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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arterial intimal thickening is common in the end-stage kidneys of patients maintained on hemodialysis. We measured the intimal thickening in patients dialyzed for varying periods and in patients with the malignant phase of essential hypertension and with scleroderma-associated renal failure. The ratio of intimal area to medical area in intrarenal arteries was used as a measure of intimal thickening. In the dialysis groups, intimal thickening was relatively constant in arteries of all sizes and correlated with duration of dialysis, particularly in larger arteries. In the malignant hypertension and scleroderma groups, the intimal thickening was greatest in arteries less than 200 mu in diameter and least in those over 500 mu in diameter. There was much less intimal thickening in arteries of all sizes in kidneys of patients with end-stage polycystic disease than in other end-stage kidneys from patients with a similar diastolic blood pressure and similar duration of dialysis. We believe that the intimal thickening in dialyzed patients is probably a disuse type of change and may be related to reduction in the area of the renal microvascular bed.
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PMID:A morphometric study of arterial intimal thickening in kidneys of dialyzed patients. 45 27

The pathological changes in blood vessels observed in primary (essential hypertension) are similar to those seen in secondary hypertension due to renal disease or other causes. In benign hypertension, the major changes are in the small arteries and arterioles especially in the kidney. Interlobular arteries exhibit intimal thickening and duplication of the elastic lamina (elastosis) and there is hyaline change in the media of many arterioles. In some respects these changes are an accentuation of vessel ageing. Malignant hypertension usually presents in a younger age group (35--50 years) and is characterized pathologically by fibrous endarteritis in the interlobular arteries of the kidney and fibrinoid necrosis in the walls of a proportion of the efferent glomerular arterioles. Similar vessel changes are seen in other organs but many of the pathological changes in the heart and brain of patients with benign hypertension are related to the accentuation of arterosclerosis. There is an increased mortality from cardiac failure, myocardial infarction, cerebral haemorrhage and subarachnoid haemorrhage due to ruptured berry aneurysms in patients with benign hypertension. Although there is ischaemic damage to the kidneys in benign hypertension, death from renal failure is uncommon. Severe ischaemic damage to renal glomeruli and renal failure does, however, occur in malignant hypertension.
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PMID:Vascular pathology in hypertension. 46 85

Renal biopsies obtained from 20 adult patients within 30 days after onset of acute renal failure with microangiopathic hemolytic anemia ("the hemolytic-uremic syndrome") were studied. Lesions were graded independently by two observers without knowledge of the clinical history. All patients who did not have refractory hypertension were treated with heparin. Ten of the patients died, and four developed end-stage renal failure requiring chronic dialysis. Six patients, however, had a relatively good outcome: two recovered completely and four developed mild-to-moderate chronic renal failure not requiring dialysis. The six patients with a good outcome had significantly less severe arterial intimal thickening on biopsy compared with the remaining patients with a poor outcome. The patients with a good outcome and those with a poor outcome did not differ in the severity of glomerular lesions. The clinical features did not allow a prediction of late outcome. These results suggest that early renal biopsies may be helpful in predicting prognosis in the "hemolytic-uremic syndrome." This clinical syndrome may occur either in apparently healthy people, or may complicate the course of a chronic essential hypertension.
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PMID:Prognostic importance of vascular lesions in acute renal failure with microangiopathic hemolytic anemia (hemolytic-uremic syndrome): clinicopathologic study in 20 adults. 48 Jul 87

In 196 adult patients with chronic renal disease or primary hypertension, the evaluation of glomerular filtration rate (GFR) by means of creatinine clearance, 'predicted' creatinine clearance and [125I]-iothalamate clearance was performed. Iothalamate clearance was evaluated after subcutaneous injection of the substance . In patients with normal or upper borderline plasma creatinine values, the iothalamate clearance ranged from 44 to 117 ml/min/1.73 m2 and the overestimation of GFR from creatinine clearance was negligible. In patients with mild or advanced renal failure, the overestimation of GFR from creatinine clearance increased up to 18 and 32%, respectively. The clinical usefulness of iothalamate clearance is evident especially in patients with mild renal failure, in whom an accurate evaluation of GFR is often important for a correct dietary and therapeutic approach.
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PMID:125I-iothalamate and creatinine clearances in patients with chronic renal diseases. 49 7

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.
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PMID:Hypertension and hyperkalaemia responding to bendrofluazide. 50 50

In 14 of 204 consecutive cadaveric renal allograft recipients, the primary diagnosis was essential hypertension. Four patients had manifest ischemic heart disease before transplantation. Three of these patients died within 31 months of transplantation from recurrent myocardial infarction, and the fourth experienced coronary insufficiency. Cadaveric renal transplantation does not prevent the progression of coronary artery disease in patients whose renal failure was due to essential hypertension. In the presence of angina or previous myocardial infarction, these patiemts may be better treated by maintenance hemodialysis.
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PMID:Renal transplantation. Effect on the ischemic heart disease of essential malignant hypertension. 77 41

The nature of the original renal disease was determined in 403 consecutive cases of end-stage renal failure, in 317 of which the clinical diagnosis was corroborated by histological examination of the kidney. Five diseases accounted for 20 or more cases--glomerulonephritis (31% of the total), analgesic nephropathy (29%), primary vesicoureteral reflux (8%), essential hypertension (6%), and polycystic kidneys (5%). In only four cases did renal failure result from chronic pyelonephritis without a demonstrable primary cause. Greater use of micturating cystography and cystoscopy and routine urine testing for salicylate are advocated for earlier diagnosis of the major causes of "pyelonephritis". The incidence of end-stage renal failure in people aged 15-55 in New South Wales was estimated to be at least 34 new cases per million of total population each year.
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PMID:Diseases causing end-stage renal failure in New South Wales. 109 Mar 38

The effect of propranolol therapy on the mean arterial pressure (MAP) and plasma renin activity (PRA) was studied in three groups of hypertensive patients who were also treated with saliuretics. Group A: In 14 patients with essential hypertension on chlorthalidone treatment, an additional daily dose of 640 mg propranolol for two months led to a significant reduction of the MAP (from 124 to 105 mm Hg) and PRA (from 5.3 to 2.0 ng AI/ml/hr standing). There was no correlation between MAP reduction and either the original levels or change in PRA. Group B: In 14 patients with essential hypertension and 5 with renal artery stenosis studied on a fixed salt intake, the plasma and extracellular volumes, PRA, and blood pressures were recorded before and after three days of diuretic induced salt depletion and, with maintenance of the depleted state, after three days of propranolol. Salt depletion resulted in a decrease in MAP from 132 to 128 mm Hg (NS), and PRA increased from 3.4 to 22.3 ng AI/ml/hr (P less than 0.01). There was no correlation between change in MAP and PRA control values, PRA change, or any of the volume parameters. Addition of propranolol was followed by a rapid MAP decrease to 111 mm Hg (P less than 0.01), and the PRA dropped to a mean of 8.5 (P less than 0.01). No correlation was found between change in MAP and change in PRA. The patients with renal artery stenosis did not differ in their reactions from those with essential hypertension. Group C: In five patients with moderate renal failure and normal to expanded 82-Br distribution volume, propranolol lowered MAP by 10% and lowered the PRA in all five. Salt depletion by furosemide to 82-Br volumes below normal resulted in a 10% decrease of MAP and a marked rise in PRA. In this state propranolol was followed by a further MAP reduction of 18% and a decrease in PRA. There was no quantitative relationship between MAP and PRA change during either of the treatment regimes. It is concluded that in various forms of hypertension, the blood pressure can be effectively lowered by combining diuretics and propranolol regardless of the pretreatment PRA level.
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PMID:Effect of salt depletion and propranolol on blood pressure and plasma renin activity in various forms of hypertension. 109 56

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

Hypertension and diabetes mellitus are strongly associated conditions from epidemiologic, genetic, and pathophysiologic points of view. The prevalence of hypertension is high in patients with diabetes, and, conversely, many patients with essential hypertension are glucose intolerant. Proteinuria appears in 40-50% of patients with insulin-dependent diabetes mellitus and 20-30% of patients with non-insulin-dependent diabetes mellitus. Progressive renal failure occurs in 30-40 and 3-8% of patients, respectively, hypertension being a leading factor in its rate of progression. In various animal experiments, ACE inhibitors are able to prevent proteinuria and glomerular sclerosis, presumably by lowering transglomerular capillary pressure. In the diabetic human, ACE inhibitors are powerful antihypertensive drugs, devoid of metabolic side effects. Clinical studies indicate that ACE inhibitors reduce proteinuria and possibly slow the rate of decline in renal function. Such an effect is not observed with beta-blockers. Large-scale studies are needed to confirm this very important hypothesis.
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PMID:Angiotensin-converting enzyme inhibition and diabetic nephropathy. 138 63


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