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  • 1
    Electronic Resource
    Electronic Resource
    Abnormal radiofurosemide binding by Tamm Horsfall glycoprotein of diabetic patients (1985)
    Springer
    Diabetologia 28 (1985), S. 827-830 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; renal sodium transport ; Tamm Horsfall glycoprotein ; furosemide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the present study, 8 Type 1 diabetic patients with normal creatinine clearance and 8 matched controls were examined. Tamm Horsfall glycoprotein was isolated with the NaCl precipitation procedure. Its purity was checked by gelelectrophoresis, immunodiffusion and isoelectric focussing. Tamm Horsfall glycoprotein of diabetic patients had higher glucose (p〈0.05) and lower N-acetylneuraminic acid content (p〈0.01) than controls. 14C-furosemide binding by Tamm Horsfall glycoprotein was examined using an Amicon ultrafiltration system at 0 °C. In nominally sodium-free medium, furosemide binding by Tamm Horsfall glycoprotein was significantly (p〈0.01) higher in diabetic patients than in matched controls. The increment of binding capacity with sodium was similar in controls and diabetic patients so that maximal binding capacity in a NaCl system was 1.7±0.3 in controls and 3.64±0.5 in diabetic patients (p〈0.025). Half maximal furosemide binding by Tamm Horsfall glycoprotein occured at 1.4±0.2mmol Na/l in controls and 0.52±0.12 in diabetic patients (p〈0.01). Abnormal radiofurosemide binding of Tamm Horsfall glycoprotein of diabetic patients may be the consequence of abnormal postribosomal modification of the glycoprotein which is synthesized in an insulin- and glucose-sensitive nephron segment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00291072
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  • 2
    Electronic Resource
    Electronic Resource
    Blood pressure and metabolic control as risk factors for nephropathy in Type 1 (insulin-dependent) diabetes (1985)
    Springer
    Diabetologia 28 (1985), S. 6-11 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; diabetic nephropathy ; blood pressure ; metabolic control
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The respective rôles of arterial blood pressure and metabolic control in different stages of diabetic nephropathy were analyzed retrospectively in 52 sequentially-followed Type 1 (insulin-dependent) diabetic patients. A negative correlation was found between median post-prandial blood glucose and median duration of diabetes until onset of persistent proteinuria (p〈0.01). Systolic blood pressure was higher in patients who subsequently developed persistent proteinuria than those who did not (140 versus 121 mmHg; p〈0.05), but duration of the interval until onset of persistent proteinuria was not related to blood pressure. After onset of persistent proteinuria, hypertensive diabetic patients developed elevated serum creatinine concentrations more frequently than normotensive diabetic patients (67% versus 14%, p〈0.05). In these patients, the delay until elevation of serum creatinine concentration was negatively correlated with blood glucose (p〈0.01). Once serum creatinine was raised, decay of renal function occurred faster in patients with persistent than intermittent hypertension (p〈0.05). No effect of metabolic control was demonstrable at this stage of nephropathy. It is concluded that metabolic control determines the early course of diabetic nephropathy, whereas blood pressure is more important in advanced stages of nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276992
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  • 3
    Electronic Resource
    Electronic Resource
    Medikamentöse Behandlung der chronisch verlaufenden Glomerulonephritiden: Contra (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 978-987 
    Details
    ISSN: 1432-1440
    Keywords: Glomerulonephritis ; Extramembraneous glomerulonephritis ; Membranoproliferative glomerulonephritis ; Lupus erythematosus ; Steroids ; Antiplatelet agents ; Glomerulonephritis ; Extramembranöse Glomerulonephritis ; Membranoproliferative Glomerulonephritis ; Lupus erythematodes ; Steroide ; Plättchenhemmer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Thema der therapeutischen Beeinflussung der entzündlichen Pathomechanismen bei chronisch-idiopathischer Glomerulonephritis bedarf einiger kritischer Anmerkungen. Eine ätiologische Behandlung ist nur in Ausnahmefällen möglich (infektiöse Tropenkrankheiten, infizierter ventrikuloatrialer Shunt etc.). Einer erfolgreichen Beeinflussung der Pathomechanismen, welche die glomeruläre Entzündung auslösen und unterhalten, steht unsere Unkenntnis über die im einzelnen verantwortlichen Schritte entgegen. Neuere Untersuchungen legen Schlüsselrollen für die terminale Komponente des Komplementsystems, Produkte des Lipoxygenaseabbauweges der Arachidonsäure sowie Sauerstoffradikale nahe, welche therapeutisch nicht oder nur beschränkt beeinflußbar sind. Ferner beruht die Progredienz glomerulärer Entzündungen in die Niereninsuffizienz in der Regel auf fortschreitender Sklerosierung von Glomerulus, Gefäßen und Interstitium und nicht auf zunehmenden aktiv entzündlichen glomerulären Läsionen. Beispielhaft wurden bei der Sichtung der veröffentlichten kontrollierten Therapiestudien die Untersuchungen bei extramembranöser und membranoproliferativer Glomerulonephritis herausgegriffen. Hierbei wurde eine im Ausmaß nur beschränkte, und nicht in allen Studien gesicherte, Beeinflussung der Nierenfunktion gefunden, der andererseits erhebliche Nebenwirkungen gegenüberstehen. Eine abschließende Wertung kommt zu dem Urteil, daß eine medikamentöse Beeinflussung der entzündlichen Pathomechanismen fragwürdig ist, daß jedoch ein therapeutischer Nihilismus nicht angezeigt ist angesichts der Beeinflußbarkeit unspezifischer Schädigungsmechanismen (antihypertensive Behandlung, diätetische Intervention).
    Notes: Summary It is controversial whether the pathomechanisms involved in chronic idiopathic glomerulonephritis are susceptible to therapeutic intervention. Etiological therapy, i.e. elimintion of the responsible antigen, is possible only in exceptional cases, e.g. tropical diseases, infected ventriculoatrial shunt etc. Antiinflammatory therapy directed against pathomechanisms initiating or maintaining glomerular inflammation has an uncertain theoretical foundation because of lack of knowledge relating to the exact steps mediating tissue injury. Recent studies suggest keyroles for terminal components of complement system, products of lipoxygenase pathway of arachidonic acid and oxygen radicals — all of which are not readily influenced by available therapeutic modulaties. Finally, progression of glomerular inflammation to renal failure is usually not the cause of cumulative acute inflammatory glomerular lesions but rather the consequence of progressive sclerosis of glomeruli, arterioles and interstitium. As examples of controlled intervention trials, studies on extramembranous and membranoproliferative glomerulonephritis are discussed. The studies show limited and not always statistically significant influence on renal function, however, at the expense of considerable side effects. It is concluded that it is highly questionable whether inflammatory pathomechanisms are influenced by currently available drugs. However, therapeutic nihilism is not appropriate given modalities to influence mechanisms of nonspecific damage, e.g. by antihypertensive medication or dietary intervention.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01738153
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  • 4
    Electronic Resource
    Electronic Resource
    Nierenfunktion bei Bleibelastung (1986)
    Springer
    Journal of molecular medicine 64 (1986), S. 871-875 
    Details
    ISSN: 1432-1440
    Keywords: Lead ; Gout ; Renal failure ; Hyperparathyroidism ; Blei ; Gicht ; Niereninsuffizienz ; Hyperparathyreoidismus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Schrumpfnierenbildung bei Blei-Intoxikation (Nephropathia saturnina) wird derzeit praktisch nicht mehr beobachtet. Trotzdem hat in den letzten Jahren die Besorgnis zugenommen, daß die vor allem durch umweltbedingte Faktoren gestiegene Bleibelastung langfristig zu Hochdruck und Nierenfunktionsveränderungen führen kann, selbst wenn klinisch manifeste Symptome einer Intoxikation fehlen. Diese Besorgnis stützt sich (a) auf epidemiologische Untersuchungen, in denen ein Zusammenhang zwischen Blut-Bleispiegeln und Blutdruck gefunden wurde; (b) auf experimentelle Untersuchungen, in denen Blei verschiedene pressorische Mechanismen aktivierte; (c) sowie auf den häufigen Nachweis erhöhter Bleibelastung bei Patienten mit Niereninsuffizienz, insbesondere wenn gleichzeitig eine Gicht vorliegt. Aus verschiedenen Gründen sind die angeführten Befunde zur nephrotoxischen und Blutdrucksteigernden Wirkung bei dem gefundenen Grad der Bleibelastung nicht beweisend. Weitere Untersuchungen zur Klärung der Frage sind zweifellos von hoher gesundheitspolitischer Bedeutung.
    Notes: Summary Renal failure as a consequence of manifest lead intoxication (nephropathia saturnina) has almost completely desappeared in the FRG. However, there has been rising concern that increased lead burden, primarily as a result of environmental pollution, may adversely affect blood pressure and renal function even in the absence of extrarenal signs of lead intoxication. Such concern is based on epidemiological studies which demonstrated a relation between blood lead level and blood pressure and on experimental studies which showed that lead activates several pressor mechanisms. Furthermore, increased body lead burden is found in a substantial proportion of patients with renal failure, particularly when concomitant gout is present. Unfortunately, none of the above findings constitute irrefutable evidence and further studies are clearly necessary.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01725560
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  • 5
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of ramipril in hypertensive patients with renal insufficiency (1989)
    Springer
    European journal of clinical pharmacology 37 (1989), S. 249-256 
    Details
    ISSN: 1432-1041
    Keywords: ramipril ; renal insufficiency ; hypertension ; pharmacokinetics ; ramiprilat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary In an open trial, the pharmacokinetics of ramipril and its active metabolite ramiprilat were studied in 25 hypertensive patients with various degrees of renal insufficiency given 5 mg ramipril p.o. for 14 days. Ramipril was rapidly absorbed and reached a peak concentration after 1–2 h. Cmax was greater in patients with severe renal insufficiency, which might indicate a reduced renal elimination rate, although, the rapid decline of the concentration-time curve for ramipril was almost independent of renal function. The mean initial apparent half-lives on Days 1 and 12, respectively, were 2.8 and 3.4 h (Group I: creatinine clearance 5–15 ml/min), 1.8 and 2.3 h (Group II: creatinine clearance 15–40 ml/min), and 1.9 and 1.9 h (Group III: creatinine clearance 40–80 ml/min). No accumulation was observed after multiple dosing. In contrast, the kinetics of its active acid metabolite ramiprilat was significantly influenced by renal function. The mean times to the peak plasma concentration were 5.7 h in Group I, 4.4 h in Group II and 3.8 h in Group III. The initial decline in plasma ramiprilat was dependent upon renal function; the mean initial apparent half-lives (Days 1 and 12, respectively) were 16.0 and 14.8 h (Group I), 10.1 and 9.5 h (Group II) and 10.6 and 8.0 h (Group III). Mean trough concentrations and absolute accumulation also increased with worsening renal function, and the renal clearance of ramiprilat was significantly correlated with the creatinine clearance. The subsequent long terminal phase at low plasma ramiprilat concentrations represented slow dissociation of the ACE-inhibitor complex. The study indicates that in patients with severe renal insufficiency (creatinine clearance below 30 ml/min) smaller doses of ramipril are required than in patients with normal or borderline renal function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00679779
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  • 6
    Electronic Resource
    Electronic Resource
    Role of diuretics, hormonal derangements, and clinical setting of hyponatremia in medical patients (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 662-669 
    Details
    ISSN: 1432-1440
    Keywords: Hyponatremia ; Vasopressin ; Thirst ; Diuretics ; Cardiac failure ; Cirrhosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Because hyponatremia is frequently associated with preceding diuretic treatment and unrestricted fluid indake — conditions which have not been addressed sufficiently in published literature — we studied the pathophysiology and the clinical setting of such hyponatremia in a large group of internal medicine patients. We observed: a) Of an initial 310 patients with chemical hyponatremia only 204 (64%) had an associated plasma hypoosmolality. Sience a normal plasma osmolality excludes a disturbance of water metabolism only the 204 patients with hypoosmolar hyponatremia were included in the study. This data shows that plasma osmolality is an essential measurement in any evaluation of hyponatremia. b) In 204 consecutive patients with hypoosmolar hyponatremia the electrolyte disturbance was related to advanced congestive cardiac failure in 25%, decompensated liver cirrhosis in 18%, volume contraction in 28%, syndrome of inappropriate antidiuretic hormone secretion in 19% and renal insufficiency in 4%. c) Plasma vasopressin was measurable in 90% of the 204 patients. It is known that radioimmunoassays to measure vasopressin fail to reliably detect low concentrations of circulating vasopressin (〈0.5 pg/ml). It may therefore be stated that hypoosmolar hyponatremia was generally characterized by a failure of antidiuretic hormone suppression. d) Mean daily fluid intake of hyponatremic patients was 2.35±0.15 l. In the presence of stimulated vasiopressin this large a fluid intake is bound to worsen the severity of hyponatremia. e) Of 204 patients 126 were treated with diuretics at the time of study. In these patients hyponatremia worsened during such treatments and was associated with evidence of prerenal azotemia. However there were no significant differences between diuretic-treated and -untreated patients with respect to plasma vasopressin stimulation and amount of fluid intake. In conclusion, stimulated vasopressin and high fluid intake explain the hyponatremia observed in the present study. This applied similary to diuretictreated and -untreated patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01726923
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  • 7
    Electronic Resource
    Electronic Resource
    Renin-Angiotensin System beim diabetischen Patienten (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 883-891 
    Details
    ISSN: 1432-1440
    Keywords: Diabetes mellitus ; Renin ; Angiotensin II ; ACE inhibitors ; Renal function ; Blood pressure ; Diabetes mellitus ; Renin ; Angiotensin II ; ACE-Hemmer ; Nierenfunktion ; Blutdruck
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird eine Übersicht gegeben über in der Literatur berichtete Befunde bei Diabetikern bezüglich der Aktivität der Komponenten des Renin-Angiotensin Systems (RAS), der Organansprechbarkeit auf Angiotensin II (ANG II), des ANG II-Rezeptorbestandes und der Auswirkungen einer Hemmung des RAS durch Angiotensin I Konversionsenzym (ACE)-Hemmer. Die Literaturübersicht zeigt, in Übereinstimmung mit eigenen Befunden, daß die Aktivität des RAS bei Diabetikern mit ausreichender Stoffwechselkontrolle normal oder eher gesteigert ist. Auch beim nephropathischen Diabetiker wird eine erhöhte, aber auch eine verringerte Aktivität des RAS angegeben. Dies widerspricht der häufig vorgetragenen Vermutung, daß das RAS bei Diabetes mellitus generell supprimiert und funktionell inaktiv ist. Letzteres wurde vor allem aus Befunden eines erniedrigten ANG II-Rezeptorbestandes bei anorektischen, schwerst hyperglykämischen Ratten geschlossen. Diese Befunde lassen sich beim Menschen nicht bestätigen, wo eher ein erhöhter ANG II-Rezeptorbestand beobachtet wurde. Dies steht im Einklang mit den häufigen Berichten, daß die Pressorantwort auf infundiertes ANG II beim Diabetiker deutlich gesteigert ist. Die gesteigerte Ansprechbarkeit hat wahrscheinlich funktionelle Bedeutung, da beim Diabetiker trotz eines erhöhten Körper-Natriumbestandes das RAS dennoch nicht, wie erwartet, supprimiert ist. Eine Reihe von Befunden sprechen auch dafür, daß die Widerstandsgefäße der Niere beim Diabetiker auf AN-G II vermehrt ansprechen. Hier könnte möglicherweise eine Ursache für die Hyperfiltration liegen. Jedenfalls wird übereinstimmend eine Verminderung der Mikroalbuminurie nach Hemmung des RAS mit ACE-Hemmern gefunden, ein möglicher indirekter Hinweis auf eine Verminderung des glomerulären kapillären Drucks.
    Notes: Summary We review available data on the activity of the renin-angiotensin system (RAS), responsiveness to angiotensin II (ANG II), ANG II receptor number, and effects of inhibition of the RAS by angiotensin I converting enzyme (ACE) inhibitors in patients with diabetes mellitus. Most authors, including ourselves, observed a normal or enhanced activity of the RAS in metabolically stable diabetics. Increased but also reduced activity of the RAS was described in nephropathic diabetes. This is in contrast to the common suggestion that the RAS of diabetics is generally suppressed and functionally inactive. The last assumption was mainly based on the finding of reduced ANG II receptor numbers in anorectic, severely hyperglycemic rats. These findings could not be reproduced in man, and a higher ANG II receptor concentration on platelets of diabetics goes in parallel with the frequent finding of an enhanced pressor response to infused ANG II in diabetes. This increased responsiveness is most probably of functional importance since the RAS is not suppressed — as one would expect — in the face of a supranormal body sodium content. A number of data also indicate that renal resistance vessels display increased responsiveness to ANG II in diabetics. This may be a reason for hyperfiltration. This notion is further supported by the reduction of albuminuria which is usually observed following inhibition of the RAS with ACE inhibitors, and which may be an index of reduction of glomerular capillary pressure in human diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01728950
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