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CRESCENTIC IGA NEPHROPATHY IN RENAL ALLOGRAFT: A CASE REPORT
NKF 2014 Spring Clinical Meetings Abstracts
BEDSIDE ULTRASONOGRAPHY FOR DIFFICULT AV FISTULA CANNULATION Patel Roshan, Ellena Linden, Maritza Brown, Aaron Stern, Bhatti Saad Elmhurst Hospital, Icahn School of Medicine, NY Difficulty in cannulating an AV fistula is a common clinical problem in hemodialysis patients which often leads to urgent referral to interventional radiology(IR) or vascular surgery. We present a case of successful use of bedside ultrasonography for a difficult AVF cannulation. 77 year old male with a PMH of HTN, DM-2, CVA and ESRD on HD had a new AVF creation on the right upper extremity and tunneled dialysis catheter placement in April 2013.In July the patient was admitted to Elmhurst Hospital with fever, chills and malaise. Catheter was removed secondary to Stenotrophomonas maltophilia bacteremia. A decision was made by the renal team to begin HD via the AVF as it was deemed to be mature. However, the most experienced nursing staff member in dialysis unit had difficulty with cannulating it.IR was unavailable due to urgent cases in IR room. The initial plan was to return the patient to his room and delay HD pending IR availability. One of the renal physicians trained in critical care with experience in ultrasonography utilized bedside ultrasonography and cannulated the AVF successfully without any complication. Venous tract of AVF in this patient was more than 1 cm deep which was the reason for failed cannulation. With use of bedside real time ultrasonogarphy the vein was easily visualized and cannulated.
(Image before and after cannulation with needle tip in vein)
282
ERLOTINIB DELAYS RECOVERY FROM ACUTE TUBULAR NECROSIS: Anyeri Peguero, Cherise Cortese, Nabeel Aslam; Mayo Clinic Florida, Jacksonville, FL USA Erlotinib is a specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is used for chemotherapy of non-small cell lung cancer. Animal studies have shown marked activation of EGFR in kidney ischemia-reperfusion injury. Inhibition of EGFR with Erlotinib leads to persistent dilatation of renal proximal tubules and delay in the renal cell proliferation in mice model. We report a case of Acute Kidney Injury (AKI) due to Acute Tubular Necrosis (ATN) with delayed recovery during the administration of Erlotinib. 67-year-old female with history of non-small cell lung cancer, CKD (baseline creatinine 2.2mg/dL), hypertension, and diabetes was being treated with Erlotinib. She developed nausea, vomiting, diarrhea and progressive rise in creatinine over several weeks while taking Erlotinib. On exam, Pulse 96/min, BP 132/80 mm (Hg), no orthostatic changes, clear lung fields, and no edema. UA showed 1+ protein, granular casts, random urine sodium 31mmol/L, Prot/Cr 0.4. Serum Cr 6.5 mg/dL and serologies were negative. She received IVF with partial improvement in creatinine (S Cr 4.5 mg/dL). Renal biopsy showed acute tubular necrosis, 50% glomerulosclerosis with significant interstitial fibrosis and tubular atrophy (Fig 1). Erlotinib was discontinued with only partial recovery of renal function (S Cr 4.1 three months later). We speculate that our patient developed ATN due to volume depletion (vomiting, diarrhea) and renal recovery was delayed due to ongoing use of Erlotinib similar to studies in animal models. We suggest discontinuing the Erlotinib in patients with volume depletion/AKI to avoid delay in renal recovery that can lead to CKD. Further studies are needed to explore the effect of Erlotinib on renal tubular cell proliferation.
284 PATTERNS OF ANEMIA MANAGEMENT IN PATIENTS UNDERGOING PERITONEAL DIALYSIS Yi Peng,1 Allyson Kats,1 David T. Gilbertson,1 Deborah Kim,2 Keri L. Monda,2 James B.Wetmore,1 Brian D. Bradbury,2 Allan J. Collins.1 1 Chronic Disease Research Group, Minneapolis, MN, USA; 2Amgen, Inc, Thousand Oaks, CA, USA. Most data on anemia management in dialysis patients are from hemodialysis (HD) patients. We aimed to describe anemia management trends, 2009-2011, in peritoneal dialysis (PD) patients. Quarterly cohorts of prevalent PD patients with Medicare coverage and at least 3 months of PD before enrollment were created to evaluate anemia management practices. Patients were followed from the first day of each quarter to the first of death, kidney transplant, change to HD, or last day of the quarter. Epogen (EPO) was administered to 68% of patients in Q1 2009 (09Q1) (n=15,043), decreasing to 64% in Q4 2011 (11Q4) (n=17,842). Darbepoetin (DPO) use decreased from 9.2% in 09Q1 to 6.2% in 11Q4; iron use increased from 21% to 36%. Mean hgb decreased from 11.3 to 10.6 g/dL and transfusions increased from 5.4% to 6.6%. Mean EPO dose per 30 outpatient days decreased 20% from 44,567 to 35,623 units, and mean DPO dose decreased from 176 to 128 mcg (27%). Between 09Q1 and 10Q4, mean iron dose per 30 OP days increased from 126 to 144 mg, declining to 130 mg by 11Q4. Continued monitoring of these trends will be important, as use of home therapies continues to increase.
Percent (%)
CRESCENTIC IGA NEPHROPATHY IN RENAL ALLOGRAFT: A CASE REPORT Shashikant Patel, Samir Parikh, Jon Von Visger. Ohio State University, Columbus, Ohio. Aggressive IgAN is rare in the renal allograft. We report a case of recurrent IgAN that manifested as a necrotizing and crescentic glomerulonephritis (GN). 31 year old male received deceased donor renal transplant (Tx) after developing ESRD due to IgAN. Induction therapy included ATG, steroids (5 days) and sirolimus. Nine months after Tx he developed acute cellular and antibody mediated rejection with mild IgA staining which improved with steroids. Graft function again worsened and repeat biopsy showed crescentic GN but no IgA. Therapy was started but due to worsening disease a 3rd biopsy was done and showed crescentic IgAN. Graft function returned to baseline after treatment with oral cyclophosphamide and steroids (figure 1). We report a case of crescentic IgAN in a renal allograft successfully treated with oral cyclophosphamide. Crescentic IgAN in the renal allograft is rare. Reports from our institution suggest steroid free regimen and sirolimus may increase risk. Treatment with cyclophosphamide appears to be effective with response similar to native IgAN. Crescentic IgAN is a devastating manifestation that can cause graft failure. Early recognition and aggressive treatment provides the best chance for graft survival.
283
80% 70% 60% 50% 40% 30% 20% 10% 0%
12 11 EPO use Iron use Hgb
DPO use Transfusion
10 9
Hgb (g/dL)
281
8 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 2009
Figure 1: Graft function vs Time
Am J Kidney Dis. 2014;63(5):A1-A121
2010 Year (Quarter)
2011
A89
BEDSIDE ULTRASONOGRAPHY FOR DIFFICULT AV FISTULA CANNULATION Patel Roshan, Ellena Linden, Maritza Brown, Aaron Stern, Bhatti Saad Elmhurst Hospital, Icahn School of Medicine, NY Difficulty in cannulating an AV fistula is a common clinical problem in hemodialysis patients which often leads to urgent referral to interventional radiology(IR) or vascular surgery. We present a case of successful use of bedside ultrasonography for a difficult AVF cannulation. 77 year old male with a PMH of HTN, DM-2, CVA and ESRD on HD had a new AVF creation on the right upper extremity and tunneled dialysis catheter placement in April 2013.In July the patient was admitted to Elmhurst Hospital with fever, chills and malaise. Catheter was removed secondary to Stenotrophomonas maltophilia bacteremia. A decision was made by the renal team to begin HD via the AVF as it was deemed to be mature. However, the most experienced nursing staff member in dialysis unit had difficulty with cannulating it.IR was unavailable due to urgent cases in IR room. The initial plan was to return the patient to his room and delay HD pending IR availability. One of the renal physicians trained in critical care with experience in ultrasonography utilized bedside ultrasonography and cannulated the AVF successfully without any complication. Venous tract of AVF in this patient was more than 1 cm deep which was the reason for failed cannulation. With use of bedside real time ultrasonogarphy the vein was easily visualized and cannulated.
(Image before and after cannulation with needle tip in vein)
282
ERLOTINIB DELAYS RECOVERY FROM ACUTE TUBULAR NECROSIS: Anyeri Peguero, Cherise Cortese, Nabeel Aslam; Mayo Clinic Florida, Jacksonville, FL USA Erlotinib is a specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor that is used for chemotherapy of non-small cell lung cancer. Animal studies have shown marked activation of EGFR in kidney ischemia-reperfusion injury. Inhibition of EGFR with Erlotinib leads to persistent dilatation of renal proximal tubules and delay in the renal cell proliferation in mice model. We report a case of Acute Kidney Injury (AKI) due to Acute Tubular Necrosis (ATN) with delayed recovery during the administration of Erlotinib. 67-year-old female with history of non-small cell lung cancer, CKD (baseline creatinine 2.2mg/dL), hypertension, and diabetes was being treated with Erlotinib. She developed nausea, vomiting, diarrhea and progressive rise in creatinine over several weeks while taking Erlotinib. On exam, Pulse 96/min, BP 132/80 mm (Hg), no orthostatic changes, clear lung fields, and no edema. UA showed 1+ protein, granular casts, random urine sodium 31mmol/L, Prot/Cr 0.4. Serum Cr 6.5 mg/dL and serologies were negative. She received IVF with partial improvement in creatinine (S Cr 4.5 mg/dL). Renal biopsy showed acute tubular necrosis, 50% glomerulosclerosis with significant interstitial fibrosis and tubular atrophy (Fig 1). Erlotinib was discontinued with only partial recovery of renal function (S Cr 4.1 three months later). We speculate that our patient developed ATN due to volume depletion (vomiting, diarrhea) and renal recovery was delayed due to ongoing use of Erlotinib similar to studies in animal models. We suggest discontinuing the Erlotinib in patients with volume depletion/AKI to avoid delay in renal recovery that can lead to CKD. Further studies are needed to explore the effect of Erlotinib on renal tubular cell proliferation.
284 PATTERNS OF ANEMIA MANAGEMENT IN PATIENTS UNDERGOING PERITONEAL DIALYSIS Yi Peng,1 Allyson Kats,1 David T. Gilbertson,1 Deborah Kim,2 Keri L. Monda,2 James B.Wetmore,1 Brian D. Bradbury,2 Allan J. Collins.1 1 Chronic Disease Research Group, Minneapolis, MN, USA; 2Amgen, Inc, Thousand Oaks, CA, USA. Most data on anemia management in dialysis patients are from hemodialysis (HD) patients. We aimed to describe anemia management trends, 2009-2011, in peritoneal dialysis (PD) patients. Quarterly cohorts of prevalent PD patients with Medicare coverage and at least 3 months of PD before enrollment were created to evaluate anemia management practices. Patients were followed from the first day of each quarter to the first of death, kidney transplant, change to HD, or last day of the quarter. Epogen (EPO) was administered to 68% of patients in Q1 2009 (09Q1) (n=15,043), decreasing to 64% in Q4 2011 (11Q4) (n=17,842). Darbepoetin (DPO) use decreased from 9.2% in 09Q1 to 6.2% in 11Q4; iron use increased from 21% to 36%. Mean hgb decreased from 11.3 to 10.6 g/dL and transfusions increased from 5.4% to 6.6%. Mean EPO dose per 30 outpatient days decreased 20% from 44,567 to 35,623 units, and mean DPO dose decreased from 176 to 128 mcg (27%). Between 09Q1 and 10Q4, mean iron dose per 30 OP days increased from 126 to 144 mg, declining to 130 mg by 11Q4. Continued monitoring of these trends will be important, as use of home therapies continues to increase.
Percent (%)
CRESCENTIC IGA NEPHROPATHY IN RENAL ALLOGRAFT: A CASE REPORT Shashikant Patel, Samir Parikh, Jon Von Visger. Ohio State University, Columbus, Ohio. Aggressive IgAN is rare in the renal allograft. We report a case of recurrent IgAN that manifested as a necrotizing and crescentic glomerulonephritis (GN). 31 year old male received deceased donor renal transplant (Tx) after developing ESRD due to IgAN. Induction therapy included ATG, steroids (5 days) and sirolimus. Nine months after Tx he developed acute cellular and antibody mediated rejection with mild IgA staining which improved with steroids. Graft function again worsened and repeat biopsy showed crescentic GN but no IgA. Therapy was started but due to worsening disease a 3rd biopsy was done and showed crescentic IgAN. Graft function returned to baseline after treatment with oral cyclophosphamide and steroids (figure 1). We report a case of crescentic IgAN in a renal allograft successfully treated with oral cyclophosphamide. Crescentic IgAN in the renal allograft is rare. Reports from our institution suggest steroid free regimen and sirolimus may increase risk. Treatment with cyclophosphamide appears to be effective with response similar to native IgAN. Crescentic IgAN is a devastating manifestation that can cause graft failure. Early recognition and aggressive treatment provides the best chance for graft survival.
283
80% 70% 60% 50% 40% 30% 20% 10% 0%
12 11 EPO use Iron use Hgb
DPO use Transfusion
10 9
Hgb (g/dL)
281
8 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 2009
Figure 1: Graft function vs Time
Am J Kidney Dis. 2014;63(5):A1-A121
2010 Year (Quarter)
2011
A89