R. A. K. Stahl

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Eine arterielle Hypotonie renalen Ursprungs wurde als Folge einer niedrigen Plasma-Reninaktivität bei bestehendem Mangel an Natrium und extrazellulärer Flüssigkeit beobachtet. Als experimentelles Modell, an dem eine sekretorische Insuffizienz der Renin-produzierenden juxtaglomerulären Zellen und eine Natrium- und Volumenverarmung gleichzeitig erzeugt werden(More)
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,(More)
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(More)
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(More)
Mesangial cell hypertrophy is one of the earliest morphological abnormalities of diabetic nephropathy. We have previously shown that high glucose induces p27Kip1 by a post-transcriptional mechanism and that mesangial cell hypertrophy depends on G1-phase arrest mediated by this CDK-inhibitor. However, it remains poorly understood how high glucose stimulates(More)
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(More)
There is accumulating evidence from clinical and experimental studies that inflammatory cells which infiltrate the glomerulus or the tubulointerstitium may play a pivotal role during the induction and progression of renal disease or participate in the reconstruction of injured tissue. Recently, particular interest has focused on the role which(More)
G. Wolf, Jena Nephrologe 2006 · 1:103–105 DOI 10.1007/s11560-006-0007-5 Online publiziert: 17. Mai 2006 © Springer Medizin Verlag 2006 U. Wenzel1 · R. Stahl1 · G. Adam2 · G. Wolf3 1 Zentrum Innere Medizin, III. Medizinische Klinik, Universitätsklinikum HamburgEppendorf 2 Klinik für Diagnostische und Interventionelle Radiologie, Universitätsklinikum(More)
Die diabetische Nephropathie ist die häufigste Ursache der terminalen Niereninsuffizienz. Im Zentrum der diabetischen Nephropathie steht die Glomerulosklerose. Sie bildet das morphologische Korrelat der Proteinurie. Pathogenetisch sind gesteigerte glomeruläre Matrixbildung und Hyperglykämie eng miteinander verknüpft. Qualitativ gleichartige diabetische und(More)
Ein Posttransplantationslymphom (PTLD) ist eine schwere Komplikation nach Organtransplantationen. Wir berichten den Fall eines 45-jährigen Patienten, der ein EBV-assoziiertes B-Zelllymphom in der transplantierten Niere entwickelte, was die Notwendigkeit hervorhebt, die Möglichkeit von PTLD in die differenzialdiagnostischen Überlegungen bei Verschlechterung(More)