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J I Scheinman

Publications and source records attributed to J I Scheinman.

53 records · Page 3Linked to original sources
PubMed1980

The immunohistology of glomerular antigens. V. The collagenous antigens of the glomerulus.

Distinct antigenic loci are present within the human glomerulus as demonstrated by high resolution epifluorescent and phase-contrast microscopic techniques using affinity-purified antibody to characterized collagens. Type IV mouse tumor procollagen and type V collagen are present within the mesangium and along the endothelial aspect of the glomerular basement membrane, demonstrating antigenic continuity between these two glomerular zones. In contrast, antiserum to type IV collagen from bovine lens capsule reacts with the full thickness of the glomerular basement membrane, as well as in the tubular basement membrane and Bowman's capsule. Types I procollagen and collagen are found within the epithelium; and types III collagen and procollagen are not detected within the glomerulus. The functional role of the multiple distinct "basement membrane" collagens in the glomerular capillary wall is unknown. A complex structure is suggested, especially in the mesangial-subendothelial continuity, and in the differential localization of two forms of type IV collagen within the glomerular basement membrane.

Animals↗
PubMed1978

Collagen synthesis by human glomerular cells in culture.

Collagen synthesis was studied in three subcultured human glomerular cell types, by radiolabeled incorporation of [14C]proline and [3H]lysine. The epithelioid circular glomerular cells secrete a collagen with a single size of chain (possibly type IV) with a high ratio of hydroxyproline to proline, hydroxylysine to lysine, and 11--17% of hydroxyproline as the 3-isomer. The smooth muscle-like rhomboid glomerular cells secrete collagen with a chain pattern suggesting types III and I collagen, distinct from that found in the media of fibroblasts. Small ovoid glomerular cells are morphologically and biochemically intermediate between circular glomerular cells and rhomboid glomerular cells, and may represent an in vitro modification of either circular glomerular cells or rhomboid glomerular cells.

Basement Membrane↗
PubMed1978

The immunohistopathology of glomerular antigens. III. Increased mesangial actomyosin in experimental diabetes in the rat.

Antisera to rat smooth muscle actomyosin (AMY) and myosin localize in the rat glomercular mesangium. The width of mesangial staining for AMY is increased in rats diabetic for four months (p less than 0.01) and seven months (p less than 0.0005) compared with age-matched controls. Mesangial AMY staining of unilaterally nephrectomized control animals was moderately increased after seven months, whereas unilaterally nephrectomized diabetic rats had prominently increased AMY mesangial width at four months, when they were compared with intact diabetic animals (p less than 0.05). Thus, a distinctive alteration that is found in human diabetic nephropathy also occurs in experimental (streptozotocin) diabetes in the rat. Further, this alteration appears to be accelerated by the changes in nephron hemodynamics resulting from unilateral nephrectomy. While the function of mesangial AMY is unknown, it may be related to intrarenal regulation of glomerular ultrafiltration, which appears to be altered in diabetic nephropathy in man.

Actomyosin↗
PubMed1978

The immunohistopathology of glomerular antigens. II. The glomerular basement membrane, actomyosin, and fibroblast surface antigens in normal, diseased, and transplanted human kidneys.

Immunofluorescent studies have demonstrated that actomyosin (AMY) is present in the mesangium in a restrictive pattern, whereas fibroblast surface antigen (FSA) has a more extensive mesangial distribution. Antibody to glomerular basement membrane (GBM) is localized to the GBM. One hundred ninety-six tissue samples, including 17 from normal subjects, 94 from patients with primary renal diseases, and 85 from transplanted kidneys, were examined for changes in distribution of AMY, FSA, and GBM antigens. The distribution of AMY and FSA in the mesangium is markedly increased in width in patients with diabetic nephropathy, and the GBM is thickened. AMY and FSA are mildly increased in patients with glomerulonephritis and GBM is normal. Patients with membranoproliferative glomerulonephritis (MPGN) show a loss of all glomerular antigens. Increased mesangial AMY was found in 12 of 37 transplanted kidneys in diabetic patients vs 4 of 33 nondiabetics 0 to 4 years after transplantation (P < 0.025). This difference is more notable at 2 to 4 years, with 5 of 9 diabetics showing increased AMY vs 0 of 6 nondiabetic patients (P < 0.0005). In MPGN, 5 of 8 tissues showed decreased mesangial AMY vs 3 of 36 diabetic patients (P < 0.0005) and 1 of 32 patients with other glomerulopathies (P < 0.0005). GBM thickening is not associated with specific pretransplant diseases. In transplanted kidneys, the pattern of FSA is dissociated from that of AMY: over half of all patients have increased FSA, even when AMY is normal. Whether this unique finding in transplanted kidneys reflects an increase in the synthesis of FSA by mesangial cells or the failure to clear this (circulating) antigen from the mesangial matrix is unknown.

Actomyosin↗
PubMed1978

Human glomerular cells in culture. Three subcultured cell types bearing glomerular antigens.

In this paper, we describe three cell types from the explanted human glomerulus: the circular glomerular cell (CGC), the rhomboid glomerular cell (RGC), and the small ovoid glomerular cell (SOGC). These cells were compared with subcultured human umbilical vein endothelial and smooth muscle cells, uterine smooth muscle cells, and skin fibroblasts. Immunochemical comparisons utilized antiserums to antigens in the human glomerulus: antiglomerular basement membrane, antifibroblast surface antigen (FSA) (reactive extensively with the mesangium), antiactomyosin (AMY) localizing more restrictively in the mesangium, and antihemophilic factor (AHF) localizing to the endothelium. No cultured glomerular cells bore the AHF marker of endothelial cells. The epithelioid CGC excrete most GBM antigen as an orderly palisade of granules from the cell surface. FSA is rapidly lost from the cell surface. RGC have a typical multilayered smooth muscle morphology and have a most prominent complex AMY pattern of periodic aggregates and fibrils. FSA adheres to the cell surface. SOGC form an initial nonoverlapped monolayer resembling endothelial cells but elongate and form multilayers after confluency. The AMY fibril pattern of SOGC is distinctively multidirectional. The translation of in vitro characteristics into in vivo identification must be interpreted cautiously: CGC may derive from glomerular epithelial cells; RGC may derive from mesangial cells; and SOGC may represent a more rapidly proliferating, less differentiated form of the epithelial cell or another, unidentified, glomerular cell type.

Antigens↗
PubMed1978

C3b receptors on human glomeruli in vitro. Loss in culture.

C3b receptors, easily demonstrated on isolated human infant glomeruli, are lost as cells grow in culture. This suggests that epithelial cells are dedifferentiated or that the C3b receptor is not intrinsic to the epithelial cell.

Cells, Cultured↗
PubMed1976

Immunopathological studies of the ruptured human renal allograft.

The immunopathology of five cases of spontaneous allograft rupture has been studied. All kidneys were edematous on exploration and routine histological sections showed interstitial edema and mononuclear cell infiltration characteristic of acute rejection. Immunofluorescence revealed, at most, scattered vascular deposition of IgM and mild mesangial C3 deposition. These findings are compared with findings in normal kidneys and kidneys which had been hyperacutely rejected. The normal kidney showed focal afferent arteriolar and proximal mesangial stalk deposition of C3 without IgM. The kidneys of patients with hyperacute rejection showed brilliant staining for fibrin and IgM in all arterial and arteriolar walls with lesser amounts of C3 and IgG; IgM and C3 were prominent in the glomerulus. These findings suggest that mechanisms other than circulating preformed antibodies are responsible for the pathogenesis of spontaneous allograft rupture.

Fluorescent Antibody Technique↗
PubMed1976

Human glomerular smooth muscle (mesangial) cells in culture.

Glomerular smooth muscle cells were grown and subcultured from human glomeruli in vitro. These cells, stained with antiserum to smooth muscle actomyosin and examined by immunofluorescence, had brightly stained intracellular fibrils similar to those seen in smooth muscle cells. Actomyosin fibrils were altered by conditions affecting actomyosin in vitro. Glomerular smooth muscle cells lacked the antihemophilic factor and blood group antigens present in endothelial cells, and are, therefore, most likely derived from the smooth muscle cells of the glomerular mesangium. By radio-labeled amino acid analysis, they synthesize a collagen differing from that of fibroblasts, and which probably differs from basement membrane collagen. Other cell types could be grown and subcultured using a different glomerular isolation technique, culture medium and method of subculture.

Actomyosin↗
PubMed1974

The immunohistopathology of glomerular antigens. The glomerular basement membrane, collagen, and actomyosin antigens in normal and diseased kidneys.

The immunofluorescent localization of antisera to human glomerular basement membrane (GBM), collagen, and smooth muscle actomyosin was examined in 15 specimens of normal renal tissue and 98 specimens from patients with renal disease. The anti-GBM and anticollagen antisera normally localize to GBM, while antiactomyosin localizes to the mesangium. Diabetic nephropathy revealed a striking expansion of mesangial material reacting with antiactomyosin. In contrast, the expanded mesangium in membranoproliferative glomerulonephritis did not react with antiactomyosin, and the GBM localization of anti-GBM and anticollagen sera was similarly lost. The thickened GBM in diabetes mellitus and membranous nephropathy reacted with anti-GBM and anticollagen, but with accentuation of staining on the inner aspect of the GBM. In proliferative glomerulonephritis there was a moderate increase in the distribution of actomyosin. Glomerular sclerosis and hyalinization in all diseases studied was accompanied by a loss of immunofluorescent staining for all glomerular antigens, including collagen.

Actomyosin↗
PubMedDate not supplied

Hypercholesterolemia and growth hormone in renal diseases.

The interrelationships of hypercholesterolemia, progression of renal disease to renal failure, and to risks of nephrotic syntrouse are emerging. Both hypercholesterolemia and growth hormone are progression factors, and, in the chronically nephrotic patient, these factors may help to explain the progression to renal failure. Treatment of such patients with growth hormone even though growth retarded should be approached with caution.

Animals↗
PubMedDate not supplied

Perspective of a pediatric nephrology program: an 18 year retrospective.

We analyzed the patient profile in a pediatric nephrology training program, along with data collected over an 18 year period, to determine whether there is merit in the proposition that clinical training can be obtained equally well in internal medicine nephrology training programs. We also compared the rate of patient referral in an U.S. metropolitan area with a population of 1.2 million, in the first 9 years without the "gatekeeper" health insurance system and the next 9 years with managed care competition. Finally, we discussed guidelines for renal biopsy in the child and approaches to treatment as practiced in a pediatric nephrology program of almost two decades. We used the same NIH clinical data form throughout the 18 years of data collection to record clinical, laboratory and biopsy diagnosis, dialysis/ transplantation and other treatment data of patients entering our outpatient and inpatient services. Between 1977 and 1996, 3,150 new patients were examined for disorders related to the kidney. Twenty-one per cent of the patients were in the first year of life and 50% were younger than seven years of age. The majority of the 389 percutaneous renal biopsies were done in children under 10 years of age. In addition, almost half of the 112 pediatric dialysis/transplant patients presented before 10 years of age. Thus, the majority of patients were in the early years of life, with an unique pattern of renal diseases and issues regarding therapy which are clearly different from adulthood. Therefore we concluded that the existing data did not support the proposition that pediatric nephrology training be absorbed into internal medicine nephrology programs. The introduction of managed care competition did not affect the rate of patient enrollment. In fact, the rate of referrals in the latter 9 years paralleled the first 9 years. The factors which contribute to this outcome are discussed. Such data should be useful to those trying to meet the challenges of this competitive era. Finally, we discussed guidelines for renal biopsies in children and approaches to specific diseases.

Adolescent↗
PubMedDate not supplied

Recent data on results of isolated kidney or combined kidney/liver transplantation in the U.S.A. for primary hyperoxaluria.

Renal transplant for primary hyperoxaluria (PH) has been problematic. K/L-Tx is used almost exclusively in Europe. In USRDS data 235 patients had PH diagnosed at ESRD, another 47 found later. Since 1994, there were 176, since our modern management protocol, 96 under age 55. Of 82 non-K/L-Tx, 40 of 49 were alive after K-Tx, 14 of 33 without Tx. By lifetable analysis, survival was better for K-Tx (85% at 5 yrs, 75% at 10 yrs) than for non-Tx patients (40% at 5 yrs, 75% at 10 yrs) (P < .001). First Tx graft lifetable survival was 70% for LRD, 50% for CAD Tx at 3 yrs, both 40-45% at 5 years (N.S.). Twenty-eight K/L-Tx PH patients from the UNOS database had projected survival 50% at 5 yrs. Overall, transplant is better for patient survival than no transplant. While curative, K/L-Tx still has considerable risk in the U.S., but could follow failed K-Tx. Confirmation of PH and ruling out B6 sensitivity must precede K/L-Tx to justify its risk. Post Tx management for K/L-Tx must follow protocols developed to prevent oxalate recurrence for K-Tx.

Databases, Factual↗