the detrimental effects of high salt to the SS/Mcw rats.
Hypertension 2001 Feb
PMID:Brown Norway chromosome 13 confers protection from high salt to consomic Dahl S rat. 1123 Mar 18

Ischemia is an inciting factor in 50% of incidences of acute renal failure, and it increases the risk of organ rejection after renal transplantation. We have previously demonstrated that resveratrol (RSV) reduces ischemia-reperfusion (I/R) injury of rat kidney both by antioxidant and anti-inflammatory mechanisms. However, a clear morphological demonstration of this activity has not been made. To answer this question we have performed a new set of experiments following the experimental protocol reported below to investigate the effects of I/R injury and RSV pretreatment on kidney morphology by computerized morphometric analysis. Both renal arteries were clamped for 40 minutes in 40 male Wistar rats (b.w. 220 +/- 20 g); 20 rats were pretreated with RSV 1 microM e.v. 40 minutes before clamping. All animals were reperfused for 24 hours and then sacrificed. Histological examination showed tissue conservation in treated rats. I/R-induced glomerular collapse (as revealed by mean glomerular volume and glomerular shape factor) was significantly reduced by RSV pretreatment. Capillary tuft/Bowman's capsule area ratio was enhanced in the I/R group suggesting tubular hypertension. RSV pre-treatments significantly reduced this parameter to the control value. The number of platelet clots in the capillary tuft and tubular necrosis were also reduced by RSV versus I/R group. L-NAME administration worsened both functional and structural damage. Finally, cGMP urinary levels were markedly reduced from 12.1 +/- 8.4 nmol/day to 0.10 +/- 0.10 nmol/day in the I/R group. RSV provided cGMP (5.01 +/- 1.5 nmol/day, P < 0.05). As expected, L-NAME administration significantly reduced cGMP in urine (0.71 +/- 0.6 nmol/day). The present study confirms the protective effect of RSV pretreatment in I/R injury of rat kidney and suggests multiple mechanisms of action.
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PMID:Resveratrol, a component of wine and grapes, in the prevention of kidney disease. 1207 75


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