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  • 1
    Electronic Resource
    Electronic Resource
    Effects of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 622-627 
    Details
    ISSN: 1432-1440
    Keywords: Angiotensin-converting enzyme inhibitors ; Cilazapril ; Furosemide ; Natriuresis ; Antinatriuresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The goal of this study was to quantitate the effect of angiotensin-converting enzyme inhibition on renal sodium handling after furosemide injection. The study was carried out on low and normal salt intake to assess potential interaction with salt balance. Eighteen healthy normotensive volunteers were examined in a double placebo-controlled parallel group design. Subjects were randomly put on either low-salt (20 mmol/day) or normal-salt (110 mmol/day) diet. In either arm of the diet volunteers were first treated orally with placebo for 1 week and subsequently with 2.5 mg/day of the angiotensin-converting enzyme inhibitor cilazapril for another 1 week. Cumulative 24-h urinary sodium excretion was measured on the 6th day of the respective week after sham injection and on the 7th day after injection of 40 mg furosemide. Compared to pretreatment with placebo, pretreatment with cilazapril resulted in a higher cumulative sodium excretion after furosemide injection (day 7) than after the sham injection (day 6) on both salt intakes. The difference in natriuresis (cilazapril versus placebo) was evident 2 and 3 h after injection of furosemide. Neither the time of onset nor the magnitude of antinatriuresis were affected by cilazapril. Following furosemide angiotensin II increased significantly even after cilazapril pretreatment. Cilazapril tended to reduce urinary furosemide excretion. At any given urinary furosemide concentration, the increment in urinary sodium excretion was significantly greater with cilazapril irrespective of salt intake. The study shows that (a) cilazapril increases furosemide-induced natriuresis irrespective of salt intake, (b) antinatriuresis is not affected by cilazapril, and (c) angiotensin II levels rise after furosemide on cilazapril in therapeutic doses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184489
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  • 2
    Electronic Resource
    Electronic Resource
    Pharmacokinetics and pharmacodynamics of lisinopril in advanced renal failure (1994)
    Springer
    European journal of clinical pharmacology 46 (1994), S. 537-543 
    Details
    ISSN: 1432-1041
    Keywords: Lisinopril ; Dose adjustment ; ACE inhibitors ; pharmacokinetics ; pharmacodynamics ; renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract To prevent drug accumulation and adverse effects the dose of hydrophilic angiotensin-converting enzyme (ACE) inhibitors, e. g. lisinopril, must be reduced in patients with renal failure. To obtain a rational basis for dose recommendations, we undertook a prospective clinical trial. After 15 days of lisinopril treatment pharmacokinetic and pharmacodynamic parameters were determined in patients with advanced renal failure (n=8; endogenous creatinine clearance [CLCR]: 18 ml·min−1·1.73m−2) and in healthy subjects with normal renal function (n=16; CLCR: 107 ml·min−1·1.73m−2). The volunteers received 10 mg lisinopril once daily, the daily dose in patients (1.1–2.2 mg) was adjusted to the individual CLCR according to the method of Dettli [13]. After 15 days of lisinopril treatment the mean maximal serum concentration (C max) in patients was lower than in volunteers (30.7 vs 40.7 ng·ml−1, while the mean area under the concentration-time curve (AUC 0–24 h) was higher (525 vs 473 ng·h−1·ml−1). ACE activity on day 15 was almost completely inhibited in both groups. Plasma renin activity, angiotensin I and angiotensin II levels documented marked inhibition of converting enzyme in volunteers and patients. Furthermore, average mean arterial blood pressure in patients decreased by 5 mmHg and proteinuria from 3.9–2.7 g per 24 h after 15 days of treatment with the reduced dose of lisinopril. Adjustment of the dose of lisinopril prevents significant accumulation of the drug in patients with advanced renal failure during chronic therapy. Mean serum levels did not exceed this in subjects with normal renal function receiving a standard dose. Despite substantial dose reduction, blood pressure and proteinuria decreases were observed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00196112
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  • 3
    Electronic Resource
    Electronic Resource
    Renal handling of drugs in the healthy elderly Creatinine clearance underestimates renal function and pharmacokinetics remain virtually unchanged (1999)
    Springer
    European journal of clinical pharmacology 55 (1999), S. 205-211 
    Details
    ISSN: 1432-1041
    Keywords: Key words Elderly ; Pharmacokinetics ; Renal function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Objective: It is commonly assumed that renal function, and in parallel the excretion of drugs, is considerably reduced in the elderly. Endogenous creatinine clearance or indirect estimates of this parameter are generally recommended for adapting drug dosage. The present study evaluates the validity of both assumptions. Methods: We compared pharmacokinetics (and pharmacodynamics) of 50 mg atenolol, 800 mg piracetam and 25 mg hydrochlorothiazide plus 50 mg triamterene in ten healthy young [25 (2) years] and 11 healthy elderly subjects [68 (5) years]. Inulin (Cin) and para-aminohippurate [PAH (CPAH)] clearance (infusion clearance technique), endogenous (CCr) and calculated (Cockroft-Gault) creatinine clearance, analysis of drugs and their metabolites (HPLC), were performed. Renal haemodynamics and the pharmacokinetics of β-adrenergic blocking agent, diuretics and the nootropic agent piracetam, respectively, were measured on separate days. Results: Cin was significantly (P 〈 0.01) lower in the healthy elderly subjects [104 (12) vs 120 (14) ml · min−2 · 1.73 m−2 in the young], but remained within the normal range (〉90 ml · min−2 · 1.73 m−2). In contrast, CCr was even lower in healthy elderly subjects [95 (24) vs 121 (20) ml · min−1 in the young], and the Cockroft-Gault clearance underestimated true glomerular filtration rate (GFR) even more seriously [74 (17) vs 122 (16) ml · min−1]. For atenolol the mean area under the curve (AUC) was similar in both groups [3.16 (0.48) μg · h−1 · ml−1 in the elderly vs 3.01 (0.30) in the young], as was the mean maximal plasma concentration [0.42 (0.07) vs 0.44 (0.06) μg · ml−1], but the proportion of the drug excreted in urine was marginally (P 〈 0.025) lower in the elderly. Similar results were obtained for hydrochlorothiazide, whereas no marked differences between the groups were found for triamterene and its metabolite. Furthermore, the pharmacodynamic action of diuretics was not significantly altered in the elderly. Conclusions: The true GFR of the healthy elderly remains within the normal range and is underestimated by creatinine clearance and more so by its surrogate (Cockroft-Gault clearance). In parallel, pharmacokinetics of renally excreted drugs are not affected in the healthy elderly to a clinically significant extent. For drugs with a narrow therapeutic window, indirect estimates of GFR appear to be an unreliable means for calculating correct dosage in the elderly.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002280050619
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  • 4
    Electronic Resource
    Electronic Resource
    OACE inhibition does not interfere with acute extrarenal or renal potassium disposal in chronic renal failure (1994)
    Springer
    European journal of clinical pharmacology 46 (1994), S. 185-189 
    Details
    ISSN: 1432-1041
    Keywords: ACE Inhibition ; Renal failure ; Perindoprilat ; potassium ; extrarenal disposal ; renal excretion ; hyperkalaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract The influence of angiotensin converting enzyme (ACE) inhibition on acute extrarenal and renal potassium elimination in stable chronic renal failure has been examined in 10 male patients median age 44 y; mean CLCR 42 ml·min−1·1.73 m−2. In a double blind, placebo-controlled cross-over study, K+ 0.3 or 0.4 mmol·kg−1 body weight was infused IV on two occasions while the patients also received an infusion either of placebo or 0.5 mg of the ACE inhibitor perindoprilat in random order. Plasma K+ levels and urinary K+ excretion were measured at regular intervals. During the study patients adhered to an isocaloric diet providing a standardised daily intake of potassium and sodium (50 mmol K+ and 40 mmol Na+). The median rise in plasma K+ was not significantly different after placebo (Δ K 0.66 mmol·1−1) compared with to the infusion of perindoprilat (Δ K 0.66 mmol·1−1). The median baseline urinary K+ excretion rate was 6.5 mmol·3 h−1 before the placebo infusion and 5.9 mmol·3 h−1 before infusion of perindoprilat. During the potassium load, the urinary excretion rate rose to 16.1 mmol·3 h−1 (after placebo) and 15.1 mmol·3 h−1 after perindoprilat in the first 3 h, and it returned almost to the baseline value within the next 3 h (5.6 mmol·3 h−1 after placebo and 5.7 mmol·3 h−1 after perindoprilat); the differences were not statistically significant. With perindoprilat a decrease in mean arterial blood pressure and ACE activity, an increase in renin plasma activity and a decrease in aldosterone concentrations were observed compared to the placebo infusion. There was no significant differences plasma in adrenaline or insulin levels after either infusion. Thus, ACE inhibition did not interfere either with the extrarenal or the renal disposal of an acute potassium load in patients with chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00192546
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of moxonidine on urinary electrolyte excretion and renal haemodynamics in man (1995)
    Springer
    European journal of clinical pharmacology 48 (1995), S. 203-208 
    Details
    ISSN: 1432-1041
    Keywords: Moxonidine ; Renal haemodynamics ; imidazoline receptors ; natriuresis ; blood pressure ; healthy volunteers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract Moxonidine and related compounds have been recently introduced into antihypertensive therapy. It is thought that these drugs exert their blood pressure lowering effect through interaction with nonadrenergic receptors in the central nervous system, i.e. imidazoline receptors, although the contribution of specific interaction with α2-receptors is still under debate. Imidazoline receptors have recently been documented in the renal proximal tubule. In experimental studies, interaction of imidazolines with these receptors decreased the activity of the Na+/H+ antiporter and induced natriuresis. To quantitate the effect of the imidazoline receptor agonist moxonidine on renal sodium handling and renal haemodynamics in man, we examined ten healthy normotensive males (aged 25 ± 4 years) in a double blind placebo-controlled study using a crossover design. Subjects were studied on a standardized salt intake (50 mmol per day). On the 7th and 10th study day they were randomly allocated to receive either i.v. placebo or i.v. 0.2 mg moxonidine. Urinary electrolyte excretion, lithium clearance (as an index of proximal tubular sodium handling), glomerular filtration rate (GFR), effective renal plasma flow (ERPF), renal vascular resistance (RVR), mean arterial blood pressure (MAP), plasma renin activity (PRA) and plasma noradrenaline (NA) levels were assessed. Injection of moxonidine did not increase fractional sodium excretion or lithium clearance. Specifically, antinatriuresis was not observed after injection of moxonidine despite a significant decrease in MAP from 91 to 85 mmHg and a significant increase in PRA. MAP and PRA did not change with administration of placebo. Injection of moxonidine did not affect GFR and RVR; ERPF decreased slightly but not significantly. Acute administration of 0.2 mg i.v. moxonidine decreased blood pressure in healthy volunteers on standardized salt intake, but did not affect natriuresis, proximal tubular sodium reabsorption or glomerular filtration rate. The absence of an antinatriuretic response despite a decrease in blood pressure suggests a direct facilitation of natriuresis by moxonidine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00198299
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  • 6
    Electronic Resource
    Electronic Resource
    Clinical relevance of albuminuria in hypertensive patients (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. S114 
    Details
    ISSN: 1432-1440
    Keywords: Albuminuria ; Microalbuminuria ; Proteinuria ; Essential hypertension ; Nephrosclerosis ; Renal dysfunction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Albuminuria (including the form not detectable by conventional tests, i.e., microalbuminuria) as well as renal dysfunction have recently been recognized as important complications in the patient with essential hypertension. The presence of albuminuria predicts cardiovascular events. Albuminuria is associated with more severe hypertension, with evidence of more advanced target organ damage (e.g., left ventricular hypertrophy), and is more prevalent in high-risk groups (e.g., the elderly). On the other hand, albuminuria may also be associated with generalized endothelial barrier dysfunction and thus predispose to accelerated atherogenesis. Ischemic nephropathy from nonmalignant nephrosclerosis has emerged as an important cause of terminal renal failure in the elderly patient with essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00207621
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  • 7
    Electronic Resource
    Electronic Resource
    Nephropathie bei Diabetes mellitus Typ 2 (2000)
    Springer
    Der Internist 41 (2000), S. 1363-1373 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Typ-2-Diabetes mellitus ; Nephropathie ; Mikroalbuminurie ; Arterielle Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Die renalen Komplikationen bei Patienten mit Typ-2-Diabetes wurden lange Zeit unterschätzt. Die steigende Zahl dialysepflichtiger Typ-2-Diabetiker zeigt jedoch die Bedeutung einer rechtzeitigen Diagnose, besseren Prävention und konsequenten Therapie der diabetischen Nephropathie. Dadurch kann nicht nur die Dialysepflichtigkeit verhindert bzw. verzögert werden, sondern auch das hohe kardiovaskuläre Risiko des Patienten mit Typ-2-Diabetes gesenkt werden. Die vorliegende Übersicht beschreibt zunächst die Stadien der diabetischen Nephropathie und mögliche Probleme bei der Diagnosestellung beim Typ-2-Diabetes. Anschließend werden die derzeit etablierten Ansätze zur Prävention und Therapie der Nephropathie beim Typ-2-Diabetes mellitus zusammengefasst.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050702
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  • 8
    Electronic Resource
    Electronic Resource
    Störungen des Kalzium- und Phosphathaushalts (1998)
    Springer
    Der Internist 39 (1998), S. 825-830 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Kalziumstoffwechsel ; Phosphatstoffwechsel ; Hyperkalzämie ; Hypokalzämie ; Hyperphosphatämie ; Hypophosphatämie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Bei epidemiologischen Querschnittsuntersuchungen findet sich eine Prävalenz der Hyperkalzämie von etwa 1%; sie ist somit eine relativ häufig anzutreffende Störung des Elektrolythaushalts. Durch routinemäßige Kalziumbestimmungen werden heute auch asymptomatische Verlaufsformen diagnostiziert. Da eine Hyperkalzämie ursächlich oft ein primärer Hyperparathyreoidismus oder ein Tumor zugrunde liegt, sollte diesbezüglich stets eine gründliche Abklärung erfolgen. Die Hypokalzämie ist seltener, aber ein Hyperventilationssyndrom mit Abfall des ionisierten Kalziums (Tetanie) ist relativ häufig. Eine klinisch bedeutsame Hyperphosphatämie tritt meist nur bei Patienten mit eingeschränkter Nierenfunktion auf, eine Hypophosphatämie ist gelegentlich bei intensivpflichtigen Patienten anzutreffen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050251
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  • 9
    Electronic Resource
    Electronic Resource
    Renal function and fluid-electrolyte homeostasis changes with age (1993)
    Springer
    Geriatric nephrology and urology 3 (1993), S. 107-116 
    Details
    ISSN: 1573-7306
    Keywords: renal hemodynamics ; electrolyte and water metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01509279
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  • 10
    Electronic Resource
    Electronic Resource
    Störungen des Kalzium- und Phosphathaushalts (1999)
    Springer
    Der Urologe 38 (1999), S. 285-295 
    Details
    ISSN: 1433-0563
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Eine Hyperkalzämie liegt bei einer Erhöhung der Serum-Gesamtkalziums über 2,6 mmol/l und der biologisch aktiven ionisierten Kalziumfraktion über 1,3 mmol/l vor. Bei epidemiologischen Querschnittsuntersuchungen findet sich eine Prävalenz der Hyperkalzämie von etwa 1%; sie ist somit eine relativ häufig anzutreffende Störung des Elektrolythaushalts. In der Mehrzahl der Fälle findet sich eine maligne Erkrankung oder ein primärer Hyperparathyreoidismus. Der erste diagnostische Schritt bei unklarer Hyperkalzämie ist die Messung des intakten Parathormons – ein supprimiertes Parathormon sollte immer Anlaß zum Tumorausschluß sein. Die kausale Therapie der Hyperkalzämie (Tumortherapie, Parathyreoidektomie) ist wichtigstes Ziel, eine symptomatische Therapie mittels forcierter Diurese und/oder Hemmung der Osteolyse mit Biphosphonaten sollte spätestens ab einer Serum-Kalziumkonzentration von etwa 3,0 mmol/l durchgeführt werden, um ein hyperkalzämisches Syndrom zu verhindern. Eine Hypokalzämie (Serum-Gesamtkalzium unter 2,2 mmol/l; ionisiertes Kalzium unter 1,0 mmol/l) kann Folge eines Ausfalls der PTH-Aktivität (Hypokalzämie mit Hyperphosphatämie) oder verminderter Vitamin D-Wirkung (Hypokalzämie mit Hypophosphatämie) sein. Auch ein Hyperventilationssyndrom mit Abfall des ionisierten Kalziums (Tetanie) ist relativ häufig. Der hypokalzämische tetanische Krampf wird akut mit 10%-iger Kalziumlösung i.V. behandelt. Die klinisch wichtigste Erscheinungsform einer Hyperphosphatämie (Serumphosphat-Konzentration über 1,6 mmol/l) sind metastatische Gefäß- und Organverkalkungen – vor allem bei Patienten mit eingeschränkter Nierenfunktion und autonomem Hyperparathyreoidismus. Das Risiko steigt ab einem Wert des Kalzium-Phosphat-Produktes von 5,5 mmol/l deutlich an; orale Phosphatbinder sind Mittel der Wahl. Eine klinisch relevante Hypophosphatämie liegt meistens bei einer Serumphosphat-Konzentration von unter 0,5 mmol/l vor. Eine normale Nierenfunktion vorausgesetzt, deutet eine Urin-Phosphatausscheidung unter 20 mmol/Tag auf eine verminderte gastrointestinale Absorption oder auf ein Umverteilungsproblem hin, wohingegen Werte über 50 mmol/Tag einen renalen Phosphatverlust (z.B. Störungen mit Tubuluspartialfunktionen bei Fanconi-Syndrom) anzeigen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001200050284
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