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PubMed1990

The evolution of benign arterionephrosclerosis from age 6 to 70 years.

Arterionephrosclerosis is diagnosed at autopsy by assessing the severity and extent of certain structural features in the renal cortical arteries seen in tissue sections. These features are characterized by fibrotic intimal thickening and medial shrinkage, a progressive change from the youthful muscular pattern to the elderly sclerotic pattern. Intimal fibrosis can be quantified by expressing intimal thickness as a percentage of the arterial outer diameter (% OD). The magnitude of arterionephrosclerosis, found by averaging the measures of intimal fibrosis seen in a kidney, can be calculated from age and mean blood pressure, using a standard prediction function. This function is a quantitative statement of a fundamentally important principle: just as blood pressure is a continuous variable that can range from low to high levels, arterionephrosclerosis is also a continuous variable that can take any degree of abnormality of arterial structure from minimal to maximal. Furthermore, a correspondence exists between the two quantities so that each can be calculated from the other. In this study, a correlation of 0.966 was found between the observed and the calculated magnitudes of arterionephrosclerosis over 10-year age groups from 25 to 34 years to 65 to 74 years, using group average data within age groups. For individuals, however, the correlations between observed and calculated magnitudes of arterionephrosclerosis were about 0.6 in a former study of elderly subjects and about 0.1 in the subjects aged 6 to 27 years in this study. The average growth rate of arterionephrosclerosis was found to be about 0.25 %OD per year from ages 15 to 54 years, and about 0.13 %OD per year from ages 55 to 70 years; the growth rate did not increase in the oldest age groups when blood pressure averaged higher than blood pressure in more youthful subjects. These and other findings are consistent with the view that the reason a correlation exists between blood pressure and arterionephrosclerosis could be because the magnitude of arterionephrosclerosis is one of the determinants that sets the level of blood pressure. From this perspective, each individual can be viewed as having other determinants of blood pressure, methodologic or biologic, which add to or subtract from the values set by age and arterionephrosclerosis. When subjects are pooled into groups, so that individual determinants balance out, the group average levels of mean blood pressure could be interpreted as reflecting little other than the magnitude of arterionephrosclerosis at each specific age.

Adolescent↗
PubMed1975

Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years.

The purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the

Adult↗
PubMed1989

[A patient with psoriatic arthritis and secondary amyloidosis].

A case of a man suffering from psoriasis vulgaris is presented. The onset of the disease was at the age of 5. From the age of 14 all joints were gradually affected by the type of severe, symmetrical psoriatic arthritis which led to aseptic necrosis of the hip joints. In the course of the disease, from 1988 on, proteinuria and nephrotic syndrome were found. The renal biopsy proved amyloidosis which is considered secondary, developed on the basis of psoriatic arthritis. The severe psoriatic arthritis with especially emphasized clinical activity is in this case the pathologic antigenic stimulus for the amyloid formation. The clinical course and the histologic findings from the renal biopsy point to serious structural disorders of the renal parenchyma which determine the progressing tendency toward chronic renal failure.

Adult↗
PubMed1977

Quantitative studies of immunoglobulin deposition in the kidney, glomerular cell proliferation and glomerulosclerosis in NZB/NZW F1 hybrid mice.

Using the NZB and NZB/NZW F1 (B/W) hybrid mouse as a model for systemic lupus erythematosus, an effort has been made to quantitate: (1) immune complex deposition in the glomeruli by immunofluorescent staining of immunoglobulin, (2) glomerular cellular proliferation by radioautographic measurement of [3H]Tdr incorporation into the glomerular cells in vivo, and (3) glomerular scarring by PAS staining. The relationship between these changes and increasing age has been examined. By radioautography it was observed that dividing glomerular cells were labelled in vivo after injection of [3H]Tdr. This provided a reproducible measure of the proliferative process in the nephritis of B/W mice. In C57B1/6J and CBA/J mice, which have a low incidence of glomerular disease, little change in the amount of glomerular cell proliferation was observed with increasing age. The NZB strain of animals showed a somewhat increased level of proliferation but this did not increase with age. In striking contrast, glomerular cell proliferation in the B/W mice increased rapidly with age. The earliest change observed in the kidney was the deposition of immunofluorescent material in the mesangium and glomerular capillary basement membrane beginning between 3 and 5 months of age and reaching a peak at 9 months. Increase in glomerular cell proliferation began about 2 months after the onset of immune complex deposition but also reached a maximum at 7 months. Glomerular sclerosis was the last change to appear and continued after the other two parameters measured has begun to decline. These data suggest that the deposition of immune complexes in the glomerulus may be an important triggering mechanism for renal cell proliferation and glomerulosclerosis in the B/W mouse. The techniques described would provide a sensitive and reproducible quantitative method for analysing the differential effects of various types of treatment of immune complex nephritis in animals.

Age Factors↗
PubMed1978

[The importance of echography in the differential diagnosis of renal insufficiency (author's transl)].

Experience with echographic investigation of the kidney and the urinary efferent system in the diagnosis of renal insufficiency is reported. Taking into account a number of criteria (size, differentiation from the surrounding tissues, position of the kidney in relation to neighboring organs and to the body surface, mobility or change of shape on respiration, on altehe evaluation of the nephroechographic findings an attempt is made to rationalize the applicatinon of further diagnostic measures. The method is recommended both for the initial diagnosis of renal insufficiency and for the supervision of patients with confirmed renal insufficiency.

Adolescent↗
PubMed1986

Original disease of the recipient.

1. The influence that a patient's original disease had on the outcome of kidney transplantation was small when recent transplants (1983 to present) were examined. A difference of only 5% was seen in one-year graft survivals of first cadaver donors. The average one-year survival was 70%; patients with pylonephritis having the best (75%) and SLE patients the worst (65%) survival rates among the major disease categories. 2. There was little difference observed in patient survivals or functional graft survivals in first cadaver transplants among patients with different original diseases. This was also the case with cadaver regrafts; with the exception of polycystic kidney patients who had quite poor graft survival (41% at one year) with regrafts. Pretransplant blood transfusions resulted in increased cadaver graft survival; however the low number of nontransfused patients in many disease categories presented difficulties in examining this effect. 3. The use of cyclosporine resulted in increased cadaver graft survival in all disease categories. One-year cadaver graft survival of cyclosporine-treated patients averaged 75% compared to 63% with noncyclosporine-treated patients. A beneficial effect of cyclosporine use was not consistently seen in transplants involving living-related donors, although perhaps larger numbers of patients are required in order to confirm this observation. 4. Graft survival in diabetic patients was quite good in this analysis of recent transplants. First cadaver one-year graft survival in diabetics was only 4% below the overall average and 2% less with cyclosporine. Patients with both juvenile (75% one-year graft survival) and adult-onset (78% one-year graft survival) forms of the disease had good graft survival when cyclosporine was used for immunosuppression.

Diabetes Mellitus↗
PubMed1988

[Disordered permeability of the glomerular filter for middle- and high-molecular serum proteins in various morphologic types and stages of chronic glomerulonephritis].

Investigation of glomerular filter permeability for serum immunoglobulins and albumins in 83 patients with chronic glomerulonephritis (CGN) with nephrotic proteinuria has shown that in mesangioproliferative glomerulonephritis permeability for IgM is rare, for IgA and IgG moderately raised; in a marked but not maximum degree of permeability for albumins, it is characterized by considerable variability. In maximum permeability for albumins there is a tendency to the reduction of the ratio of IgA and IgM clearances to albumin clearance, and variability of these indices. In membranous CGN the structure of nephron permeability for serum proteins is identical but it remains unchanged with a sharp rise of albumin fractional clearance. In mesangiocapillary CGN permeability for IgM is more frequent and enhanced for IgG. in focal-segmental glomerular hyalinosis/sclerosis and diffuse-fibroplastic GN permeability for IgG is considerably raised unrelated to a degree of permeability for albumins. Sclerotic changes are accompanied by elevated permeability for IgG.

Adolescent↗
PubMed1988

Renal glomerular and tubular abnormalities in glycogen storage disease type I.

Three children had renal histopathologic findings indicative of glycogen storage disease type I. Glomerular basement membrane (GBM) alterations were present in the three patients, particularly so in the two patients with proteinuria. Thickening, lamellation, and glycogen deposition were the characteristic alterations in the GBM. Glomerulosclerosis was prominent in one patient. We suggest that the GBM alteration is related to the glomerular sclerosis and that both are related to metabolic derangements of glycogen storage disease type I.

Adolescent↗