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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 4  |  Page : 672-673
Diabetic nephropathy with crescentic GN


Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Institute of Kidney Diseases & Research Centre and Institute of Transplantation Sciences, Civil Hospital Campus, Asarwa, Ahmedabad, India

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Date of Web Publication8-Jul-2009
 

How to cite this article:
Kanodia KV, Vanikar AV, Goplani KR, Trivedi HL. Diabetic nephropathy with crescentic GN. Saudi J Kidney Dis Transpl 2009;20:672-3

How to cite this URL:
Kanodia KV, Vanikar AV, Goplani KR, Trivedi HL. Diabetic nephropathy with crescentic GN. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2020 Jun 3];20:672-3. Available from: http://www.sjkdt.org/text.asp?2009/20/4/672/53301
To the Editor,

Diabetic nephropathy does not require biopsy for confirmation. In the presence of hematuria or other manifestations might suggest disease other than diabetic nephropathy. We present here a case of a 48 years old male with diabetes mel­litus (DM) for 8 years, presented with breath­lessness, abdominal pain and nausea for 10 days. He had high blood pressure of 160/80 mmHg and fundus examination showing grade III hyper­tensive retinopathy. Ultrasound showed normal sized kidneys with increased echogenicity and altered cortico-medullary differentiation (CMD). On investigations, his urine albumin was +4 (24 hours urine proteinuira was 1.2 gm), microscopy showed 4-6 pus cells, 15-20 RBCs/ high power field (HPF). His serum creatinine was 14.16 mg/dL, hemoglobin 9 gm/dL, total WBC count 5,000/mm 3 , platelet count 4,62,000/mm 3 , serum protein 5.1 gm % and serum albumin of 2.8 gm/dL. Vasculitis markers which included anti­neutrophilic cytoplasmic antibodies (by indirect immunofluorescence and ELISA) as well as ANA were negative. Renal biopsy was performed which showed 12 glomeruli, with majority sho­wing lobular accentuation with variably shrun­ken capillary tufts. Capillary lumina was lined by thickened, rarely reduplicated and ruptured membranes. There was presence of Kimmelsteil Wilson nodules in at least three glomeruli with peripheral rim of swollen endothelial cells in fairly open capillaries [Figure 1]. There was mild uniform accentuation of mesangial matrix accompanied by mild focal hypercellularity. Ma­jority of the glomeruli also showed well developed fibrocellular crescents occupying 75 - 90% of diameter of Bowman capsules [Figure 2]. Crescents were infiltrated by fibrin threads, few leucocytes and RBCs. Focal fibrinoid necrosis was evident in capillary tufts. Bowman capsules were segmentally thickened or ruptured and sur­rounded by periglomerular fibrosis in few tufts. Moderate focal tubular atrophy was also noted along with mild interstitial edema with scat­tered leucocytic infiltration. Blood vessels showed mild fibrointimal proliferation with small cali­ber arteries showing nodular subintimal hyaline sclerosis. Immunofluorescence studies were ne­gative.

A diagnosis of diabetic nephropathy with dif­fuse intercapillary glomerulosclerosis as well as nodular sclerosis accompanied by crescents was made. He was kept on maintenance hemodialysis after cylophosphamide and pulse methylpredni­solone management. However, he succumbed to the disease after 2 months.

It is speculated that due to functional and bio­chemical alterations the glomeruli of diabetic patients may be more susceptible to immune mediated injury. [1] Various forms of primary and secondary glomerular diseases have been repor­ted in diabetic patients including idiopathic membranoproliferative glomerulonephritis and IgA nephropathy. [2],[3],[4] This can be due to hyper­perfusion injury, mesangial matrix expansion and thickening of all extra cellular membranes. [2] Anti-GBM nephritis, pauci-immune crescentic glomerulonephritis and Churg Strauss syndrome associated with necrotizing crescentic glome­rulonephritis in diabetic patients has also been reported requiring aggressive immunosuppres­sion similar to our patient. [3] ,[5] ,[6] We present our case for its rarity.

 
   References Top

1.Cavallo T, Pinto JA, Rajaraman S. Immune complex disease complicating diabetic glome­rulosclerosis, Am J Nephrol 1984;4(6):347-54  Back to cited text no. 1    
2.Grcevska L, Petrusevska G, Dzikova S. Kosta­dinova S, Polenakovic M. Membranoprolife­rative glomerulonephritis complicating diabetic nephropathy. Prilozi 2005;26 (2):53-61.  Back to cited text no. 2    
3.Kitazawa M, Tomosugi N, Ishii T, et al. Rapidly progressive glomerulonephritis concomitant with diabetic nephropathy, Intern Med 1997;36(12): 906-11.  Back to cited text no. 3    
4.Orfila C, Lepert JC, Modesto A, Pipy B, Suc JM. IgA nephropathy complicating diabetic glome­rulosclerosis. Nephron. 1998;79 (3):279-87.  Back to cited text no. 4    
5.Ahuja TS, Velasco A, Deiss W Jr, Indrikovs AJ, Rajaraman S. Diabetic nephropathy with anti­GBM nephritis. Am J Kidney Dis 1998;31(1): 127-30.  Back to cited text no. 5    
6.Maeda Y, Tomura S, Kato K, et al. Churg Strauss syndrome associated with necrotizing crescentic glomerulonephritis in diabetic patient. Intern Med 1997; 36: 1: 68-72.  Back to cited text no. 6    

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Correspondence Address:
Kamal V Kanodia
Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Institute of Kidney Diseases & Research Centre and Institute of Transplantation Sciences, Civil Hospital Campus, Asarwa, Ahmedabad
India
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PMID: 19587517

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