Membranous nephropathy after bone marrow transplantation in ciclosporin treatment.
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Adult↗
Biomedical subjects
A Bohle
Publications and source records attributed to A Bohle.
[The pathogenesis of chronic renal failure].
The pathogenesis of terminal renal failure is discussed. The following are distinguished: 1. Renal failure occurring against a background of decompensated benign nephrosclerosis, primary and secondary malignant nephrosclerosis, and stenosis of the renal artery. 2. Renal failure caused by loss of glomeruli. It is pointed out that in most glomerulopathies, including diabetic glomerulopathy and renal amyloidosis, terminal renal failure only develops when accompanying disease of the postglomerular vessels leading to interstitial fibrosis impairs the outflow of blood from the glomerulus to such an extent that no more urine is produced. 3. Renal failure in disease of the tubules themselves. It is emphasized that acute renal failure only becomes chronic when interstitial fibrosis develops from the interstitial edema occurring in the early stage of the disease. 4. Renal failure occurring in primary diseases of the renal cortical interstitium. The chronic sclerosing renal diseases arising from acute interstitial nephritis are dealt with, as also are reflux nephropathy, incomplete obstructive nephropathy, analgesic nephropathy, and chronic interstitial rejection reactions in transplanted kidneys.
Amyloidosis↗
[Clinical pathology of the glomerulus--from phenomenon to entity. The mesangial lesion].
The numerous findings discussed lead to the following conclusions: 1. The mesangial lesions, which may take a wide range of different forms, can be classified into two groups according to whether an underlying immunological pathomechanism is involved. Those that result from such a pathomechanism represent various types of glomerulonephritis. 2. Amongst these immunologically-mediated glomerulonephritides mesangioproliferative glomerulonephritis (and, of this group, IgA nephritis) is the most common. Membranoproliferative glomerulonephritis is the most severe of these diseases. Either may be idiopathic or secondary, or may occur in association with systemic disease. 3. The number of macrophages in the mesangial lesions in glomerulonephritis correlates with the severity of the glomerulonephritis, the localization of the immune complex deposits and the degree of proteinuria. If the immune complex deposits extend out of the mesangium into the subendothelial space, the number of macrophages is higher, the structural changes are more marked, and proteinuria is more severe. 4. Various pathomechanisms and nosologic entities can lead to mesangial lesions of the type seen in mesangioproliferative glomerulonephritis or membranoproliferative glomerulonephritis. On the other hand, the same entity may be associated with mesangial lesions of different severity, and consequently the prognosis varies. Differential diagnosis of the mesangial lesions, which represent heterogeneous nosologic entities, requires the use of light microscopic, immunohistochemical, and electron microscopic techniques. Exact diagnosis is necessary because of the differences in prognosis. 5. The course and prognosis of mesangial lesions are determined by immunological and nonimmunological factors. Long-term studies have demonstrated that prognostically relevant information can already be gained at the time of biopsy by the assessment of certain morphological features (e.g., immunohistological findings, severity of glomerulonephritis, the presence of focal/segmental lesions) and clinical parameters (e.g., proteinuria, hematuria, hypertension, and serum creatinine concentration). The decisive predictor of an unfavorable prognosis is the presence of interstitial fibrosis.
Glomerular Mesangium↗
Evaluation of change with time of glomerular morphology in membranoproliferative glomerulonephritis: a serial biopsy study of 33 cases.
The evolution of renal glomerular lesions was examined in biopsies taken from 33 patients with membranoproliferative glomerulonephritis (MPGN). 25 patients had a diffuse form of MPGN in the first biopsy (group A). Twenty-four of them still showed diffuse MPGN in subsequent biopsies, but one patient improved clinically and histologically 19 years after the initial biopsy. Out of 6 patients with focal MPGN in the first biopsy (group B), 4 developed diffuse MPGN, one remained with focal MPGN in the repeat biopsy, and another one was found in remission, as determined by both histological and clinical features. Group C represents two patients who had no histological findings of MPGN on initial biopsy but later showed evidence of a diffuse form of MPGN on subsequent biopsies. Thus, the focal form of MPGN may be found either in the development of diffuse MPGN or in its healing stage, and the prognosis will vary accordingly.
Adolescent↗
[Benign and malignant nephrosclerosis. Comparative clinical and morphologic studies of 792 cases].
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Glomerular Mesangium↗
Long-term prognosis of chronic idiopathic membranous glomerulonephritis. An analysis of 334 cases with particular regard to tubulo-interstitial changes.
A retrospective long-term study (average follow-up time 5.2 years) of 334 patients with idiopathic membranous glomerulonephritis (MGN) was carried out with the following results: 1) MGN was found to have a relatively good prognosis when all cases were considered together: 5-year kidney survival rate (KSR) -88%, and 10-year KSR -77%. 2) Univariate survivorship analysis showed the following morphological and clinical parameters to be associated with an increased risk of terminal renal insufficiency or death from renal disease: a) tubulo-interstitial changes; b) glomerular stage III as opposed to stages I and II; c) elevation of serum creatinine concentration at the time of the biopsy; d) arterial hypertension at the time of the biopsy. 3) Multivariate analysis showed that only tubulo-interstitial changes (interstitial fibrosis and/or acute renal failure) found at the time of the biopsy and their clinical correlate, serum creatinine concentration, were significant and therefore of definite prognostic importance. 4) Unsystematic therapy with steroids and/or cytostatic agents does not improve the long-term prognosis of MGN. 5) The cause of disease in the tubulo-interstitial system in MGN is discussed. Interstitial fibrosis is considered to develop possibly as a consequence of unresorbed interstitial edema which can develop during an episode of acute renal failure. Coexisting T-cell-mediated disease in the region of the intertubular capillaries is also considered as a possible factor in the development of interstitial fibrosis.
Acute Kidney Injury↗
[Acute renal failure--clinical aspects and morphology].
This study reports the pathological-anatomical diagnoses in 180 cases in which a diagnosis of acute renal failure (ARF) had been made on clinical grounds. The clinical and pathological diagnoses were in agreement in 43.3% of the cases. In 56.7%, the pathological-anatomical diagnosis differed from the clinical diagnosis. Glomerulonephritis (GN) was particularly often concealed behind ARF, in particular rapidly progressive GN, but also acute interstitial nephritis or hemolyticuremic syndrome. In addition, the clinical diagnoses in cases with a pathological-anatomical diagnosis of ARF are presented. Finally, the clinical diagnoses made in cases with a pathological-anatomical diagnosis of GN with ARF are reported. It is thus shown that the pathologist is in a position to distinguish GN with true compensated retention from GN with transient ARF simulating compensated retention.
Acute Kidney Injury↗
Peripolar cells in the avian kidney.
Four white leghorn chickens were injected with furosemide (20 mg per kg body weight) three times at 12 h intervals and the kidneys fixed by perfusion after 36 h. Five chickens were injected with DOCA (desoxycortone trimethylacetate, 75 mg per kg body weight) three times at 12 day intervals and the kidneys fixed by perfusion after 36 days. Serial sections from the kidneys of these two groups of birds were made and the number of peripolar cells recorded. These recordings were compared with the number of peripolar cells in four normal, untreated chickens. A significant increase in the number of peripolar cells was recorded in the furosemide treated group. No significant change was seen in the DOCA treated group. However, in the DOCA-group heavily granulated podocytes were found. No distinct morphological difference was found between the granules in the podocytes and the granules in the peripolar cells. A possible lysosomal nature of the peripolar cell granules is discussed.
Animals↗
Transmission and scanning electron microscopy investigations on the structure of the ultrafilter of glomeruli in human acute renal failure.
In 4 cases of human acute renal failure (ARF) with oligo-anuria, normuria and polyuria the following findings were made. (1) The diameter of endothelial cell fenestrae is on average larger than that of the control values, but not significantly. (2) In ARF the ratio of the endothelial cell fenestral area to the total endothelial area is not significantly lower than in control kidneys. (3) In ARF the average density of fenestrae per unit of area is not significantly lower than in control kidneys. (4) The structure of the podocytes does not differ from that of control kidneys.
Acute Kidney Injury↗
Hyperperfusion injury of the human kidney in different glomerular diseases.
Investigations of biopsy material from human kidneys with different forms of glomerulonephritis (n = 1,240) and with diabetic glomerulosclerosis (n = 406) performed in order to find changes caused by hyperperfusion of the kidney tissue gave the following results: (1) Hyperperfusion injury occurs in the different forms of glomerulonephritis with varying frequency. It was rarely found in immunologically negative mesangioproliferative glomerulonephritis. The highest incidence was found in patients with membranoproliferative glomerulonephritis type I. (2) Hyperperfusion injury was also found in kidneys with diabetic glomerulosclerosis. The frequency of this finding increased with the degree of the diabetic changes. (3) The hyperperfusion injury was seen as a complication of glomerulonephritis or diabetic glomerulosclerosis only when the patient clinically had developed malignant hypertension and when the serum creatinine level was elevated, a sign of compensated retention. (4) In patients with glomerulonephritis, the hyperperfusion changes occurred more frequently in males than in females. Diabetic glomerulosclerosis was complicated by hyperperfusion injury with the same frequency in both sexes. (5) Patients with hyperperfusion changes of the kidneys always excrete large amounts of protein in the urine. (6) Hyperperfusion changes occur first in the juxtamedullary glomeruli. The intermediate glomeruli are affected later and the subcapsular glomeruli last.
Adolescent↗
Role of hyperperfusion in different glomerular diseases.
In various forms of glomerulonephritis, diabetic glomerulosclerosis and decompensated benign nephrosclerosis hyperperfusion injury of the glomeruli may be found in addition to the basic disease in patients with malignant hypertension. The changes consist of adhesions, subendothelial capillary hyalinosis and fat droplets in the hyalin material and in endothelial cells. They occur far more often in males than in females. The highest frequency of hyperperfusion injury was found in patients with membranoproliferative glomerulonephritis type I. The lowest frequency was found with membranous glomerulonephritis. The juxtamedullary part of the kidney, which is not autoregulated, is earlier and more severely affected than the subcapsular part. Hyperperfusion changes occur in the middle and eventually in the subcapsular part of the cortex only when the glomeruli in the juxtamedullar cortex are sclerotic.
Diabetic Nephropathies↗
Kidney function and protein excretion in relation to pathomorphology of glomerular diseases.
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Adolescent↗
On benign and malignant nephrosclerosis.
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Adult↗
Plasma exchange and immunosuppression in rapidly progressive glomerulonephritis: a controlled, multi-center study.
In a randomized study of 26 patients with histologically confirmed rapidly progressive crescentic glomerulonephritis, 12 patients were treated with immunosuppressants alone (corticosteroids, cyclophosphamide and azathioprine) while the other 14 patients received not only the identical immunosuppressive treatment but also plasma exchange therapy for four weeks. No statistically significant difference was found between the two groups. After 8 weeks, 73% and 69% of the patients in each respective group showed recompensation of renal function; serum creatinine fell from initially 7.0 and 6.2 mg/dl mean to 2.7 and 2.3 mg/dl mean, and under continued immunosuppression did not rise in the following months. Thus, in non-autoantibody induced rapidly progressive glomerulonephritis, kidney function could be improved substantially by immunosuppressive therapy, but an advantage of supplementary plasma exchange could not be shown.
Adult↗
Is there any tubular secretion of protein?
Immunohistological investigations performed with the PAP method on tubular casts in the thick Henle loops and in the distal convoluted tubules led to the following results. 1) In control kidneys, casts consisting of sIgA and IgM occur, mostly isolated, in 30% and 20%, respectively, of cases. On the other hand IgG casts, likewise isolated, are only observed in 7% of cases. 2) In the case of mesangioproliferative glomerulonephritis of the IgA and non-IgA nephritis type, casts consisting of sIgA and IgM are observed more often than in control kidneys, especially when the serum creatinine concentration exceeds 1.3 mg%; i.e., the glomerular filtration is reduced. 3) In kidneys with inflammatory and non-inflammatory glomerular diseases which had led to nephrotic syndrome, casts consisting of sIgA and IgM are not observed more often than in kidneys with glomerulonephritides which had not been accompanied by nephrotic syndrome. 4) In kidneys with severe impairment of the excretory function (rapidly-progressive glomerulonephritis, primary malignant nephrosclerosis, acute renal failure) casts consisting of sIgA and IgM are observed more often than in controls but not more often than in IgA and non-IgA nephritides with increased serum creatinine concentration. 5) In kidneys which had become aglomerular as a result of scarring of the glomeruli, with atrophic proximal tubules and preserved epithelia of the ascending loop of Henle, casts consisting of sIgA and IgM as well as secretory component occur in a large quantity.(ABSTRACT TRUNCATED AT 250 WORDS)
Female↗
Contribution on the correlation between morphometric parameters gained from the renal cortex and renal function in IgA nephritis.
The following findings were obtained in a comparative morphometric and clinical study of 130 adult men and women with immunologically confirmed IgA nephritis: (a) IgA nephritis develops in varying frequency as minimal proliferating intercapillary glomerulonephritis, low-grade mesangioproliferative glomerulonephritis, moderate to severe mesangioproliferative glomerulonephritis, or variously severe mesangioproliferative glomerulonephritis with signs of focal accentuation. (b) Tubular epithelial surface area and interstitial width in 62 of 130 cases of IgA nephritis was the same as in normal kidneys. IgA nephritis was complicated in 33 cases by interstitial cortical fibrosis, in 23 cases by acute renal failure, and in 12 cases by acute renal failure and interstitial fibrosis. (c) In IgA nephritis with acute renal failure, the tubular epithelium (only proximal tubular epithelium was measured) was significantly swollen. In IgA nephritis with interstitial fibrosis, the epithelial surface area of the proximal tubules was significantly smaller than the normal surface area. In IgA nephritis with acute renal failure (ARF) and interstitial fibrosis, tubular swelling was less severe than in ARF. Proximal tubular epithelial surface area, however, was significantly larger than the normal surface area. (d) In IgA nephritis, like in other inflammatory and noninflammatory glomerular diseases, a significant positive correlation existed between width of the cortical interstitium and height of serum creatinine level. Moreover, in IgA nephritis, significantly negative correlation existed between width of the cortical interstitium and C creatinine. (e) In IgA nephritis, significant negative correlations existed between C creatinine and age. (f) In IgA nephritis, a significant correlation existed between proximal tubular epithelial surface area and serum creatinine level and a significant negative correlation, between C creatinine and proximal tubular epithelial surface area, when ARF cases were excluded from the total group of IgA nephritis. (All correlations are closer when the cases with accompanying ARF are eliminated.) The discrepancy between the findings of Bennett et al. (Bennett WM, Walker RG, Kincaid-Smith P: Lab Invest 47:330, 1982) and ours is clarified when it is presumed that the group of patients investigated by Bennett et al. (N = 85) included just as many ARF cases as our material. Consequently, there is no reason to correct our interpretation of the influence of tubulointerstitial changes on glomerular function.
Acute Kidney Injury↗
The granular epithelioid cells in the kidney of the lemon sole (Pleuronectes microcephalus Donovani).
Serial sections from kidneys of 5 aglomerular lemon soles (Pleuronectes microcephalus) demonstrated the presence of anastomosing arteriolar networks in the caudal half of the organs. There was no preferred location of the networks, which were found both near the surface and in the deeper parts of the kidney. The size of the networks varied; the largest measured more than 900 micrometers in the longest axis and covered an area larger than 500,000 micrometers2, whereas the smallest measured about 60 micrometers in diameter with an area of 2040 micrometers2. The larger networks were invariably located close to large intrarenal veins. Anastomoses were found between the arteriolar networks and the peritubular capillaries and also associated with veins. The walls of the arterioles were composed of granulated epithelioid cells, exhibiting numerous intracytoplasmic granules. These granules occasionally had a rod-like appearance with a paracrystalline substructure. Using antibodies directed against murine and human renin, the epithelioid cells in the walls of the arteriolar networks and the cytoplasmic granules revealed a positive immunoreaction. The results suggest that the renin-angiotensin system in the aglomerular lemon sole may be important for both the regulation of the systemic blood pressure and the blood supply to the peritubular capillaries of the kidney.
Animals↗
Tubulo-interstitial alterations in type I membranoproliferative glomerulonephritis. An investigation of 259 cases.
A total of 259 kidney biopsies with type I membranoproliferative glomerulonephritis (MPGN) were evaluated, and five grades of glomerular alterations were compared to the following four categories of tubulo-interstitial findings: no changes, interstitial fibrosis (IF), acute renal failure (ARF), ARF and IF combined. The tubulo-interstitial findings proved to be unrelated to the severity of the glomerular alterations. Severe glomerular lesions can be associated with completely normal interstitium and tubules. Conversely, low-grade glomerular lesions may be accompanied by severe tubular and/or interstitial lesions. When the renal cortical interstitium and tubules were normal, then creatinine and blood pressure values were within the normal range; however, these values were significantly elevated in the presence of IF and/or ARF. It is concluded from these findings that in MPGN type I the disturbance in the excretion function of the kidney is caused primarily by tubulo-interstitial changes rather than by glomerular lesions.
Acute Kidney Injury↗