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

One hundred and eight patients suffering from hypertension due to a unilateral parenchymatous neophropathy were studied over a period of one to eight years after treatment was starded. The aetiologies were diverse: harmonious hypoplasia, segmental hypoplasia, pyelonephritis, reflux nephropathy, hydronephrosis and tuberculosis. Thirty nine patients were treated surgically, with 50% good results. In 82 cases medical treatment was continued for at least a year with a 52% success rate. Such success was recorded in 94% of cases in which beta-blockers were used (38 cases). Surgical success was not dependent upon the period for which hypertension had been present. The best results were seen in cases of hydronephrosis and pyelonephritis and the worst in tuberculosis. Thirteen patients underwent surgery event though there was no unilateral increase in plasma renin levels. Seven were improved or cured. Ten patients underwent surgery with a renin activity 50% greater than on the healthy side, 9 being improved or cured. Treatment with beta-blockers, alone or in association with diuretics, controlled blood pressure in 90% of cases, regardless of the renin activity. Plasma renin activity in the renal veins is of good prognostic value in terms of the effectiveness of nephrectomy against hypertension. In Call cases, beta-blockers were more effective than surgery.
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PMID:[Hypertension due to unilateral parenchymatous nephropathy (author's transl)]. 3 35

Severe renin-mediated hypertension was noted in 2 children as a result of selective renal damage from vesicoureteral reflux during the early years of life. In each case the reflux had been corrected successfully long before hypertension developed. In 1 case the late damage involved only 1 kidney and nephrectomy resulted in immediate relief of the hypertension. In the second case, even though both kidneys showed segmental scarring from calicectasis and chronic pyelonephritis, removal of the atrophied lower pole of 1 kidney made hypertension amenable to medical treatment and reduced excessive renin output to a fraction of the original high levels. The mechanism of renin-mediated hypertension in kidneys with segmental scars of chronic pyelonephritis is believed to be ischemia of the relatively normal renal cortex in proximity to areas of interstitial fibrosis, within which are tortuous interlobular and smaller arterioles with severe intimal thickening. Hypertrophy of normal renal segment occurs in young patients with segmental chronic pyelonephritis. To accommodate this enlargement the original calix develops an extension or elongation readily distinguishable from other dilated calices.
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PMID:Malignant hypertension in children secondary to chronic pyelonephritis: laboratory and radiologic indications for partial or total nephrectomy. 61 6

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.
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PMID:Elevated plasma renin activity in patients with acute pyelonephritis. 69 21

Eight cases are reported of female children presenting with hypertension and found to have primary vesicoureteral reflux with chronic pyelonephritis. In 6 patients renal function was essentially normal while 2 had azotemia and progessive renal deterioration. As a result of early surgical intervention in the form of antireflux procedures, occasionally combined with unilateral nephrectomy for renin-dependent lesions, 5 of the 8 had complete disappearance or amelioration of hypertension with stabilization of renal function. The interactions of each member of the triad--vesicoureteral reflux, pyelonephritis, and hypertension--are reviewed with emphasis on pertinent pathophysiologic concepts regarding their roles in the production of progressive renal deterioration.
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PMID:Hypertension as complication of vesicoureteral reflux in children. 93 78

The present authors conducted a series of experiments with mongrel dogs, in which unilateral chronic pyelonephritis was induced and postoperative changes in blood pressure and plasma renin activity were observed over a period of 3 months. The pyelonephritis infection was brought about by a method involving vesicoureteral reflux and ureteral dysfunction, as described in a previous paper. Pre- and postoperative levels of systolic pressure were compared, but no definite trends were found for the first 3 weeks after operation. At 30, 60 and 90 days the pressures were found to have risen by 21.2 +/- 14.6 and 17.1 +/- 16.7 mm Hg, respectively. No appreciable change in the plasma renin activity was found, however, at any stage. From these results it was concluded that experimentally induced chronic pyelonephritis in dogs caused a rise in blood pressure. No connection between the pyelonephritis and the renin angiotensin system was found.
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PMID:Hypertension and plasma renin activity in experimentally induced chronic pyelonephritis. 94 Jun 27

Hypertension resulting from chronic pyelonephritis has been shown in clinical as well as experimental cases, although some authors deny that there is a pathogenic relationship between the two. To throw light on this problem the present authors conducted a series of experiments with mongrel dogs, in which chronic pyelonephritis was induced and postoperative changes in blood pressure and plasma renin activity were observed over a period of 3 months. The pyelonephritis infection was brought about by a method involving vesicoureteral reflux and ureteral dysfunction, as described in a previous paper. Preoperative and postoperative levels of systolic pressure wer compared, but no definit trends were found for the first 3 weeks after operation. At 30, 60 and 90 days the pressures were found to have risen by 21.2 plus or minus 11.2 mmHg, 21.7 plus or minus 14.6 mmHg and 17.1 plus or minus 16.7 mmHg, respectively. Thus there was a significant elevation (p smaller than 0.01). No appreciable change in the plasma renin activity was found, however, at any stage. From these results it was concluded that experimentally induced chronic pyelonephritis in dogs caused a rise in blood pressure. No connection between the pyelonephritis and the renin angiotensin system was found.
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PMID:The relation between experimentally induced pyelonephritis and hypertension. 114 21

The role of the split kidney function tests in the diagnosis of renal hypertension is reviewed, and a new technique is described which is designed to diminish the number of false negative results sometimes encountered in unilateral pyelonephritis and segmental renal arterial stenosis. Split kidney function tests still have an important role in diagnosis of renal hypertension, particularly when the results of other investigations are equivocal and when facilities for differential renal renin assay are not available.
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PMID:Reconsideration of split kidney function tests in hypertension: a new technique. 115 Mar 95

Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline-depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and 11 patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion ("low renin hypertension"). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.
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PMID:[Plasma aldosterone and plasma renin activity in patients with essential and renal hypertension under acute stimulation with saline depletion and acute suppression with saline infusion]. 115 49

It is apparent that the split function study and renal vein renin determination are complementary and afford valuable information for selecting patients with potentially curable renovascular hypertension. The split function study, when interpreted with the recently defined split function ratio, offers the clinician a highly accurate means of diagnosing significant renal ischemia. Because the split function ratio shows the disparity between the ischemic and contralateral kidney to a greater degree, the chance of misdiagnosis due to laboratory or physician error is minimized. The split function study, however, is of limited value in patients with pyelonephritis since the water- and salt-losing characteristics of the pyelonephritic kidney may mask significant renal ischemia. In these patients, as well as those with a nonfunctioning kidney or hydronephrosis, the renal vein renin determination is the test of choice. In addition, the added morbidity of the split function study is not warranted in a patient with an elevated peripheral renin which, for interpretation, requires an accurate 24 hour urine for sodium, a renal vein renin ratio outside the range of patients with essential hypertension (renal vein renin ratio greater than 1.7) and evidence of suppression of renin secretion from the contralateral kidney. If, however, the renin determination does not afford convincing evidence of significant renal ischemia in a patient with radiographic evidence of renal arterial stenosis, a split function ratio definitely should be determined to more completely define the pathology. The attendant morbidity of a carefully performed split renal function study does not approach the morbidity and mortality associated with unnecessary surgery or inadequately treated hypertension.
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PMID:Ureteral catheterization studies. 115 55

Blood pressure changes were followed up for 1-12 years (average; 3.8 years) in 46 cases of confirmed postoperative chronic pyelonephritis which had undergone ureterocutaneostomy, nephrostomy or other urologic operations. Diastolic blood pressure levels averaged 82 mmHg before operation, and 89 mmHg in the chronic stage after the operation. The incidence of hypertension (over 100 mmHg diastolic pressure) was 7% before the operation, but rose to 30% in the chronic stage. Application of an "age- and sex-adjusted score" also served to confirm a mean increase in blood pressure through the development of chronic pyelonephritis. No correlation was found between renal function and blood pressure. Nor was there any definite relationship between family history of hypertension and high blood pressure. In the 14 cases observed for plasma renin activity, values were found to be in the normal range.
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PMID:Pyelonephritis and hypertension. 120 57


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