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ANTICOAGULATION RELATED NEPHROPATHY PRESENTING AS GROSS HEMATURIA AND OLIGURIC AKI
NKF 2015 Spring Clinical Meetings Abstracts
253 ANTICOAGULATION RELATED NEPHROPATHY PRESENTING AS GROSS HEMATURIA AND OLIGURIC AKI. Pallavi Shirsat, Chyi Chyi Chong, Ramesh Marahatta, Neeraj Singh.Department of Nephrology & Hypertension, Louisiana State University- University Health, Shreveport, Louisiana, USA. Anticoagulation related nephropathy is a newly described entity presenting with painless gross hematuria and AKI in patients treated with anticoagulants. It has been associated with irreversible kidney injury and has an increased risk of mortality. We report a 64 years old white male with history of hypertension and coronary artery disease who underwent aortic valve replacement, was put on warfarin. Patient presented 3 months after the surgery with gross hematuria and AKI of unexplained etiology. His baseline serum creatinine was 0.8-1.0 mg/dL. Patient developed sudden onset painless gross hematuria and oliguric AKI. Serum creatinine subsequently rose to 3.3 mg/dL. The INR was found to be elevated at 6. The urinalysis showed innumerable RBCs, no WBCs, no bacteria and no casts or crystals. Spot urine protein to creatinine ratio showed 4 grams proteinuria. Renal ultrasound was unremarkable. CT scan abdomen and pelvis was negative for stones. Serum complements and serological work-up (ANCA, Anti GBM antibody etc.) were within normal limits. Warfarin was then put on hold and daily INR was followed. Serum creatinine peaked at 8.1 mg/dL after about a week of hospitalization after which it started trending down as the INR normalized. Hematuria resolved and proteinuria decreased to 0.1. The kidney biopsy was not performed due to the risk of bleeding. During a follow up visit in the clinic two months after discharge, patient’s creatinine was back to baseline of 0.8 mg/dL. We conclude that anticoagulation related nephropathy should be considered in the differential diagnosis in patients with coagulopathy and AKI after excluding other causes. It may be reversible if diagnosed early with correction of coagulopathy and supportive care.
255 IRON STORES ARE INCREASED WITHIN THE FIRST 24 WEEKS AND MAINTAINED FOR 80 ADDITIONAL WEEKS WITH LONGTERM USE OF ORAL FERRIC CITRATE (FC) AS A PHOSPHATE BINDER. M Sika1, MJ Koury1, R Niecestro2, JP Dwyer1, JB Lewis1 for the Collaborative Study Group, 1Vanderbilt University, Nashville, TN, USA, 2Independent Consultant, Pocono Pines, PA, USA A randomized clinical trial (KRX304) comparing FC to active controls (calcium acetate and/or sevelamer carbonate) in dialysis patients showed that FC was safe and effectively bound phosphate (P), raised iron stores, and decreased the use of IV iron and erythropoiesis stimulating agents over 52 weeks. FC subjects then entered a 4-week placebo-controlled period. Eligible subjects who completed this trial on either treatment arm were invited to participate in a long-term, 48week, safety extension trial (KRX307). The primary objective of KRX307 was to investigate the long-term safety of FC. Twenty-eight subjects who received FC in both 304 and 307 without interruption between the trials were evaluated for the effects of longterm use of FC as a phosphate binder on phosphorus control and iron parameters (Ferritin, Transferrin saturation (TSAT), and serum iron). Hemoglobin (Hgb) and serum calcium were also investigated. FC controlled serum phosphorus over 104-week trial. Serum iron, TSAT, and Ferritin increased in the first 24 weeks and remained stable over the next 80 weeks. Hemoglobin and serum calcium remained unchanged throughout 104 weeks.
Oral FC used as a phosphate binder in dialysis patients maintains phosphorus control while increasing iron stores over the first 24 weeks. These effects remain stable for an additional 80 weeks.
254 RECURRENT MEMBRANOUS NEPHROPATHY WITH CRESCENTIC GLOMERULONEPHRITIS IN RENAL ALLOGRAFT Noaman Siddiqi, Clifton Kew, University of Alabama, Birmingham, AL, USA. This interesting case shows recurrence of membranous nephropathy with crescentic glomerulonephritis as a cause of AKI which responded to high dose steroids and cyclophosphamide. 34 year old African American male with history of ESRD secondary to membranous nephropathy S/P living related donor kidney transplant ( brother) in 2003 maintained on cyclosporine, cellcept and prednisone with baseline serum Cr of 2.2-2.6mg/dl was found to have elevated Creatinine of 4.6 on routine lab work. His urinalysis showed +2 protein and UPCR 0.9 that was normal earlier. Allograft ultrasound and perfusion scan was unremarkable. DSA came back negative. Other investigations including ANA, double stranded DNA antibody, complements, ANCA serologies, BK virus titer, came back negative as well. He underwent allograft biopsy that showed membranous nephropathy with crescents, no rejection was found. Pt got total of 2000mg IV methylprednisolone over 4 days followed by cyclophosphamide. He responded well with decrease in serum creatinine which came back to baseline and improvement in UPCR from 0.9 to 0.4.
A78
256 AN UNUSUAL CASE OF IGA NEPHROPATHY AND LEUKOCYTOCLASTIC VASCULITIS, COMPLICATED BY PAUCI-IMMUNE RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN) Jaswinder Singh, Aaron Stern, George Coritsidis, Elmhurst Hospital Center, Icahn School of Medicine at Mount Sinai, New York, USA Crescentic IgA nephritis is an infrequent cause of RPGN. We describe a case of a rapidly progressive cresentic IgA nephropathy which occurred during treatment for a systemic IgA negative leukocytolastic vasculitis (LCV) in the setting of stable IgA nephropathy. A 54 year old female with biopsy proven IgA nephropathy and immunofluorescence negative LCV diagnosed several years prior was admitted to our hospital for treatment of LCV flare with IVIG and Rituximab. During her hospitalization, her clinical course was complicated by development of massive proteinuria (up to 25 gm/day), gross hematuria and a rapid loss of renal function, rise in creatinine from a baseline of 1.1mg/dl to 5 mg/dl by the fifth hospital day. She was promptly treated with pulse steroid therapy followed by prednisone but required several sessions of hemodialysis over the next ten days. A kidney biopsy was performed revealing marked crescent formations (upto 80% involvement), mesangial expansion with immunoflorescent IgA deposits, and mild interstitial scarring. She responded favorably to treatment with steroids, and ACE inhibitor with resolution of hematuria over a few days, urine protein decreasing over several weeks to less than 3gm/day, and serum creatinine returning to her baseline level of 1.1 mg/dl. The patient presented had been diagnosed with two small-vessel vasculitides. Gastrointestinal (GI) biopsies from multiple sites -stomach body, antrum, caecum, and ascending colon performed two years ago for GI bleeding were immunofluorescence negative. Despite suspicion for Henoch-Schönlein Purpura, negative IgA deposition in the skin or GI tract mitigates it. Her sudden clinical deterioration with a diagnosis of RPGN from Crescentic IgA nephritis is an uncommon manifestation of that disease, but in her case we were able to treat quickly with a positive clinical outcome.
Am J Kidney Dis. 2015;65(4):A1-A93
253 ANTICOAGULATION RELATED NEPHROPATHY PRESENTING AS GROSS HEMATURIA AND OLIGURIC AKI. Pallavi Shirsat, Chyi Chyi Chong, Ramesh Marahatta, Neeraj Singh.Department of Nephrology & Hypertension, Louisiana State University- University Health, Shreveport, Louisiana, USA. Anticoagulation related nephropathy is a newly described entity presenting with painless gross hematuria and AKI in patients treated with anticoagulants. It has been associated with irreversible kidney injury and has an increased risk of mortality. We report a 64 years old white male with history of hypertension and coronary artery disease who underwent aortic valve replacement, was put on warfarin. Patient presented 3 months after the surgery with gross hematuria and AKI of unexplained etiology. His baseline serum creatinine was 0.8-1.0 mg/dL. Patient developed sudden onset painless gross hematuria and oliguric AKI. Serum creatinine subsequently rose to 3.3 mg/dL. The INR was found to be elevated at 6. The urinalysis showed innumerable RBCs, no WBCs, no bacteria and no casts or crystals. Spot urine protein to creatinine ratio showed 4 grams proteinuria. Renal ultrasound was unremarkable. CT scan abdomen and pelvis was negative for stones. Serum complements and serological work-up (ANCA, Anti GBM antibody etc.) were within normal limits. Warfarin was then put on hold and daily INR was followed. Serum creatinine peaked at 8.1 mg/dL after about a week of hospitalization after which it started trending down as the INR normalized. Hematuria resolved and proteinuria decreased to 0.1. The kidney biopsy was not performed due to the risk of bleeding. During a follow up visit in the clinic two months after discharge, patient’s creatinine was back to baseline of 0.8 mg/dL. We conclude that anticoagulation related nephropathy should be considered in the differential diagnosis in patients with coagulopathy and AKI after excluding other causes. It may be reversible if diagnosed early with correction of coagulopathy and supportive care.
255 IRON STORES ARE INCREASED WITHIN THE FIRST 24 WEEKS AND MAINTAINED FOR 80 ADDITIONAL WEEKS WITH LONGTERM USE OF ORAL FERRIC CITRATE (FC) AS A PHOSPHATE BINDER. M Sika1, MJ Koury1, R Niecestro2, JP Dwyer1, JB Lewis1 for the Collaborative Study Group, 1Vanderbilt University, Nashville, TN, USA, 2Independent Consultant, Pocono Pines, PA, USA A randomized clinical trial (KRX304) comparing FC to active controls (calcium acetate and/or sevelamer carbonate) in dialysis patients showed that FC was safe and effectively bound phosphate (P), raised iron stores, and decreased the use of IV iron and erythropoiesis stimulating agents over 52 weeks. FC subjects then entered a 4-week placebo-controlled period. Eligible subjects who completed this trial on either treatment arm were invited to participate in a long-term, 48week, safety extension trial (KRX307). The primary objective of KRX307 was to investigate the long-term safety of FC. Twenty-eight subjects who received FC in both 304 and 307 without interruption between the trials were evaluated for the effects of longterm use of FC as a phosphate binder on phosphorus control and iron parameters (Ferritin, Transferrin saturation (TSAT), and serum iron). Hemoglobin (Hgb) and serum calcium were also investigated. FC controlled serum phosphorus over 104-week trial. Serum iron, TSAT, and Ferritin increased in the first 24 weeks and remained stable over the next 80 weeks. Hemoglobin and serum calcium remained unchanged throughout 104 weeks.
Oral FC used as a phosphate binder in dialysis patients maintains phosphorus control while increasing iron stores over the first 24 weeks. These effects remain stable for an additional 80 weeks.
254 RECURRENT MEMBRANOUS NEPHROPATHY WITH CRESCENTIC GLOMERULONEPHRITIS IN RENAL ALLOGRAFT Noaman Siddiqi, Clifton Kew, University of Alabama, Birmingham, AL, USA. This interesting case shows recurrence of membranous nephropathy with crescentic glomerulonephritis as a cause of AKI which responded to high dose steroids and cyclophosphamide. 34 year old African American male with history of ESRD secondary to membranous nephropathy S/P living related donor kidney transplant ( brother) in 2003 maintained on cyclosporine, cellcept and prednisone with baseline serum Cr of 2.2-2.6mg/dl was found to have elevated Creatinine of 4.6 on routine lab work. His urinalysis showed +2 protein and UPCR 0.9 that was normal earlier. Allograft ultrasound and perfusion scan was unremarkable. DSA came back negative. Other investigations including ANA, double stranded DNA antibody, complements, ANCA serologies, BK virus titer, came back negative as well. He underwent allograft biopsy that showed membranous nephropathy with crescents, no rejection was found. Pt got total of 2000mg IV methylprednisolone over 4 days followed by cyclophosphamide. He responded well with decrease in serum creatinine which came back to baseline and improvement in UPCR from 0.9 to 0.4.
A78
256 AN UNUSUAL CASE OF IGA NEPHROPATHY AND LEUKOCYTOCLASTIC VASCULITIS, COMPLICATED BY PAUCI-IMMUNE RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN) Jaswinder Singh, Aaron Stern, George Coritsidis, Elmhurst Hospital Center, Icahn School of Medicine at Mount Sinai, New York, USA Crescentic IgA nephritis is an infrequent cause of RPGN. We describe a case of a rapidly progressive cresentic IgA nephropathy which occurred during treatment for a systemic IgA negative leukocytolastic vasculitis (LCV) in the setting of stable IgA nephropathy. A 54 year old female with biopsy proven IgA nephropathy and immunofluorescence negative LCV diagnosed several years prior was admitted to our hospital for treatment of LCV flare with IVIG and Rituximab. During her hospitalization, her clinical course was complicated by development of massive proteinuria (up to 25 gm/day), gross hematuria and a rapid loss of renal function, rise in creatinine from a baseline of 1.1mg/dl to 5 mg/dl by the fifth hospital day. She was promptly treated with pulse steroid therapy followed by prednisone but required several sessions of hemodialysis over the next ten days. A kidney biopsy was performed revealing marked crescent formations (upto 80% involvement), mesangial expansion with immunoflorescent IgA deposits, and mild interstitial scarring. She responded favorably to treatment with steroids, and ACE inhibitor with resolution of hematuria over a few days, urine protein decreasing over several weeks to less than 3gm/day, and serum creatinine returning to her baseline level of 1.1 mg/dl. The patient presented had been diagnosed with two small-vessel vasculitides. Gastrointestinal (GI) biopsies from multiple sites -stomach body, antrum, caecum, and ascending colon performed two years ago for GI bleeding were immunofluorescence negative. Despite suspicion for Henoch-Schönlein Purpura, negative IgA deposition in the skin or GI tract mitigates it. Her sudden clinical deterioration with a diagnosis of RPGN from Crescentic IgA nephritis is an uncommon manifestation of that disease, but in her case we were able to treat quickly with a positive clinical outcome.
Am J Kidney Dis. 2015;65(4):A1-A93