Histological Findings in Renal Involvement of Microscopic Form of Panarteritis

2015 ◽  
pp. 115-122
Author(s):  
V. Colombo ◽  
R. Confalonieri ◽  
E. Minola ◽  
B. Brando
Keyword(s):  
Renal Involvement ◽  
Histological Findings

Adrenocortical Scintigraphy with 131I-6-Beta-Iodomethyl-NorchoIesterol (NP 59) in Bilateral Adrenocortical Carcinoma

1998 ◽  
Vol 37 (04) ◽  
pp. 141-145
Author(s):  
F. J. C. Pallarés ◽  
A. R. Bartual ◽  
Susana Tenes Rodrigo ◽  
F. J. Ampudia-Blasco ◽  
C. R. de Ávila y Ávalos ◽  
...  
Keyword(s):  
Case Report ◽  
Literature Review ◽  
Adrenocortical Carcinoma ◽  
Rapid Progression ◽  
Histological Findings ◽  
Mr Images ◽  
Imaging Procedure ◽  
Adrenocortical Scintigraphy

SummaryA case of a 49-year-old man suffering from bilateral adrenocortical carcinoma with local and secondary rapid progression is reported. The results of adrenocortical scintigraphy (NP 59) and histological findings allowed the diagnosis. This case report and a literature review showed the importance of using adrenocortical scintigraphy as a complementary imaging procedure of CT or MR images.

Histological Findings of Arsenical Keratosis

1977 ◽  
Vol 39 (4) ◽  
pp. 567-573 ◽  
Author(s):  
Nobuko ISE ◽  
Harue ARAI
Keyword(s):  
Histological Findings

Histological Findings in Ménière Cases

1948 ◽  
Vol 36 (sup78) ◽  
pp. 108-108
Author(s):  
S. Berggren
Keyword(s):  
Histological Findings

Ventricular premature beats in young subjects without evidence of cardiac disease: histological findings

1992 ◽  
Vol 13 (6) ◽  
pp. 732-737 ◽  
Author(s):  
M. DI BIASE ◽  
A. CHIDDO ◽  
G. CARUSO ◽  
M. TRITTO ◽  
A. MARCHESE ◽  
...  
Keyword(s):  
Cardiac Disease ◽  
Histological Findings ◽  
Ventricular Premature Beats ◽  
Young Subjects ◽  
Premature Beats

Renal Involvement in Neuropathy, Ataxia, Retinitis Pigmentosa (NARP) Syndrome: A Case Report

2018 ◽  
Vol 71 (5) ◽  
pp. 754-757 ◽  
Author(s):  
Sandrine Lemoine ◽  
Marine Panaye ◽  
Maud Rabeyrin ◽  
Elisabeth Errazuriz-Cerda ◽  
Bénédicte Mousson de Camaret ◽  
...  
Keyword(s):  
Case Report ◽  
Retinitis Pigmentosa ◽  
Renal Involvement

scholarly journals PGNMID in a patient with diabetes mellitus

2021 ◽  
pp. 239936932098478
Author(s):  
Joana Marques ◽  
Patrícia Cotovio ◽  
Mário Góis ◽  
Helena Sousa ◽  
Fernando Nolasco
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Renal Disease ◽  
Renal Involvement ◽  
Organ Damage ◽  
Therapeutic Implications ◽  
Stage Renal Disease

Diabetic nephropathy is a well known complication of diabetes mellitus and the leader cause of end -stage renal disease worldwide. Nonetheless, other forms of renal involvement can occur in diabetic population. Since it has prognostic and therapeutic implications, differentiating non-diabetic renal disease from diabetic nephropathy is of great importance. We report an 80-year-old man with well-controlled type 2 diabetes mellitus and hypertension, who presented with rapid deterioration of renal function, nephrotic proteinuria, microscopic hematuria and leukocyturia. The atypical clinical presentation prompted us to perform a kidney biopsy. A diagnosis of proliferative glomerulonephritis with monoclonal immunoglobulin deposits (light chain only variant) was made, with however some chronic histological aspects which made us took a conservative therapeutic attitude. We emphasize that other causes of chronic proteinuric kidney disease should be considered in patients with type 2 diabetes mellitus, based on clinical suspicion, absence of other organ damage and mostly if an atypical presentation is seen. We review the spectrum of monoclonal gammopathies of renal significance, focusing on this rare and newly describe entity.

scholarly journals OP0038 SPLICEOSOME ALTERATIONS IN LEUCOCYTES FROM APS, SLE AND SLE+APS PATIENTS ARE CLOSELY RELATED TO THEIR MAIN CLINICAL FEATURES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 20.2-20
Author(s):  
A. M. Patiño-Trives ◽  
C. Perez-Sanchez ◽  
A. Ibañez-Costa ◽  
P. S. Laura ◽  
M. Luque-Tévar ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Clinical Features ◽  
Antiphospholipid Syndrome ◽  
Immune Cells ◽  
Inflammatory Mediators ◽  
Clustering Analysis ◽  
Renal Involvement ◽  
Molecular Clustering ◽  
Cluster 2 ◽  
Splicing Machinery

Background:To date, although multiple molecular approaches have illustrated the various aspects of Primary Antiphospholipid Syndrome (APS), systemic lupus erythematosus (SLE) and antiphospholipid syndrome plus lupus (APS plus SLE), no study has so far fully characterized the potential role of posttranscriptional regulatory mechanisms such as the alternative splicing.Objectives:To identify shared and differential changes in the splicing machinery of immune cells from APS, SLE and APS plus SLE patients, and their involvement in the activity and clinical profile of these autoimmune disorders.Methods:Monocytes, lymphocytes and neutrophils from 80 patients (22 APS, 35 SLE and 23 APS plus SLE) and 50 healthy donors (HD) were purified by immunomagnetic selection. Then, selected elements of the splicing machinery were evaluated using a microfluidic qPCR array (Fluidigm). In parallel, extensive clinical/serological evaluation was performed, comprising disease activity, thrombosis and renal involvement, along with autoantibodies, acute phase reactants, complement and inflammatory molecules. Molecular clustering analyses and correlation/association studies were developed.Results:Patients with primary APS, SLE and APS plus SLE displayed significant and specific alterations in the splicing machinery components in comparison with HD, that were further specific for each leukocyte subset. Besides, these alterations were associated with distinctive clinical features.Hence, in APS, clustering analysis allowed to identify two sets of patients representing different molecular profile groups with respect to the expression levels of splicing machinery components. Principal component analyses confirmed a clear separation between patients. Clinically, cluster 1 characterized patients with higher thrombotic episodes and recurrences than cluster 2 and displayed a higher adjusted global APS score (aGAPSS). Accordingly, these patients showed higher levels of inflammatory mediators than cluster 2.Similarly, in patients with APS plus SLE, clustering analysis allowed to identify two sets of patients showing differential expression of splicing machinery components. Clinical and laboratory profiles showed that cluster 2 characterized patients that had suffered more thrombotic recurrences, most of them displaying an aGAPSS over 12 points and expressing higher levels of inflammatory mediators than cluster 1. The incidence of lupus nephropathy was similarly represented in both clusters.Lastly, in SLE patients, molecular clustering analysis identified two sets of patients showing distinctive clinical features. One cluster characterized most of the patients positive for anti-dsDNA antibodies, further suffering lupus nephropathy, and a high proportion of them also presenting atheroma plaques and high levels of inflammatory mediators.Correlation studies further demonstrated that several deranged splicing machinery components in immune cells (i.e. SF3B1tv1, PTBP1, PRP8 and RBM17) were linked to the autoimmune profile of the three autoimmune diseases, albeit in a specific way on each disorder. Accordingly, in vitro treatment of HD lymphocytes with aPL-IgG or anti-dsDNA-IgG changed the expression of spliceosome components also found altered in vivo in the three autoimmune diseases. Finally, the induced over/downregulated expression of selected spliceosome components in leukocytes modulated the expression of inflammatory cytokines, changed the procoagulant/adhesion activities of monocytes and regulated NETosis in neutrophils.Conclusion:1) The splicing machinery, profoundly altered in leukocytes from APS, APS plus SLE and SLE patients, is closely related to the activity of these diseases, their autoimmune and inflammatory profiles. 2) The analysis of the splicing machinery allows the segregation of APS, APS plus SLE and SLE, with specific components explaining the CV risk and renal involvement in these highly related autoimmune disorders.Acknowledgements:Funded by ISCIII, PI18/00837 and RIER RD16/0012/0015 co-funded with FEDERDisclosure of Interests:None declared

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