Dieter S. Meyer

The structure of the human juxtaglomerular apparatus

49 juxtaglomerular apparatuses were examined using 1.9 μ thick Giemsastained serial sections from human renal tissue embedded in plexiglass. In 43 juxtaglomerular apparatus the direct contact areas between the different juxtaglomerular structures and the basal area of the macula densa were calculated. A positive, significant correlation was found between the size of the macula densa and the direct contact area between macula densa and Goormaghtighs cell field on the one hand, and between the macula densa and the direct contact area between Goormaghtighs cell field and the afferent arteriole on the other. There was also a significant, positive correlation between the direct contact area of Goormaghtighs cell field with the macula densa and that of Goormaghtighs cell field with the afferent arteriole. On the efferent side none of these correlations were significant. Thus a “flow of information” from the macula densa via the Goormaghtigh cells to the afferent arteriole is morphologically possible. The direct contact areas between macula densa and the afferent or the efferent arterioles were not correlated with any of the other parameters. Epithelioid cells were present in the interlobular arteries, prior to and within the juxtaglomerular apparatus in the afferent arterioles, as well as within and beyond the juxtaglomerular apparatus in the efferent arterioles.

Über die primäre und sekundäre maligne Nephrosklerose

SummaryAs a result of examining kidneys from 54 patients suffering from malignant nephrosclerosis it proved to be necessary to divide the material into to groups differing with respect to morphological findings and to the clinical course.The first group consists of patients with malignant nephrosclerosis secondary to a long-standing hypertension. In the other group the renal vascular lesions preceded, at least in 5 out of 22 cases, the malignant hypertension. This type is called primary malignant nephrosclerosis and separated from the secondary malignant nephrosclerosis caused by hypertension.From a clinical point of view a primary malignant nephrosclerosis has to be taken into consideration if—frequently after an infectious disease—an acute renal failure associated with a mostly severe anaemia and normal or increased blood pressure rapidly develops. On the other hand a progressive renal failure evolving within several weeks or months of hypertensions is typical of secondary malignant nephrosclerosis.Morphologically, it was shown that in primary malignant nephrosclerosis on an average the afferent arterioles are affected more frequently than in secondary malignant nephrosclerosis. Moreover in primary malignant nephrosclerosis according to the sudden onset of this disease acute, often thrombotic vascular lesions are prevalent in contrast to chronic vascular alterations (e.g. Fahrs productive endarteriitis) in secondary malignant nephrosclerosis.Furthermore our investigations proved a higher frequency of primary malignant nephrosclerosis in younger patients, especially in females, whereas in males more often a secondary malignant nephrosclerosis may be found.The relations of primary malignant nephrosclerosis to Gassers haemolytic-uraemic syndrome are discussed. An attempt is made to distinguish between primary malignant nephrosclerosis and the syndrome of Moschcowitz, the generalised Shwartzman reaction and the microangiopathic haemolytic anaemia.ZusammenfassungDie Untersuchung der Nieren von 54 Patienten mit maligner Nephrosklerose ergab, daß aufgrund unterschiedlicher morphologischer und klinischer Befunde eine Differenzierung dieses Krankheitsbildes in zumindest 2 Gruppen erforderlich ist.Bei der ersten Gruppe handelt es sich um Patienten, bei denen sich die maligne Nephrosklerose sekundär im Verlauf einer meist mehrjährigen Hochdruckanamnese entwickelt hatte. Bei der zweiten Gruppe gingen die für die maligne Nephrosklerose kennzeichnenden renalen Gefäßveränderungen, zumindest in einigen Fällen (5 von 22), der malignen Hypertonie voraus. Die letztere Form der malignen Nephrosklerose wird als primäre maligne Nephrosklerose von der hochdruckbedingten sekundären malignen Nephrosklerose abgegrenzt.Von klinischer Seite muß der Verdacht auf eine primäre maligne Nephrosklerose geäußert werden, wenn sich, meist nach uncharakteristischem Infekt, sehr schnell eine Niereninsuffizienz im Sinne des akuten Nierenversagens mit schwerer Anämie bei normalem oder erhöhtem Blutdruck entwickelt.Eine progrediente Entwicklung einer Niereninsuffizienz in mehreren Wochen bzw. Monaten bei Bestehen eines Hypertonus spricht dagegen für eine sekundäre maligne Nephrosklerose.Durch Analyse der vasculären Läsionen bei den beiden Formen der malignen Nephrosklerose konnte gezeigt werden, daß bei der primären malignen Nephrosklerose die Vasa afferentia im Durchschnitt häufiger erkrankt sind als bei der sekundären malignen Nephrosklerose. Die Akuität des Krankheitsverlaufes bei primärer maligner Nephrosklerose bringt es darüber hinaus mit sich, daß bei dieser Erkrankung akute, oft mit Thrombenbildungen einhergehende Gefäßwandschäden dominieren, während bei der sekundären malignen Nephrosklerose die chronischen Gefäßwandläsionen (z. B. produktive Endarteriitis Fahr) stärker hervortreten.Darüber hinaus ergaben unsere Untersuchungen, daß die primäre maligne Nephrosklerose bei im Durchschnitt jüngeren Patienten auftritt als die sekundäre maligne Nephrosklerose, ferner, daß an der primären malignen Nephrosklerose überwiegend Frauen, an der sekundären malignen Nephrosklerose vorwiegend Männer erkranken.Die Beziehungen zwischen primärer maligner Nephrosklerose und dem hämolytisch-urämischen Syndrom Gasser werden aufgezeigt. Ferner wird eine Abgrenzung der primären malignen Nephrosklerose vom Moschcowitz-Syndrom, vom generalisierten Shwartzman-Phänomen sowie von der sog. mikroangiopathischen hämolytischen Anämie versucht.

The normal juxtaglomerular apparatus in the human kidney

Out of 49 serially studied juxtaglomerular apparatuses, 6 typical variants from two normal human kidneys were reconstructed graphically. The agranular Goormaghtigh cells filled the entire space between the macula densa, the afferent and the efferent arterioles and the glomerular mesangium. The Goormaghtigh cells were always in direct contact with all the other structures. They also invariably continued into the glomerular mesangium. The distal tubule regularly showed widening in the macula densa segment and, at this level, there was considerable variation in the shape of the distal tubule. Direct contact between the macula densa and the hilar arterioles was not always present, the area of contact was usually greater with the afferent than with the efferent arteriole.

The structure of the juxtaglomerular apparatus in Addison's disease, Bartter's syndrome, and in Conn's syndrome

Continuing and supplementing previous morphometric studies on the Juxtaglomerular apparatus (JGA) of normal kidneys we have now investigated semi-thin serial sections of each 10 hyperplastic and hypertrophied JGAs in Addisons disease and in Bartters syndrome, as well as 8 atrophic JGAs in Conns syndrome. With the exception of Bartters syndrome, where in only two out of ten JGAs the efferent arteriole, and in none of them the afferent arteriole touches immediately the macula densa, there is an almost regular direct contact between the hilar arterioles and the macula densa like in normal kidneys. The Goormaghtigh cell field invariably touches the macula densa. In Bartters syndrome, but not in Addisons disease, a considerable enlargement of the macula densa was measured, associated with an exceptional enlargement of the Goormaghtigh cell field. In all cases examined here about 40–60% of the basal area of the macula densa do not have any direct contact with other structures forming the JGA.

Über Beziehungen zwischen Struktur und Funktion der Niere beim akuten Nierenversagen

Lange Zeit ist angenommen worden, das bei der Krankheit, die wir heute als akutes Nierenversagen (a.N.) bezeichnen, die Struktur der Niere nicht verandert ist (Nonnenbruch 1949 u.a.).

The glomerular mesangium in hypertension

Glomerular changes were morphometrically studied in renal biopsies of 27 cases of nephrosclerosis showing clinically benign or malignant hypertension and of 15 cases of mild mesangioproliferative glomerulonephritis with hypertension. In nephrosclerosis, there was a mild increase in mesangial matrix without cell proliferation. The degree of the mesangial changes varied little despite a large variation in blood pressure and showed no significant difference between benign and malignant hypertension. In mild mesangioproliferative nephritis with hypertension, mesangial matrix, as well as the number of mesangial cells, showed an increase of varying degree. A quantitative assessment of the mesangium was proved effective in differentiating the glomerular changes in nephrosclerosis from those in mesangioproliferative nephritis with hypertension.