PubMed Health⌕ Search

Biomedical subjects

R L Vernier

Publications and source records attributed to R L Vernier.

At least 73 records · Page 4Linked to original sources
PubMed1976

Development of diabetic vascular lesions in normal kidneys transplanted into patients with diabetes mellitus.

We examined renal-transplant tissue from 12 diabetic and 28 nondiabetic patients who had had a renal graft for at least two years. In 10 diabetic patients arteriolar hyalinosis lesions developed in the graft. In six these lesions involved both afferent and efferent limbs of glomerular arterioles - a pathological finding virtually diagnostic of diabetes mellitus. In all cases these lesions were present within five years of transplantation. Only three of the 28 nondiabetic patients had hyaline vascular changes (P less than 0.001), which occurred only in rare vessels, did not appear within the first five years after transplantation and did not involve both afferent and efferent arterioles, One diabetic patient had nodular glomerulosclerosis. Thus, the first clearly distinguishable lesion of diabetes to occur with frequency in normal kidneys transplanted into diabetic patients is arteriolar hyalinosis.

Adolescent↗
PubMed1976

Natural remission of nephrotic syndrome in a dog with immune-complex glomerular disease.

A nephrotic syndrome caused by immune-complex glomerular disease was diagnosed in a 4-year-old male Great Dane. The syndrome was characterized by proteinuria, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, and subcutaneous edema. Renal biopsy revealed segmental membranous glomerular disease. The edema underwent complete remission 18 days after admission. Two months after admission, there was no clinical or laboratory evidence of glomerular disease. Periodic reevaluation of the dog during the next 2 years revealed recurrence of proteinuria, but no other clinical or laboratory abnormalities. Serial renal biopsies revealed persistence, but no appreciable increase, in the severity of the segmental membranous glomerular disease. The natural course of the nephrotic syndrome and immune-complex glomerular disease has been associated with unpredictable variability. It was concluded that the widespread use of corticosteroid or immunosuppressant therapy in dogs with immune complex glomerular disease should be withheld until the natural course of the disease has been evaluated in a significant number of patients and until the results of well-controlled clinical studies confirm or deny their therapeutic value.

Animals↗
PubMed1976

Recurrence of membranoproliferative glomerulonephritis following kidney transplantation. Serum complement component studies.

Sixteen patients with membranoproliferative glomerulonephritis who required kidney transplantation because of renal failure were evaluated for evidence of recurrence of the original disease by serologic and morphologic studies. Of the 12 patients with transplant tissue available for study, seven showed membranoproliferative glomerulonephritis by light morphology. Four of these seven also had hypocomplementemia, and this hypocomplementemia was characterized by decreased serum CH50, C3 beta1A or C3-C9 but norma serum C1, C4 and C2 by hemolytic assay. Immunofluorescent microscopy demonstrated more intense glomerular deposition of C3 and properdin in the hypocomplementemic patients. Ultrastructural studies demonstrated intramembranous deposits typical of dense deposit disease in one patient who also had marked hypocomplementemia. One patient who had two transplant biopsies and persistent hypocomplementemia showed progression from predominantly mesangial glomerular changes to both capillary wall and mesangial abnormalities. This study has shown a high rate of recurrence of membranoproliferative glomerulonephritis in the transplanted kidneys. A high death rate was noted in persistently hypocomplementemic patients. The serum C profile in hypcomplementemic patients who received translants was similar to that seen before transplantation, but the signficance of this finding remains unknown.

Adolescent↗
PubMed1976

Extramembranous glomerulonephritis in childhood: relationship to systemic lupus erythematosus.

Extramembranous glomerulonephritis is an uncommon but distinct pathologic lesion in children. The diagnosis is established by the characteristic light, immunofluorescent, and ultrastructural abnormalities in renal biopsy specimens. This report describes seven of the ten children with this lesion studied in the past 11 years. Emphasis is given to the comparison of four children with idiopathic membranous glomerulonephritis with three others who presented with a nephrotic syndrome but subsequently developed evidence of systemic lupus erythematosus. Two of the latter three children, and three others with SLE and MGN not described in detail, demonstrated deposition of IgA by immunofluorescence along glomerular capillaries. Five of six children with SLE and MGN had microtubular structures in glomerular endothelial cells demonstrable by electron microscopy. These observations suggest that children with MGN require careful and continuing study for evidence of SLE.

Adolescent↗
PubMed1976

The glomerular mesangium: uptake and transport of intravenously injected colloidal carbon in rats.

Collodial carbon, 70 mg/100 g, was injected into rats which were sacificed for histologic study of the kidneys at intervals of five minutes to seven weeks. Transient thrombocytopenia and albuminuria were observed. Uptake of carbon by the mesangium of glomeruli was maximal at 32 hr and gradually decreased thereafter. Semiquantitative analysis of the distribution of carbon particles within glomeruli revealed a predominately peripheral localization during early time periods, and increased relative concentration of particles within more central zones and in the lacis area at the vascular pole of the glomerulus at two to seven weeks, indicating that one of the mechanisms for clearance of materials from the mesangium was movement of particles in the direction of the lacis area. Sequential electron microscopic studies showed that carbon particles moved through fenestrae in the endothelium covering the mesangium into channels between mesangial cells. Observations at later intervals suggested that carbon eventually reached the vascular pole by being passed on from one mesangial cell to the next. Vasoactive amines or other substances derived from platelets may play an important role in initiating the process of mesangial uptake.

Albuminuria↗
PubMed1976

Unilateral renal disease in the rat. II. Glomerular mesangial uptake of colloidal carbon in unilateral aminonucleoside nephrosis and nephrotoxic serum nephritis.

Unilateral renal disease was produced in rats by left renal perfusion in situ with the aminonucleoside of puromycin or with nephrotoxic serum. The uptake of colloidal carbon by the glomerular mesangium was increased in kidneys perfused with aminonucleoside or nephrotoxic serum compared to contralateral kidneys. The quantities of carbon within the glomerular mesangium remained increased in aminonucleoside perfused kidneys 14 days later. These studies demonstrate that alterations in glomerular mesangial function in aminonucleoside nephrosis and nephrotoxic serum nephritis are related to renal factors rather than differences in host milieu and may be involved in the pathogenesis of the morphologic lesions seen in chronic proteinuria.

Animals↗
PubMed1976

Normal development and experimental models of cystic renal disease.

From a review of renal development and experimental cystic disease, the following observations can be made: 1. The previous theories developed to explain cystic renal disease (nonunion, failure of regression, and obstruction to urine flow) do not adequately fit with the numerous recent observations made in studies of most experimental models or in human renal cystic disease. 2. The most acceptable theory to date for most types of renal cystic abnormalities (except those due to known obstruction of urine flow) is that abnormalities of the tubular supporting wall occur, probably as a result of toxic or metabolic injury to the tubular cells of the wall and the related interstitial tissues, which are exposed to the highest concentrations of these compounds. This theory would also help explain the etiology of cystic renal diseases in man and should lead to attempts to isolate toxic factors or enzyme abnormalities in susceptible families and in early cases. 3. Induction of cystic abnormalities through a variety of experimental manipulations and drugs reveals impressive strain, sex, and species variability, and these differences should be more carefully examined. 4. The same chemical that induces a cystic change in the mature, fully developed kidney may cause changes which are quite different (location, severity, etc.) in both the fetal and newborn kidney, in which continual nephrogenesis is occurring. 5. Many of the previous explanations of cystic changes require careful reinterpretation of the findings (to reconcile certain differences), and confirmatory studies should be performed to help piece together some of the puzzling observations noted, such as the cystic changes seen with adrenocorticosteroids, and their relationship to potassium depletion.

Adrenal Cortex Hormones↗
PubMed1975

Acute eosinophilic interstitial nephritis and renal failure with bone marrow-lymph node granulomas and anterior uveitis. A new syndrome.

We describe two patients with a unique granulomatous syndrome who presented with renal failure secondary to diffuse eosinophilic interstitial nephritis. Both had bilateral anterior uveitis, bone marrow granulomas, hypergammaglobulinemia and an increased sedimentation rate. One patient had lymph node granulomas and an immunoglobulin G (IgG) rheumatoid factor. An extensive investigation for an etiologic agent was unrewarding, and neither patient could be placed into any existing diagnostic category. Over a period of 2 years both patients have experienced improved renal function and dissolution of their bone marrow granulomas.

Acute Kidney Injury↗
PubMed1975

Human glomerular cells in tissue culture.

Cells from human glomeruli explanted in tissue culture were grown and subcultivated up to 12 to 13 times. Light and electron microscopic studies revealed these cells to be morphologically distinct from fibroblasts. By electron microscopy, an extracellular material resembling basal lamina was seen and prominent intracellular microfilaments were evident. Immunofluorescent microscopy demonstrated reactivity of heterologous antiglomerular basement membrane antibody with aggregates of extracellular material. Absorption experiments using antiglomerular basement membrane antibody showed that the extracellular materiial shared some antigenic components with glomerular basement membrane. Antibody to cultured glomerular cells stained the mesangium and glomerular basement membrane of normal human kidney. This antibody was nephrotoxic in monkeys, induced proteinuria with proliferative glomerulonephritis, and localized to the mesangium and glomerular basement membrane of monkey glomeruli. These findings and the presence of prominent intracellular microfilaments (contractile elements) suggest that the glomerular cells may be of mesangial origin.

Adult↗
PubMed1974

Hematogenous Streptococcus faecalis pyelonephritis in the rat. A histologic, immunopathologic and bacteriologic study.

The demonstration of bacterial antigens in active pyelonephritis in man has been inconsistent. In this paper we have studied 110 rats with experimental pyelonephritis induced by a single intravenous injection of Streptococcus faecalis. The animals were studied at intervals up to 1 year; bacteremia, urine and renal parenchymal bacterial counts were monitored. In these animals it was observed that bacteriuria and positive bacterial cultures of renal tissue persisted up to 1 year in some rats. Bacteria and their antigenic products in small foci were detected by immunofluorescence in the pyelonephritic lesions. The highly focal distribution of the bacterial antigens in bacteriologically positive tissues of this model suggest the need for careful fixation technics, availability of large tissue specimens and careful control of immunologic factors. These specific requirements to detect bacterial antigens may preclude the practical study of human pyelonephritic kidneys.

Animals↗
PubMed1974

The nail-patella syndrome-pathogenesis of the kidney lesion.

The nail-patella syndrome is an inheritable disorder of connective tissue in which multiple osseous abnormalities are frequently associated with renal dysfunction and proteinuria. This paper describes a unique abnormality of glomerular basement membranes (GBM) in eight patients. The abnormality consists of fibrils and bundles of cross-striated collagen within the GBM of each patient, including children with minimal proteinuria. This ultrastructural lesion may provide increased understanding of the pathogenesis of the basic defect underlying both the osseous and renal lesion.

Basement Membrane↗