Kamal V Kanodia1, Aruna V Vanikar2, Rashmi D Patel3, Kamlesh S Suthar4, Lovelesh K Nigam4, Himanshu V Patel5, Vivek Kute6, Hargovind L Trivedi7. 1. Professor, Department of Pathology, Lab Medicine, Transfusion Services and Immunohematology, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 2. Professor and Head, Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 3. Professor, Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 4. Associate Professor, Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 5. Professor, Department of Nephrology and Transplantation, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 6. Associate Professor, Department of Nephrology and Transplantation, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India . 7. Professor, Department of Nephrology and Transplantation Medicine and Director, G.R. Doshi and K.M. Mehta Institute of Kidney Diseases & Research Centre and Dr. H.L. Trivedi Institute of Transplantation Sciences , Civil Hospital Campus, Asarwa, Ahmedabad, India .
Abstract
INTRODUCTION: Collapsing Glomerulopathy (CG) is recognized as distinct pattern of proliferative parenchymal injury with poor response to empirical therapy. AIM: A single center retrospective study was carried out to find out clinicopathological features of idiopathic CG. MATERIALS AND METHODS: A total of 3335 native renal biopsies were analyzed retrospectively which were performed from 2008 to 2014 with emphasis on clinicopathological correlation and histopathological presentation. RESULTS: Idiopathic CG constituted 0.75% incidence (25 out of 3335 biopsies) of all biopsies, adults constituting major study part with 88%. The duration of the symptoms at the time of biopsy was 34.12±26.09 days and 35±22.91 days respectively in adults and children. Hypertension was noted in 9(40.9%) and oliguria in 8(36.4%) in adults. Urinalysis revealed microscopic haematuria 12(54.5%) in adults. Nephrotic range proteinuria was reported in 10 (45.5%) adult patients. Glomerular collapse with hyperplasia/ hypertrophy of podocytes was seen in 4.54±3.11 glomeruli. Tubular microcystic dilation was seen in 16(64%) patients. Tubular atrophy involving mild (t1) in 15(60%), moderate (t2) in 4(16%) and severe (t3) in 6(24%) patients. Interstitial fibrosis was mild (i1) in 17(68%), moderate (i2) in 2(8%) and severe (i3) in 6(24%) patients. CONCLUSION: Idiopathic CG is a morphological pattern of grave podocyte injury with poor prognosis. However, there are chances of remission/ recovery if the tubular atrophy and interstitial fibrosis are of grades ≤ t1 i1.
INTRODUCTION:Collapsing Glomerulopathy (CG) is recognized as distinct pattern of proliferative parenchymal injury with poor response to empirical therapy. AIM: A single center retrospective study was carried out to find out clinicopathological features of idiopathic CG. MATERIALS AND METHODS: A total of 3335 native renal biopsies were analyzed retrospectively which were performed from 2008 to 2014 with emphasis on clinicopathological correlation and histopathological presentation. RESULTS: Idiopathic CG constituted 0.75% incidence (25 out of 3335 biopsies) of all biopsies, adults constituting major study part with 88%. The duration of the symptoms at the time of biopsy was 34.12±26.09 days and 35±22.91 days respectively in adults and children. Hypertension was noted in 9(40.9%) and oliguria in 8(36.4%) in adults. Urinalysis revealed microscopic haematuria 12(54.5%) in adults. Nephrotic range proteinuria was reported in 10 (45.5%) adult patients. Glomerular collapse with hyperplasia/ hypertrophy of podocytes was seen in 4.54±3.11 glomeruli. Tubular microcystic dilation was seen in 16(64%) patients. Tubular atrophy involving mild (t1) in 15(60%), moderate (t2) in 4(16%) and severe (t3) in 6(24%) patients. Interstitial fibrosis was mild (i1) in 17(68%), moderate (i2) in 2(8%) and severe (i3) in 6(24%) patients. CONCLUSION: Idiopathic CG is a morphological pattern of grave podocyte injury with poor prognosis. However, there are chances of remission/ recovery if the tubular atrophy and interstitial fibrosis are of grades ≤ t1 i1.
Entities:
Keywords:
End stage renal disease; Idiopathic collapsing glomerulopathy; Podocyte; Proteinuria
Authors: Aruna V Vanikar; Hargovind L Trivedi; Pankaj R Shah; Kamal V Kanodia; Rashmi D Patel; Pranjal R Modi; Shruti D Dave; Atin M Singhai; Veena R Shah; Varsha B Trivedi; V Shankar Journal: Saudi J Kidney Dis Transpl Date: 2013-01
Authors: Érico Murilo Monteiro Cutrim; Precil Diego Miranda de Meneses Neves; Marcos Adriano Garcia Campos; Davi Campos Wanderley; Antonio Augusto Lima Teixeira-Júnior; Monique Pereira Rêgo Muniz; Francisco Rasiah Ladchumananandasivam; Orlando Vieira Gomes; Rafael Fernandes Vanderlei Vasco; Dyego José de Araújo Brito; Joyce Santos Lages; Natalino Salgado-Filho; Felipe Leite Guedes; José Bruno de Almeida; Marcelo Magalhães; Stanley de Almeida Araújo; Gyl Eanes Barros Silva Journal: Front Med (Lausanne) Date: 2022-03-03