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Quality control aims to analyze not only the results of therapy but the efficiency and cost effectiveness of diagnostic procedures. In a catamnestic analysis of the outcome in 97 patients with acute pericarditis seen at this hospital from 1982 to 1992, we tried to answer the question whether a conservative diagnostic strategy might harm the patient. The outcome in 33 patients after limited diagnostic activity (patient story, clinical status; WBC differential count, ESR; creatinine and creatine kinase; ECG and chest x-ray) was the same as in 33 patients who underwent additional diagnostic procedures. Moreover, in patients in whom after limited diagnostic activity the etiology of acute pericarditis (precordial pain and friction rub) remained unclear, additional diagnostic procedures did not settle the problem. We conclude that extensive and even invasive diagnostic procedures are justified in selected patients and in special circumstances only (fever38 degrees and protracted course of disease, marked pericardial effusion or threatening tamponade; epidemiological or scientific interest).

Overt renal disease is a rare complication of infectious mononucleosis (MI). In contrast, up to 16% of patients with MI have been shown to exhibit abnormalities in urinary sediment. Histological abnormalities--usually interstitial nephritis, and occasionally glomerular lesions--are rather common. Clinical symptoms include in rare cases isolated macrohematuria, occasionally a nephrotic or nephritic syndrome, and more commonly acute renal failure due to rhabdomyolysis, hepatorenal syndrome or acute interstitial nephritis. We report two observations of acute renal failure with a typically benign course and discuss these observations in the light of an updated literature survey of 34 patients.

Eight patients with life threatening hyperkalemia were treated in the intensive care unit over a period of 2 years. Serum potassium at admission was 7.1-11.2. Two patients had to be resuscitated and 3 exhibited quadriplegia or paralyses but were alert. Seven showed marked ECG change: in 5 the QRS-complexes were extremely broadened and in one case an AV-rhythm was observed; the atrial wave was absent in all 7 patients. Renal failure was present in 7 of 8 patients. In 6 of these 8 cases drugs were also involved in the development of hyperkalemia. The following therapeutic procedure is recommended for hyperkalemia: (1) injection of calcium, (2) inhalation or injection of beta 2-mimetics (well documented in the literature; clinical experience limited), (3) insulin and glucose i.v., (4) sodium bicarbonate, but only in case of metabolic acidosis, (5) hemodialysis, (6) cation exchange resins or furosemide in non-acute situations.

The haemodynamic effects of angiotensin II and noradrenaline were studied in the rat kidney. These pressors were given by intravenous infusion in stepwise increasing doses. Intrarenal haemodynamics were analyzed by the 133xenon washout technique, 85krypton autoradiography and silastic casting of the renal vascular tree. Angiotensin II induced significant changes in intrarenal haemodynamics before any changes in systemic blood pressure were detected. The decrease in mean renal blood flow (2.91 ml.min-1.g-1 in controls, 1.76 ml.min-1.g-1 in rats given 50 mug of angiotensin II.kg-1.h-1) reflects a reduction in component I blood flow rate (from 3.9 to 2.9 ml.min-1.g-1) as well as a decrease in the fraction of total renal blood flow supplied to component I of the washout curve (from 84% to 62%). With noradrenaline an increase in total renal resistance occurred simultaneously with the elevation of mean arterial blood pressure. The resulting reduction in mean renal blood flow (from 2.76 ml.min-1.g-1 in controls to 1.55 ml.min-1.g-1 in rats given 1000 mug of noradrenaline kg-1.h-1) reflects a decrease in component I blood flow rate with lower infusion rates and a drop in component I flow fraction (from 82% to 52%) whith higher doses. In contrast to canine kidneys, no evidence for a patchy cortical vasoconstriction was found in the rat. Using autoradiography it was possible to attribute component I to the renal cortex and subcortical area of the kidney.

Haemorrhagic hypotension (HH) causes a redistribution of intrarenal blood flow characterized by a patchy cortical hypoperfusion. Previous studies indicated that the sYmpathoadrenergic system is mainly responsible for these redistribution processes. The relative role of renal nerves and of circulating catecholamines was studied in the present experiments. Intrarenal haemodynamics were analysed by means of the 133 Xenon washout technique and 83 Krypton autoradiographics. 8 autotransplanted (and, therefore, chronically denervated) kidneys showed the same typical response to severe and prolonged HH as 11 normal control organs. In 2 additional dogs, the intrarenal distribution of blood flow (IDBF) and local blood flow rates (Fi ) of an acutely denervated kidney before and during HH did not show any differences as compared with the contralateral control organ. It is concluded that the patchy cortical hypoperfusion observed in the dog during severe haemorrhagic hypotension does not depend on an intact innervation of the kidney, but that it is mainly mediated by circulating catecholamines.

The inert gas washout technique of Thorburn et al. has been adapted to the rat. The left kidney was exposed and placed in a micropuncture type lead spoon. A lead ring, a fenestrated

Das Verstandnis der pathophysiologischen Charakteristica der insuffizienten Niere ermoglicht erst die richtige Einschatzung der zu erwartenden besonderen Probleme des chronisch niereninsuffizienten Pa

Eine genaue Analyse der Anatomie der Korperflussigkeiten und der Dynamik des Wasserhaushaltes eines Patienten mit chronischer Hyperosmolaritat, fehlendem Durstgefuhl, unauffalligen Trink- und Urinmengen und HVL-Insuffizienz bei ektopischem Pinealom im Boden des dritten Ventrikels wird im Hinblick auf die Pathogenese des Diabetes insipidus hypersalaemicus occultus diskutiert. Die Befunde fuhren zum Nachweis einer schweren Beeintrachtigung der Osmoregulation mit „Neueinstellung der Osmoreceptoren“, bzw. gestorter, aber fix gekoppelter Beziehung zwischen Osmolaritat und Diurese.

Untersuchungen der intrarenalen Hamodynamik an normalen (nicht-transplantierten), autotransplantierten und homotransplantierten Hundenieren zeigten folgende Resultate: 1. Transplantation per se fuhrt

Wird bei narkotisierten Hunden der arterielle Mitteldruck akut und uber mehrere Stunden auf 50 mm Hg gesenkt, so konnen folgende Veranderungen der intrarenalen Hamodynamik beobachtet werden: Die corticale Flowfraktion sinkt von einem Ausgangswert um 80% auf Werte um 10% der Gesamtdurchblutung der Niere ab. Gleichzeitig steigt der corticomedullare Durchflus von 14 auf 80% des Gesamtstroms, wahrend sich die Anteile der inneren Markzone und des perirenalen Fettgewebes nur unwesentlich verandern. Ebenso zeigen die lokalen Stromstarken keine signifikanten Veranderungen. Daraus wird auf eine Abnahme des perfundierten Rindengewebes geschlossen. Autoradiographisch zeigt sich das Bild einer fleckigen Rindenischamie, die mit der Dauer der hypotensiven Phase an Ausdehnung zunimmt. Nach Normalisierung des Blutdruckes kommt es, selbst nach stundenlanger Hypotension, zu einer raschen Reversion der hamodynamischen Verschiebung, wobei sich allerdings erst nach Tagen wieder vollig normale Verhaltnisse einstellen.

Auf Grund von Untersuchungen an 17 Patienten und Kontrollpersonen werden die Beziehungen zwischen Aldosteron- und Natrium-ausscheidung bzw. Natriumbilanz unter langdauernder Einwirkung von saluretisch wirksamen Pharmaka analysiert. 1. Beim Gesunden wie beim Odemkranken fuhrt die Verabreichung von Diuretica zu einer vorubergehenden Steigerung der Aldosteronausscheidung. Diese tritt in dem Moment auf, da die rasch mobilisierbaren Natrium- bzw. Korperflussigkeitsreserven erschopft sind, d. h. keine weiteren odeme mehr ausgeschwemmt werden konnen. 2. Die Diskrepanz zwischen dem Verlauf der Aldosteronausscheidung und der Natriumbilanz unter langdauernder Einwirkung von Diuretica weist auf das Eingreifen neuer, noch unbekannter natriumbewahrender Mechanismen hin. 3. Es wird die Bedeutung einer erhohten Aldosteronaktivitat bei therapierefraktaren Odemen und sekundarem Wirkungsverlust der Diuretica diskutiert.