[Comparative karyometric studies in minimally proliferating intercapillary glomerulonephritis (minimal chage lesions) with and without nephrotic syndrome].
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Biomedical subjects
Publications and source records attributed to A Bohle.
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48 cases of renal amyloidosis (grade I-IV) were investigated morphologically (point-counting method). Statistically significant positive correlations exist between relative interstitial volume and serum creatinine concentration at the time of biopsy. In amyloidosis there are furthermore connections (positive rank correlations) between the extent of glomerular amyloidosis and renal insufficiency, although single cases of grade III show normal serum creatinine concentrations if the interstitium is not enlarged. With regard to interstitial alterations only fibrosis, not amyloid masses, seems to influence renal function, especially in the case of predamaged glomeruli (grade II to IV). The diminished renal function - reduction of the glom. filtr. rate - may be explained in the case of interstitial fibrosis by slowing of renal blood flow caused by a decreasing cross-sectional area of postglomerular vessels. Renal insufficiency seems to depend upon both the glomerular and the interstitial factor, but in grades II-IV the interstitial fibrosis is thought to be of more importance for renal function.
Renal biopsies of 44 patients with endocapillary acute glomerulonephritis (gn) and 64 patients with moderately severe mesangioproliferative gn were investigated morphometrically (point-counting-method, tubulometry). In both gn's statistically significant positive corrleations between relative interstitial volume and the concentration of serum creatinine at the time of biopsy were found. Despite severe glomerular lesions the serum creatinine concentration is not increased in most cases of endocapillary acute gn, providing the relative interstitial volume is not increased by more than 15%. Increased serum creatinine concentration without a markedly enlared interstitium was found in 11 cases of endocapillary acute gn with clinically and morphologically proven acute renal failure. In these cases the glomerular function is probably impaired by the Thurau-mechanism. In all other patients, especially in those with moderately severe mesangioproliferative gn, the serum creatinine concentration rises with an enlargement of relative interstitial volume. This reduction of renal function may be explained by a decrease to the total cross-sectional area of postglomerular vessesl, caused by interstitial fibrosis. That may possible lead to diminished renal blood flow and glomerular filtration with an increase of the serum creatinine concentration.
Morphometric investigations in 33 patients suffering from membranoproliferative glomerulonephritis at different grades of glomerular involvement showed that there is no certain relationship between the severity of glomerular lesions and the serum creatinine level. On the other hand there is a significant positive correlation between the relative interstitial volume and the level of serum creatinine. The best congruence (r=+0,87, p less than 0.0001) showed an exponential function y=0.563-e0.049x. We therefore conclude that in membranoproliferative glomerulonephritis which is generally considered to be a glomerular disease, interstitial changes have to be taken into account as a cause of renal insufficiency. Glomerular lesions alone cannot explain the functional impairment. The pathophysiologic factors concerning increased interstitial volume as a cause of renal insufficiency - probably immunologic in origin - are yet to be completely clarified.
In order to study the lympho-epithelial relationships in human oviducts, lymphocytes situated in the epithelium were counted and the values found were correlated with differing physiological and pathological changes. In this process the following observations were made: 1. In the secretory phase there are significantly more lymphocytes to be found in the epithelium than during the proliferative phase. 2. In nonspecific purulent salpingitis the number of lymphocytes is not significantly different from that in a normal proliferative phase. 3. The values for fallopian pregnancy are significantly lower than those of a normal secretory phase and do not differ significantly from those of a normal proliferative phase. 4. The values observed for the reproductive period are significantly higher than those found postmenopausally. Examination by electron-microscopy showed that the lymphocytes in the epithelium of the uterine tube are intercellular. Pointers towards degenerative changes were not seen. It is presumed that the number of lymphocytes appearing in the epithelium of the fallopian tube depends on the hormonal activity of the ovaries.
Morphometric investigations in 40 patients suffering from perimembranous glomerulonephritis at different stages showed that there is no certain relationship between the severity of glomerular lesions and the serum creatinine level. In 19 cases in stages I-III, with serum creatinine level less than 1.2 mg/100 ml on biopsy, the renal interstitium was less enlarged than in 21 cases in the same stages, but with serum creatinine level higher than 2 mg/100 ml. There is a significant positive correlation between the relative interstitial volume and the level of serum creatinine. The best congruence was demonstrated in the lin/log-plotting indicating that our values correlate best with an exponential function. We therefore conclude that in perimembranous glomerulonephritis, generally considered to be a glomerular disease, functional impairment cannot be explained by the glomerular lesions alone; interstitial changes have also to be taken into account as a cause of renal insufficiency. The following hypothesis is proposed; that the increase in renal interstitium and possible shrinking of collagen fibres may lead to a narrowing of intertubular capillaries. This may result in slowing of glomerular blood flow and may lead to renal insufficiency.
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This report presents information about a method to construct a wax-sheet model of rat and human glomerula, able to be divided into several segments. Based on the wax model consisting of segments a glomerula model is developed, showing the axis of the glomerula capillaries formed by an ironwire. By means of this model it will be possible to follow the course of the capillaries precisely.
Five personal cases and many reports in the literature demonstrate the not rare development of hypertension after oral contraceptives or an increase of an existing hypertension. In addition, the drug may also cause vascular changes in the kidneys with development of benign or malignant nephrosclerosis, similar to the increased risk of thrombo-embolic complications of the venous-arterial system. It is, therefore, necessary to check the blood pressure of women on oral contraceptive and, if hypertension exists or develops, discontinue these drugs.
Morphometrical and clinical investigations were performed in 34 patients with the so-called hypercellular form of focal glomerulosclerosis (FGS), i.e., a form showing clear diffuse mesangial hypercellularity beside focal sclerosis with the light microscopy. This form was compared with focal glomerulosclerosis without remarkable mesangial hypercellularity, with mild mesangioproliferative glomerulonephritis (gn), as well as with normal kidneys. The results were as follows: 1. Morphometrically both the increase in relative mesangial volume as well as in mesangial cell count is statistically significant in the hypercellular form compared with the nonhypercellular form and with controls. Comparison with mild mesangioproliferative gn shows no difference. 2. Even the so-called nonhypercellular form contains more mesangial matrix and mesangial cells than the controls. 3. The frequency of the hypercellular form is higher in males and in older patients. 4. All of our patients with hypercellular FGS had at the time of biopsy manifested nephrotic syndrome. The frequency of additional clinical symptoms (hematuria, hypertension, renal insufficiency) corresponds with the nonhypercellular form, but is different in mild mesangioproliferative gn. 5. Therapeutic response and prognosis is worse in the hypercellular form. The hypercellular form of FGS has to be separated from the nonhypercellular form as a defined entity.
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 Addison's disease and in Bartter's syndrome, as well as 8 atrophic JGAs in Conn's syndrome. With the exception of Bartter's 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 Bartter's syndrome, but not in Addison's 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.
From repeat biopsies of 291 patients with glomerulonephritis, the clinical and morphological course of the individual forms of glomerulonephritis were compared with one another. From these results we concluded that: 1. Every form of glomerulonephritis has in all probability its individual course and prognosis, which can only be very slightly influenced by therapy. 2. The prognosis is considerably worsened, when either hypertension develops or tubular lesions in the morphological sense of an acute renal failure.
Comparative morphological and clinical studies of 2,500 patients suffering from glomerulonephritis, enabled us to divide the different forms of diffuse glomerulonephritis into 3 distinct groups and to separate these groups from the focal glomerulonephritides. The different forms of diffuse glomerulonephritis in group I are: 1. endocapillary (acute) glomeruloenphritis (of the post-streptococcal type), 2. mesangioproliferative glomerulonephritis, 3. mesangioproliferative glomerulonephritis with focal crescents, 4. mesangioproliferative glomerulonephritis with focal scarring, 5. minimal proliferating intercapillary glomerulonephritis without nephrotic syndrome. It is emphasised that these forms can transform into one another, that they seldom occur with nephrotic syndrome, and with varying frequency with hypertension. Group II consists of: 1. minimal proliferating intercapillary glomerulonephritis with nephrotic syndrome, 2. focal sclerosing glomerulonephritis, 3. perimembranous glomerulonephritis, 4. membranoproliferative glomerulonephritis, 5. lobular glomerulonephritis. It is stressed that these glomerulonephritis forms usually do not develop out of group I type glomerulonephritis forms, and that in this group a nephrotic syndrome is the most prominent clinical syndrome. In the third group are 1. mesangioproliferative glomerulonephritis with diffuse crescents, 2. necrotising glomerulonephritis. It is shown that this form of glomerulonephritis does not usually develop from either group I of II forms. The fourth group of focal glomerulonephritis is uncommon. This disease is characterized by a necrotising and proliferative inflammatory lesion found segmentally and focally in the glomeruli. Most of the other glomeruli appearing normal. It is emphasised that in the literature the diagnosis focal glomerulonephritis is made far too often. This is because glomeruli in which the inflammatory process in a few lobules is of varying prominence, are included in the focal glomerulonephritis group. The classification of the different forms of glomerulonephritis into 3 groups here described, is thought of as a basic classification. It is compared with Ellis' classification (1942), with which it has much in common.
1. As proposed by Schürmann & MacMahon (1933), we suggest that two types of malignant nephrosclerosis exist. 2. In the type called primary malignant nephrosclerosis, renal vascular lesions precede hypertension. 3. In the second type, called secondary malignant nephrosclerosis, renal vascular lesions are considered to be the consequence of malignant hypertension.