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Biomedical subjects

A Bohle

Publications and source records attributed to A Bohle.

At least 109 records · Page 6Linked to original sources
PubMed1979

Shock kidney.

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Acute Kidney Injury↗
PubMed1979

The normal juxtaglomerular apparatus in the human kidney. A morphological study.

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.

Adult↗
PubMed1979

The role of the interstitium of the renal cortex in renal disease.

Morphometrical investigations (point-counting method) showed that in different inflammatory (endocapillary -- acute -- GN, mesangioproliferative GN, membranoproliferative GN) glomerulonephritides and in non-inflammatory glomerular diseases (perireticular amyloidosis), there are statistically significant correlation between serum creatine concentrations at the time of biopsy and the enlargement of the cortical interstitium by fibrosis. Similar results were obtained in investigating different grades of benign nephrosclerosis with transition into secondary malignant nephrosclerosis conditioned by hypertension and in chronic diffuse sclerosing interstitial nephritides of different etiologies. As hypothesis, we assume that a narrowing of the postglomerular vessel network by interstitial fibrosis take place. This could lead to an increase resistance of the renal cortical blood flow. In spite of an elevated effective filtration pressure, the slowing of the glomerular blood flow may lead to the reduction of GRF and to an increase of the serum creatinine concentration. Additionally, in the case of interstitial fibrosis the tubules look atrophied. This could be the consequence of the reduced GFR as a sign of inactivity. On the other hand, tubular atrophy could result from malnutrition in the case of interstitial fibrosis. The resorptive capacity of these atrophied-looking tubules could be lowered and the GFR could be diminished by the so-called Thurau mechanism.

Amyloidosis↗
PubMed1978

Renal insufficiency in nephrosclerosis (benign nephrosclerosis resp. transition from benign to secondary malignant nephrosclerosis) correlations between morphological and functional parameters.

62 tissue specimens with the only diagnosis benign nephrosclerosis (or benign nephrosclerosis with transition to secondary malignant nephrosclerosis) were investigated attempting to correlate morphological findings (relative interstitial volume of the renal cortex, types of hyalinisation and kinds of periglomerular changes, vessel index) with each other and with the serum creatinine concentration as a parameter of renal function. There are significant correlations in form of exponential and parabolic functions between relative interstitial volume of the renal cortex and the serum creatinine concentration at the time of biopsy. Furthermore 5 types of glomerular and periglomerular changes, which could be discriminated, seem to influence renal function in a different way and at different stages of the disease. An additional factor are the arteriolar changes. There are positive rank correlations between vessel index and serum creatinine concentration as well as between vessel index and relative interstitial volume. In cases with a higher percentage of hyalinized glomeruli more pronounced arteriolar lesions (partly alterations which can be found in secondary malignant nephrosclerosis) were observed. No connections seem to exist between mean blood pressure and the mentioned morphological and functional parameters. The reduction of renal function seems to be caused by tubular and interstitial factors: the often observed atrophy of tubules in fibrotic areas possibly impairs resorptional capacity. The mechanisms of the glomerular-tubular-balance may lead to a diminished glomerular filtration. On the other hand alterations of the capillaries may induce perivascular edema, which, if not reabsorbed, leads to interstitial fibrosis. The produced collagen fibres may reduce the cross sectional area of the postglomerular vessel network. This may lead to a slowing of the renal cortical and glomerular blood flow, thus inducing an increase of the serum creatinine concentration. Weighing all factors, the interstitial fibrosis seems to be the most important.

Arterioles↗
PubMed1978

Correlations between the morphological and clinical findings in a patient recovering from secondary generalised amyloidosis with renal involvement. Light- and electron microscopic investigations on serial biopsies.

We report light- and electron microscopic findings in glomerular amyloidosis (secondary amyloidosis), which occurred after recurrent empyema of the pleura. After healing of the empyema, the clinical symptoms disappeared, over a period of eight years. During the acute stage of the disease (grade II-III amyloidosis) when the nephrotic syndrome was present, amyloid deposits were seen in the mesangium and on both sides of the basement membrane of the glomerular capillaries. Furthermore, denuded basement membrane areas showing the passage of amyloid into the urinary space, and invaginations of the podocyte by straightened amyloid fibrils were found. After clinical recovery (except for a trace of proteinuria), the renal amyloidosis had electronmicroscopically transformed from an active into an inactive or resting form, while the amount of amyloid present was almost the same. In the areas of amyloid deposits, reparative changes were observed, espcially in the area of the mesangial cells and of the podocytes. The podocytes were separated from the persisting amyloid deposits by newly formed basement membrane material.

Adult↗
PubMed1978

Investigations on the cause of the nephrotic syndrome in renal amyloidosis. A discussion of electron microscopic findings.

Systematic electron microscopic investigation of glomeruli of 35 patients with renal amyloidosis (grade I-III), among them 26 with nephrotic syndrome, reveals the following: 1. The extent of the area of basement membrane denuded of its epithelial covering is correlated significantly with the reduction of plasma protein concentration at the time of renal biopsy. 2. In amyloid free regions of the glomerular capillary loops, the foot processes of the epithelial cells remain intact despite the presence of the nephrotic syndrome. From these findings we conclude that the high glomerular protein losses in amyloidosis occur in areas of the basement membrane which are penetrated by amyloid and denuded of their epithelial covering. With increasing number of these lesions per unit area, the permeability of the capillary network for protein increases to a degree which is significantly correlated with the reduced plasma protein concentration at the time of biopsy.

Adolescent↗
PubMed1978

Simultaneous occurrence of perimembranous glomerulonephritis and glomerular amyloidosis.

The results of electron microscopic examination of renal biopsies from 3 patients with rheumatoid arthritis treated with penicillamine are presented. All 3 patients developed a nephrotic syndrome upon discontinuation of penicillamine therapy. When viewed with the electron microscope, segmental forms of perimembranous glomerulonephritis (Stages I-II of Ehrenreich and Churg) and glomerular renal amyloidosis Grade I-III were observed. In all three cases the nephrotic syndrome was considered to be due to the simultaneous occurrence of the two disease processes. In 2 cases perimembranous glomerulonephritis with immuno-complex-deposits was assumed to be the dominant factor in the causation of the disease, in the other case amyloidosis was the principle abnormality.

Amyloidosis↗
PubMed1978

[Are clotting disorders a pathogenetic factor in nephrosclerosis and hypertension? (author's transl)].

The clinical course of the haemolytic-uraemic syndrome in four patients suggests that hypertension may result from it. The morphological changes in the kidney are those of primary malignant nephrosclerosis. Hypercoagulability is thought to be an important pathogenetic factor in the development of the disease. But irreversible renal failure is not, contrary to typical primary malignant nephrosclerosis, an inevitable sequel. Abortive forms with predominant involvement of glomerular vessels have a more favourable prognosis than those forms with additional preglomerular vascular changes, in which a more or less marked impairment of renal function and hypertension persists. These forms are of particular interest because they indicate a renal pathogenetic mechanism of chronic hypertension. The described observations--taken together with those on the pathogenesis of hypertension caused by oral contraceptives--provide a pointer to the importance of clotting disorders in the initiation and development of some forms of hypertension.

Adult↗
PubMed1978

The juxtaglomerular apparatus in a human kidney with polar artery stenosis.

Juxtaglomerular apparatuses (JGA) of a human kidney with stenosis of a polar artery from a hypertensive 18-year-old male patient were studied qualitatively and quantitatively on 2 mu thick serial sections from plastic embedded renal tissue. 11 JGA from juxtamedullary and 9 JGA from subcapsular cortical zones were photographed serially, the copies taped together and the cells and relationships within the JGA studied. On the copies the lenght of contact between the different juxtaglomerular structures and the basement membrane of the macula densa was measured. Futhermore we calculated the areas of surface contact and the macula densa basal area. In the juxtamedullary JGA affected by the polar artery stenosis all Goormaghtigh cells were transformed into epitheloid cells and the Goormaghtigh cell field was significantly larger than in the JGA of the subcapsular cortex, which obviously had been exposed to the systemic hypertension. The macula densa basal area was significantly greater in the juxtamedullary JGA than in the subcapsular JGA, but neither of these differed significantly from the macula densa in the normal JGA reported previously.

Adolescent↗