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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiographic and histological studies of the intrarenal circulation have been undertaken in 20 patients following complicated pregnancies: 12 patients had had hypertension of pregnancy (group 1); 7 acute renal failure due to either ante- or post-partum haemorrhage and 1 patient post-partum renal failure (group 2). 3 months after delivery all patients had angiographic evidence of structural and functional abnormalities involving intrarenal blood vessels and cortical blood flow. The severity of the structural changes was related to the degree of microangiopathic haemolytic anaemia noted in the acute obstetric complication but not to the height of the blood pressure at this stage. Histological abnormalities of the cortical blood vessels were minimal. At the time of the renal angiogram and biopsy, 3 of the 12 group 1 patients were hypertensive and 3 had impaired renal function, compared with 5 and 1, respectively, in the 8 group 2 patients. Although during the follow-up period (mean 5 years) no further deterioration in renal function in either group has been observed, hypertension developed in 50% of the group 1 patients compared with only 1 of the patients in group 2. The relationship between the late onset of hypertension and the intrarenal vascular and haemodynamic abnormalities is discussed.
Nephron 1979
PMID:Structural and functional changes in the renal circulation after complicated pregnancy. 31 35

End-stage kidneys in patients who are receiving long-term intermittent treatment with hemodialysis are metabolic structures that participate in many body processes and that themselves develop and change despite severe excretory deficiencies. Nephron loss is severe. Other lesions in such kidneys include the following: smooth muscle nodules that arise in necrotic arteries and arterioles; embryonal hyperplasia of Bowman's capsular epithelium; remodeling of the arteries and veins; tubular atrophy; dilation and cyst formation (acquired cystic disease); arteriolar granular cell hyperplasia and hypertension; deposits of oxalate, calcium, and immune complexes; interstitial fibrosis with collagen and smooth muscle; mucoid change; and cellular infiltration. This list does not include all pathologic conditions found in the end-stage--dialysis kidney. The necessity of and the criteria for an experimental model of human long-term intermittent hemodialysis for end-stage renal disease, presently lacking, are indicated.
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PMID:New therapies and new pathologies: end-stage--dialysis kidneys. 36 73

The authors investigated post-renal transplantation hypertension behaviour in 20 patients with primary malignant hypertension (PMH), in 42 patients with secondary malignant hypertension (SMH) and in 62 controls (without malignant hypertension). All cases of malignant hypertension required removal of primary kidneys, either before or after transplantation. Hypertension was noticed at different periods of the post-renal transplantation phase, in 93% of PMH cases, 90% of SMH cases and in only 31% of the controls. After a period of time following transplantation, a decrease of hypertension incidence in the SMH and control groups was noticed, and persistence of hypertension was observed in the PMH group. The long-term development of PMH patients was worse than that of the other two groups.
Nephron 1978
PMID:Blood pressure behaviour in patients with malignant hypertension submitted to kidney transplantation. 37 Jun 28

18 patients undergoing renal transplantation were studied prospectively to determine the incidence and mechanism of blood pressure elevations which sometimes occur after release of vascular clamps from the grafts. No patients became as severely hypertensive as noted in previous reports. A weak, but statistically significant (r=0.56, p less than 0.05) positive correlation was found between changes in plasma renin activity and small incremental changes in blood pressure. 2 patients in whom the greatest change in renin occurred showed little or no increase in blood pressure. In view of the small blood pressure changes seen in the face of significant changes in plasma renin activity, it appears unlikely that acute hyperreninemia alone is sufficient explanation for postdeclamping hypertension which is sometimes observed during renal transplantation.
Nephron 1978
PMID:Hyperreninemia during renal transplantation. 37 Jun 29

The pattern of renal disease and its basic principles of management are essentially the same in the tropics as in the temperate environment. Glomerulonephritis and pyelonephritis with concomitant hypertension account for most cases of renal failure. Malaria is now well recognised as a cause of the nephrotic syndrome. Economic and manpower factors dictate a conservative approach to therapy. Maintenance haemodialysis and renal transplantation are not realistic in the present context, having regard to the order of priorities in health care delivery.
Nephron 1978
PMID:Nephrology in the tropical setting. 37 Jun 31

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
Nephron 1979
PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

Hypertension in children is a rare disorder with reliable estimates of annual incidence that do not exceed 0.1%. At least one third of these cases have no definable etiology when all of the presently available diagnostic studies are used. Major invasive or expensive evaluations are indicated when hypertension is sustained or severe, and should be directed toward the renal and renovascular areas. Serum potassium and calcium estimates are essential in every case, but the more extensive evaluations of thyroid, parathyroid, adrenal cortical and adrenal medullary hormones should be reserved for patients with specific indications of malfunction in those systems.
Nephron 1979
PMID:Hypertension in children: endocrine aspects. 44 May 7

A critical survey of the literature suggests that elevated serum uric acid is definitely associated with hypertension and may function as an independent risk factor in the development of this disease. The possible role of an elevated serum uric acid as an independent risk factor for the development of ischemic heart disease remains controversial and the association of these two factors may depend on the relationship between uric acid and hypertension. There is no evidence available to define the metabolic turnover of uric acid in hypertensives. The exact mechanisms underlying elevated serum uric acid values during diuretic treatment are unclear, but depend initially upon diuretic-induced extracellular volume depletion.
Nephron 1979
PMID:Elevated serum uric acid. A cardiovascular risk factor? 47 Nov 50

Subtotal nephrectomy was produced in male Wistar rats and the evolution of arterial pressure, water distribution and electrolytic composition of muscle and arterial tissue were studied. Also, the modifications produced by a chronic administration of saline load were evaluated. The incidence of hypertension is higher in the group that received saline load but the levels of the blood pressure were similar in both groups of hypertensive animals. The total water is increased in all the groups, except at the fourth week in the animals that did not receive saline load, in which it was decreased. The extracellular space is augmented in all groups and the plasma volume increased in the early phases of the experimental period with exception of the normotensive rats without saline load. No alterations were observed in the electrolytic muscle content, and the total water and potassium and chloride content of the arterial tissues was increased without modifications in the sodium content. The possible relationship of these alterations with the development of hypertension are discussed.
Nephron 1979
PMID:Body fluid changes in hypertensive rats. Their modifications by saline load. 50 66

Arteriovenous fistula of the kidney is a common complication of percutaneous needle biopsy with a reported incidence of as high as 15% in some series. Although a few cases eventually may develop hypertension, cardiomegaly, or congestive heart failure, most heal spontaneously within 1-18 months. Those which do not heal within this time are usually treated surgically and consequently there is little available information concerning the long-term conservative management of this problem. The subject of this report is a patient who has been followed medically for 10 years and who, despite the persistence of a large fistula, remains in good health.
Nephron 1979
PMID:Natural history of post-biopsy renal arteriovenous fistula: a 10-year follow-up. 50 68


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