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DE NOVO MULTIPLE MYELOMA AFTER KIDNEY TRANSPLANTATION
NKF 2014 Spring Clinical Meetings Abstracts
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RETROPERITONEAL FIBROSIS CAUSING ACUTE KIDNEY INJURY WITHOUT ANATOMIC OBSTRUCTION: Salah Sabbagh, Narendranath Epperla, Rosemary Nwoko: Marshfield Clinic, Marshfield, WI, USA We present a case of a 79-year-old male with a history significant for non-small cell lung cancer status-post resection without radiation or chemotherapy and a 6-month history of progressive weakness, fatigue and malaise who was admitted with pneumonia At presentation, he had an elevated creatinine of 3.6 mg/dL (baseline 1.2). He underwent a CT scan of abdomen and pelvis (without contrast) for evaluation of back and abdominal pain. CT scan revealed large soft tissue peri-renal masses in both kidneys surrounding the renal hila with complete encasement and mass effect on the collecting system but no overt hydronephrosis. No anatomical ureteral blockage was noted. This was a new finding compared to a CT scan performed two years prior. Extensive work-up for vasculitis and paraneoplastic syndromes was negative. Urinalysis was bland and urine protein quantification was nominal. An ultrasound-guided biopsy of the mass showed a nonmalignant lymphoplasmacytic infiltrate with a normal IgG4/IgG ratio making IgG4-related disease unlikely. Bone marrow biopsy was unremarkable as was PET scan. Based on the imaging study and negative workup, he was diagnosed with idiopathic retroperitoneal fibrosis and initiated on 60 mg of prednisone. His creatinine improved from a peak of 4 to1.2 mg/dl within one month of steroid therapy. Multiple attempts to wean his prednisone below 20 mg daily led to recurrences of acute renal failure and he was initiated on Tamoxifen 20 mg twice daily. Retroperitoneal fibrosis is characterized by inflammatory and fibrous tissue that often encases the ureters and other abdominal organs. It can either be idiopathic or secondary to drugs, malignancy, infection or granulomatous disease. Renal failure is often from obstructive uropathy though it may also rarely occur without obstruction as in our case. Diagnosis is by imaging and biopsy. Treatment is surgical and/or medical with prednisone, tamoxifen and other immunosuppresants.
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$% ./6/ -5,4)0,% -9%,/-! !&4%2 +)$.%9 42!.30,!.4!4)/. 3AMI 3AFADI -$ .ELSON ,EUNG -$ &ERNANDO #OSIO -$ (ATEM !MER -$ -ORIE 'ERTZ -$ 6INCENT 2AJKUMAR -$ 3UZANEE (AYMAN -$ -ARTHA ,ACY -$ !NGELA $ISPENZIERI -$ -AYO #LINIC 2OCHESTER -. 53! )NTRODUCTION $ATA REGARDING MULTIPLE MYELOMA -- THAT DEVELOPS AFTER KIDNEY TRANSPLANTATION +4X IS SCARCE IN THE LITERATURE 7E EVALUATED THE OUTCOMES OF THESE PATIENTS IN A SINGLE CENTER RETROSPECTIVE STUDY -ETHODS 0ATIENTS WITH NEWLY DIAGNOSED -- AFTER +4X WERE SELECTED 4HEIR RECORD WAS QUERIED FOR MONOCLONAL GAMMOPATHY AND PLASMA CELL DYSCRASIA PRIOR TO +4X TREATMENT RECEIVED FOR -- AND PATIENT SURVIVAL 0ATIENTS WITH A DIAGNOSIS OF -- OR THOSE WHO RECEIVED TREATMENT FOR MONOCLONAL GAMMOPATHY OF RENAL SIGNIFICANCE PRIOR TO +4X WERE EXCLUDED 2ESULTS "ETWEEN AND PATIENTS WERE IDENTIFIED OF DEVELOPING -- AND SMOLDERING -- AFTER +4X 2EASONS FOR %32$ INCLUDED !$0+$ #Q NEPHROPATHY -0'. ,# TUBULOPATHY WITH &ANCONIS SYNDROME HYPERTENSIVE NEPHROSCLEROSIS AND CHRONIC INTERSTITIAL NEPHRITIS HAD EVIDENCE OF MONOCLONAL GAMMOPATHY BEFORE +4X AND OF THEM HAD EVIDENCE OF CLONAL PLASMA CELLS IN THEIR BONE MARROW BEFORE +4X 4HIS INFORMATION WAS MISSING FOR THE OTHER PATIENTS /F THE PATIENTS ARE STILL ALIVE -EDIAN FOLLOW UP AFTER THE DIAGNOSIS OF -- WAS MONTH )12 TO -EDIAN SURVIVAL WAS MONTHS )12 TO -EDIAN TIME FROM +4X TO DIAGNOSIS OF -- WAS YEARS )12 TO +IDNEY ALLOGRAFT FAILED IN PATIENTS DUE TO MONOCLONAL GAMMOPATHY RELATED KIDNEY DISEASES RECEIVED LENALIDOMIDE RECEIVED THALIDOMIDE RECEIVED BORTEZOMIB AND UNDERWENT !3#4 #ONCLUSION -- AFTER +4X IS RARE -OST PATIENTS WHO DEVELOP -- HAD A MONOCLONAL GAMMOPATHY PRIOR TO +4X 3URVIVAL DOES NOT APPEAR WORSE WHEN COMPARED TO -- WITHOUT +4X &URTHER STUDIES ARE NEEDED TO EXPLAIN THE RELATIONSHIP BETWEEN -- AND 04,$ AND TO IDENTIFY THE BEST THERAPY OPTIONS
A96
LACTIC ACIDOSIS IN ASSOCIATION WITH GASTRIC CARCINOMA – A CASE REPORT Sami Safadi, MD, Christopher D. Janish, MD, Qi Qian, MD, Mayo Clinic, Rochester, MN, USA. Type B Lactic acidosis is associated with some malignancies. The mortality is usually high because of advanced disease, and high tumor burden. Increased awareness of this complication in certain malignancies is important because early initiation of chemotherapy may improve LA and increase patients’ chances of survival. We describe here a case of type B LA in association with gastric carcinoma. A 56 y/o male presents with progressive lower abdominal pain, nausea, and cough for a month duration. His PMH is notable for CKD stage 3B secondary to autosomal dominant polycystic kidney disease (ADPKD). His exam revealed dry mucous membranes, and abdominal distension. Initial labs revealed known secondary polycythemia (Hgb of 17.3), thrombocytopenia (platelets of 117,00/μL), hyponatremia (sodium of 131), and lactic acidosis(lactate of 3.9). He was admitted and received IVF resuscitation. Extensive workup for intra-abdominal infection, and sepsis were negative. Over the next few days, his lactic acidosis persisted along with AG metabolic acidosis. He required initiation of CVVH and significant bicarbonate repletion. A CT chest was then performed and revealed marked mediastinal lymphadenopathy. CT-guided biopsy of a retroperitoneal lymph node was performed. The following day, the patient decompensated, and passed away. Final pathology returned the next day showing adenocarcinoma with signet ring cells consistent with gastric adenocarcinoma.
IN-PATIENT HEMODIALYSIS WITHOUT HEPARIN: S Sahota, R Rodby, Rush University Medical Center (RUMC), Chicago, IL, USA. Because hemodialysis (HD) requires extracorporeal blood flow, heparin use during treatment is standard practice. All adult in-patient HD treatments at RUMC are performed using a standardized heparinfree protocol (HFP). We thus performed a retrospective chart review to determine the incidence of HD circuit clotting during the procedure. A chart review was done on all adult RUMC in-patient HD treatments, both end-stage renal disease (ESRD) and acute kidney injury (AKI) from 12/12 to 10/13. Patients were excluded if they were on a heparin drip, clopidogrel, warfarin or direct thrombin inhibitors. We identified 400 patients and evaluated the first HD treatment of their hospitalization. The HFP begins with priming the hemodialyzer with 0.9% normal saline (NS) at a pump speed (PS) of 200 ml/min, recirculating the saline at PS 500 ml/min for 30 seconds or until all air has been removed from the blood lines and hemodialyzer, followed by continued recirculation of the NS at PS 200 ml/min for 10 min. During the HD treatment, the hemodialyzer is flushed every 15 min with 100 ml of 0.9% NS the total amount of which is pre-calculated into the total ultrafiltration fluid removal during the HD treatment. PATIENT CHARACTERISTICS ESRD/AKI 84.5% / 15.5% Age (mean) 55.9 ± 15.3 BMI (mean) 28.3 ± 8.1 Male / Diabetes 52% / 45% History of Peripheral Blood Clot 11% Access: Catheters / Fistulas / Grafts 44% / 41% / 15% ASA use 44% Platelet count (mean) 183x103 ± 88.7 INR (mean) 1.2 ± 0.76 The average HD blood flow rate was 378 ± 46 ml/min with 4.7% of (88% catheters; 12% grafts) treatments requiring bloodline “reversal” because of high venous or arterial pressures. Only 0.8% of the HD treatments were associated with clotting of the hemodialyzer circuit. In conclusion, a HFP allows adult in-patient HD to be performed across all access types without heparin and without circuit clotting.
Am J Kidney Dis. 2014;63(5):A1-A121
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RETROPERITONEAL FIBROSIS CAUSING ACUTE KIDNEY INJURY WITHOUT ANATOMIC OBSTRUCTION: Salah Sabbagh, Narendranath Epperla, Rosemary Nwoko: Marshfield Clinic, Marshfield, WI, USA We present a case of a 79-year-old male with a history significant for non-small cell lung cancer status-post resection without radiation or chemotherapy and a 6-month history of progressive weakness, fatigue and malaise who was admitted with pneumonia At presentation, he had an elevated creatinine of 3.6 mg/dL (baseline 1.2). He underwent a CT scan of abdomen and pelvis (without contrast) for evaluation of back and abdominal pain. CT scan revealed large soft tissue peri-renal masses in both kidneys surrounding the renal hila with complete encasement and mass effect on the collecting system but no overt hydronephrosis. No anatomical ureteral blockage was noted. This was a new finding compared to a CT scan performed two years prior. Extensive work-up for vasculitis and paraneoplastic syndromes was negative. Urinalysis was bland and urine protein quantification was nominal. An ultrasound-guided biopsy of the mass showed a nonmalignant lymphoplasmacytic infiltrate with a normal IgG4/IgG ratio making IgG4-related disease unlikely. Bone marrow biopsy was unremarkable as was PET scan. Based on the imaging study and negative workup, he was diagnosed with idiopathic retroperitoneal fibrosis and initiated on 60 mg of prednisone. His creatinine improved from a peak of 4 to1.2 mg/dl within one month of steroid therapy. Multiple attempts to wean his prednisone below 20 mg daily led to recurrences of acute renal failure and he was initiated on Tamoxifen 20 mg twice daily. Retroperitoneal fibrosis is characterized by inflammatory and fibrous tissue that often encases the ureters and other abdominal organs. It can either be idiopathic or secondary to drugs, malignancy, infection or granulomatous disease. Renal failure is often from obstructive uropathy though it may also rarely occur without obstruction as in our case. Diagnosis is by imaging and biopsy. Treatment is surgical and/or medical with prednisone, tamoxifen and other immunosuppresants.
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$% ./6/ -5,4)0,% -9%,/-! !&4%2 +)$.%9 42!.30,!.4!4)/. 3AMI 3AFADI -$ .ELSON ,EUNG -$ &ERNANDO #OSIO -$ (ATEM !MER -$ -ORIE 'ERTZ -$ 6INCENT 2AJKUMAR -$ 3UZANEE (AYMAN -$ -ARTHA ,ACY -$ !NGELA $ISPENZIERI -$ -AYO #LINIC 2OCHESTER -. 53! )NTRODUCTION $ATA REGARDING MULTIPLE MYELOMA -- THAT DEVELOPS AFTER KIDNEY TRANSPLANTATION +4X IS SCARCE IN THE LITERATURE 7E EVALUATED THE OUTCOMES OF THESE PATIENTS IN A SINGLE CENTER RETROSPECTIVE STUDY -ETHODS 0ATIENTS WITH NEWLY DIAGNOSED -- AFTER +4X WERE SELECTED 4HEIR RECORD WAS QUERIED FOR MONOCLONAL GAMMOPATHY AND PLASMA CELL DYSCRASIA PRIOR TO +4X TREATMENT RECEIVED FOR -- AND PATIENT SURVIVAL 0ATIENTS WITH A DIAGNOSIS OF -- OR THOSE WHO RECEIVED TREATMENT FOR MONOCLONAL GAMMOPATHY OF RENAL SIGNIFICANCE PRIOR TO +4X WERE EXCLUDED 2ESULTS "ETWEEN AND PATIENTS WERE IDENTIFIED OF DEVELOPING -- AND SMOLDERING -- AFTER +4X 2EASONS FOR %32$ INCLUDED !$0+$ #Q NEPHROPATHY -0'. ,# TUBULOPATHY WITH &ANCONIS SYNDROME HYPERTENSIVE NEPHROSCLEROSIS AND CHRONIC INTERSTITIAL NEPHRITIS HAD EVIDENCE OF MONOCLONAL GAMMOPATHY BEFORE +4X AND OF THEM HAD EVIDENCE OF CLONAL PLASMA CELLS IN THEIR BONE MARROW BEFORE +4X 4HIS INFORMATION WAS MISSING FOR THE OTHER PATIENTS /F THE PATIENTS ARE STILL ALIVE -EDIAN FOLLOW UP AFTER THE DIAGNOSIS OF -- WAS MONTH )12 TO -EDIAN SURVIVAL WAS MONTHS )12 TO -EDIAN TIME FROM +4X TO DIAGNOSIS OF -- WAS YEARS )12 TO +IDNEY ALLOGRAFT FAILED IN PATIENTS DUE TO MONOCLONAL GAMMOPATHY RELATED KIDNEY DISEASES RECEIVED LENALIDOMIDE RECEIVED THALIDOMIDE RECEIVED BORTEZOMIB AND UNDERWENT !3#4 #ONCLUSION -- AFTER +4X IS RARE -OST PATIENTS WHO DEVELOP -- HAD A MONOCLONAL GAMMOPATHY PRIOR TO +4X 3URVIVAL DOES NOT APPEAR WORSE WHEN COMPARED TO -- WITHOUT +4X &URTHER STUDIES ARE NEEDED TO EXPLAIN THE RELATIONSHIP BETWEEN -- AND 04,$ AND TO IDENTIFY THE BEST THERAPY OPTIONS
A96
LACTIC ACIDOSIS IN ASSOCIATION WITH GASTRIC CARCINOMA – A CASE REPORT Sami Safadi, MD, Christopher D. Janish, MD, Qi Qian, MD, Mayo Clinic, Rochester, MN, USA. Type B Lactic acidosis is associated with some malignancies. The mortality is usually high because of advanced disease, and high tumor burden. Increased awareness of this complication in certain malignancies is important because early initiation of chemotherapy may improve LA and increase patients’ chances of survival. We describe here a case of type B LA in association with gastric carcinoma. A 56 y/o male presents with progressive lower abdominal pain, nausea, and cough for a month duration. His PMH is notable for CKD stage 3B secondary to autosomal dominant polycystic kidney disease (ADPKD). His exam revealed dry mucous membranes, and abdominal distension. Initial labs revealed known secondary polycythemia (Hgb of 17.3), thrombocytopenia (platelets of 117,00/μL), hyponatremia (sodium of 131), and lactic acidosis(lactate of 3.9). He was admitted and received IVF resuscitation. Extensive workup for intra-abdominal infection, and sepsis were negative. Over the next few days, his lactic acidosis persisted along with AG metabolic acidosis. He required initiation of CVVH and significant bicarbonate repletion. A CT chest was then performed and revealed marked mediastinal lymphadenopathy. CT-guided biopsy of a retroperitoneal lymph node was performed. The following day, the patient decompensated, and passed away. Final pathology returned the next day showing adenocarcinoma with signet ring cells consistent with gastric adenocarcinoma.
IN-PATIENT HEMODIALYSIS WITHOUT HEPARIN: S Sahota, R Rodby, Rush University Medical Center (RUMC), Chicago, IL, USA. Because hemodialysis (HD) requires extracorporeal blood flow, heparin use during treatment is standard practice. All adult in-patient HD treatments at RUMC are performed using a standardized heparinfree protocol (HFP). We thus performed a retrospective chart review to determine the incidence of HD circuit clotting during the procedure. A chart review was done on all adult RUMC in-patient HD treatments, both end-stage renal disease (ESRD) and acute kidney injury (AKI) from 12/12 to 10/13. Patients were excluded if they were on a heparin drip, clopidogrel, warfarin or direct thrombin inhibitors. We identified 400 patients and evaluated the first HD treatment of their hospitalization. The HFP begins with priming the hemodialyzer with 0.9% normal saline (NS) at a pump speed (PS) of 200 ml/min, recirculating the saline at PS 500 ml/min for 30 seconds or until all air has been removed from the blood lines and hemodialyzer, followed by continued recirculation of the NS at PS 200 ml/min for 10 min. During the HD treatment, the hemodialyzer is flushed every 15 min with 100 ml of 0.9% NS the total amount of which is pre-calculated into the total ultrafiltration fluid removal during the HD treatment. PATIENT CHARACTERISTICS ESRD/AKI 84.5% / 15.5% Age (mean) 55.9 ± 15.3 BMI (mean) 28.3 ± 8.1 Male / Diabetes 52% / 45% History of Peripheral Blood Clot 11% Access: Catheters / Fistulas / Grafts 44% / 41% / 15% ASA use 44% Platelet count (mean) 183x103 ± 88.7 INR (mean) 1.2 ± 0.76 The average HD blood flow rate was 378 ± 46 ml/min with 4.7% of (88% catheters; 12% grafts) treatments requiring bloodline “reversal” because of high venous or arterial pressures. Only 0.8% of the HD treatments were associated with clotting of the hemodialyzer circuit. In conclusion, a HFP allows adult in-patient HD to be performed across all access types without heparin and without circuit clotting.
Am J Kidney Dis. 2014;63(5):A1-A121