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Biomedical subjects

J Churg

Publications and source records attributed to J Churg.

At least 91 records · Page 5Linked to original sources
PubMed1976

Glomerular morphology in nephrotic heroin addicts.

Renal biopsies of 23 heroin addicts who presented with the nephrotic syndrome were examined by light and electron microscopy. The majority of patients (14) showed focal segmental glomerular sclerosis on light microscopy, four patients showed "minimal change", and two were classified as "focal global sclerosis." In one case focal mesangial proliferation was the outstanding feature; one patient had diabetic glomerulosclerosis; and one had mesangiocapillary glomerulonephritis and dysproteinemia. Visceral epithelial swelling and proliferation were present in 14 patients on light on light microscopy. Electron microscopy showed distinct podocyte changes consisting of loss of foot processes, vacuolization, and cytoplasmic degeneration; focal separation of podocytes from basement membranes was found in 11 of 18 cases. In some instances a few electron-dense deposits were present in the mesangium. Membranous nephropathy was not encountered, although it occurs in 30 to 40% of unselected adult nephrotic individuals. Of 15 patients followed for 2 months to 5 years, one died of heroin overdose, eight went into renal failure, two improved, and four continued to have proteinuria. It is concluded that nephrotic syndrome of heroin addicts is most often associated with focal segmental glomerular sclerosis and occasionally with minimal change disease or focal global sclerosis. Conceivably these three conditions represent different phases of one disease process, although different reactions to heroin or its various vehicles and contaminants cannot be excluded. The morphologic resemblance to experimental aminonucleoside and N,N'-diacetylbenzidine-induced nephrosis suggests a possible toxic origin.

Adolescent↗
PubMed1976

Mesangial involvement in hemolytic-uremic syndrome. A light and electron microscopic study.

Electron microscopic analysis of the mesangial injury in the hemolytic-uremic syndrome was performed in 10 patients. Proteinaceous material similar to that found in the subendothelial region was also seen focally in the mesangium altering the matrix and imparting a reticular appearance. This degenerative process was associated with reparative changes in the glomerular tuft. Many of the mesangial cells were hypertrophied and demonstrated phagocytic activity and peripheral extension of their cytoplasmic processes. Mitotic figures in endothelial as well as mesangial cells were regarded as evidence of a reparative process. Severe mesangial insudation of material containing fibrinogen derivatives resulted in segmental tuft necrosis with almost complete replacement and destruction of the mesangial matrix. On some occasions, a break of the glomerular basement membrane was accompanied by the escape of intraluminal contents into the urinary space, leading to crescentic epithelial cell proliferation.

Adolescent↗
PubMed1975

Radiation nephritis: a review.

Radiation nephritis is a process of necrosis, atrophy and sclerosis that follows exposure of the kidney to ionizing radiation. Experimental studies with electron microscopy demonstrate that this process begins as degeneration of the glomerular endothelium and the tubular epithelium, and their basement membranes, leading to collapse of these structures and the development of interstitial fibrosis. Rather late and complicating events are necrosis and thrombosis of arteries and arterioles, contributing to the destruction of the renal parenchyma. The process is the same with large doses (5,000 to 10,000 rads) and with medium doses (1,000 to 3,000 rads), the only difference being the extent and the speed with which the lesions develop and the frequency of arterial necrosis.

Abdominal Neoplasms↗
PubMed1975

Focal glomerular sclerosis in nephrotic patients: an electron microscopic study of glomerular podocytes.

Renal biopsy specimens of 16 adult patients with nephrotic syndrome and focal glomerular sclerosis were examined by light and electron microscopy. Particular attention was paid to alterations of podocytes. Except for loss of foot processes, five patients had no podocyte changes, five had mild changes and six had severe changes. Of the last group (group III), four patients were heroin addicts, the fifth had infectious mononucleosis and the sixth, an apparent idiopathic disease; five patients were males, 16 to 25 yr old. Podocyte changes consisted of cytoplasmic degeneration, detachment of epithelial cells from basement membranes, with filling of resulting space by cell debris and new membranes. Underlying capillaries were often collapsed. Repeat biopsies in three patients in group III revealed progression of lesions, paralleling rapid clinical deterioration. It is concluded that some cases of focal glomerular sclerosis are associated with severe damage to podocytes which may be caused by drugs, infection or unknown factors and may contribute to the development and progression of the glomerular lesions.

Adolescent↗
PubMed1975

Recurrent hemolytic-uremic syndrome: a case report.

A girl who developed HUS at 2 years of age had four further episodes of the disease during the next 2 1/2 years. No renal or hematologic abnormalities were detected during or between the attacks. Reduced levels of serum complement were found during three of the episodes.

Child, Preschool↗
PubMed1974

Electron microscopic studies in hereditary nephritis.

A characteristic electron microscopic lesion-longitudinal splitting of the glomerular basement membranes with accumulation of dark particles-was found in some cases of hereditary nephritis, especially in Alport syndrome. A somewhat similar but less specific alteration was present in the tubular basement membranes and in the Bowman capsule. The lesions tended to exhibit a familial segregation. The possible pathogenesis of the lesions and their relation to physiologic abnormalities are briefly discussed.

Basement Membrane↗
PubMed1973

Structure and development of the glomerular crescent.

Twenty patients with idiopathic extracapillary glomerulonephritis and 16 patients with other forms of crescentic glomerulonephritis were examined by light and electron microscopy. Crescents were found to be composed of several types of cells which can be divided roughly into two groups: light and dark cells. Most of the crescent cells are apparently derived from the pariental epithelial cells of the Bowman's capsule, but at least in some cases podocytes participate in the cresent formation. Breaks in the glomerular capillary basement membrane were frequently seen (in 11 of 15 patients with idiopathic disease and in 4 of 15 other patients). Such breaks may significantly contribute to the leakage of fibrinogen and red blood cells into the Bowman's space and thus accelerate crescent formation. Proliferation of the epithelial cells appears to be related to precipitation of fibrin, though it is uncertain whether the actual stimulus is provided by the fibrin or by a coprecipitate of some normal or abnormal serum protein. Some of the proliferated cells acquire features of fibroblasts and are presumably responsible for laying down of collagen in the crescent, while other cells demonstrate phagocytic properties. These metaplastic changes of the epithelial cells are briefly discussed.

Adolescent↗