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Biomedical subjects

H D Feiner

Publications and source records attributed to H D Feiner.

At least 55 records · Page 3Linked to original sources

Congenital cystic adenomatoid malformation of the lung in adults.

Congenital cystic adenomatoid malformation of the lung presents mainly in neonates, is rare in children beyond infancy, and has not been reported in adults. Two adult males (aged 24 and 35) had congenital cystic adenomatoid malformation of the right and left lower lobes respectively. A third case, that of a 7-year-old girl, provided the link between the typical neonatal and these adult cases. All three lesions consisted of single or multiple macroscopic cysts, as well as a network of interconnecting spaces (the adenomatoid component). The lining varied from pseudostratified columnar ciliated, to simple mucinous and cuboidal epithelium. Abundant smooth muscle was present in two cases. Cartilage was absent in all three cases. The absence of inflammation is typical of the lesion in neonates. By contrast, all three of our patients had clinical and pathologic evidence of chronic inflammation. We postulate that congenital cystic adenomatoid malformation, when confined to a lobe or segment, may be clinically silent in infancy and may present as pneumonia associated with a cystic lesion on chest x-ray in childhood or later life.

Adult↗

Late presentation of congenital cystic adenomatoid malformation of the lung.

Although most often recognized in neonates and young children, congenital cystic adenomatoid malformation of the lung (CCAM) occasionally appears in later years. Three patients, aged 35, 24, and 7 years, are reported. Chest radiographs in each case suggested a localized patchy density, a cystic mass, or a multicystic mass, but computed tomography (CT) best demonstrated the cystic and solid components while ruling out bronchiectasis or major bronchial obstruction. Bronchography contributed no further diagnostic information compared with CT. Each patient underwent lobectomy. Histologically, the characteristic overgrowth of bronchiolar elements replacing normal parenchymal architecture was accompanied by some superimposed inflammatory change. Each patient had a history of pneumonia, and in such patients, characteristic radiographic features should suggest the possibility of late presentation of CCAM.

Adult↗

Relationship of tissue deposits of cryoglobulin to clinical features of mixed cryoglobulinemia.

Two patients with type 2 mixed cryoglobulinemia had tissue deposits of serum cryoproteins. Patient 1, a 72-year-old man, had purpura and glomerulonephritis. The serum cryoglobulin consisted of monoclonal IgM kappa and polyclonal IgG. Renal biopsy revealed diffuse proliferative glomerulonephritis with abundant IgG, IgM, kappa light chain, and complement in glomerular capillary walls. These immunoglobulins, but no complement, were also present in histologically normal cutaneous blood vessels. Ultrastructurally, cutaneous vascular deposits were identical to the renal deposits and to the crystalline mixed IgM-IgG serum cryoprecipitates and renal deposits previously described. Patient 2 was a 68-year-old man with sensorimotor peripheral polyneuropathy and purpura. His serum cryoglobulin consisted of monoclonal IgA lambda and polyclonal IgG. Sural nerve and skin biopsies revealed vasculitis involving small arteries and arterioles. Immunoglobulin A and complement were present in perineurial arteriolar walls of the sural nerve. Cryoprecipitates in both cases had strong rheumatoid factor activity. These findings support the view that in type 2 cryoglobulinemia tissue deposits consist of cryoprotein immune complexes. The presence of these deposits in histologically normal blood vessels in patient 1 suggests that deposition of cryoproteins precedes and may initiate tissue damage.

Aged↗

Amelioration of experimental glomerulonephritis by dietary protein restriction.

We have examined the effects of various levels of dietary protein intake on the course of nephrotoxic serum nephritis in the rat by feeding low (4.6% casein), standard (23% casein), and high (57.5% casein) protein diets which were identical in calorie, mineral, and electrolyte content. Nephritic rats on a high protein diet manifested heavy proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia, and elevated serum creatinine levels. In those subjected to dietary protein restriction, proteinuria remitted and azotemia did not develop. While mesangial widening, interstitial abnormalities, and segmental proliferation and sclerosis of glomeruli occurred regularly in nephritic rats fed high protein diets, histologic abnormalities were virtually absent in those on low protein intake. Animals on a standard protein intake manifested histologic and clinical features intermediate in severity. We conclude that the renal functional and histologic consequences of nephrotoxic serum nephritis can be averted by dietary protein restriction.

Animals↗

Aggravation of experimental glomerulonephritis by superimposed clip hypertension.

To evaluate the possible enhancing effect of hypertension on the clinical and morphologic features of glomerulonephritis, two-kidney clip hypertension (CH) was superimposed on a mild form of nephrotoxic serum nephritis (NSN) in female Sprague-Dawley rats. The following parameters were assessed regularly over a 6-month period: blood pressure (BP), heart weight, proteinuria (UpV), and renal morphology. Blood pressure and heart weights were increased equally in clip hypertension and in nephrotoxic serum nephritis combined with clip hypertension. While only moderate proteinuria occurred in nephrotoxic serum nephritis (49 +/- 28 mg/24 hr) or clip hypertension (40 +/- 22 mg/24 hr) alone, the superimposition of clip hypertension on nephrotoxic serum nephritis resulted in heavy proteinuria (161 +/- 36 mg/24 hr) (P less than 0.001) after 5 months of hypertension. Glomerular histology in nephrotoxic serum nephritis showed infrequent focal and segmental proliferation and minimal sclerosis; vessels were normal. Clip hypertension was characterized by infrequent and mild vascular sclerosis and glomerular proliferation and sclerosis. Severe glomerular endo- and extracapillary proliferation and widespread glomerular and vascular sclerosis occurred in the majority of rats when nephrotoxic serum nephritis was combined with clip hypertension. The data demonstrate that clip hypertension enhances glomerular proliferation and sclerosis and results in the development of vascular sclerosis in experimental nephritis.

Animals↗

Giant lymph node hyperplasia. An immunopathologic and ultrastructural study of a case of the multicentric plasma cell variant.

A case of the multicentric plasma cell variant of giant lymph node hyperplasia (Castleman's disease) was studied. The left supraclavicular and axillary lymph nodes were affected. The parafollicular region of the lymph nodes was greatly expanded by sheets of mature plasma cells and by regionally concentrated as well as singly occurring immunoblasts. Both plasma cells and immunoblasts were polyclonal, as judged by the heterogeneity of immunoglobulin light-and heavy-chain components documented by immunofluorescence microscopy and immunohistochemistry. Ultrastructurally, free ribosomes and polyribosomes were the predominant cytoplasm organelles seen in immunoblasts. In plasma cells, rough endoplasmic reticulum was typically abundant and often contained electron-dense secretory product.

Female↗

Intrarenal vascular sclerosis in IgA nephropathy.

In this analysis of 43 patients with IgA nephropathy, renal morphology was correlated with clinical data. Gross hematuria and mild proteinuria were typical among younger patients. Among older individuals the clinical spectrum was wider. A comparison with data previously obtained from the normal population indicated that disease-related glomerular sclerosis was present in 1/3 of initial biopsy specimens. The prevalent pattern of glomerular sclerosis was that of global tuft collapse, the type of sclerosis known to result from ischemia. Intrarenal vascular sclerosis was present in 1/3 of initial biopsies. Follow-up specimens from 6 patients showed progression of glomerular sclerosis, vascular sclerosis or both. Hypertension occurred in over 1/4 of patients. It is proposed that progressive renal damage in IgA nephropathy may not be solely immunologically mediated. Glomerular sclerosis may also be mediated by vascular sclerosis, or alterations in intrarenal hemodynamics in glomerulonephritis may have a direct damaging effect on both the glomerulus and the intrarenal vasculature.

Adolescent↗

Nephrotoxicity of nitrosoureas.

Irreversible and progressive renal parenchymal damage and functional impairment occurred in the majority of patients receiving at least six courses (200 mg/m2 of BCNU and/or methyl CCNU at eight-week intervals) of nitrosoureas for therapy of malignant brain tumors. Seventeen of 18 patients who received at least six courses and all nine patients who received more than ten courses developed impaired renal function as judged by elevation of blood urea nitrogen and/or serum creatinine or decrease in filtration rate as determined by inulin clearance. Four patients have developed uremia. Renal tissue obtained from seven patients demonstrated tubular atrophy, interstitial fibrosis and glomerular sclerosis. This remarkably high incidence of renal damage occurred without a phase of acute renal failure and in the absence of significant urinary abnormalities, while producing an insidiously progressive interstitial renal lesion.

Adolescent↗

Acquired cystic disease of kidney in chronic dialysis patients.

Eight cases of acquired cystic disease of the kidney (ACDK) associated with chronic renal failure and hemodialysis are described. No patient had a family history or clinical evidence of congenital adult polycystic kidney disease (CAPKD). Glomerulonephritis was the cause of renal failure in 6, and pyelonephritis in 2. Massive renal and perirenal hemorrhage necessitated 3 nephrectomies in 2 patients. Single kidney weights did not exceed 280 Gm., a major feature in the distinction of ACDK from CAPKD. Morphologically, in addition to the usual stigmata of end-stage kidneys, 40 to 80 per cent of the renal parenchyma was replaced by small cysts. Continuity of cysts with tubules was established by nephron dissection.

Female↗

CT in B-thalassemia: iron deposition in the liver, spleen, and lymph nodes.

The authors report the striking increase in lymph node density due to hemochromatosis observed with computed tomography (CT) in nine patients with Cooley anemia treated with multiple blood transfusions. The CT appearance and pathologic findings of hemochromatosis of the liver and spleen in three of these patients were also observed and correlated with pathologic specimens. CT density of the liver seemed to relate to the degree of hepatic fibrosis or cirrhosis, rather than the amount of iron. Previous reports have not emphasized dense ferritinized lymph nodes in treated Cooley anemia patients.

Adolescent↗

Acute cholecystitis: sonographic-pathologic analysis.

The study was performed to assess the pathogenic basis of sonographically demonstrable changes in the gallbladder wall in acute cholecystitis in an attempt to predict the degree of inflammation and to define a set of sonographic criteria for the diagnosis of acute cholecystitis. Sonograms in a control group of 30 patients (group A) without biliary tract symptoms, ascites, or cholelithiasis and 24 patients (group B) with proven diagnosis of acute cholecystitis were reviewed. The histologic sections of the gallbladder wall in the cholecystitis patients were correlated with sonographic findings. None of the gallbladders showed perforation at the time of pathologic evaluation. Data failed to show a correlation between the pathologic severity of the inflammatory process in the gallbladder wall and the degree of sonographic wall thickening and wall anechoicity. Of patients with acute cholecystitis, 70% met all of the following sonographic criteria: (1) gallbladder wallthickening of 5 mm or greater, (2) gallbladder wall anechoicity, (3) gallbladder distension, as determined by an external anteroposterior width of 4 cm or greater, and (4) cholelithiasis.

Acute Disease↗

Nodular glomerulopathy associated with nonamyloidotic kappa light chain deposits and excess immunoglobulin light chain synthesis.

A nodular glomerulopathy characterized by mesangial deposits of monoclonal kappa light chains was detected by immunofluorescence in a renal biopsy from a patient with proteinuria and hypertension. These nodules lacked the tinctorial and morphologic features of amyloid. Ultrastructurally, the nodules contained electron-dense granular deposits as well as fibrils in parallel arrangement. The fibrils measured 110-140 A in diameter. They were consistent in size with amyloid fibrils. However, they differed in lacking the randomly oriented network of typical amyloid fibrils and more closely resembled fibrils intrinsic to mesangial matrix. The patient had no bone marrow or X-ray evidence of myeloma and no evidence of free monoclonal light chains in serum or concentrated urines. Biosynthetic studies of the patient's bone marrow cells demonstrated unbalanced immunoglobulin synthesis with excess production of monoclonal kappa light chains. These observations suggest that the observed glomerulopathy results from direct deposition of monoclonal light chains. Deposits with kappa light chain determinants have been found in 7 other patients with similar nodular glomerulopathies, 4 of whom had diagnosed clinical myeloma. The lesion of nonamyloidotic nodular glomerulopathy previously described in 19 patients, nor examined by immunopathologic techniques or not shown to contain light chain determinants, may have a similar pathogenesis.

Adult↗

Role of intrarenal vascular sclerosis in progression of poststreptococcal glomerulonephritis.

A comparison has been made of the percentage of sclerotic glomeruli found in normal subjects and in 31 patients 6 months to 15 years after an episode of acute poststreptococcal glomerulonephritis (PSGN). The findings establish that a greater than expected incidence of glomerular sclerosis occurs in the course of PSGN. The pattern of glomerular sclerosis frequently was that of contracted collapsed tufts, one known to result from ischemia. In the majority of specimens with significant glomerular sclerosis, there was co-existent vascular sclerosis (arterioles and/or prearterioles), and the incidence of both glomerular and vascular sclerosis increased with time from onset of PSGN. Intrarenal vascular sclerosis may thus be of major importance in the genesis and progression of glomerular sclerosis in PSGN.

Adolescent↗

Membranes nephropathy associated with renal cell carcinoma. Evidence against a role of renal tubular or tumor antibodies in pathogenesis.

A patient with the nephrotic syndrome due to membranous nephropathy was found to have renal cell carcinoma. Since membranous nephropathy in patients with malignancies has been attributed to a tumor antigen-antibody complex form of glomerulonephritis, an attempt was made to implicate tumor antigens and/or renal tubular epithelial antigens in the pathogenesis of membranous nephropathy in our patient with renal cell carcinoma. Antibodies directed against tumor antigens and renal tubular antigens and renal tubular eipthelial antigens were sought in his serum and in eluates of his glomeruli; no such antibodies were found. The concurrence of the two renal lesions may have been fortuitous in this patient. However, their association temporally suggests that they were related, and our immunologic studies demonstrate that tumor antigen-antibody complexes are not invariably involved in the pathogenesis of malignancy-associated membranous nephropathy.

Adenocarcinoma↗

Pseudomonas cepacia endocarditis and ecthyma gangrenosum.

A case of right-sided Pseudomonas cepacia endocarditis in a heroin addict is presented in which septic cutaneous vasculitis (ecthyma gangrenosum) is a prominent feature. Ecthyma gangrenosum, most commonly associated with sepsis due to P aeruginosa, has not been previously described with P cepacia septicemia.

Adult↗