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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of PGE2, PGF2 alpha and renin activity were measured in renal venous blood of 29 patients with essential hypertension (EH), 23 patients with renovascular hypertension (RVH) and 10 patients with unilateral pyelonephritis and high arterial hypertension. The pattern of change in renal venous PG content was found to be related to the type of renal lesion: the level of PGE2 was lowered and PGF2 alpha/PGF2 ratio increased in the blood outflow from the kidneys of EH patients and from ischemized kidneys of RVH patients as compared to similar parameters in the outflow from contralateral kidneys of patients with RVH and pyelonephritis. Venous levels of both PGs were the highest in pyelonephritis-affected kidneys. Renal venous PG levels go down in all cases as the disease grows older. An acute drop in arterial pressure is accompanied with increased withdrawal of PGF2 alpha from the kidneys and enhanced renin activity in renal veins, while PGE2 drops simultaneously. PGF2 and PGE2 showing different trends of change in response to falling arterial pressure suggests increased transition of PGE2 to PGF2 alpha under the effect of enhanced PG-9-ketodehydrogenase activity. In the abdominal aorta, the scope of drop in arterial pressure correlates to the change in PGF2 alpha level, that is an evidence of PG direct involvement in the autoregulation of renal blood flow.
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PMID:[Prostaglandins in the renal vascular bed in arterial hypertension of different etiologies]. 634 86

We report the experience of a regional centre serving a population of 3 millions in the management of patients with hypertension and unilateral scarred kidneys between 1972 and 1981. Thirty one patients were studied, fifteen have been subjected to nephrectomy and sixteen managed conservatively. The medically and surgically treated patients differed only in that the diseased kidney was smaller, 7.7 +/- 1.9 vs 9.9 +/- 1.7 cm, (p less than 0.01), and systolic blood pressure higher, 224 +/- 34 vs 198 +/- 30 mmHg, (p = 0.05), in the surgically treated group. Following nephrectomy blood pressure was normal without drugs in four patients, control was made easier in 10 patients and only one patient, who had bilateral disease, failed to benefit. In the non-surgical group drugs could be withdrawn in only one patient and control became easier in only five. Serum creatinine did not increase following nephrectomy, but had increased significantly at the time of the most recent follow up in the medically treated patients (89 +/- 20 to 102 +/- 32 mumol 1(-1), p less than 0.05). We conclude that nephrectomy is of value in the management of some patients with unilateral chronic pyelonephritis and need not result in loss of renal function. Renal vein renin studies may be helpful in selecting patients for surgery but examination of the effect of nephrectomy in patients without differences in renal vein renin is necessary to establish this.
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PMID:Experience in the management of hypertension with unilateral chronic pyelonephritis: results of nephrectomy in selected patients. 635 27

The renin-angiotensin (juxtaglomerular apparatus--JGA) and prostaglandin [interstitial cells (IC) of renal medulla and nephrocytes of collecting tubules (NCT)] systems of the kidneys were studied in 72 patients (renal biopsies, nephrectomy, morphofunctional correlations) with the nephrogenic arterial hypertension (vasorenal hypertension, chronic glomerulonephritis, pyelonephritis). Histological and electron-microscopic methods were used; the renin activity was determined in the peripheral blood and blood from the renal veins. The results were analysed mathematically and statistically using an original programme. It is shown that stereotype cyclic changes develop in the endocrine renal system of patients with renal hypertension and they reflect the stages of initial hyperfunction (ultrastructural hyperplasia of JGA cells with appearance of numerous immature granules; ultrastructural moderate hyperplasia of medulla IC; increase of blood renin activity), discoordination of functions (progressing JGA hyperfunction and depletion of prostaglandin synthetic function of medulla IC; compensatory activation of NCT; further increase of the blood renin activity) and depletion (atrophy and fibroblastic transformation of the JGA of the majority of nephrons and of medulla IC). The stages of renal endocrine system alterations in the arterial hypertension are the manifestation of compensatory and adaptive response. Morphofunctional analysis with the use of morphometry and mathematical statistics are necessary for the objective evaluation of this response.
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PMID:[Endocrine system of the kidneys in nephrogenic arterial hypertension: functional and morphological analysis]. 639 31

The long-term results of nephrectomy were evaluated in 27 patients with malignant renal hypertension. The hypotensive effect of nephrectomy, function of the remaining kidney, central hemodynamics, and peripheral blood renin were investigated. It was found that hypertension remitted in subjects with an unaffected remaining kidney which completely compensated for the function of the removed kidney and maintained blood pressure within normal. Nephrectomy performed during malignant arterial hypertension that developed because of unilateral pyelonephritis and unilateral stenosing of the renal artery with a sufficient total renal function before surgery led to a prolonged remission of arterial hypertension and reverse development of the symptoms of its malignancy. Hypertension did not remit during chronic pyelonephritis of a single kidney. Renal function was substantially decreased as compared with the control group.
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PMID:[Hypotensive effect of nephrectomy in malignant renal hypertension and the function of the remaining kidney at late follow-up]. 651 45

The distribution of renin in two cases of segmental renal hypoplasia was investigated by immunofluorescence and the peroxidase anti-peroxidase (PAP) method using an anti-human renin antiserum. Renin-containing cells were found only in hypoplasic segments in the vicinity of altered glomeruli and small arteries. Well-preserved renal cortex and areas of chronic atrophic pyelonephritis failed to show any demonstrable site of renin production. Whatever is the mechanism of the disease, the characterization of large numbers of renin-containing cells in the affected kidney support a role for the renin-angiotensin system stimulation in this form of hypertension.
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PMID:Renin localization in segmental renal hypoplasia. Immunohistochemical demonstration in two cases. 701 53

The etiology of persistent hypokalemia and renal potassium loss was investigated in three children. Each had normal blood pressure but low plasma aldosterone values in relation to elevated plasma renin activity. None had a history of licorice abuse, laxative or diuretic use, persistent vomiting or diarrhea, pyelonephritis, or diabetes insipidus. Additional studies in one patient showed low prostaglandin E excretion and a normal platelet aggregation response to epinephrine and ADP. Although certain aspects of this condition resemble Bartter syndrome, the low concentrations of aldosterone and the absence of evidence for mineralocorticoid excess suggest a previously undescribed syndrome.
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PMID:Hypokalemia, normal blood pressure, and hyperreninemia with hypoaldosteronism. 702 99

It was found that hypertension in patients with stenosis of the renal artery is of a renopressor character which is maintained by increased renin secretion by the kidney with the stenosed artery. High arterial hypertension is conducive to the maintenance of the function of the kidney with the stenosed artery at the most optimum level and has an effect on the contralateral kidney. After surgery (nephrectomy), in addition to normalization of arterial pressure the blood flow in the remaining kidney becomes almost equal to the blood flow in two kidneys, i.e. the remaining kidney compensates for the function of the removed kidney. The incidence of malignant course of arterial hypertension in combination of an occlusive lesion of the renal artery and pyelonephritis of this kidney is twice that in isolated stenotic lesion of the renal artery.
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PMID:[Separate and summary renal hemodynamics in renovascular hypertension (before and after surgery)]. 742 Aug 46

During the past decade, experimental and clinical evidence has indicated an important role for the renin-angiotensin system in the progressive destruction of nephrons in a wide variety of chronic renal diseases. Studies have indicated that in the subtotally nephrectomized rat model of progressive glomerulosclerosis, in experimental diabetes mellitus, in the chronic phase of puromycin aminonucleoside-induced nephrotic syndrome and in Heymann's nephritis, angiotensin-converting enzyme (ACE) inhibitors dramatically preserve both nephron structure and function. Clinical studies have similarly noted that chronic administration of ACE inhibitors inhibits progression of renal failure in type I diabetes and type II diabetes as well as primary glomerulopathies, sickle cell nephropathy, systemic lupus erythematosis, chronic pyelonephritis and adult polycystic kidney disease. Current evidence suggests that the beneficial effect of ACE inhibitors is primarily due to inhibition of angiotensin II production, and there is strong suggestive evidence for increases in local intrarenal activation of the renin-angiotensin system in these conditions. In obstructive uropathy, activation of the renin-angiotensin system has also been shown to be an important aspect of the early functional changes and may be of importance in the subsequent generation of interstitial fibrosis. In the obstructed kidney, renin and angiotensinogen production increase and type I angiotensin receptors decrease. Inhibitors of angiotensin II production and angiotensin II action partially reverse the vasoconstriction and the reduced renal blood flow, and abolish the changes in expression of AT1 MRNA induced by obstruction. Studies suggest that the angiotensin-mediated increases in tubulointerstitial fibrosis may be mediated by increased production of transforming growth factor-beta.
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PMID:Angiotensin II-mediated renal injury. 756 81

The authors examined 150 patients with pronounced arterial hypertension: 73 with essential hypertension, 42 with chronic glomerulonephritis, 26 with chronic pyelonephritis and 10 with diabetic glomerulosclerosis. In addition to conventional tests, measurements were made of renin activity, levels of plasma aldosterone and hydrocortisone, IgA, IgG, IgM, CIC. A significant rise in concentrations of aldosterone, hydrocortisone against a significant fall in those of plasma renin were registered in all the patients irrespective of the disease. Significant differences between the groups by the renin profile, aldosterone and hydrocortisone levels were absent. It is suggested that changes in the hormonal spectrum and immunological indices are independent of renal affections in hypertension, while involvement of renin-angiotensin-aldosterone system in hypertension stabilization has no nosological specificity. The pattern of the immunity shifts evidences for their important pathogenetic role in maintenance and progression of arterial hypertension.
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PMID:[Changes of the renin-angiotensin-aldosterone system and immunologic parameters in essential and symptomatic arterial hypertension]. 814 96

Arterial hypertension is frequent among chronically dialyzed patients. The kidney obviously plays a major role in arterial blood pressure control. There is a large number of experimental data emphasizing different factors (in addition to renin important in renal hypertension prognosis) such as: sodium balance, angiotensin, etc [1-8]. Sympathetic activity disorders or lack of vasodilatory prostaglandins and quinine may also play a certain role. In uremic patients peripheral arteriolar resistance is increased, unlike normotensive uremic patients or those who prove to be normotensive upon clinical examinations [8, 11-15]. Hypertension occurs in approximately 80% of patients with chronic renal failure, producing a number of complications primarily affecting the CNS and systemic circulation [5-8, 10, 11, 13]. The study concerned patients on chronic dialysis, with a male to female ratio of 69.9%:32.1%. In most of them the underlying disease, which caused chronic renal failure, was glomerulonephritis (60.0%), then pyelonephritis (17.0%) and nephrosclerosis, nephrolithiasis, polycystic kidney and, finally, renal tumours. The effect of permanent haemodialysis during the first year of treatment, was efficacious on hypertension in 1704 (65.1%) patients; in 672 (25.7%) patients therapeutical effects were achieved by dialysis and antihypertensive drugs, while in 240 (9.2%) subjects there was no improvement. General observations suggest that two types of arterial hypertension persisted in patients with chronic renal failure: volume-dependent arterial hypertension which is more frequent (90-95%) among haemodialyzed patients and renin-dependent hypertension. Such findings are of utmost importance indicating that hypervolaemia is one of the major factors in the development of arterial hypertension in patients with chronic renal failure, with renin playing the secondary role. Salt-free diet should be used in the treatment of arterial hypertension for years, a well conducted haemodialysis is highly effective in the control of arterial hypertension among these patients. In our series of patients dialysed three times a week; normalization of blood pressure was faster with lower incidence of hypertensive crises during haemodialysis and with few complications. Water and sodium excess was reduced by frequent haemodialyses and sudden changes in electrolyte, hydrostatic and other metabolic effects were minimized. Increased values of plasma renin activity were observed in a small number of patients. Ultrafiltration is insufficient for normalization of blood pressure. Hypertensive crises were frequent in these patients. Their response to medicaments such as methyldopa, beta-adrenergic blockers or other antihypertensive drugs, was good. Severe changes in blood vessels, especially in fundus oculi blood vessels were frequent in these patients. The life of hypertensive glomerulonephritis patients was especially endangered (graphs 1-6). In addition to the mentioned factors arterial hypertension during haemodialysis may also be of cardiac origin, including increase in cardiac output due to arteriovenous anastomosis, disequilibrium syndrome, changes in osmotic gradient of both extra- and intracellular spaces with resultant arteriolar wall oedema, erythrocyte amount, hypoxia, composition of dialysis fluid (sodium concentration), plasma osmotic pressure, metabolic acidosis and other factors. More recently, natriuretic hormone has also been indentified as a cause of vascular refraction. Peripherial arteriolar resistance as a cause of arterial hypertension among uremic patients must not be forgotten, because the genesis of arterial hypertension in patients with chronic renal failure is multifactorial. The highest percentage refers to volume-dependent arterial hypertension, whereas the percentage of other aetiologic factors is lower. Haemodialysis enables the normalization of blood pressure in most of hypertensive patients.
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PMID:[Arterial hypertension in patients on chronic hemodialysis]. 910 57


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