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  • 1
    Electronic Resource
    Electronic Resource
    Angiotensinase A gene expression and enzyme activity in isolated glomeruli of diabetic rats (1996)
    Springer
    Diabetologia 39 (1996), S. 275-280 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418342
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  • 2
    Electronic Resource
    Electronic Resource
    Angiotensinase A gene expression and enzyme activity in isolated glomeruli of diabetic rats (1996)
    Springer
    Diabetologia 39 (1996), S. 275-280 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy. [Diabetologia (1996) 39: 275–280]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00418342
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  • 3
    Electronic Resource
    Electronic Resource
    Angiotensin converting-enzyme inhibitor treatment reduces glomerular p16INK4 and p27Kip1 expression in diabetic BBdp rats (1999)
    Springer
    Diabetologia 42 (1999), S. 1425-1432 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy, cyclin-dependent kinase inhibitors, glomerular hypertrophy, cell cycle arrest, angiotensin II, progression of renal failure.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Renal hypertrophy occurs early in diabetes mellitus and precedes the development of glomerulosclerosis and tubulointerstitial fibrosis. We have previously shown that cultured mesangial cells exposed to high glucose are arrested in the G1-phase of the cell cycle and undergo cellular hypertrophy. High glucose-mediated induction of p27Kip1, an inhibitor of cyclin-dependent kinases, is essential in this process. Further investigations have also shown that p27Kip1 and p21Cip1, other cyclin-dependent kinase inhibitors, are up regulated in the kidneys of mice with Type I (insulin-dependent) as well as Type II (non-insulin-dependent) diabetes mellitus. Our study was undertaken to test a potential effect of short-term treatment with the angiotensin-converting enzyme inhibitor enalapril on the glomerular expression of the cyclin-dependent kinase inhibitors p16INK4, p21Cip1, and p27Kip1 in BBdp rats, an autoimmune model of Type I diabetes.¶Methods. We evaluated p16INK4, p21Cip1, and p27Kip1 protein expression in isolated glomeruli by western blots. We also assessed p27Kip1 positive glomerular cells by immunohistochemistry.¶Results. Glomerular expression of all three cyclin-dependent kinase inhibitors were stimulated in BBdp rats compared with non-diabetic BBdr animals. Enalapril treatment for 3 weeks, started after the onset of diabetes, reduced the glomerular expression of p16INK4 and p27Kip1 but not of p21Cip1. Enalapril also prevented the increase in kidney weights observed in BBdp rats but had no effect on systolic blood pressure or glucose concentrations.¶Conclusion/interpretation. Our data show that enalapril attenuates the glomerular expression of cyclin-dependent kinase inhibitors in diabetes and suggest a molecular mechanism of how angiotensin-converting enzyme inhibitors prevent renal hypertrophy in diabetes. [Diabetologia (1999) 42: 1425–1432]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051314
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  • 4
    Electronic Resource
    Electronic Resource
    Sodium chloride as regulator of renal prostaglandin E2 production in patients with essential hypertension (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 579-581 
    Details
    ISSN: 1432-1440
    Keywords: Renal prostaglandins ; Essential hypertension ; Sodium choride intake ; Renale Prostaglandine ; essentielle Hypertonie ; Kochsalzdiät
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 16 Patienten mit essentieller Hypertonie wurde der Einfluß diätetischer Kochsalzzufuhr (5 Tage NaCl-arm, 4 Tage NaCl-reich) auf den Blutdruck (BD), die Plasmareninaktivität (PRA) und die Urinausscheidung von Prostaglandin E2 und F2α untersucht. Kochsalzarme Kost (35 mEq/24 h) erniedrigte den systolischen und diastolischen Blutdruck von 162±11 auf 145±10 mm Hg bzw. 102±6 auf 90±9 mm Hg. Anschließende kochsalzreiche Kost erhöhte den systolischen und diastolischen Blutdruck wieder auf 167±14 bzw. 102±10 mm Hg. Die PRA stieg unter Kochsalzrestriktion von 0,83±0,33 auf 2,82±1,12 ng/AI/ml/h und fiel unter hoher Natriumzufuhr wieder auf 0,45±0,31 ng AI/mI/h ab. Na-Verarmung steigerte die Urinausscheidung von Prostaglandin E2 von 151±76 auf 328±94 ng/24 h. Am vierten Tag der kochsalzreichen Diät war die PGE2-Ausscheidung wieder auf 114±41 ng abgefallen. Die Prostaglandin-F2α-Urinausscheidung wurde während des Versuches nicht signifikant beeinflußt. Die Ergebnisse zeigen, daß diätetische Kochsalzzufuhr die renale PGE2-Produktion bei Patienten mit essentieller Hypertonie beeinflußt. Die erniedrigte PGE2-Synthese unter Bedingungen hoher Kochsalzzufuhr könnte eine Rolle bei der Regulation des renalen Gefäßwiderstandes der Niere spielen und pathogenetische Bedeutung bei der chronischen Hochdruckkrankheit besitzen.
    Notes: Summary The effect of dietary sodium intake (5 days' low salt, 4 days' high salt) on 24-h urinary prostaglandin E2 (PGE2) and prostaglandin F2α (PGF2α) excretion, blood pressure (BP), and plasma renin activity (PRA) was evaluated in 16 patients with essential hypertension. Sodium restriction significantly increased urinary PGE2 excretion (p〈0.05) from 151±76 to 328±94 ng/24 h, while high salt intake reduced renal PGE2 production to 114±41 ng/24 h (p〈0.05). There was a moderate but not significant increase in urinary PGF2α excretion on the low salt regimen, which was reversed under high salt diet. Systolic and diastolic blood pressure fell from 162±11 to 145±10 mm Hg, i.e., 102±6 to 90±9 mm Hg on low sodium intake (35 mEq/day) and returned to levels close to control after 4 days on a high salt diet (250 mEq/day). Under low salt conditions, PRA increased significantly (p〈0.001) from 0.83±0.33 to 2.82±1.12 ng AI/ml/h and fell to 0.45±0.31 ng AI/ml/h on high salt regimen (p〈0.001). The results demonstrate that dietary sodium chloride intake modulates renal PGE2 production in patients with essential hypertension. The depressed PGE2 production under high salt conditions may play a role in regulation of renal vascular resistance and influence sustainment of chronic hypertensive disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01724215
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  • 5
    Electronic Resource
    Electronic Resource
    Die Bedeutung von Eicosanoiden bei glomerulären Erkrankungen (1986)
    Springer
    Journal of molecular medicine 64 (1986), S. 813-823 
    Details
    ISSN: 1432-1440
    Keywords: Prostanoids ; Leukotrienes ; Glomerular Disease ; GFA ; Proteinurie ; Prostanoide ; Leukotriene ; Glomerulopathien GFR ; Proteinurie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Eicosanoide sind Syntheseprodukte der Zyklooxygenase und Lipoxygenase, Enzymkomplexe, die in fast allen Körperzellen vorkommen und ihr Hauptsubstrat, die mehrfach ungesättigte Arachidonsäure (AS), verstoffwechseln. Prostaglandine (PG) E2, I2 und Thromboxan (Tx) A2 sind Zyklooxygenaseprodukte mesangialer und epithelialer Zellen des Glomerulus, die direkte und indirekte vasodilatatorische und vasokonstriktorische Effekte am Glomerulus ausüben. Vasodilatatorische Prostaglandine E2 und I2 sind verantwortlich für die Aufrechterhaltung der GFR bei kritischer renaler Perfusion. Diese Prostanoide (PGE2 und PGI2) vermitteln darüberhinaus aber auch die glomeruläre Hyperperfusion nach experimenteller Nierenablation und bei Patienten mit chronischen Glomerulopathien. Die Induktion verschiedener tierexperimenteller Glomerulonephritiden steigert die glomeruläre PG- und Txsynthese. Der stimulatorische Einfluß auf den vasokostriktorischen Metaboliten TxA2 ist ausgeprägter als auf die Synthese der vasodilatatorischen PGE2 und I2. Einige Befunde weisen darauf hin, daß die erhöhte glomeruläre TxA2 Produktion mitverantwortlich ist für die reduzierte GFR, die bei experimentellen Nephritiden beobachtet wird. Bei einer Reihe von Glomerulopathien des Menschen ist die Produktion vasodilatatorischer Prostaglandine gesteigert. Die Gabe eines Zyklooxygenasehemmers führt bei diesen Patienten zur Reduktion der Proteinurie. Neben hämodynamischen Effekten scheint die erhöhte vasodilatatorische PG Produktion bei diesen Patienten auch die Permselektivität der glomerulären Filtrationsbarriere zu beeinflussen. Hauptsyntheseorte für Lipoxygenaseprodukte sind Granulozyten und Monozyten. Pharmakologische Untersuchungen zeigen, daß Lipoxygenaseprodukte (Leukotriene) vasokonstriktorische Effekte am Glomerulus haben. Leukotriene beeinflussen darüberhinaus das Wachstum mesangialer Zellen in Kultur und erhöhen die Adhäsion von Monozyten an mesangiale Zellen. Sie können deshalb bei zellvermittelten Glomerulonephritiden von Bedeutung sein.
    Notes: Summary Prostanoids are local cyclooxygenase products, synthesized by mesangial and epithelial cells of the glomerulus as well as by a variety of inflammatory cells and platelets. Prostaglandins and thromboxane have direct vasodilatory and vasoconstrictory effects and can modulate glomerular function. Arachidonic acid, the main substrate for cyclooxygenase, can also be metabolized by the lipoxygenase pathway to leukotrienes, substances which are primarily synthesized in inflammatory cells. In several models induction of immunologic glomerular injury is associated with an increased glomerular formation of cyclooxygenase and lipoxygenase products. The changes in cyclooxygenase products have been shown to account for some hemodynamic changes found in some of these models. Increased renal prostanoid formation is also present in patients with glomerular disease. There is some evidence that increased renal PG-formation in patients with moderate glomerular disease regulates GFR and mediates proteinurie in some of these patients. Leukotrienes are chemotactive substances which modulate the function of inflammatory cells, stimulate the growth of mesangial cells, and constrict mesangial cells in culture. Thus, these compounds might be mediators in the induction of immune mediated glomerular disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01725553
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  • 6
    Electronic Resource
    Electronic Resource
    Progressive renal failure in a patient after one and two-thirds nephrectomy (1988)
    Springer
    Journal of molecular medicine 66 (1988), S. 508-510 
    Details
    ISSN: 1432-1440
    Keywords: Nephrectomy ; Hyperfiltration ; Progressive renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report on a patient who lost one and two-thirds of his kidneys following surgery because of bilateral renal cell carcinoma. The serum creatinine following surgical intervention increased to about 7 mg% and fell to serum values of about 3 mg% in the year after one and two-thirds nephrectomy. The patient's renal function remained stable for 18 months, then it started to deteriorate and the patient developed progressive renal failure with proteinuria. The course of the disease suggests that an intrinsic renal mechanism was operative, which relates to glomerular hyperfiltration following surgical loss of renal tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01876174
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  • 7
    Electronic Resource
    Electronic Resource
    Mild proteinuria in patients with unilateral kidney (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 1048-1051 
    Details
    ISSN: 1432-1440
    Keywords: Reduced renal mass ; Glomerular hyperperfusion ; Proteinuria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Arterial blood pressure, 24 h urinary excretion, and glomerular filtration rate (GFR) in 24 patients with unilateral kidney were compared with an age and sex matched control group of healthy persons. Of the patients with unilateral kidney, 13 were uninephrectomized and 11 patients had a congenital unilateral kidney. The 24 h urinary protein excretion in patients with one kidney was significantly higher (630±51 mg/24 h) compared to the control group (206±36 mg/24 h). The arterial systolic and diastolic blood pressures and GFR did not differ in both groups. Furthermore, no differences were found between patients with unilateral kidneys following nephrectomy or renal agenesis. This study shows that mild proteinuria occurs in patients with unilateral kidney. An increased risk for deterioration in renal function or severe arterial hypertension was not detected in this investigation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01739671
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  • 8
    Electronic Resource
    Electronic Resource
    Akutes Nierenversagen Isolierte Manifestation einer Systemerkrankung (1997)
    Springer
    Der Internist 38 (1997), S. 606-609 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Sarkoidose ; Niereninsuffizienz ; Kalziumnephropathie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Eine Sarkoidose der Niere kann isoliert oder im Rahmen einer Systemerkrankung auftreten. Als diagnostisches Leitsymptom dient eine Nierenfunktionsverschlechterung, deren Ursache interstitielle Nephritiden, Glomerulonephritiden oder eine Kalziumnephropathie sein können. Eine Nierenbiopsie ist als wertvolles, differentialdiagnostisches Kriterium frühzeitig indiziert. Störungen des Kalziumstoffwechsels können ebenfalls diagnostisch wegweisend sein. Unter Therapie mit Steroiden kommt es in den meisten Fällen einer Sarkoidose der Niere zu einer guten Restitution der Nierenfunktion. Wesentlich ist, bei einer Niereninsuffizienz unklarer Ätiologie eine Sarkoidose in die differentialdiagnostischen Überlegungen einzubeziehen und frühzeitig mit einer adäquaten Therapie zu beginnen, um Spätschäden zu verhindern.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050073
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  • 9
    Electronic Resource
    Electronic Resource
    The possible role of chemotactic cytokines in renal disease (1994)
    Springer
    Journal of molecular medicine 72 (1994), S. 711-712 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00212998
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  • 10
    Electronic Resource
    Electronic Resource
    Eine 73jährige Patientin mit hypertensiver Krise War der Einsatz des Kalziumantagonisten Nifedipin gerechtfertigt? (1999)
    Springer
    Der Internist 40 (1999), S. 205-209 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter Nifedipin ; Kalziumantagonisten ; Koronare Herzkrankheit ; Hypertensive Krise ; Hypertensive Dringlichkeit ; Evidence Based Medicine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zusammenfassung Eine 73jährige Patientin erwachte in der Nacht mit linksthorakalen Schmerzen und Herzklopfen. Der herbeigerufene Notarzt diagnostizierte eine hypertensive Krise. Der Blutdruck war 260/120 mm Hg, und der Notarzt verabreichte 50 mg Urapidil i.v.. Es folgte der Transport in die Klinik. In der Notaufnahme war der Blutdruck mit 190/120 mm Hg weiterhin erhöht. Die Patientin war beschwerdefrei. Das EKG zeigte keine Ischämie-typischen oder Infarkt-verdächtigen Veränderungen. Nach Gabe von 10 mg Nifedipin als Kapsel kam es zum schnellen Abfall des Blutdrucks auf 120/80 mm Hg. Es entwickelte sich eine Tachykardie, und heftige linksthorakale Schmerzen traten auf. Das EKG zeigte eine Sinustachykardie mit Ischämie-typischen ST-Streckensenkungen von 0.3 mV in den Brustwandableitungen. Die Symptomatik besserte sich nach i.v. Gabe von Nitroglycerin und Frequenzkontrolle. Das 12 h später geschriebene EKG zeigte keine Ischämie-typischen Veränderungen. Nach Intensivierung der antihypertensiven Therapie wurde die Patientin beschwerdefrei entlassen. Bei der Patientin waren durch die Gabe von Nifedipin Angina pectoris Beschwerden und ischämietypische EKG-Veränderungen ausgelöst worden. Wir diskutieren, warum wir trotz dieser Beobachtung den Gebrauch von Nifedipinkapseln bei der hypertensiven Krise für gerechtfertigt halten.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050325
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