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

Statistical analysis of the realtion between blood pressure and renal function in 421 patients with CGN, referred to the Second Internal Medicine at Nihon University Hospital, and in 253 Hypertensive patients with CGN by questionaires sent to 29 Medical Universities were investigated. The relationship between survival rate and blood pressure of 84 patients with CGN in Surugadai Nihon University Hospital was also examined. These data show that antihypertensive therapy for CGN with hypertension has an important effect on prognosis. Propranolol was given to 10 hypertensive patients with CGN and hypotensive effect on renal function was observed. Our experience suggests that propranolol may be useful for treating a high renin component in the hypertension with non renal failure, and renal function does not become worse. But in renal failure, propranolol therapy must be used carefully because of inducement to cardiac failure.
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PMID:Therapy and prognosis of hypertension in chronic nephritis. 115 36

Twenty-nine patients with terminal renal failure were treated by periodic hemodialysis for 2 to 18 months. Serial determinations of blood pressure, blood volume, cardiac output, exchangeable sodium and plasma renin activity were performed. Bilateral nephrectomy was performed in 17 patients and followed by a fall in blood pressure. Cardiac index was elevated in all patients but the blood pressure changes were mainly related to resistance changes. In non-nephrectomized patients, mean arterial pressure was directly correlated to plasma volume (P less than 0.0001), exchangeable sodium (P less than 0.01) and plasma renin activity (P less than 0.001). In anephric patients, mean arterial pressure was only directly correlated to plasma volume (P less than o.005). The slope of the curve relating arterial pressure to plasma volume was significantly shallower in nephrectomized than in non-nephrectomized patients, indicating a lower sensitivity of pressure to volume changes. The study provides evidence that, in hypertensive patients with chronic renal failure, the positive pressure-volume relationship is the fundamental cause of the high blood pressure and that the renin-angiotensin system acts mainly by changing the sensitivity of this mechanism.
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PMID:Overhydratation and renin in hypertensive patients with terminal renal failure: a hemodynamic study. 119 20

Continuing interest in the mechanism of hypertension have produced considerable new information on the underlying pathophysiologic processes involved. Elucidation of the role of renal malperfusion, the renin-angiotensin-aldosterone mechanism, and renal medullary antihypertensive substances continues to clarify our understanding of renal hypertension. Current evidence suggests that angiotensin can produce hypertension by a direct effect on peripheral blood vessels in malignant hypertension and in renin-secreting renal tumors and by an intrarenal mechanism influencing intrarenal distribution of blood flow, and, thereby, sodium resorption in chronic renovascular hypertension. The current diagnostic techniques used to determine the presence of renal atery stenosis and its functional significance are reviewed. Arteriographic evidence of renal artery collaterals and a positive differential venous renin ratio are the two parameters whose usefulness and practicality have been best documented in recent years. The results of surgical procedures reported in the world literature show a 50 per cent rate with a further 30 per cent improvement rate in terms of control of hypertension. When functional significance of stenosis is demonstrated before surgical procedures, cure rates of the order of 80 per cent can be achieved. Recent developments of technique of operating room upon less extensive lesions of the renal artery branch extend the possibilities of surgical benefit which should also be considered in the presence of renal failure of renovascular origin.
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PMID:Renal hypertension. 120 80

In 14 patients with terminal renal failure who underwent dialysis with a solution containing potassium in a concentration of 2 mmol/l, the aldosterone concentration in plasma decreased significantly during haemodialysis. On the other hand a clear increase of plasma aldosterone was observed during haemodialysis in two patients who were dialysed with a solution containing potassium in a concentration of 4 mmol/l. This observation demonstrates the importance of plasma potassium for the regulation of plasma aldosterone concentration during haemodialysis. It suggests that the renin-angiotensin system has no major role in the regulation of aldosterone despite sodium and fluid losses.
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PMID:[Plasma aldosterone during haemodialysis in patients with terminal renal failure]. 127 56

Thirty-four cases of combined abdominal aortic aneurysm (AAA) and renal artery stenosis (RAS) are reported. Hypertension was found at admission in 32 subjects, the other two being well responsive to drug therapy. Angiography and selective renal vein renin assay were always performed: renal artery stenosis was unilateral in 21 (61.7%) subjects and bilateral in 13 (38.3%). In 9 cases renal artery stenosis was not correlated to the hypertensive state. Mild chronic renal insufficiency was demonstrated preoperatively in 20 patients (58.8%). Simultaneous surgical treatment was carried out in 25 cases (73.5%). Mortality was 4% (one subject), severe renal insufficiency 8% (two subjects) and permanent renal failure 4% (one subject) All complications occurred among the group with bilateral RAS. While surgical repair of AAA is always mandatory, simultaneous surgical treatment of AAA and RAS should be carried out in carefully selected cases, due to elevated mortality rates reported in the literature, in order to cure renovascular hypertension, when it is demonstrated as related to RAS, or to preserve renal functionality, when RAS is contralateral to a functionally excluded or hypotrophic kidney or it exceeds 80% of the diameter of the artery.
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PMID:Surgical approach to combined abdominal aortic aneurysm and renal artery stenosis. 129 47

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

Treatment with angiotensin-converting enzyme (ACE) inhibitors can begin at any time when a left ventricular dysfunction has been diagnosed. In the absence of rare contra-indications (renal artery stenosis, connective tissue disease, severe renal failure), all patients with asymptomatic or, a fortiori, symptomatic chronic heart failure can benefit from ACE inhibitors, whatever the origin of the heart failure. Among the ACE inhibitors now available, the benefits of captopril (3 daily doses) and of enalapril (2 daily doses) on all the targets of cardiac failure treatment are now well established. The effects of lisinopril on mortality are not yet known, but the haemodynamic and symptomatic benefits of this drug are also well established (with the advantage of once daily administration). Other ACE inhibitors with less numerous and less convincing trial reports can be used or rejected depending on the physician's faith in the effects of this pharmaceutical class. With all ACE inhibitors the initial dose must be very low, to be gradually increased over several days or even weeks until the highest dose tolerated is reached. ACE inhibitors can be associated with the classical treatment of cardiac failure. A previous diuretic treatment with sodium depletion may increase the risks of first dose effect and renal intolerance due to the introduction of the ACE inhibitors. Theoretically, the combination of ACE inhibitors and spironolactone is to be avoided for fear of hyperkalaemia and renal deterioration. Yet, provided some precautions are taken this combination may improve the benefits of ACE inhibition when the renin-angiotensin-aldosterone system inhibition is not optimal. However, this has yet to be demonstrated by prospective clinical trials.
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PMID:[Management of the treatment with converting enzyme inhibitors in chronic heart failure]. 129 41

To elucidate the mechanism of hyperkalemia in diabetic patients without renal failure, we investigated (Na(+)-K+) adenosine triphosphatase (ATPase) activity in erythrocyte membrane, erythrocyte Na+ and K+ content, and plasma endogenous digitalis-like substance in control subjects (n = 16) and non-insulin-dependent diabetes mellitus (NIDDM) patients (n = 62). NIDDM patients were divided into normokalemic patients (NKDM, n = 48) and hyperkalemic patients (HKDM, n = 14). There was no difference in plasma glucose or hemoglobin A1c (HbA1c) levels, plasma renin activity (PRA), and plasma aldosterone concentrations (PAC) between NKDM and HKDM patients. (Na(+)-K+)ATPase activities in NIDDM patients were significantly reduced compared with those in control subjects (0.336 +/- 0.016 mumol-inorganic phosphate [Pi]/mg protein/h, mean +/- SEM, P less than .05), and (Na(+)-K+)ATPase activities in HKDM patients (0.243 +/- 0.015 mumol Pi/mg protein/h) were significantly reduced compared with those in NKDM patients (0.295 +/- 0.008 mumol Pi/mg protein/h, P less than .01). Plasma K+ content had a significant negative correlation with (Na(+)-K+)ATPase activity in diabetic patients (r = -.365, P less than .01). Erythrocyte Na+ content had a significant negative correlation with (Na(+)-K+)ATPase activity in control subjects (r = -.619, P less than .05). There was no difference in plasma endogenous digitalis-like substance among the three groups. (Na(+)-K+)ATPase activity was not significantly correlated with plasma endogenous digitalis-like substance in control subjects and diabetic patients. These findings suggest that the reduction of (Na(+)-K+)ATPase activity, which was not related to plasma digitalis-like substance, may be partly responsible for hyperkalemia in diabetic patients.
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PMID:Reduction of erythrocyte (Na(+)-K+) ATPase activities in non-insulin-dependent diabetic patients with hyperkalemia. 131 28

The pathogenesis of hypertension in autosomal-dominant polycystic kidney disease (ADPKD) is unclear, but increased activity of the renin-angiotension system may contribute. The renal and systemic hemodynamic response to lisinopril, an angiotension converting enzyme (ACE) inhibitor, in patients with ADPKD without renal failure was compared with the response in matched unaffected family members. Mean blood pressure and renal vascular resistance decreased in the affected group after lisinopril, with no significant change in the unaffected group. Glomerular filtration rate (GFR) was unchanged and therefore filtration fraction fell significantly. Changes in urinary excretion of 6-keto-PGF1 alpha and kallikrein suggested that increased renal synthesis of PGI2 or activation of the renal kallikrein-kinin system were not likely to be responsible for the hemodynamic effects. The acute decrease in renal vascular resistance without change in GFR suggests that ACE inhibition may have a particular value in the treatment of hypertension associated with ADPKD which should be assessed by further long-term studies.
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PMID:Effects of angiotensin converting enzyme inhibition in adult polycystic kidney disease. 131 77

Lead may exert toxic effects on several organ systems, but those in the kidney are the most insidious. Acute lead nephropathy is characterized by proximal tubular dysfunction with the development of a Fanconi-type syndrome, alterations in mitochondrial structure and the development of cytosolic and nuclear inclusion bodies. Intracellular lead is associated with specific high affinity proteins and can also bind to metallothionein. Chronic lead nephropathy is irreversible and is typically accompanied by interstitial fibrosis, both hyperplasia and atrophy of the tubules, glomerulonephritis and, ultimately, renal failure. In addition, lead produces renal neoplasms in experimental animals. Chronic lead exposure is also implicated in the development of saturnine gout and hypertension. The metal interacts with renal membranes and enzymes and disrupts energy production, calcium metabolism, glucose homeostasis, ion transport processes and the renin-angiotensin system. This review summarizes the biochemical effects of lead on the kidney to understand the mechanisms of lead-induced nephropathy and other associated disorders.
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PMID:Lead nephrotoxicity and associated disorders: biochemical mechanisms. 131 92


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