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  • 1
    Electronic Resource
    Electronic Resource
    Pharmakokinetik von Triamteren bei Probanden und Patienten mit Leber- und Nierenfunktionsstörungen (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 883-891 
    Details
    ISSN: 1432-1440
    Keywords: Triamterene ; Pharmacokinetics ; Metabolism ; Bioavailability ; Determination ; Liver disease ; Renal disease ; Age
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The knowledge about the pharmacokinetics of triamterene (TA) was limited until recently. The metabolic pathway of TA is the formation of p-hydroxytriamterene (OH-TA), which is subsequently conjugated with active sulfate to form p-hydroxytriamterene sulfuric acid ester (OH-TA-ester). The phase-II-metabolite is surprisingly pharmacologically active. TA and its metabolites were measured concomitantly by a specific and sensitive tlc-method. The i.v. kinetics of TA were determined after application of a newly developed lactic acid solution of the drug. Comparing these data with results after oral application of TA the bioavailability of TA was 52% and the extent of absorption 83%. The bioavailability of different dosage forms was correlated with in vitrotests. In liver disease the pharmacokinetics of TA are markedly altered. While in cirrhosis the hydroxylation of TA was decreased, the biliary excretion of this agent was strongly reduced in hepatitis. In renal disease the excretion of TA and OH-TA-ester was reduced proportional to the reduction of endogenous creatinine clearance. In older patients the elimination of TA was impaired.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01537528
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  • 2
    Electronic Resource
    Electronic Resource
    Excretion of the mono- and divalent ions in relation to flow rate in bartter's and pseudo bartter's syndromes in parotid saliva. comparative studies to the syndrome of conn (1972)
    Springer
    Journal of molecular medicine 50 (1972), S. 959-966 
    Details
    ISSN: 1432-1440
    Keywords: Salivary electrolytes ; Bartter's syndrome ; pseudo-Bartters syndrome ; Conn's syndrome ; Speichelelektrolyte ; Bartter-Syndrom ; Pseudo-Bartter-Syndrom ; Conn-Syndrom
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Im pilocarpinstimulierten Parotisspeichel wurde beim Bartter- (n=1), Pseudo-Bartter- (n=2) und Conn-Syndrom (n=2) die Konzentration der mono- und bivalenten Ionen als Funktion der Flußrate untersucht. Des weiteren wurde nach einem mathematischen Ansatz von Knauf und Frömter (1970) die gesamte aktive Na+-Rückresorption einer Parotis sowie die passive Leckpermeabilität des Gangsystems für Na+ berechnet. Führendes speichelchemisches Symptom desBartter- undPseudo-Bartter-Syndroms war eine Steigerung der aktiven K+-Sekretion, wobei der Normbereich um mehr als das Doppelte überschritten wurde. Die Na+-Reabsorption, die im Kontrollkollektiv mit 171±12 µ Äq/min berechnet wurde, verhielt sich unterschiedlich: leicht erniedrigt beim eehten Bartter-Syndrom, gering erhöht beim Pseudo-Bartter-Syndrom. Die flußratenbezogene Exkretion von Ca und z.T. auch Mg war bei allen Bartter-Kranken gesteigert. In ähnlicher Weise bestanden für die Anionen HCO − 3 und anorg. Phosphat deutlich erhöhte Werte. Im Unterschied zu diesen Befunden war der Elektrolyttransport beimConn-Syndrom durch eine exzessive Zunahme der Na+-Reabsorption gekennzeichnet. Trotz vermehrter Leckpermeabilität des Gangsystems wurde der Normbereich um den Faktor 2–3 überschritten. Die flußratenbezogene Konzentration von K+ und anorg. P war leicht, die des Ca stark erhöht. Erniedrigte Werte kennzeichneten die Bicarbonatsekretion — im Gegensatz zum Bartter-Syndrom. Aufgrund der qualitativen und quantitativen Differenzen in der Speichelchemie beider Krankheitsbilder ist es zweifelhaft, daß Aldosteron allein für den veränderten Elektrolyttransport beim Bartter-Syndrom verantwortlich ist.
    Notes: Summary In three patients, one with Bartter's syndrome and two with pseudo-Bartter's syndrome, the excretion pattern of mono- and divalent ions of the parotid saliva was studied as a function of flow rate. The results were compared with those observed in normal adults and in two patients with Conn's syndrome. In both Bartter's and pseudo-Bartter's syndromes, salivary K+ secretion was more than two times higher if compared with the corresponding flow rates. Other symptoms of the complex alterations of electrolyte transport in Bartter's and pseudo-Bartter's syndromes were the increased salivary excretion of calcium, magnesium, bicarbonate and inorganic phosphorus. Na+ reabsorption was slightly decreased in the patient with true Bartter's syndrome, and moderately increased in pseudo-Bartter's syndrome. The typical feature in the two patients with Conn's syndrome showed to be an excessive increase of salivary sodium reabsorption. The total amount of sodium actively reabsorbed by the duct system (J*ac), exceeded the normal range by about a factor of 2–3. Simultaneously, and in contrast to Bartter's syndrome, the flow-dependent concentrations of bicarbonate were markedly and those of magnesium slightly lower. The concentrations of potassium and inorganic phosphorus were moderately elevated, whereas those of calcium were markedly increased. Quantitative as well as qualitative differences in the salivary electrolyte patterns in these diseases provide strong arguments against an exclusive role of aldosterone in the pathogenesis of the electrolyte disturbances in Bartter's and pseudo-Bartter's syndrome. Experiments on human parotid glands clearly demonstrate that alterations of transepithelial electrolyte transport in this disease are not only confined to the different segments of the renal tubulus, but seem to be a symptom of a generalized disturbance of electrolyte transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01488069
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  • 3
    Electronic Resource
    Electronic Resource
    Modelling of electrolyte transport in renal and intestinal epithelia (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 1191-1200 
    Details
    ISSN: 1432-1440
    Keywords: Solute transport ; Leaky and tight epithelia ; Membrane porter systems ; Transport disorders ; Aminoaciduria ; Glucosuria ; Rickets ; Fanconi syndrome ; Bartter's syndrome ; Renal tubular acidosis ; Diabetes insipidus ; Chloridorrhea ; Stofftransport ; Lecke und dichte Epithelien ; Membrancarrier ; Tubulopathien ; Aminoazidurie ; Glucosurie ; Phosphatdiabetes ; Fanconi-Syndrom ; Bartter-Syndrom ; Renal-tubuläre Azidosen ; Diabetes insipidus ; Chloriddiarrhoe
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Epitheliale Strukturen können als „leck“ oder „dicht“ klassifiziert werden entsprechend ihren Eigenschaften beim Salz- und Wassertransport. Sowohl die proximalen Anteile des Nephrons wie auch des Darmtraktes gelten als „leck“, während das distale Nephron und der Dickdarm als „dichte Epithelien“ angesehen werden. Entsprechend dieser Klassifikation manifestieren sich angeborene Störungen des Stofftransportes als auch Defekte durch exogene Noxen meist in analoger Ausprägung sowohl im proximalen Nierentubulus als auch im Dünndarm. Darüberhinaus bestehen große Ähnlichkeiten in der Beeinflußbarkeit und Regulation des Salz- und Wassertransportes des distalen Nephrons wie auch des Dickdarms. In der vorliegenden Übersicht werden Modelle des Stofftransportes durch lecke und dichte Epithelien entwickelt, die auf bekannte in Säugerzellen nachgewiesene Transportsysteme zurückgreifen. Die renalen Tubulopathien als auch die intestinalen Transportstörungen werden auf Defekte der epithelialen Transportsysteme zurückgeführt.
    Notes: Summary Epithelia can be classified as “leaky” and “tight epithelia” due to their conductive properties and their modes of solute transport. Both the proximal segment of the nephron and the intestinal tract are “leaky” whereas the distal nephron and the colon are “tight”. Consequently, inborn errors and exogenous disorders of solute transport often involve both the proximal tubule and the small intestine. In addition, effects on ion and water transport in the distal nephron closely resemble those in the large intestine. Models of solute transport in leaky and tight epithelia are presented employing porter systems known in mammalian tissues. These porter systems are discussed as possible sites of transport defects and as targets for pharmacological agents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01716722
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  • 4
    Electronic Resource
    Electronic Resource
    Die Bedeutung der HCO 3 − -ATPase in der H+/HCO 3 − -Sekretion (1976)
    Springer
    Journal of molecular medicine 54 (1976), S. 97-104 
    Details
    ISSN: 1432-1440
    Keywords: H+-secretion, stomach, kidney ; HCO 3 − -secretion, pancreas, salivary glands ; membrane-bound HCO 3 − -ATPase ; pathology of buffer transport ; H+-Sekretion, Magen, Niere ; HCO 3 − -Sekretion, Pankreas, Speicheldrüse ; membrangebundene HCO 3 − -ATPase ; Störungen des Puffertransportes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Dem aktiven Puffertransport, der an Magen und Niere zur H+-Sekretion, am Pankreas und Speicheldrüse zur HCO 3 − -Sekretion führt, ist eine ATP-Phosphohydrolase zugeordnet, die typischerweise durch HCO 3 − -Ionen stimuliert wird. Im Gegensatz zur (Na+-K+)-ATPase, dem Transportenzym des Na+-Transportes, benötigt dieses Enzym nurein Ion und ist Ouabain unempfindlich. Die HCO 3 − -ATPase ist an die Plasmamembran der einzelnen Epithelien gebunden, jedoch im Gegensatz zur (Na+-K+)-ATPase luminal lokalisiert. Das Enzym ändert seine Aktivität proportional zur Rate des aktiven Puffertransportes, was seine Bedeutung als Transportenzym unterstreicht. Es werden Krankheitsbilder des gestörten Puffertransportes aufgeziegt, bei denen möglicherweise der Defekt im HCO 3 − -ATPase-System zu suchen ist.
    Notes: Summary Active buffer transport, e.g. H+-secretion by stomach and kidney and HCO 3 − -secretion by pancreas and salivary glands, is linked with the presence of a HCO 3 − stimulated ATP-Phosphohydrolase. In contrast to (Na+-K−)-ATPase which is considered to be equivalent to the Na+ pump, the HCO 3 − -ATPase requires onlyone ion for activation and is insensitive to ouabain. The HCO 3 − -ATPase is found in the plasma membrane of the epithelia, but in contrast to the (Na+-K+)-ATPase it is located in the luminal cell border. The activity of the HCO 3 − -ATPase changes in parallel along with the rate of active buffer transport, a finding which underlines its importance as a transport enzyme. Several disorders of buffer transport are described which are possibly associated with a defect of the HCO 3 − -ATPase system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01468786
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  • 5
    Electronic Resource
    Electronic Resource
    Prediction of diuretic mobilization of cirrhotic ascites by pretreatment fractional sodium excretion (1990)
    Springer
    Journal of molecular medicine 68 (1990), S. 545-551 
    Details
    ISSN: 1432-1440
    Keywords: Ascites ; Liver cirrhosis ; Xipamide ; Spironolactone ; Furosemide ; Resistance to diuretics ; Fractional sodium excretion ; Side effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a randomized prospective study the efficacy and side effects of xipamide versus the combination spironolactone/furosemide in the treatment of cirrhotic ascites were studied. Out of 27 patients four responded to a basic treatment consisting of salt and water restriction and one had to be excluded because of deterioration of kidney function. The remaining 22 patients were randomized to additional treatment with either 20 mg xipamide/day (group I) or 200 mg spironolactone/ day combined with 40 mg of furosemide every other day (group II). A response to treatment during the first 4 days was seen in 7 of 11 patients of group I versus only 3 of 11 patients in group II. In the latter group 7 of 11 patients finally responded after 8 days of treatment. Responsiveness to either diuretic treatment strongly depended on pretreatment fractional Na excretion, FENa. The resistance to diuretic treatment can be predicted by a FENa〈0.2%, and could be overcome by additional strategies known to reduce avid proximal Na reabsorption. Xipamide frequently induced hypokalemia, whereas hyperkalemia was seen following treatment with spironolactone/furosemide. Kidney function remained stable during either diuretic treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01667146
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  • 6
    Electronic Resource
    Electronic Resource
    Pharmacodynamics and kinetics of etozolin/ozolinone in hypertensive patients with normal and impaired kidney function (1984)
    Springer
    European journal of clinical pharmacology 26 (1984), S. 687-693 
    Details
    ISSN: 1432-1041
    Keywords: etozolin ; ozolinone ; furosemide ; hypertension ; renin ; catecholamines ; chronic renal failure ; steady state kinetics ; plasma levels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect on urinary electrolyte excretion, renin release and plasma norepinephrine of single oral doses of 400 mg etozolin (E) and of 40 mg furosemide (F) were studied in hypertensive patients with normal (n=6) and impaired kidney function (n=6). E caused a marked saluresis up to 24 hours, showing its long duration of action. F, however, displayed a brief, brisk peak diuresis, followed by a rebound from the 4th to the 24th hours. The brisk peak diuresis induced by F was associated with pronounced release of renin, almost twice that induced by E. In chronic renal failure the renin release in relation to the magnitude of the diuresis was increased, i.e. the sensitivity of these patients to changes in water homeostasis was increased. E and F stimulated the sympathetic system to roughly the same extent. Patients with essential hypertension had higher plasma levels of norepinephrine than hypertensive patients with chronic renal failure. In addition, hypertensive patients with normal renal function (n=4) and varying degrees of renal impairment (n=11) were also given 400 mg daily for 2 weeks. Effects on blood pressure and electrolyte homeostasis were monitored, as well as the plasma kinetics of metabolite I, ozolinone. At the end of the 2 week treatment E had significantly lowered systolic (−12 mm Hg) and diastolic (−9 mm Hg) blood pressure, and had produced a significant loss of body weight, without altering plasma electrolytes or blood chemistry. There was no accumulation of the effective metabolite ozolinone under conditions of severe impairment of kidney function. It is concluded that E can effectively control high blood pressure in patients with normal and impaired kidney function. Its effective metabolite ozolinone did not accumulate in chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00541926
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  • 7
    Electronic Resource
    Electronic Resource
    Saluretic effect of the loop diuretic torasemide in chronic renal failure (1990)
    Springer
    European journal of clinical pharmacology 39 (1990), S. 337-343 
    Details
    ISSN: 1432-1041
    Keywords: Torasemide ; chronic renal failure ; electrolyte excretion ; tubulo-glomerular feedback ; rebound ; loop diuretic ; renal function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effects of torasemide have been studied in 7 healthy controls and 9 patients with stable chronic renal failure of various degrees. After a control period of 3 days torasemide 20 mg i. v. caused a dramatic increase in diuresis and electrolyte excretion without affecting the glomerular filtration rate. The duration of action of torasemide, τ, averaged 6 h and was independent of the creatinine clearance, CLCR. When related to τ the drug-induced excretion of Cl−, Na+, K+, Ca2+ and Mg2+ showed strong linear dependence on CLCR. Both the kaliuresis and the calciuresis during τ were tightly correlated with the natriuresis over the broad range of CLCR. Similarly, the excretion of Mg2+ was dependent on the kaliuresis. The torasemide-induced kaliuresis amounted to 12% of natriuresis, as after furosemide. The kaliuretic effect of loop diuretics is smaller than that of the thiazides. After τ, e. g. over a 24 h period, kaliuresis was not correlated with natriuresis. The magnitude of the rebound effect was diminished with increasing renal impairment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00315406
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  • 8
    Electronic Resource
    Electronic Resource
    Constant K+/Na+ excretion ratio during peak diuresis after piretanide but insignificant K+ loss during 24 hours (1992)
    Springer
    European journal of clinical pharmacology 43 (1992), S. 23-27 
    Details
    ISSN: 1432-1041
    Keywords: Piretanide ; natriuresis ; kaliuresis ; chronic ; renal failure ; renal haemodynamics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of piretanide on Na+ and K+ excretion and on renal haemodynamics has been studied in 14 subjects with a GFR (Inulin clearance) ranging from 140 to 2 ml · min−1. After a two day fluid and salt balance control period, oral piretanide 6 mg induced a natriuresis and kaliuresis, which was proportional to the GFR of the patients. The ratio of drug-induced K+ to Na+ excretion was always 0.13, independent of individual GFR. This was only true for the duration of the action of piretanide,τ, which was 6 h in subjects with normal GFR and 5 h in patients with impaired kidney function. Surprisingly, afterτ, i. e. for 24 h after drug administration, less potassium was lost than in the pretreatment period. Neither the GFR nor the renal blood flow (PAH clearance) of the patients were affected by piretanide. In conclusion, piretanide given once a day was an effective natriuresic agent, even in end-stage renal disease, and it produced relatively little K+-loss when given once daily.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02280749
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  • 9
    Electronic Resource
    Electronic Resource
    Pharmacodynamics and pharmacokinetics of xipamide in patients with normal and impaired kidney function (1984)
    Springer
    European journal of clinical pharmacology 26 (1984), S. 513-520 
    Details
    ISSN: 1432-1041
    Keywords: xipamide ; electrolyte excretion ; bioavailability ; elimination ; extrarenal clearance ; chronic renal failure ; furosemide ; hydrochlorothiazide ; amiloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of a single oral dose of 40 mg xipamide on urinary excretion of Na+, K+, Cl−, Ca2+ and Mg2+ in healthy subjects and in patients with varying degrees of renal impairment was compared with various conventional diuretics. Xipamide caused marked excretion of Na+ and Cl−, whereas the diuretic produced only moderate kaliuresis; urinary excretion of Ca2+ was increased in proportion to Na+, like the loop diuretics. Xipamide affected electrolyte excretion even in patients with a creatinine clearance below 30 ml/min, as do the loop diuretics, too. Therefore, the pharmacodynamic characteristics of xipamide are more like those of a loop diuretic than of a thiazide. Xipamide was good bioavailable, its t1/2β was 7 h and urinary recovery of the undegraded drug was 40% of the given dose. In renal insufficiency, t1/2β increased from 7 to only 9 h, yielding a moderate increase in the AUC. Urinary recovery of the drug was reduced in proportion to the reduction in the creatinine clearance of the patient. Therefore, significant extrarenal elimination of the diuretic must be postulated, which suffices to prevent significant drug accumulation in renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00542150
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  • 10
    Electronic Resource
    Electronic Resource
    Delayed elimination of triamterene and its active metabolite in chronic renal failure (1983)
    Springer
    European journal of clinical pharmacology 24 (1983), S. 453-456 
    Details
    ISSN: 1432-1041
    Keywords: triameteren ; renal failure ; hydroxytriamterene sulphate ; pharmacokinetics ; plasma protein binding ; urinary excretion ; renal tubular secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The kinetics of triamterene and its active phase II metabolite were studied in 32 patients with various degrees of impaired renal function; the creatinine clearances ranged from 135 to 10 ml/min. The area under the plasma concentration-time curves (AUC) for triamterene were not influenced by kidney function, but the AUCs for the effective metabolite OH-TA-ester were significantly elevated in renal failure, indicating accumulation of the metabolite. Urinary recovery of triamterene and its metabolite over a 48 h collection period was significantly reduced in renal failure. This is considered to be due to delayed urinary excretion, corresponding to reduced renal clearance. The renal clearance of the native drug exceeded that of the metabolite, because of their different protein binding, 55% for triamterene and 91% for the metabolite. The latter is eliminated almost exclusively via tubular secretion and extrarenal elimination is less important. Administration of this antikaliuretic is therefore considered hazardous in patients with impaired kidney function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00609885
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