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Biomedical subjects

A Modesto

Publications and source records attributed to A Modesto.

At least 37 records · Page 2Linked to original sources
PubMed1997

VariGlass fluoride release and uptake by an adjacent tooth.

PURPOSE: To quantitatively analyze in vitro the fluoride release from proximal VariGlass restorations and resulting uptake by the enamel of adjacent teeth. MATERIALS AND METHODS: Sixty impacted third molars were used and assigned to three groups: C: control, teeth without restorations; RC: teeth with resin composite restorations (Prisma APH); and PMRC: teeth with polyacid-modified resin composite restorations (VariGlass). Each group consisted of four sets of five teeth each. In the latter two sets, by alternating restored and unrestored teeth, the proximal surfaces of three unrestored teeth with an area of exposed enamel were in contact with the restored proximal surfaces of two other teeth. The sets were submitted to high caries challenge conditions with demineralizing and remineralizing solutions for 14 days. The fluoride of each solution and the fluoride uptake were determined and statistical analyses were carried out (ANOVA and Tukey's test). RESULTS: The highest mean fluoride concentration occurred with Group PMRC in both kinds of solutions (P < 0.01), but this value was higher in the demineralizing solution (P < 0.01). Over the 14 days, however, this mean gradually decreased in both solutions (P < 0.01). Group PMRC also showed the highest mean fluoride uptake (P < 0.01), which gradually decreased with depth in the enamel (P < 0.01).

Acrylic Resins↗
PubMed1996

Henoch-Schönlein purpura and membranoproliferative-like glomerulonephritis.

A 17-year-old man presented Henoch-Schönlein purpura with renal impairment, nephrotic syndrome needing transitory hemodialysis and hematuria. By light microscopy, the renal biopsy revealed membranoproliferative-like lesion associated with massive subendothelial deposits, some subepithelial deposits, hyalin thrombi and intracapillary neutrophils. By immunofluorescence, intense nodular and segmental deposits of IgG, IgM, IgA, C3, fibrinogen and C1q were found to be present in the intracapillary area and the mesangium. By electron microscopy, large subendothelial and rare subepithelial deposits were observed. A skin biopsy demonstrated leukocytoclastic skin vasculitis with IgA deposits in the arterial walls. Treatment with corticosteroids resulted in return renal to normal renal function but persistent proteinuria and hematuria. A second renal biopsy, performed after 2 months, showed a marked decrease in lesions and deposits. Fifteen months later, the patient presented normal serum creatinine level but proteinuria and hematuria persisted. At this time, a third renal biopsy was performed and showed segmental mesangial sclerosis and the decrease of disappearance of deposits. Two years after the first hospitalization, no abnormal serum creatinine or urinalysis were present. This report describes a detailed study of a case presented with Henoch-Schönlein purpura and morphologic features consistent with membranoproliferative-like lesion, who recovered normal renal function and urinalysis; repeat biopsies performed at intervals of 2 months and 1 year confirmed the disappearance of mesangial proliferation, double contours and deposits.

Adolescent↗
PubMed1996

Acute renal failure in kidney transplant patients treated with interferon alpha 2b for chronic hepatitis C.

Sixteen kidney transplant (KT) patients (10 men, 6 women, aged 49 +/- 10 years) with chronic hepatitis C alpha-interferon (IFN-alpha) therapy (Intron A, Schering Plough) at a dose of 3 x 10(6) units subcutaneously 3 times a week. The treatment was scheduled for 24 consecutive weeks. Each patient had had stable renal function for at least 12 months prior to IFN-alpha therapy (mean serum creatinine, SCr, 121 +/- 38 mmol/l). Fourteen patients were receiving cyclosporin-A (CsA)-based immunosuppression and 2 patients were on conventional therapy. The patients' SCr was checked every 2 weeks while on IFN-alpha, or weekly if it increased more than 15% from baseline. IFN-alpha was withdrawn if SCr increased more than 25% from baseline, in which case a kidney biopsy was performed. Six patients experienced either acute (n = 5) or subacute (n = 1) renal failure within 7-24 weeks after the onset of IFN-alpha therapy. Their mean SCr increased from 105 +/- 31 to 207 +/- 63 mmol/l (p = 0.02) with de novo proteinuria in 1 case (1 g/day) and an increase in preexisting proteinuria in 2. The other 3 patients did not develop proteinuria. In each case, histological study showed diffuse interstitial edema associated with dilation of the peritubular capillaries, whereas mild inflammatory infiltrates were present in only 3 cases and mild glomerular lesions were not always found (glomerular ischemia, mesangial hypertrophy). There were no vascular lesions. IFN-alpha was withdrawn in these 6 patients, in association with methylprednisolone pulses in 5 cases. Renal function improved in 2 cases, stabilized in 1 and progressed to end-stage renal failure in 3 within 4-12 months. Four of these patients had iterative renal biopsies which showed diffuse interstitial fibrosis in each case. The patients who developed renal failure did not statistically differ at the start of the study from those who did not, with respect to the following: baseline immunosuppression, HLA matching, total peripheral blood lymphocyte count or peripheral blood lymphocyte subtypes. IFN-alpha therapy was associated with acute or subacute renal failure in 37% of the patients. The most prominent histological finding was diffuse interstitial edema of rapid onset, without signs of cellular or vascular rejection. In conclusion, we do not recommend IFN-alpha therapy for KT patients with chronic hepatitis C, until the mechanisms of the subsequent renal failure are better understood.

Acute Kidney Injury↗
PubMed1996

[Acute renal insufficiency in renal transplants treated with interferon-alpha for chronic hepatitis C].

Sixteen renal transplant (RT) patients (10 men, 6 women, aged 49 +/- 10 years) with chronic hepatitis C received alpha interferon (IFN alpha) therapy (Intron A, Schering Plough) at a dose of 3 x 10(6) units s.c. 3 times a week, scheduled for 24 consecutive weeks. At the beginning of the study all had a stable renal function since at least 12 months (mean serum creatinine -SCr- 121 +/- 38 mmol/l). Fourteen patients were receiving cyclosporin A (CsA) either alone (1) or in combination with steroids and/or azathioprine -AZA- (double therapy: 8; triple therapy: 5); two patients were on conventional therapy. The mean daily doses of CsA were 2.6 mg/kd i.e. a mean whole blood trough level of 104 ng/ml. Six patients experienced renal failure either acute (5) or subacute (1) within 7 to 24 weeks after the start of IFN alpha therapy. Their mean SCr increased from 105 +/- 31 mmol/l to 207 +/- 63 mmol/l (p = 0.02) with de-novo proteinuria in one case (1 g/d) and an increase in pre-existing proteinuria in 2; 3 remained without proteinuria. The histological study showed in all cases a diffuse interstitial edema associated with dilatation of peritubular capillaries; mild inflammatory infiltrates were present in only 3 cases; mild glomerular lesions were not always found (glomerular ischemia, mesangial hypertrophy). There was no vascular lesions IFN alpha was withdrawn in these 6 patients, associated with methylprednisolone pulses in 5 cases. Renal function improved in two cases, stabilized in one and progressed to end stage renal failure in 3 within 4 to 12 months. Four patients had iterative renal biopsies showing in all cases diffuse interstitial fibrosis. This subgroup of patients did not statistically differ at the start of the study from those who did not develop renal failure according to baseline immunosuppression, HLA matching, total peripheral blood lymphocyte (PBL) count. PBL subtypes. INF alpha therapy was associated with acute or subacute renal failure in 37% of patients. The most prominent histological finding was a diffuse interstitial edema of rapid onset, without signs of cellular or vascular rejection. Thus we do not recommend to use IFN alpha therapy in RT patients with chronic hepatitis C, until the mechanisms of the subsequent renal failure be more understood.

Acute Kidney Injury↗
PubMed1995

[Nephro-angiosclerosis in the graft: impact on graft survival. Study of 33 cases].

UNLABELLED: When early kidney transplant biopsies showed benign hypertensive nephrosclerosis, i.e. hyalin arteriosclerosis and/or interlobular arteries intimal thickening, they are thought to be of donor origin. Between 1987 and 1992, 439 cadaveric renal transplantations have been performed in our department: amongst them 97, i.e. 22% patients underwent a graft biopsy before the end of the first post transplant month (13 +/- 9.5 days). To ascertain if findings of early renal biopsy was predictive of eventual clinical outcome we analyzed renal function and blood pressure (BP) in the short and mid term. Nephrosclerosis lesions were found in 33 cases (group I) and were absent in the remaining 64 cases (group II). The 2 groups were not statistically different according to the time on dialysis, the recipient's age, the HLA matching, the cold ischemia time. The only statistically significant difference was the donor's age: 39.1 +/- 7 years in group I vs 26.9 +/- 8 years in group II (p = 0.0001). Delayed graft function was not different in the 2 groups (13 +/- 9 days group I vs 11 +/- 6 days group II). On the other hand, 30% of group I, patients required hemodialysis (9.8% in group II; p < 0.005). The incidence in graft rejection episodes was similar in both groups (50%) as well as surgical complications. Renal function was assessed by creatinine clearance at 1 and 2 years and at last follow-up visit (mean follow-up: 50.5 +/- 44 months in group I and 46.9 +/- 24 months in group II; p = Ns): it was similar in both groups (see table). The prevalence of hypertension (HTA) was significantly higher in group I than in group II at two years and last follow-up (*: p < 0.005). [table: see text] CONCLUSIONS: The age of donor is of importance in determining nephrosclerosis of the graft observed on early biopsies. Donor-related nephrosclerosis is a risk factor for the recipient of developing HTA without impairment of graft function in the mid term. In the context of early nephrosclerosis, the occurrence of acute rejection episode(s) is detrimental for the graft function.

Adult↗
PubMed1994

[Systemic embolism of cholesterol crystals].

Systemic cholesterol crystal emboli (SCCE) are no longer a rare complication of severe atheroma. Sixty-year old men, with many vascular problems are typically involved. SCCE, released from atheromatous ulcerated "plaques", invade one or more arteriolar beds. Clinical presentation is polymorphic: skin, muscle, kidney, digestive tract and other abdominal organs, retina, bone narrow ... may be embolized. SCCE are associated with triggering conditions: vascular surgery, anticlotting agents and fibrinolysis, femoral retrograd catheterization by radiologists or cardiologists. This last factor is presently predominant. Clinical signs depend on atheroma localization, intensity and repetition of embols and topography of arteriolar beds susceptible to be embolized: livedo reticularis, acute renal failure with high blood pressure, limbs or abdominal pain, periarteritis nodosa-like syndrome. Diagnosis is based on the discovery of ocular fundi (cholesterol crystals in arterioles) and evidence of cholesterol crystals in various biopsies: skin, muscle, kidneys. Prognosis and curative treatment are poor. Mortality is greater than 80% in systemic forms. Surgical palliative treatment was recently proposed (bypass). Prevention is essential: triggering manipulations i.e. retrograd femoral catheterism have to be avoided by radiologists or cardiologists in exposed patients. In high risk atheromatous patients symptomatic treatment including repetitive dialysis is able to induce significative survival.

Embolism, Cholesterol↗
PubMed1994

Henoch-Schönlein purpura in a patient with diabetic nephropathy.

A 46-year-old man presented with Henoch-Schönlein purpura and diabetic nephropathy. At 30 years of age, the patient had presented with an acute and severe nephritic syndrome with severe renal impairment. The renal function returned to normal 6 months after this first attack. At the age of 38 years, the patient was diagnosed as having type II diabetes and was treated with diet alone. At 44 years of age, a renal biopsy was performed because of proteinuria and hematuria. In this renal biopsy, mesangial expansion, medial arterial hyperplasia, and focal interstitial fibrosis were found to be present. Mesangial and subendothelial deposits of immunoglobulin A (IgA) were demonstrated by immunofluorescence. At 45 years of age, cutaneous vasculitis appeared, and at 47 years of age, the patient presented with necrotic purpura, non-insulin-dependent diabetes, renal impairment, proteinuria, and hematuria. A skin biopsy demonstrated leukocytoclastic skin vasculitis with IgA deposits in the arterial walls. A second renal biopsy was performed that showed diabetic glomerulosclerosis associated with a marked vascular and interstitial fibrosis. Mesangial and subendothelial deposits of IgA and C3 and linear IgG deposits along the glomerular basement membranes were demonstrated by immunofluorescence. Electron microscopy showed that the glomerular basement membranes were thickened; a fusion of foot processes was observed and electron-dense deposits were present in the widened mesangium. In summary, we describe a patient with a history of ancient glomerulonephritis who presented with an IgA mesangial nephropathy consistent with Henoch-Schönlein purpura associated with diabetic glomerulosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 2↗
PubMed1994

Long-term follow-up of monoclonal gammopathy of undetermined significance in transplant patients.

We report the long-term follow-up of 5 patients (4 kidney, 1 heart recipients) having a pretransplant monoclonal gammopathy of undetermined significance (MGUS). The follow-up of MGUS before transplantation was 41.2 +/- 40.7 months (range 2-108). The monoclonal component isotype was IgG-kappa in 3 cases and IgA-lambda in 2. The pretransplant level of the monoclonal component was 11.1 +/- 4.8 g/l (range 4-15.6). The transplant recipients who had MGUS were older than our other transplant patients. All but one of them received ciclosporine A. They did not experience more rejection or infectious complications than the others. Their posttransplant follow-up ranged from 3 to 9 years. The monoclonal component level remained stable in 2 patients but increased in 3 (33-225%). This was not correlated with bone marrow plasmocytosis. Two patients developed smoldering myeloma indicated by bone marrow immunochemistry studies which showed monomorph monoclonal plasma cells; nevertheless, they did not have cytopenia or bone lytic lesions. This percentage is higher than in the Kyle study but we cannot assume that it is due to ciclosporine A since our study sample is too small. In conclusion, MGUS is not a contraindication to organ transplantation.

Contraindications↗
PubMed1994

[Renal involvement in POEMS syndrome].

We described a patient with a POEMS syndrome (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal grammapathy and Skin changes) who was found to have renal involvement with peculiar renal pathological findings. Hitherto, 17 other cases, most of them from Japan, of POEMS syndrome with renal involvement, have been published. Clinical features are variable: acute renal failure with anasarca or moderate chronic renal insufficiency with mild proteinuria. This latter presentation often passes unnoticed. There is no severe HTA, no microangiopathic hemolytic anemia. Renal biopsy shows prominent glomerular changes which are unusual and distinct from membranoproliferative glomerulonephritis (MPGN) and from glomerular thrombotic microangiopathy (TMA). Mesangial proliferation and thickening of the capillary wall with double contour evoke by light microscopy a MPGN. By immunofluorescent microscopy, no immunoglobulins or complement deposits are found. The finding of mesangiolytic lesions has led to the term of "mesangiolytic glomerulonephritis". The presence, on electron microscopy, of lucent subendothelial space could evoke TMA. But there is neither thrombi, nor arteriolar changes. We are inclined to presume that microangiopathic lesions are due to chronic injury of glomerular endothelial cells, exacerbated at outbreaks of the disease. An increased production of IL-6 could support the efficacity of corticosteroid therapy, particularly in acute clinical situations.

Adult↗
PubMed1993

Rapidly progressive glomerulonephritis associated with bacterial endocarditis: efficacy of antibiotic therapy alone.

A 65-year-old woman presented rapidly progressive glomerulonephritis with purpura and mitral insufficiency. Blood cultures grew Streptococcus mitis. By light microscopy, the renal biopsy revealed necrotizing glomerulonephritis 56% associated with cellular crescents and tubulointerstitial changes. By immunofluorescence, deposits of IgM and C3 were found to be present in the mesangium. Electron-microscopic study showed subendothelial and intramembranous deposits. Treatment with antibiotics alone resulted in renal recovery with disappearance of proteinuria, circulating immune complexes and cryoglobulinemia. A 2nd renal biopsy, performed after 3 months, showed segmental sclerosis and tubulointerstitial lesions. Eight months after the first hospitalization, cardiac insufficiency occurred. Four years later, a valve replacement was performed. No abnormal serum creatinine, serum creatinine clearance or urinalysis levels were present. These data suggest that rapidly progressive glomerulonephritis associated with bacterial endocarditis may be treated by antibiotics alone and result in normal and stable renal function.

Aged↗
PubMed1993

[Anti-cytoplasm antibodies to polynuclear neutrophils: specificity in renal vasculitis].

We present a retrospective study of all patients with a positive anti-neutrophil cytoplasm autoantibodies (ANCA) result from July 1987 to December 1990. The aims of the study were to assess specificity of ANCA in renal vasculitis and to correlate ANCA immunofluorescence subtypes with clinical aspect, diagnosis, severity and outcome. Anti-myeloperoxidase antibody (A-MPO) was sought in 31 cases. Specificity was 86% and false-positive results were 11%. ANCA subtypes varied with the clinical picture. C-ANCA were more often present when renal vasculitis was associated with pulmonary and ear, nose and throat involvement; P-ANCA were more often present when there was no respiratory tract involvement. Thus C-ANCA were preferentially associated with Wegener's granulomatosis and P-ANCA with microscopic polyarteritis and pauci-immune necrotizing and crescentic glomerulonephritis. No correlation was found between ANCA subtypes and severity or outcome. A-MPO were positive in 14 cases (especially in micropolyarteritis and necrotizing glomerulonephritis).

Autoantibodies↗
PubMed1992

[Micropolyarteritis].

Micropolyarteritis are defined as necrotizing inflammatory lesion of the wall of small vessels affecting different organs. A necrotizing crescentic glomerulonephritis without immuno-deposits is observed in the kidney, frequently involved in this microscopic form of systemic vasculitis. Micropolyarteritis are regrouped with Wegener's syndrome and isolated pauci-immune necrotizing crescentic glomerulonephritis as "ANCA-related vasculitis", whose diagnosis is assessed throw renal biopsy and prognosis dependent on immuno-suppressive treatment. Sixty-one patients treated in our nephrology department for a RPGN during these ten recent years have been retrospectively studied. Among them, twenty-five patients presented clinical and morphologic aspects compatible with the diagnosis of micropolyarteritis. We present their clinical aspects and evolution under treatment.

Antibodies, Antineutrophil Cytoplasmic↗