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  • 1
    Electronic Resource
    Electronic Resource
    Vitamin D-Metabolismus bei Niereninsuffizienz — Störung eines endokrinen Regelkreises (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 1053-1059 
    Details
    ISSN: 1432-1440
    Keywords: Niereninsuffizienz ; Vitamin D-Stoffwechsel ; Osteomalazie ; Parathormon ; Myopathie ; Uremia ; Vitamin D ; Osteomalacia ; Parathyroid hormone ; Myopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The vitamin metabolite 25(OH)D is transformed into the active secosterole 1.25(OH)2D3 in the proximal tubular epithelium of the kidney. This transformation is disturbed in patients with renal insufficiency. However, this review shows that presumably not all vitamin D dependent disturbances in patients with renal insufficiency are explicable merely as the consequence of reduced renal synthesis of 1.25(OH)2D3 secondary to nephronal loss. In incipient renal failure, vitamin D dependent functions (calcemic action of PTH, intestinal absorption of Ca) are disturbed. Yet, circulating 1.25(OH)2D3 levels are slightly elevated. This finding is compatible with an inadequate response of the renal 1-alpha-hydroxylase system to activating stimuli (hyperparathyroidism, hypocalcemia, fasting hypophosphatemia) and/or end-organ resistance to the action of 1.25(OH)2D3. Osteomalacia in renal insufficiency cannot entirely be explained as the consequence of a reduction of the serum-concentration of any of the known vitamin D metabolites [25(OH)D3; 1.25(OH)2D3; 24.25(OH)2D3]. The relatively poor response of osteomalacia of uremic patients to the administration of 1.25(OH)2D3 leads to the question of whether other vitamin D metabolites or non-vitamin D related factors are important in its genesis. Critical information is lacking with respect to 1.25(OH)2D3 receptors, post receptor events and interaction between vitamin D metabolites and PTH in bone cells of such patients. A specific action of 1.25(OH)2D3 on longitudinal growth of uremic children has been described. However, several clinical and experimental studies failed to provide evidence of normalization of growth by 1.25(OH)2D3 and failed to show differences in this respect between vitamin D and 1.25(OH)2D3. Currently, it remains undecided whether vitamin D metabolites affect PTH secretion, and if so which vitamin D metabolite is involved. Clarification of this problem is of paramount importance for therapeutic suppression of the parathyroids of uremic patients. Vitamin D metabolites play an important role in some organ functions unrelated to homeostasis of Ca-Pi-metabolism (e.g. muscle, testis, pancreas, etc). The loss of such function is of potential importance in the genesis of the uremic syndrome and its imcomplete reversal by hemodialysis.
    Notes: Zusammenfassung In den proximalen Tubulusepithelien der Niere wird der Vitamin D-Metabolit 25(OH)D in das aktive Secosterol 1,25(OH)2D3 umgewandelt. Diese Umwandlung ist bei niereninsuffizienten Patienten beeinträchtigt, jedoch sind möglicherweise nicht alle Vitamin D-abhängigen Störungen bei Niereninsuffizienz allein durch den Ausfall der Synthese von 1,25(OH)2D3 zu erklären. Bei initialer Niereninsuffizienz, bei der bereits Vitamin D-abhängige Funktionen (calzämische Wirkung von PTH, Calziumabsorption) gestört sind, liegen die 1,25(OH)2D3-Spiegel im Serum geringfügig oberhalb des Normalbereichs. Dieser Befund ist mit einer inadäquaten Antwort der 1-alpha-Hydroxylase auf aktivierende Stimuli (Hyperparathyreoidismus, Hypocalzämie, Hypophosphatämie) und/oder einer möglichen Endorganresistenz gegenüber 1,25(OH)2D3 vereinbar. Die Osteomalazie bei niereninsuffizienten Patienten ist nicht ausschließlich als Folge der Erniedrigung der Serum-Konzentration eines der bekannten Vitamin D-Metabolite [25(OH)D3; 24,25(OH)2D3; 1,25(OH)2D3] zu erklären. Das schlechte Ansprechen der Osteomalazie urämischer Patienten auf 1,25(OH)2D3 legt die Frage nach der möglichen Wirkung zusätzlicher Vitamin D-Metabolite oder dem Vorhandensein nicht Vitamin D-abhängiger Zusatzfaktoren nahe. Bislang fehlen Informationen zum Verhalten der 1,25(OH)2D3 Rezeptoren und nachgeschalteter Ereignisse an Knochenzellen und Einzelheiten einer möglichen Wechselwirkung zwischen 1,25(OH)2D3 und PTH bleiben noch unklar. Obwohl ein spezifischer wachstumsfördernder Effekt von 1,25(OH)2D3 auf das Längenwachstum urämischer Kinder beschrieben wurde, zeigten mehrere klinische und experimentelle Untersuchungen keine Normalisierung durch 1,25(OH)2D3 resp. keinen Wirkunterschied zwischen Vitamin D und 1,25(OH)2D3. Gegenwärtig ist noch unklar, ob Vitamin D-Metabolite, und gegebenenfalls welcher Vitamin D-Metabolit, die PTH-Sekretion der Parathyreoidea hemmen. Die Klärung dieser Frage erscheint dringend für eine optimale medikamentöse Suppression der Parathyreoidea niereninsuffizienter Patienten. Auch außerhalb der Homöostase des Ca-Pi-Stoff-wechsels spielen Vitamin D-Metabolite eine wichtige Rolle in der Funktion einiger Organe, z.B. Muskel, Hoden, Pankreas etc. Der Ausfall dieser Funktionen ist möglicherweise bedeutsam zum Verständnis des urämischen Syndroms und seiner mangelnden Rückbildung unter Hämodialysebehandlung.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01479991
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  • 2
    Electronic Resource
    Electronic Resource
    Long-term therapy with cyclosporin A does not influence serum concentrations of vitamin D metabolites in patients with multiple sclerosis (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 595-599 
    Details
    ISSN: 1432-1440
    Keywords: Cyclosporin A ; 1,25-Dihydroxyvitamin D3 ; Calcium metabolism ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Animal studies have shown that cyclosporin A (CyA) stimulates renal 25-hydroxyvitamin D3 [25(OH)D3]-1α-hydroxylase activity; in contrast, studies in renal transplant recipients indirectly suggest that CyA reduces 1α,25-dihydroxyvitamin D3 [1,25 (OH)2D3] production. To clarify the effect of CyA on vitamin D metabolite concentrations, we measured parameters of calcium metabolism in 37 CyA-treated patients (median trough whole blood levels 171–222 ng/ml) with multiple sclerosis and initially normal kidney function. The patients participated in a randomized double-blind study to assess the efficacy of CyA in multiple sclerosis. An age- and sex-matched control group (n = 39) received azathioprine (Aza). Measurements were made at the end of a 2-year treatment period. The 1,25(OH)2D3 serum concentrations were not significantly different between the two groups, although they were numerically lower in CyA-treated patients [median (range), 28.4 pg/ml (7.8–85.9) vs 41.0 pg/ml (9.2–105.1) in Aza-treated patients]. The 25(OH)D3 levels were comparable in both groups. There was no correlation between the 25(OH)D3 and 1,25(OH)2D3 concentrations. The renal function in both groups was stable in the last 6 months of the study. At the end of the study period, the endogenous creatinine clearance was significantly lower in the CyA-treated group (85 ± 17 ml/min versus 99 ± 22 in the Aza-treated group, P 〈 0.05). The carboxyterminal parathyroid hormone (C-PTH) was within the normal range in both groups, although CyA-treated patients had significantly higher concentrations (P〈0.01). The urinary excretion of mineral ions, cations and protein was similar in both groups. Our data suggest that long-term treatment with CyA does not cause clinically important alterations of vitamin D metabolism in humans. Subtle differences in the concentrations of 1,25(OH)2D3 and C-PTH between CyA- and Aza-treated patients result presumably from a slight impairment of renal function through CyA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184801
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  • 3
    Electronic Resource
    Electronic Resource
    Subacute effects of thiazide administration on renal hemodynamics and calcium metabolism (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 686-691 
    Details
    ISSN: 1432-1440
    Keywords: Thiazides ; Glomerular filtration ; Hemoconcentration ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To elucidate the renal effects of thiazides as a function of sodium intake, 8 healthy volunteers without renal disease were studied at baseline and 1 day as well as 4 days after the administration of 100 mg hydrochlorothiazide/day. The subjects were compared on two different dietary sodium intakes (120 mmol/day and 220 mmol/day). Measurements comprised inulin clearance (Cin) and paraaminohippurate clearance (Cpah) by infusion clearance technique, total and ionised calcium, immunoreactive parathyroid hormone (1,84 iPTH), 1.25 (OH)2 vitamin D3, and indices of hemoconcentration. Acute administration of hydrochlorothiazide (HCTZ) caused no change in Cin (before 111 ± 3 ml/min 1.73 m2 ; 24 h after, 107 ± 2 ml/min 1.73 m2) or Cpah (before, 579 ± 9 ml/min 1.73 M2; after, 584 ± 12 ml/min 1.73 m2), while a significant (P 〈 0.01) decrease was noted on the 4th day after 100 mg HCTZ/day and normal sodium intake. No significant change of creatinine clearance (Ccr) was seen with either manouever. Renal hemodynamic changes after HCTZ administration were marginal when hemoconcentration was prevented by a high salt intake. Acute administration (1 h) of HCTZ caused suppression of 1,84 iPTH (before, 2.3 ±0.5 pmol/l; after, 1.9 ± 0.2 pmol/l; P 〈 0.01), but after 4 days a lower ionised calcium (baseline, 1.25 ± 0.01 mmol/l; day 5, 1.20 ± 0.02 mmol/l; P 〈 0.01) was noticed in parallel with hemoconcentration, metabolic alkalosis, and reduced 1,25 (OH)2 vitamin D3 concentrations. The level of 1,84 iPTH was elevated. We conclude that (i) hydrochlorothiazide does not affect the renal hemodynamics if hemoconcentration is avoided and (ii) hydrochlorothiazide acutely lowers PTH, while subacutely metabolic alkalosis and decreased ionised calcium may occur with concomitant increase in 1,84 iPTH and decrease in 1,25 (OH)2 vitamin D3 concentrations unless hemoconcentration is prevented.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180287
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  • 4
    Electronic Resource
    Electronic Resource
    Disturbed calcium metabolism in subjects with elevated diastolic blood pressure (1992)
    Springer
    Journal of molecular medicine 70 (1992), S. 748-751 
    Details
    ISSN: 1432-1440
    Keywords: Hypertension ; Calcium ; Parathyroid hormone ; 1,25-Dihydroxyvitamin D3
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 ± 6 mmHg, mean ± SD) and age-matched male subjects (n=79) with low diastolic blood pressure (62 ± 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P 〈 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 ± 0.10 vs. 2.47 ± 0.10 mmol/l, mean ± SD; P 〈 0.01). PTH concentrations were correlated with diastolic pressure (r = −0.39, P 〈 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00180741
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  • 5
    Electronic Resource
    Electronic Resource
    Hyperparathyroidism: Influence of glomerular filtration rate on urinary excretion of cyclic AMP (1977)
    Springer
    Journal of molecular medicine 55 (1977), S. 275-281 
    Details
    ISSN: 1432-1440
    Keywords: Hyperparathyroidism ; Glomerular filtration rate ; Urinary cyclic AMP ; Serum parathyroid hormone ; Cyclic AMP ; urinary ; Competitive protein binding assay ; Parathyroid hormone ; Radioimmunoassay ; GFR ; Phosphate excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Urinary cyclic AMP excretion per 24 h or per g creatinine in primary hyperparathyroidism (1° HPT) has been evaluated by several authors with conflicting results. In 50 patients with 1° HPT, 25 patients with secondary (2°) HPT and 35 healthy control persons we determined urinary cyclic AMP per 24 h or per g creatinine. These parameters did not satisfactorily discriminate patients from controls, especially when glomerular filtration rate (GFR) as determined by creatinine clearance was reduced. Since urinary cyclic AMP is derived from plasma by glomerular filtration and from kidney by tubular production—the amount of tubules is reflected by GFR—the cyclic nucleotide was related to GFR. In controls urinary cyclic AMP correlated better with GFR than with creatinine excretion. Additionally, in 45 of 50 patients with 1° HPT and in all with 2° HPT, urinary cyclic AMP/GFR was raised. In 1° HPT serum levels of parathyroid hormone correlated closer with urinary cyclic AMP/GFR than with urinary cyclic AMP/g creatinine. The ratio cyclic AMP/GFR decreased to normal or subnormal values after removal of adenomatous or hyperplastic glands in 1° HPT and during infusion of calcium in 2° HPT. In 50 patients with renal lithiasis caused by diseases other than 1° HPT (anatomical variations, pyelonephritis, immobilization after tetraplegia) the ratio cyclic AMP/GFR was not raised. Urinary cyclic AMP/GFR, therefore, reflects parathyroid hormone excess more reliably than cyclic AMP/g creatinine.
    Notes: Zusammenfassung Parathormon erhöht die renale Ausscheidung von cyclischem AMP (cAMP). Die renale Ausscheidung von cAMP/24 h oder cAMP/g Kreatinin wurde bei primärem Hyperparathyreoidismus (1° HPT) von verschiedenen Untersuchern gemessen. Die Resultate waren widersprüchlich. Wir bestimmten die renale Ausscheidung von cAMP/24 h oder cAMP/g Kreatinin bei 50 Patienten mit 1° HPT, 25 Patienten mit sekundärem (2°) HPT und 35 Kontrollpersonen. Die Patienten schieden im Mittel mehr cAMP/24 h oder cAMP/g Kreatinin aus als die Kontrollpersonen. Eine Überlappung mit dem Normalbereich wurde besonders bei reduzierter Kreatininclearance beobachtet. Da im Urin ausgeschiedenes cAMP zum Teil aus dem Plasma (glomeruläre Filtration) und zum Teil aus der Niere (tubuläre Produktion) stammt und die Anzahl der Tubuli von der GFR reflektiert wird, bezogen wir die renale Ausscheidung von cAMP auf die GFR (bestimmt als Kreatininclearance). Bei den Kontrollpersonen korrelierte die renale Ausscheidung von cAMP besser mit der Kreatininclearance als mit der Kreatininausscheidung. 45 von 50 Patienten mit 1° HPT und alle Patienten mit 2° HPT wiesen eine erhöhte renale Ausscheidung von cAMP/GFR auf. Die radioimmunologisch gemessenen Serumspiegel von Parathormon korrelierten bei 1° HPT besser mit der renalen Ausscheidung von cAMP/GFR als mit cAMP/g Kreatinin. Nach Entfernung von adenomatösen oder hyperplastischen Nebenschilddrüsen bei 1° HPT oder nach Infusion von Calcium bei 2° HPT fiel die Ausscheidung von cAMP/GFR auf normale oder erniedrigte Werte. 50 zusätzlich untersuchte Patienten mit Nephrolithiasis, die nicht durch 1° HPT bedingt war, wiesen keine Erhöhung der renalen Ausscheidung von cAMP/GFR auf. Die renale Ausscheidung von cAMP/GFR ist ein zuverlässigerer Indikator der Nebenschilddrüsenüberfunktion als die Ausscheidung von cAMP/Kreatinin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01484728
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  • 6
    Electronic Resource
    Electronic Resource
    Phosphat-Depletion (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 1-15 
    Details
    ISSN: 1432-1440
    Keywords: Phosphate ; Calcium ; Phosphate-depletion ; Parathyroid hormone ; Vitamin-D ; Rhabdomyolysis ; Cardiac insufficiency ; Haemolysis ; Osteomalacia ; Phosphat ; Calcium ; Phosphat-Depletion ; Parathormon ; Vitamin D ; Myolyse ; Herzinsuffizienz ; Hämolyse ; Osteomalazie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammensetzung Die kritische und lebenswichtige Rolle von anorganischem Phosphat ist in der Veterinärmedizin und der tierexperimentellen Forschung seit Jahrzehnten bekannt. Das Syndrom der Phosphat-Depletion fand in der Klinik jedoch erst seit kurzem stärkere Beachtung. Eine Hypophosphatämie wird bei folgenden Krankheitsbildern gehäuft beobachtet: chronischer Alkoholismus, Erholungsphase der diabetischen Ketoazidose, parenterale Ernährung mit Phosphat-freien Lösungen, schwere respiratorische Alkalose und Fruktose-Infusion. Die Organfunktionsstörungen bei Hypophosphatämie sind auf die Verarmung des Zytoplasmas an anorganischem Phosphat zurückzuführen. Eine derartige Phosphat-Verarmung kann (1) durch negative Phosphat-Bilanz des Gesamtorganismus als Folge renaler oder intestinaler Phosphat-Verluste oder (2) ohne negative äußere Phosphat-Bilanz durch Verschiebung von Phosphat aus dem extra- in den intrazellulären Raum auftreten. Die Phosphat-Depletion beeinträchtigt im Prinzip die Funktion aller Organe. Klinisch stehen bei der akuten Phosphat-Depletion Funktionsstörungen der Skelettmuskulatur (Rhabdomyolyse mit myoglobinurischem akutem Nierenversagen), Herzmuskulatur (akute Herzinsuffizienz) und des hämatologischen Systems (Hämolyse, gestörte Leukozyten- und Thrombozytenfunktion) im Vordergrund, während bei chronischer Phosphat-Depletion Skelettstörungen (Osteomalazie) vorherrschen. Die Organfunktionsstörungen sind wahrscheinlich auf verminderte Synthese von ATP und anderen organischen Phosphat-Metaboliten zurückzuführen. Verminderte 2,3-DPG-Spiegel in Erythrozyten und die hierdurch bedingte Hypoxie sind eine weitere mögliche Ursache von Organfunktionsstörungen.
    Notes: Summary The essential and critical role of inorganic phosphate has been known in veterinary medicine and experimental research on animals for decades. However, only recently has the phosphate depletion syndrome found widespread attention by clinicians. Hypophosphatemia is usually observed in the following clinical situations: chronic alcoholism, recovery phase of diabetic ketoacidosis, administration of phosphate-free solutions in parenteral nutrition, severe respiratory alkalosis, and infusion of fructose. Disturbed organ function in hypophosphatemia is the result of a depletion of inorganic phosphate in the cytoplasm of somatic cells. Such phosphate depletion may be due to either of the following mechanisms or a combination of both. (1) Negative external phosphate balance resulting from phosphate loss in urine or feces or (2) translocation of phosphate from the extracellular into the intracellular space with or without concomitant negative external phosphate balance. In principle, phosphate depletion interferes with the function of all somatic cells. In acute phosphate depletion, the clinically most important disturbances are observed in striated muscle (rhabdomyolysis with myoglobinuric acute renal failure), heart muscle (acute heart failure), and hematological systems (hemolysis, disturbed leukocyte and thrombocyte functions). In contrast, in chronic phosphate depletion skeletal abnormalities (osteomalacia) predominate. Organ disturbances are thought to result from diminished synthesis of ATP and other organic phosphate esters and/or from hypoxia secondary to changes in erythrocyte 2,3-DPG.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477138
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  • 7
    Electronic Resource
    Electronic Resource
    Lack of involvement of sarcoplasmic reticulum in myopathy of acute phosphorous depletion (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 833-837 
    Details
    ISSN: 1432-1440
    Keywords: Phosphat-Depletion ; Sarkoplasmisches Retikulum ; Calcium-Transport ; Vitamin D-Stoffwechsel ; Myopathie ; Phosphat ; Phosphate depletion ; Sarcoplasmic reticulum ; Calcium transport ; Vitamin D metabolism ; Myopathy ; Phosphate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Acute and chronic hypophosphatemia are known to cause metabolic myopathy. It has been proposed that impaired Ca transport in subcellular membranes is involved in its genesis. In the present study, calcium transport in the sarcoplasmic reticulum (SR), concentrations of ions or nucleotides and transmembrane potential were investigated in muscles of acutely hypophosphatemic rats, i.e. animals with chronic dietary phosphorous deprivation (PD) and superimposed acute hypophosphatemia resulting from the administration of insulin and glucose. Despite hypophosphatemia and low muscle phosphorous concentration, no significant change of the initial rate of Ca uptake or Ca concentrating ability was observed in the SR of PD rats. Storing capacity was decreased; this may result from altered vesicle geometry. Water content, Na concentration, the concentration of several nucleotides and transmembrane potential of muscle were unchanged in PD rats. The findings document that no intrinsic abnormality of vectorial Ca transport is present in the SR of acutely hypophosphatemic PD animals.
    Notes: Zusammenfassung Bei akuter und chronischer Hypophosphatämie tritt eine Myopathie auf, für deren Entstehung Störungen des subzellulären Calcium-Transports postuliert wurden. In der vorliegenden Studie wurden die Calcium-Transport-Kinetik im sarkoplasmischen Retikulum (SR), Ionen- und Nukleotid-Konzentrationen sowie Ruhemembran-Potential der quergestreiften Muskulatur akut hypophosphatämischer Ratten untersucht. Bei diesem Modell wurde bei Ratten mit chronischer diätetischer Phosphat-Verarmung eine akute Hypophosphatämie durch Gabe von Insulin und Glukose erzeugt. Trotz Hypophosphatämie und erniedrigter Muskel-Phosphor-Konzentration wurde keine Abweichung der Geschwindigkeit der initialen Calcium-Aufnahme oder der Calcium-Konzentrationsfähigkeit im sarkoplasmischen Retikulum beobachtet. Die Speicherfähigkeit war vermindert; dies mag Ausdruck veränderter Vesikel-Geometrie sein. Wassergehalt, Natrium-Konzentration, Konzentration energiereicher Nukleotide sowie Ruhemembran-Potential waren in der Muskulatur hypophosphatämischer Ratten unverändert. Die Befunde zeigen, daß keine primäre Störung des vektoriellen Calcium-Transports im SR phosphatdepletierter Ratten mit akuter Hypophosphatämie besteht.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01491104
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  • 8
    Electronic Resource
    Electronic Resource
    Myopathy in experimental uremia (1975)
    Springer
    Research in experimental medicine 165 (1975), S. 205-212 
    Details
    ISSN: 1433-8580
    Keywords: Myopathy ; uremia ; polyneuropathy ; histochemistry ; planimetry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary M. quadriceps and diaphragm were studied in Wistar rats 2, 3, und 4 weeks after 5/6 nephrectomy. Control animals were sham operated and pair fed. In 10 µ transverse cryostat sections, the following histochemical reactions were performed: NADH-dehydrogenase, myofibrillar ATP-ase, modified trichrom stain, hematoxylin-eosin. Three fibre types (I, II, intermediate) were analysed quantitatively by planimetry. Sarcolemnal nuclei per unit area and fibre cross section area were determined. In muscle specimens from uremic animals, a uniform atrophy of all three fibre types could be demonstrated. In contrast to findings in man, preferential atrophy of one of the three fibre types, increase of sarcolemnal nuclei per fibre cross section area or structural abnormalities within single muscle fibres could not be detected. Neurogenic damage could be excluded (electrophysiology, sciatic nerve planimetry). The fibre changes point to a primary disturbance of muscle metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01971379
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