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Nephrolithiasis Associated with Darunavir: A Case For Caution
NKF 2016 Spring Clinical Meetings Abstracts
Case Report 305
307
NEPHROLITHIASIS ASSOCIATED WITH DARUNAVIR; A CASE FOR CAUTION Anahita Sattari, Maryam Sattari, Amir Kazory Emory University, Atlanta, Georgia and University of Florida, Gainesville, Florida, USA 1,
SUCCESSFUL TREATMENT OF AN UNUSUAL CASE OF Pregnancy in a Patient With Primary Membranous Nephropathy MEMBRANOUS NEPHROPATHY WITH ADRENOCORTICOTROPIC HORMONE GEL IN HIV PATIENT. and Circulating Anti-PLA2R Antibodies: A Case Report
David Saxon, Amr El-Husseini, Stuart Jennings, Virgilius Cornea, B. Peter Sawaya, University of Kentucky, Lexington, KY, USA and
1 1 Laith Al-Rabadi, MBBS, * Rivka Ayalon, MD, Ramon G. Bonegio, MD,Center, PhD, Laurence Beck, Boston University Medical Boston, MA, USA 2,y 3 4 In adults, nephropathy MD, (MN) isPhD, a major cause of Case: A 48-year-old man withE. human immunodeficiency virus (HIV) Jennifer Ballard, MD, Alan M. Fujii, MD, Joelmembranous M. Henderson, nephrotic syndrome. While the majority1 of cases of MN are idiopathic, on antiretroviral therapy (including darunavir, a protease inhibitor 1 [PI], David J. Salant, MD, and Laurence H. Beck Jr, MD, PhD secondary forms can be seen in the setting of autoimmune disease, ritonavir, and abacavir-lamivudine) presented with 3 days of left flank
neoplasia, infection, and following exposure to certain therapeutic pain. Physical exam was unremarkable. Laboratory studies were agents. Both human immunodeficiency virus (HIV) and hepatitis C positive for serum creatinine of 1.51 mg/dL, hemoglobin of 12.8 g/dL, There littlecells information aboutfield pregnancy outcomes in patients with infections active membranous nephropathy virus (HCV) could cause MN. However, the(MN), effect of as well as 6-10 whiteisblood per high power and +1 leukocyte HIV and HCV infection on the spectrum and progression of esterase inespecially the urine. A those non-contrast tomography scan (PLA with computed circulating autoantibodies to M-typecoexisting phospholipase A2 receptor 2R), the major as wellcase as the of effect of MN treatment on HIV demonstrated a 1.1 cm proximal left ureteral stone with mild proximal autoantigen in primary MN. We present what we believe to kidney be thedisease first known successful pregnancy in and HCV infection are not well known. hydroureter and hydronephrosis and several other punctate stones at the to pregnancy, the patient Adeveloped a 39-year-old woman with PLA2R-associated MN. In the year Hereinprior we describe a patient with hemophilia and acquired HIV lower pole of the left kidney. The patient underwent cystoscopy, left hypoalbuminemia (protein excretion, Kidney bi- with and HCV infections who developed 29.2 severeg/d). nephrotic syndrome retrogradeanasarca, pyelogram, left ureteroscopy, laser(albumin, lithotripsy, 1.3-2.2 ureteral g/dL), and proteinuria and the patientrenal was seropositive for anti-PLA2R autoantibodies. opsy revealed MN with staining for PLA biopsy showing MN. 2R, balloon dilation, and left ureteral stent placement. Urine and stone workuprituximab was negative causes She didnegative, not respond to conservative therapy and was treatedThe withpatient’s intravenous (2 for doses ofof1 secondary g each). MN, and cultures remained and stone analysis demonstrated 18% he waspregnant found to be positive antiphospholipase receptor atazanavirSeveral and/or closely related andshe 55%was calcium weeks aftermetabolite(s), presentation, found to be 6 weeks and was for closely followed upA2without antibodies consistent with idiopathic MN. The patient was treated with oxalate monohydrate, 25% calcium oxalate dihydrate, andProteinuria 2% protein. remained further immunosuppressive treatment. with protein excretion in the 8to 12-g/d range. adrenocorticotropic hormone gel. He responded well with decreasing Discussion: Our patient presented with nephrolithiasis in the setting of declined but were still detectable. At 38 weeks, a healthy babyviagirl was blot born, Circulating anti-PLA2R levels antiphospholipase A2 receptor antibodies western and urine darunavir use for management of HIV. Darunavir and atazanavir are without at birth or atinher subsequent At the time of delivery, thegm/gm mother stilltherapy when protein tovisit. creatinine ratio decreasing from 6.0 preferred PIs for theproteinuria initial treatment of HIV-1 combination with 6-month postnatal was(IgG1), initiatedIgG3, to 0.4 gm/gm at 18subclasses, months of follow up. HIVatand HCV R of immunoglobulin G1 and IgG4 although had detectable circulating anti-PLA other antiretroviral drugs. While atazanavir has been2recognized as a affected by reasons treatment. for the were not adversely risk factorlow for nephrolithiasis, our knowledge the second found in cord blood. Potential titers. Only to trace amountsthis of isIgG4 anti-PLA2R wereinfections Therefore, adrenocorticotropic hormone gel might be useful in the reported case of darunavir-associated nephrolithiasis. Possible fetal circulation arecases discussed. discrepancy between anti-PLA 2R levels in the maternal and management of complex of idiopathic MN. mechanisms responsible for the association between atazanavir and Am J Kidney Dis. 67(5):775-778. ª 2016 by the National Kidney Figure:Foundation, Serum albuminInc. nephrolithiasis are urinary excretion and precipitation. Risk factors for and random urine atazanavir-associated nephrolithiasis include elevated urine pH, hepatic protein/ creatinine ratio INDEX WORDS: Membranous nephropathy (MN); nephrotic syndrome; pregnancy; M-type phospholipase A2 dysfunction, decreased fluid intake or a history of nephrolithiasis. (UPCr) duringGthe Cliniciansreceptor should be (PLA aware2of thisautoantibody; potential complication of PIrituximab; use to R); placenta; immunoglobulin (Igfollow G) subclass. up period. prevent delay in diagnosis and treatment in patients who present with
signs and symptoms of nephrolithiasis. Furthermore, changing the antiretroviral regimen should be considered due to the high risk of recurrence regnantof nephrolithiasis. patients with autoimmune disease may
P
deliver newborns with a spectrum of clinical manifestations due to the transplacental passage of 306 circulating autoantibodies. Pregnant patients with PROTEIN ENERGY WASTING IN PREDIALYSIS PATIENTS. 1 lupus or myasthenia Anita Saxena , Amit Gupta2gravis can deliver babies with 1 2 1,2 Additional Professor, Professor, of Nephrology, Sanjay corresponding disease in Department the neonate. Neonatal Gandhi Post Graduate Institute Of Medical Sceinces, Lucknow, UP, membranous nephropathy (MN) not associated with India. Protein energy wasting (PEW) a majordescribed challenge in CKD. Objective: congenital infection wasis first in 1990 and To assess presence of PEW inpredialysis patients at first visit to a attributed to the passive transfer of maternal antinephrologist. Methods: Three days dietary intake of 141 patients in 3 CKD to stages 3 and 4. renal Appetiteantigens. and diet assessment (ADAT) and bodies putative More tool than a decade subjective global assessment (SGA) were used for appetite assessment. 4 later, Debiec et al identified the first antigen involved Result: Serum albumin2.87± 2.10/3.56±0.58 g/dL; total serum protein ±1.50/6.45±0.07; of 141 patients, 52.8% had normal BMI, a in 5.59 such cases as Out neutral endopeptidase (NEP), 15% were underweight, 5.71% were severely underweight and 27.1% metalloprotease present on the surface of the podocyte overweight. Males had hyperphosphatemia and hypocalcemia.There andwasinvolved in the proteolytic vasoacsignificant difference in dietary intakeregulation of BMI groupsof in weight (p appetite (0.004), energy (0.004) carbohydrate (0.003), tive0.000), peptides. Debiec et al described a mother with a In males and females, mean dietary energy intake was 1198.6±609.6 mutation preventing NEP expression who had formed and 981.44±490.0 kcal/d i.e 19.9±9.8 and 19.6 kcal/kg/d; protein 42.57±19.3antibodies and 37.6±15.4 g/d g/kg/d and 0.8±0.43g/kg/d anti-NEP duei.e.,to0.7±0.36 fetomaternal alloimmu, fat 22.1±31.6 and 16.1 ±15.0 g/d. Based on BMI energy intake in nization from a previous miscarriage; these antibodies normals was 17.2 ±9.0/18.6±13.5, in underweight 17.0±10.0 and 12.46±10.6, in severely underweight and 15.91±11.1 and subepithelial 18.4±6.5 and in were to cross the placenta cause overweight 17.5.0±7.8 and 18.9±6.0 kcal/kg/d in males and females In deposits in theintake fetal a subsequent pregnormals protein was kidney 0.73 ±0.31 of and 0.65±0.35; in underweight 0.55±0.63 and 0.42.±0.56 and, in severely 0.57±.53 and nancy. M-type phospholipase Aunderweight receptor (PLA 2 2R) overweight 0.62±.21 and 0.67±.18. Appetite significantly was0.87±.31, later identified as the major autoantigen for pricorrelated (p 0.000) with weight, BMI, dietary energy protein, fat , 5 serumMN albumin creatinine.Little Based on appetite energy and protein mary in and adults. literature exists about intake in male patients with normal appetite was 29.9±4.6 and 1.0±.38, pregnancy outcomes in patients with nephrotic synwith average 20.7±3,9 and 0.79±.2; poor 18.8±6.4 and 0.69±0.24 and drome due to primary MN, with no data energy available anorexic in 0.39±0.36 and 9.9±6.1 respectively. In females and protein intake in patients with normal appetite was disease. 31.3 ±8.2 and about pregnancy in PLA R-associated We 0.97±.16, in average 26.3 ±8.6 and2 .94±.49, in poor 17.6±4.9 and 0.69 present what we believeandto0.64±0.45. be the first known case of ±0.17 and in anorexic12.2±5 Conclusion: in Inadequate dietary with intake, body index (BMI) and low pregnancy a patient PLAmass 2R-associated MN serum albumin and protein are markers of malnutrition in predialysis who was seropositive for anti-PLA R autoantibodies 2 population. throughout the course of her pregnancy. Am J Kidney Dis. 2016;67(5):A1-A118
CASE REPORT A 39-year-old multiparous woman with morbid obesity presented for workup of severe nephrotic syndrome several months 308
before her current pregnancy. She had been treated for resistant DELAYED DIAGNOSIS OF RENAL ARTERY THROMBOSIS: IS hypertension and lower-extremity edema duringHarish the past year, ENDOVASCULAR THERAPY STILL AN ANSWER? butSeethapathy, her proteinuria had been overlooked. presentation, Helena Levy, John Hix, Rochester At General Hospital, serum Rochester, level NY, USA. creatinine was 1.52 mg/dL (corresponding to estimated Renal artery thrombosis a serious, yet often missed We by glomerular filtration rateis of 46 mL/min/1.73 m2 diagnosis. as calculated describe a patient who, despite late diagnosis, was successfully treated thewithisotope-dilution mass spectrometry – traceable 4-variable endovascular therapy. MDRD [Modification Diet ofinCKD Renal Study equaA 55 year old male withof a history stageDisease] III, baseline tion); serum albumin g/dL; and urine protein creatinine of 1.6 mg/dL, level, atrophic1.5 right kidney and24-hour resistant HTN presented with and leftbiopsy lower quadrant abdominal pain features of 2 excretion, 29.2suprapubic g. The kidney specimen revealed days duration. He denied nausea, vomiting diarrhea.for His the typical of primary MNfever, withchills, additional strong or staining blood pressure was 184/118 mmHg. Physical exam revealed suprapubic PLA R antigen within immune deposits (Fig S1). Many of the 2 tenderness. Labs showed acute on chronic renal failure with a subepithelial completely surrounded by new creatinine of 7.1deposits mg/dL andwere urinalysis showed erythrocytes and protein. Electrolytesmembrane and blood counts were normal. basement material (Fig Lower S2), urinary and tract 35% of the obstruction was ruled out with a Foley insertion and later confirmed by cystoscopy. CT abdomen and renal ultrasound did not reveal acute abnormal findings. He was started on dialysis when his kidney function 1 Fromto the Department Medicine,ARenal and failed improve with volumeof resuscitation. nuclear Section, flow scan of the De2 kidneys revealed an obstructive pattern in the3Pediatrics, left kidney, and 4Papartments of Obstetrics andflow Gynecology, or ischemia. CT Medical suggestive tubular necrosis thology andof obstruction, Laboratoryacute Medicine, Boston University Angiogram obtained 6 days after initial presentation showed severe Center, Boston, MA. bilateral filling defects in the renal arteries, suggestive of thrombi. He * Current aspiration affiliation: Department of Internal Medicine, Division underwent of the thrombus along with stenting of the left ofrenal Nephrology, University of Utah of Medicine, Salt Lake artery. Patient was also started on School anticoagulation. A complete hypercoagulability work up failed to reveal any thrombophilias. His City, UT. y kidney function recoveredDepartment back to baseline within 2 weeks. Current affiliation: of Obstetrics and Gynecology, In a patient who presents with acute renal failure of unclear etiology, Medstar Washington Hospital Center, Washington, DC. an embolic insult should be considered. Anticoagulation for 6 months Received 29, 2015. inrecommended. revised form October 27, followed by June antiplatelet therapyAccepted is generally 2015. Originally published endovascular online December 2015. on the Effectiveness of percutaneous therapy 29, is dependent severity andcorrespondence duration of ischemia. our patientH. diagnosis and MD, PhD, Address to In Laurence Beck Jr, treatment were delayed the outcome Some Renal Section, X-504, but 650thankfully, Albany St, Boston, was MAgood. 02118. E-mail: clinicians may have argued against thrombolysis and thrombectomy [email protected] after three days of compromised renal perfusion but remarkably flow � 2016 by theinto National Kidneyand Foundation, Inc. to baseline was reestablished the left kidney function returned within two weeks of starting therapy. 0272-6386
http://dx.doi.org/10.1053/j.ajkd.2015.10.031 775 A95
Case Report 305
307
NEPHROLITHIASIS ASSOCIATED WITH DARUNAVIR; A CASE FOR CAUTION Anahita Sattari, Maryam Sattari, Amir Kazory Emory University, Atlanta, Georgia and University of Florida, Gainesville, Florida, USA 1,
SUCCESSFUL TREATMENT OF AN UNUSUAL CASE OF Pregnancy in a Patient With Primary Membranous Nephropathy MEMBRANOUS NEPHROPATHY WITH ADRENOCORTICOTROPIC HORMONE GEL IN HIV PATIENT. and Circulating Anti-PLA2R Antibodies: A Case Report
David Saxon, Amr El-Husseini, Stuart Jennings, Virgilius Cornea, B. Peter Sawaya, University of Kentucky, Lexington, KY, USA and
1 1 Laith Al-Rabadi, MBBS, * Rivka Ayalon, MD, Ramon G. Bonegio, MD,Center, PhD, Laurence Beck, Boston University Medical Boston, MA, USA 2,y 3 4 In adults, nephropathy MD, (MN) isPhD, a major cause of Case: A 48-year-old man withE. human immunodeficiency virus (HIV) Jennifer Ballard, MD, Alan M. Fujii, MD, Joelmembranous M. Henderson, nephrotic syndrome. While the majority1 of cases of MN are idiopathic, on antiretroviral therapy (including darunavir, a protease inhibitor 1 [PI], David J. Salant, MD, and Laurence H. Beck Jr, MD, PhD secondary forms can be seen in the setting of autoimmune disease, ritonavir, and abacavir-lamivudine) presented with 3 days of left flank
neoplasia, infection, and following exposure to certain therapeutic pain. Physical exam was unremarkable. Laboratory studies were agents. Both human immunodeficiency virus (HIV) and hepatitis C positive for serum creatinine of 1.51 mg/dL, hemoglobin of 12.8 g/dL, There littlecells information aboutfield pregnancy outcomes in patients with infections active membranous nephropathy virus (HCV) could cause MN. However, the(MN), effect of as well as 6-10 whiteisblood per high power and +1 leukocyte HIV and HCV infection on the spectrum and progression of esterase inespecially the urine. A those non-contrast tomography scan (PLA with computed circulating autoantibodies to M-typecoexisting phospholipase A2 receptor 2R), the major as wellcase as the of effect of MN treatment on HIV demonstrated a 1.1 cm proximal left ureteral stone with mild proximal autoantigen in primary MN. We present what we believe to kidney be thedisease first known successful pregnancy in and HCV infection are not well known. hydroureter and hydronephrosis and several other punctate stones at the to pregnancy, the patient Adeveloped a 39-year-old woman with PLA2R-associated MN. In the year Hereinprior we describe a patient with hemophilia and acquired HIV lower pole of the left kidney. The patient underwent cystoscopy, left hypoalbuminemia (protein excretion, Kidney bi- with and HCV infections who developed 29.2 severeg/d). nephrotic syndrome retrogradeanasarca, pyelogram, left ureteroscopy, laser(albumin, lithotripsy, 1.3-2.2 ureteral g/dL), and proteinuria and the patientrenal was seropositive for anti-PLA2R autoantibodies. opsy revealed MN with staining for PLA biopsy showing MN. 2R, balloon dilation, and left ureteral stent placement. Urine and stone workuprituximab was negative causes She didnegative, not respond to conservative therapy and was treatedThe withpatient’s intravenous (2 for doses ofof1 secondary g each). MN, and cultures remained and stone analysis demonstrated 18% he waspregnant found to be positive antiphospholipase receptor atazanavirSeveral and/or closely related andshe 55%was calcium weeks aftermetabolite(s), presentation, found to be 6 weeks and was for closely followed upA2without antibodies consistent with idiopathic MN. The patient was treated with oxalate monohydrate, 25% calcium oxalate dihydrate, andProteinuria 2% protein. remained further immunosuppressive treatment. with protein excretion in the 8to 12-g/d range. adrenocorticotropic hormone gel. He responded well with decreasing Discussion: Our patient presented with nephrolithiasis in the setting of declined but were still detectable. At 38 weeks, a healthy babyviagirl was blot born, Circulating anti-PLA2R levels antiphospholipase A2 receptor antibodies western and urine darunavir use for management of HIV. Darunavir and atazanavir are without at birth or atinher subsequent At the time of delivery, thegm/gm mother stilltherapy when protein tovisit. creatinine ratio decreasing from 6.0 preferred PIs for theproteinuria initial treatment of HIV-1 combination with 6-month postnatal was(IgG1), initiatedIgG3, to 0.4 gm/gm at 18subclasses, months of follow up. HIVatand HCV R of immunoglobulin G1 and IgG4 although had detectable circulating anti-PLA other antiretroviral drugs. While atazanavir has been2recognized as a affected by reasons treatment. for the were not adversely risk factorlow for nephrolithiasis, our knowledge the second found in cord blood. Potential titers. Only to trace amountsthis of isIgG4 anti-PLA2R wereinfections Therefore, adrenocorticotropic hormone gel might be useful in the reported case of darunavir-associated nephrolithiasis. Possible fetal circulation arecases discussed. discrepancy between anti-PLA 2R levels in the maternal and management of complex of idiopathic MN. mechanisms responsible for the association between atazanavir and Am J Kidney Dis. 67(5):775-778. ª 2016 by the National Kidney Figure:Foundation, Serum albuminInc. nephrolithiasis are urinary excretion and precipitation. Risk factors for and random urine atazanavir-associated nephrolithiasis include elevated urine pH, hepatic protein/ creatinine ratio INDEX WORDS: Membranous nephropathy (MN); nephrotic syndrome; pregnancy; M-type phospholipase A2 dysfunction, decreased fluid intake or a history of nephrolithiasis. (UPCr) duringGthe Cliniciansreceptor should be (PLA aware2of thisautoantibody; potential complication of PIrituximab; use to R); placenta; immunoglobulin (Igfollow G) subclass. up period. prevent delay in diagnosis and treatment in patients who present with
signs and symptoms of nephrolithiasis. Furthermore, changing the antiretroviral regimen should be considered due to the high risk of recurrence regnantof nephrolithiasis. patients with autoimmune disease may
P
deliver newborns with a spectrum of clinical manifestations due to the transplacental passage of 306 circulating autoantibodies. Pregnant patients with PROTEIN ENERGY WASTING IN PREDIALYSIS PATIENTS. 1 lupus or myasthenia Anita Saxena , Amit Gupta2gravis can deliver babies with 1 2 1,2 Additional Professor, Professor, of Nephrology, Sanjay corresponding disease in Department the neonate. Neonatal Gandhi Post Graduate Institute Of Medical Sceinces, Lucknow, UP, membranous nephropathy (MN) not associated with India. Protein energy wasting (PEW) a majordescribed challenge in CKD. Objective: congenital infection wasis first in 1990 and To assess presence of PEW inpredialysis patients at first visit to a attributed to the passive transfer of maternal antinephrologist. Methods: Three days dietary intake of 141 patients in 3 CKD to stages 3 and 4. renal Appetiteantigens. and diet assessment (ADAT) and bodies putative More tool than a decade subjective global assessment (SGA) were used for appetite assessment. 4 later, Debiec et al identified the first antigen involved Result: Serum albumin2.87± 2.10/3.56±0.58 g/dL; total serum protein ±1.50/6.45±0.07; of 141 patients, 52.8% had normal BMI, a in 5.59 such cases as Out neutral endopeptidase (NEP), 15% were underweight, 5.71% were severely underweight and 27.1% metalloprotease present on the surface of the podocyte overweight. Males had hyperphosphatemia and hypocalcemia.There andwasinvolved in the proteolytic vasoacsignificant difference in dietary intakeregulation of BMI groupsof in weight (p appetite (0.004), energy (0.004) carbohydrate (0.003), tive0.000), peptides. Debiec et al described a mother with a In males and females, mean dietary energy intake was 1198.6±609.6 mutation preventing NEP expression who had formed and 981.44±490.0 kcal/d i.e 19.9±9.8 and 19.6 kcal/kg/d; protein 42.57±19.3antibodies and 37.6±15.4 g/d g/kg/d and 0.8±0.43g/kg/d anti-NEP duei.e.,to0.7±0.36 fetomaternal alloimmu, fat 22.1±31.6 and 16.1 ±15.0 g/d. Based on BMI energy intake in nization from a previous miscarriage; these antibodies normals was 17.2 ±9.0/18.6±13.5, in underweight 17.0±10.0 and 12.46±10.6, in severely underweight and 15.91±11.1 and subepithelial 18.4±6.5 and in were to cross the placenta cause overweight 17.5.0±7.8 and 18.9±6.0 kcal/kg/d in males and females In deposits in theintake fetal a subsequent pregnormals protein was kidney 0.73 ±0.31 of and 0.65±0.35; in underweight 0.55±0.63 and 0.42.±0.56 and, in severely 0.57±.53 and nancy. M-type phospholipase Aunderweight receptor (PLA 2 2R) overweight 0.62±.21 and 0.67±.18. Appetite significantly was0.87±.31, later identified as the major autoantigen for pricorrelated (p 0.000) with weight, BMI, dietary energy protein, fat , 5 serumMN albumin creatinine.Little Based on appetite energy and protein mary in and adults. literature exists about intake in male patients with normal appetite was 29.9±4.6 and 1.0±.38, pregnancy outcomes in patients with nephrotic synwith average 20.7±3,9 and 0.79±.2; poor 18.8±6.4 and 0.69±0.24 and drome due to primary MN, with no data energy available anorexic in 0.39±0.36 and 9.9±6.1 respectively. In females and protein intake in patients with normal appetite was disease. 31.3 ±8.2 and about pregnancy in PLA R-associated We 0.97±.16, in average 26.3 ±8.6 and2 .94±.49, in poor 17.6±4.9 and 0.69 present what we believeandto0.64±0.45. be the first known case of ±0.17 and in anorexic12.2±5 Conclusion: in Inadequate dietary with intake, body index (BMI) and low pregnancy a patient PLAmass 2R-associated MN serum albumin and protein are markers of malnutrition in predialysis who was seropositive for anti-PLA R autoantibodies 2 population. throughout the course of her pregnancy. Am J Kidney Dis. 2016;67(5):A1-A118
CASE REPORT A 39-year-old multiparous woman with morbid obesity presented for workup of severe nephrotic syndrome several months 308
before her current pregnancy. She had been treated for resistant DELAYED DIAGNOSIS OF RENAL ARTERY THROMBOSIS: IS hypertension and lower-extremity edema duringHarish the past year, ENDOVASCULAR THERAPY STILL AN ANSWER? butSeethapathy, her proteinuria had been overlooked. presentation, Helena Levy, John Hix, Rochester At General Hospital, serum Rochester, level NY, USA. creatinine was 1.52 mg/dL (corresponding to estimated Renal artery thrombosis a serious, yet often missed We by glomerular filtration rateis of 46 mL/min/1.73 m2 diagnosis. as calculated describe a patient who, despite late diagnosis, was successfully treated thewithisotope-dilution mass spectrometry – traceable 4-variable endovascular therapy. MDRD [Modification Diet ofinCKD Renal Study equaA 55 year old male withof a history stageDisease] III, baseline tion); serum albumin g/dL; and urine protein creatinine of 1.6 mg/dL, level, atrophic1.5 right kidney and24-hour resistant HTN presented with and leftbiopsy lower quadrant abdominal pain features of 2 excretion, 29.2suprapubic g. The kidney specimen revealed days duration. He denied nausea, vomiting diarrhea.for His the typical of primary MNfever, withchills, additional strong or staining blood pressure was 184/118 mmHg. Physical exam revealed suprapubic PLA R antigen within immune deposits (Fig S1). Many of the 2 tenderness. Labs showed acute on chronic renal failure with a subepithelial completely surrounded by new creatinine of 7.1deposits mg/dL andwere urinalysis showed erythrocytes and protein. Electrolytesmembrane and blood counts were normal. basement material (Fig Lower S2), urinary and tract 35% of the obstruction was ruled out with a Foley insertion and later confirmed by cystoscopy. CT abdomen and renal ultrasound did not reveal acute abnormal findings. He was started on dialysis when his kidney function 1 Fromto the Department Medicine,ARenal and failed improve with volumeof resuscitation. nuclear Section, flow scan of the De2 kidneys revealed an obstructive pattern in the3Pediatrics, left kidney, and 4Papartments of Obstetrics andflow Gynecology, or ischemia. CT Medical suggestive tubular necrosis thology andof obstruction, Laboratoryacute Medicine, Boston University Angiogram obtained 6 days after initial presentation showed severe Center, Boston, MA. bilateral filling defects in the renal arteries, suggestive of thrombi. He * Current aspiration affiliation: Department of Internal Medicine, Division underwent of the thrombus along with stenting of the left ofrenal Nephrology, University of Utah of Medicine, Salt Lake artery. Patient was also started on School anticoagulation. A complete hypercoagulability work up failed to reveal any thrombophilias. His City, UT. y kidney function recoveredDepartment back to baseline within 2 weeks. Current affiliation: of Obstetrics and Gynecology, In a patient who presents with acute renal failure of unclear etiology, Medstar Washington Hospital Center, Washington, DC. an embolic insult should be considered. Anticoagulation for 6 months Received 29, 2015. inrecommended. revised form October 27, followed by June antiplatelet therapyAccepted is generally 2015. Originally published endovascular online December 2015. on the Effectiveness of percutaneous therapy 29, is dependent severity andcorrespondence duration of ischemia. our patientH. diagnosis and MD, PhD, Address to In Laurence Beck Jr, treatment were delayed the outcome Some Renal Section, X-504, but 650thankfully, Albany St, Boston, was MAgood. 02118. E-mail: clinicians may have argued against thrombolysis and thrombectomy [email protected] after three days of compromised renal perfusion but remarkably flow � 2016 by theinto National Kidneyand Foundation, Inc. to baseline was reestablished the left kidney function returned within two weeks of starting therapy. 0272-6386
http://dx.doi.org/10.1053/j.ajkd.2015.10.031 775 A95