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11. |
Calcium Channel Antagonists and Renin Release |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 32-38
Paul C. Churchill,
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摘要:
Calcium (Ca2+) is an inhibitory second messenger in the renin secretory process, and evidence suggests that first messengers can alter Ca2+ in the renin-secreting juxtaglomerular cells by altering Ca2+ influx, efflux, and mobilization pathways. Influx of Ca2+ through voltage-operated channels is one such pathway, and it has been suggested that pressure-induced changes in renin secretion (the baroreceptor mechanism) are mediated by depolarization-induced Ca2+ influx. On this basis, renin secretion should be stimulated by organic calcium channel antagonists; however, stimulation is only occasionally observed. Therefore, other effects of these substances counteract the stimulatory effects on renin secretion.
ISSN:0250-8095
DOI:10.1159/000167540
出版商:S. Karger AG
年代:1987
数据来源: Karger
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12. |
Effect of High-Dose Aldosterone Infusions on Renal Electrolyte Excretion in Patients with Renal Insufficiency |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 33-37
Ronald J. Hené,
Hein A. Koomans,
Peter Boer,
Evert J. Dorhout Mees,
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摘要:
We investigated the effect of aldosterone infusion (0.5 mg/h for 6 h) on electrolyte excretion in 11 patients with severe renal insufficiency (creatinine clearance 6–20 ml/min), with normal or elevated serum potassium levels and a wide range of plasma aldosterone levels, and compared the data with those obtained in 7 healthy subjects. The studies were done under conditions of fixed sodium and potassium intake. In the normal subjects, aldosterone infusion caused a significant rise in potassium excretion and a significant fall in sodium and chloride excretion (p < 0.01). In 1 patient with a high plasma aldosterone, virtually no response occurred to the aldosterone infusion. In the others, the increase in potassium excretion and reduction in chloride excretion were not different from the changes observed in the normals, but the fall in sodium excretion was less due to a higher urinary sodium before infusion in the normals (p < 0.05). Fractional electrolyte excretions as well as the changes in fractional excretion by aldosterone were larger in the patients (p < 0.05). Apparently, the renal tubules of patients with chronic renal failure are still responsive to maximal stimulation with aldosterone, in spite of their basically elevated fractional electrolyte output. These findings suggest that, with some exceptions, the hyperkalemia in patients with chronic renal failure is in part due to relative hypoaldosteronis
ISSN:0250-8095
DOI:10.1159/000167426
出版商:S. Karger AG
年代:1987
数据来源: Karger
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13. |
Successful Treatment of Pseudomonas Peritonitis during Continuous Ambulatory Peritoneal Dialysis |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 38-43
Vo Nguyen,
Richard D. Swartz,
Janice Reynolds,
Dorinda Wilson,
Friedrich K. Port,
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摘要:
Successful eradication of Pseudomonas peritonitis is described in 12 (57%) of 21 cases from a large continuous ambulatory peritoneal dialysis (CAPD) program at a tertiary care center. In successful cases, cure was achieved within 17 days using therapy which included aminoglycoside started routinely at the onset of symptoms and an antipseudomonal penicillin or cephalosporin derivative added as soon as pseudomonas infection was identified on culture. Of the 9 treatment failures which required catheter removal, 2 had failure of peritoneal drainage, 4 had infection with multiple and/or drug-resistant Pseudomonas strains, and 3 had persistent catheter tunnel infection which resulted in recurrent Pseudomonas peritonitis. Factors such as diabetes mellitus and pediatric age group did not prevent successful medical therapy. Predisposing factors favoring development of Pseudomonas peritonitis included technical failures and in a few cases recent antibiotic therapy. We conclude that Pseudomonas peritonitis complicating CAPD can be successfully cured without catheter removal or discontinuation of CAPD in many cases, particularly when complicating factors are not present.
ISSN:0250-8095
DOI:10.1159/000167427
出版商:S. Karger AG
年代:1987
数据来源: Karger
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14. |
Calcium-Channel-Blocking Drugs and Renal Sodium Excretion |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 39-43
Friedrich C. Luft,
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摘要:
The administration of calcium-blocking drugs exerts a natriuretic response. Acute studies in isolated perfused kidneys and in experimental animals, as well as in man, consistently demonstrate diuresis, natriuresis, calciuresis, and generally kaliuresis, even in the face of arterial blood pressure reduction. Clearance methodology suggests that calcium-blocking drugs exert their natriuretic response by exerting hemodynamic effects, as well as by acting directly on the proximal tubule. Micropuncture studies and experiments utilizing the toad urinary bladder suggest that calcium-blocking drugs impair sodium reabsorption in the distal tubule. Chronic studies in both animals and man, in which sequential urine collections were made in the face of a known sodium intake, corroborate the natriuretic effects of calcium-blocking drugs. Moreover, these studies suggest that the effects of these medications are likely to be clinically important.
ISSN:0250-8095
DOI:10.1159/000167541
出版商:S. Karger AG
年代:1987
数据来源: Karger
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15. |
Nifedipine, Sodium Intake, Diuretics, and Sodium Balance |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 44-48
Graham A. MacGregor,
Joe B. Pevahouse,
Francesco P. Cappuccio,
Nirmala D. Markandu,
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摘要:
The acute blood pressure-lowering effect of nifedipine was studied in patients on high, normal, and low sodium diets. The demonstrated decrease in blood pressure was greatest in those patients receiving the high sodium diet. Studies were then performed with a combination of nifedipine and the diuretic bendrofluazide. When nifedipine was given to patients already on bendrofluazide, there was an additional fall in blood pressure. However, when bendrofluazide was added to the regimen of patients already receiving nifedipine, there was no further reduction in blood pressure. Studies were then performed in patients receiving chronic nifedipine therapy who had their nifedipine treatment stopped while on a fixed sodium intake. All patients retained sodium and there was an increase in weight. This latter study confirms that nifedipine causes a long-term reduction in sodium balance in patients with essential hypertension. It is possible that these long-term changes in sodium balance with nifedipine could partially explain the blunting of the blood pressure-lowering effect seen when the thiazide diuretic was added to the regimen of patients already receiving nifedipine.
ISSN:0250-8095
DOI:10.1159/000167542
出版商:S. Karger AG
年代:1987
数据来源: Karger
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16. |
Early Patent and Proprietary Medicines and the Treatment of Kidney and Urinary Tract Diseases |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 45-48
Eugene E. Cunningham,
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ISSN:0250-8095
DOI:10.1159/000167429
出版商:S. Karger AG
年代:1987
数据来源: Karger
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17. |
Do Calcium Channel Blockers Protect against Renal Ischemia? |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 49-56
Jules B. Puschett,
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摘要:
Data from several studies have indicated that calcium channel blockers may prevent acute renal damage caused by ischemia. If this is true, then the obvious clinical application of this premise would be in surgical cases requiring cross-clamping of the aorta, or in patients experiencing prolonged hypotension. Evidence for the mechanism by which calcium channel blockers mitigate injury include the prevention or amelioration of renal vasoconstriction and/or their ability to inhibit calcium entry into cells, thereby possibly preventing toxic calcium ‘overload’. Studies of animal models examining ischemic acute renal failure produced either by infusion of vasoconstrictors or by interrupting renal artery blood flow have provided conflicting results. Certain calcium channel blockers afford some degree of protection only when administered prior to the ischemic episode, while others may protect even if given after the insult. Several investigations have been carried out to determine the mechnism(s) of this protective effect. The results indicate cellular calcium accumulation occurs in cells during the anoxic period; this is most pronounced during reflow. This accumulation of calcium appears to be temporally related to both mitochondrial dysfunction and cell death. The ability of the calcium channel blockers to prevent calcium entry into cells may explain their role in protecting the cell and ameliorating ischemic inj
ISSN:0250-8095
DOI:10.1159/000167543
出版商:S. Karger AG
年代:1987
数据来源: Karger
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18. |
Unilateral Nodular Diabetic Glomerulosclerosis: Recurrence of an Experiment of Nature |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 55-59
Vincent C. Béroniade,
René Lefebvre,
Pierre Falardeau,
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摘要:
The case of a 60-year-old diabetic patient with a fully developped diabetic glomerulosclerosis in one kidney, but only ischemic lesions in the contralateral one, which was ‘protected’ by a renal artery stenosis, is presented. The only other report of such a peculiar observation was made by Berkman and Rifkin on a patient who died in 1940. Because of the rather high incidence of diabetes and of renal artery stenosis, the scarcity of this ‘experiment of nature’ is astonishing and can be barely explained by a precise timing of the two pathological conditions. Despite rather detailed information on the clinical and paraclinical evolution of the present patient, the exact sequence of events could not be determined with certitude. Both cases bring a strong support for the role of glomerular hyperperfusion-hypertension in the pathogenesis and evolution of diabetic nephropathy and provide a theoretical basis for the importance of keeping the arterial pressure low in di
ISSN:0250-8095
DOI:10.1159/000167431
出版商:S. Karger AG
年代:1987
数据来源: Karger
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19. |
Calcium Channel Blockers in Systemic Hypertension |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 57-66
William H. Frishman,
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摘要:
Calcium channel blockers selectively inhibit transmembrane flux of calcium in excitable tissue. Their ability to block calcium-mediated electromechanical coupling in contractile tissue produces peripheral vasodilation and has led to their clinical use in patients with systemic hypertension. The drugs appear to be well tolerated and have excellent safety profiles. Sustained-release preparations allow the drugs to be used once or twice daily. The calcium channel blockers will play an important role in the management of patients with mild, moderate, and severe hypertension when used as monotherapy or when combined with other antihypertensive medications. They can also be used in patients with concomitant diseases, such as angina pectoris and arrhythmia.
ISSN:0250-8095
DOI:10.1159/000167544
出版商:S. Karger AG
年代:1987
数据来源: Karger
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20. |
Recurrent Hemolytic Uremic Syndrome and Metastatic Malignancy |
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American Journal of Nephrology,
Volume 7,
Issue 1,
1987,
Page 60-64
Jacques J. Sennesael,
Katherina M. Vanden Houte,
Herbert D. Spapen,
Roger M.G. de Bruyne,
Dierik L. Verbeelen,
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摘要:
A 64-year-old patient with a prostatic adenocarcinoma presented two well-documented episodes of hemolytic-uremic syndrome (HUS) occurring 8 months apart and resolving without renal sequelae. The temporal relationship between these episodes and the natural progression of the underlying disease as well as the absence of chemotherapy favor the hypothesis of cancer-associated HUS. The clinical, laboratory and pathological findings of this patient and 3 additional patients reported in the literature are discussed. These cases suggest that malignancy should be suspected in adults developing the HUS and that this form of HUS need not have a poor prognosis despite progressive cancer.
ISSN:0250-8095
DOI:10.1159/000167432
出版商:S. Karger AG
年代:1987
数据来源: Karger
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