various glomerular diseases can be caused by the deposition of monoclonal immunoglobulin g ( igg ) .
renal disease related to the deposition of monoclonal igg containing both heavy and light chains can occur in type 1 cryoglobulinemia , randall - type light- and heavy - chain deposition disease ( lhcdd ) , light- and heavy - chain amyloidosis and immunotactoid glomerulonephritis [ 15 ] .
proliferative glomerulonephritis with monoclonal igg deposits ( pgnmid ) is a relatively newly described entity mimicking immune complex glomerulonephritis ( gn ) that does not conform to any of those subtypes .
it represents a form of proliferative gn with electron - dense deposits ( edds ) localized to glomeruli and immunofluorescence ( if ) findings of monoclonal igg deposits .
recurrent pgnmid in the renal allograft has been described in a few case series [ 68 ] . in this article
pathologic features of three cases of pgnmid in the renal allograft showing the variable course and manifestation of the disease .
our three cases , like most other reported cases , have no bone marrow involvement and no evidence of monoclonal protein on electrophoresis and immunofixation studies .
a 61-year - old caucasian female developed end - stage kidney disease ( eskd ) secondary to membranoproliferative glomerulonephritis ( mpgn ) based on a native kidney biopsy in 2001 , with no further information about if or electron microscopy ( em ) . in december 2006 , her serum creatinine ( scr ) was 530 mol / l and she underwent a preemptive unrelated living kidney transplantation . in 2014 , she was found to have a random urine protein / gram creatinine ( upcr ) of 452 mg / mmol and an scr of 132 mol / l , up from 106 mol / l .
her workup for a lymphoproliferative disorder was negative , as was her serologic workup ( see table  1 ) . on biopsy , if showed diffuse granular positivity for igg , c3 and c1q .
em showed edds , mostly in the mesangium and subendothelial regions ( please see figures  17 ) .
she was later switched to carfilzomib , as she developed acute kidney injury with scr up to 247 mol / l ; after completion of therapy her scr was 150
table  1.clinical data of post  kidney transplant recipients with pgnmidpatient # 1 # 2 # 3 # 4 # 5 # 6 age ( years)617440616868race / sexcaucasian / femalecaucasian / malehispanic / femalecaucasian / malecaucasian / femalecaucasian / femalecause of eskdmpgnpgmidmpgnpgnmidunclear 
nephrotic range proteinuriapolycystic kidney disease ( pkd)transplant typeunrelated living donordeceased donordeceased donordeceased donorrelated living donordeceased donorisfk506 , prednisone , mmffk506 , prednisone , mmffk506 and azathioprinemmf , rapamycinmmf , rapamycinprednisone , cyclosporinebaseline scr ( mol / l)10626496.8114132132scr at biopsy ( mol / l)132396114237281228time from transplant to diagnosis of recurrent or de novo pgnmid ( months)9861321321158proteinuria ( mg / mmol)4001002087050150hematuria1 + 3 + 2 + 2 + 2 + 1+serum complementnormalnormalnormalnormalnormalnormalcryoglobulinnegativenegativenegativen / an / an / ahepatitis bnegativenegativenegativenegativenegativenegativehepatitis cnegativenegativenegativenegativenegativenegativehivnon - reactivenon - reactivenon - reactivenon - reactivenon - reactivenon - reactivemonoclonal protein spikenegativenegativenegativenegativenegativenegativepattern of injuryec on both biopsies with a crescent on the second biopsynative biopsy : 1st  atn2nd  ectransplant biopsy : mpmpmpgn - likempmpgn - likenumber of glomeruli sclerosednone on first , 3 of 20 on second13/364 of 101 of 91 of 275 of 8interstitial fibrosisnone on first and 15% on second50%15%1 + 3 + 3+igg subtype kappa or lambdaigg3-kappanative : igg lambda ( subtype not available)2nd transplant : igg3-lambdaigg3-kappaigg3-kappa , mild lambdaigg3-kappaigg1-kappaelectron microscopy depositsedm , eds on both biopsiesnative biopsy : eds , edmtransplant biopsy : edmedm , edsmpgn - likempmpgn - likebone marrow biopsypositive stain for plasma cells for cd138 5% cellularity ; no staining for kappa and lambda light chain by in situ hybridizationpositive stain for plasma cells for cd138 < 5% cellularity ; no staining for kappa and lambda light chain by in situ hybridization ( pre - transplant)not done due to stability of kidney functionnonenonenonetreatmentbortezomib 3 doses , dexamethasone 3 dosespatient opted for noneno changeno changechange to mmf and prednisoneno changeoutcome after allograft biopsy : scr ( mol / l)149 , proteinuria 600 mg / mmolremains on is as aboveend - stage kidney disease114proteinuria 10 mg / mmolremains on is as abovefatal mi after 20 months of kidney biopsydied with cryptococcal meningitis 15 months after biopsyend - stage kidney diseasefollow - up ( months ) after biopsy17336201520patient # 7 # 8 # 9 # 10 # 11 # 12 age245560743866race / sexcaucasian / femalecaucasian / malecaucasian / femalecaucasian / femalecaucasian / femalecaucasian / femalecause of eskddiabetic nephropathypgnmidpgnmidpgnmidpgnmidpgnmidtransplant typesimultaneous kidney 
pancreasunrelated living donordeceased donorunrelated living donorunrelated living donordeceased donorisfk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmf stopped at 1 monthbaseline scr ( mol / l)15816710612379.260.7scr at biopsy ( mol / l)290246326422106176time from transplant to diagnosis of recurrent or de novo pgnmid ( months)4312221564318proteinuria ( mg / mmol)170807405806330hematuria3+yesyesyesno3+serum complementnormalnormallow c3 and c4low c3 and c4normaln / acryoglobulinn / anegativenegativenegativenot donenegativehepatitis bnegativenegativenegativenegativenegativenegativehepatitis cnegativenegativenegativenegativenegativenegativehivnon - reactivenon - reactivenon - reactivenon - reactivenon - reactiven / amonoclonal protein spikenegativenegativenegativenegativenegativepattern of injurympgn - likefirst two biopsies showed mp , third showed diffuse ec and fourth showed focal proliferativediffuse ec on both with diffuse on first and focal on second biopsyfirst biopsy showed diffuse ec and exudative gn , next two biopsies with mpminimal to mild mpec with crescentsnumber of glomeruli sclerosed8 of 133/37 sclerosed , 16/27 crescentsinterstitial fibrosis2+mildmildmild then moderatemild then moderateigg subtype kappa or lambdaigg3-kappaigg3-kappaigg3-kappaigg3-lambdaigg3-kappakappa ( subtype not available)electron microscopy depositsmpgn - likefirst two biopsies showed edm , and edm and eds on last twoedm , edsfirst and third showed eds and second showed edm and edsedm in first two biopsies and edm and eds in others ; third and fifth biopsies showed banff 1aedm and parietal depositsbone marrow biopsynonenonenonenonenonenonetreatmentno changeprednisone , oral cyclophosphamide for 6 monthsmethylprednisolone with prednisone , rituximab 2 doses , lisinoprilmethylprednisolone with prednisone , rituximab 1 dose , with plasmapheresis 4 and hd 3methylprednisolone for acr , rituximab 2 dosesplasmapheresis , ivig 0.5 g / kg / day with methylprednisolone total 850 mg , mmf 1.5 g / dayoutcome after allograft biopsy : scr ( mol / l)29020296.811420296.8 , transplant nephrectomy in the setting of sepsis 6 months post - treatment with biopsy showing resolution of disease despite nephrectomy , disappearance of ec and cellular crescents , if staining remained kappafollow - up ( months ) after biopsyshort151183636mpgn , membranoproliferative glomerulonephritis ; pgnmid , proliferative glomerulonephritis and monoclonal immunoglobulin deposits ; mp , mesangial proliferative ; ep , endothelial proliferative ; ec , endocapillary proliferative ; scr , serum creatinine ; mmf , mycophenolate mofetil ; edm , electron - dense mesangial deposits ; eds , electron - dense subendothelial deposits ; fk506 , prograf / tacrolimus . 

the increase in cells includes increased mononuclear elements within the expanded mesangial areas and many mononuclear inflammatory cells within the glomerular capillary lumens . as a result , the capillary tufts have a distinctly lobulated appearance .
3.the peripheral capillary walls are distorted and thickened , often with the formation of double contours or basement membranes with a chain - like appearance .
5.kappa light chains stain strongly positive ( 3+/4 + ) along the peripheral capillary walls and mesangial areas .
6.if staining for the igg subtypes shows intense glomerular positivity for ( c ) igg3 with negative staining for ( a ) , igg1 ( b ) igg2 and ( d ) igg3 . 

7.glomerular capillaries are greatly distorted and thickened by the presence of numerous , sometimes large and/or confluent subendothelial electron - dense deposits .
the electron - dense deposits have a variegated (  two - toned ) appearance and are finely granular , but they do not show organized substructures
clinical data of post  kidney transplant recipients with pgnmid mpgn , membranoproliferative glomerulonephritis ; pgnmid , proliferative glomerulonephritis and monoclonal immunoglobulin deposits ; mp , mesangial proliferative ; ep , endothelial proliferative ; ec , endocapillary proliferative ; scr , serum creatinine ; mmf , mycophenolate mofetil ; edm , electron - dense mesangial deposits ; eds , electron - dense subendothelial deposits ; fk506 , prograf / tacrolimus .
the increase in cells includes increased mononuclear elements within the expanded mesangial areas and many mononuclear inflammatory cells within the glomerular capillary lumens . as a result ,
the peripheral capillary walls are distorted and thickened , often with the formation of double contours or basement membranes with a chain - like appearance .
kappa light chains stain strongly positive ( 3+/4 + ) along the peripheral capillary walls and mesangial areas .
if staining for the igg subtypes shows intense glomerular positivity for ( c ) igg3 with negative staining for ( a ) , igg1 ( b ) igg2 and ( d ) igg3 .
glomerular capillaries are greatly distorted and thickened by the presence of numerous , sometimes large and/or confluent subendothelial electron - dense deposits .
the electron - dense deposits have a variegated (  two - toned ) appearance and are finely granular , but they do not show organized substructures . magnification 12 000 , electron micrograph . a 74-year - old caucasian male developed eskd secondary to pgnmid seen on a native biopsy on september 2009 .
he received bortezomib and dexamethasone ; however , he developed eskd requiring hemodialysis ( hd ) after three doses .
he received a diseased donor transplant ( ddt ) in may 2013 , with his course complicated by biopsy - proven acute tubular injury .
his scr improved to 265 mol / l until 6 months post - transplant , at which time his scr was  530
if from his biopsy showed positivity for igg3 , c3 , c1q and lambda light chains .
kappa was negative , as were peritubular capillaries for c4d ( see table  1 ) .
his kidney disease progressed and he declined therapy and restarted hd 9-month post - transplantation .
a 40-year - old hispanic female received a ddt in june 2001 after developing eskd . in 1995
there were no if data for reevaluation . in june 2012 , she had hematuria and her scr was 114 mol / l , up from her baseline scr of 97
her allograft biopsy showed a mesangioproliferative pattern of injury by light microscopy ( see table  1 ) . if revealed mesangial deposits restricted to igg3-kappa .
a 61-year - old caucasian female developed end - stage kidney disease ( eskd ) secondary to membranoproliferative glomerulonephritis ( mpgn ) based on a native kidney biopsy in 2001 , with no further information about if or electron microscopy ( em ) . in december 2006 , her serum creatinine ( scr ) was 530
mol / l and she underwent a preemptive unrelated living kidney transplantation . in 2014 , she was found to have a random urine protein / gram creatinine ( upcr ) of 452 mg / mmol and an scr of 132 mol / l , up from 106 mol / l .
her workup for a lymphoproliferative disorder was negative , as was her serologic workup ( see table  1 ) .
em showed edds , mostly in the mesangium and subendothelial regions ( please see figures  17 ) .
she was later switched to carfilzomib , as she developed acute kidney injury with scr up to 247 mol / l ; after completion of therapy her scr was 150
table  1.clinical data of post  kidney transplant recipients with pgnmidpatient # 1 # 2 # 3 # 4 # 5 # 6 age ( years)617440616868race / sexcaucasian / femalecaucasian / malehispanic / femalecaucasian / malecaucasian / femalecaucasian / femalecause of eskdmpgnpgmidmpgnpgnmidunclear  nephrotic range proteinuriapolycystic kidney disease ( pkd)transplant typeunrelated living donordeceased donordeceased donordeceased donorrelated living donordeceased donorisfk506 , prednisone , mmffk506 , prednisone , mmffk506 and azathioprinemmf , rapamycinmmf , rapamycinprednisone , cyclosporinebaseline scr ( mol / l)10626496.8114132132scr at biopsy ( mol / l)132396114237281228time from transplant to diagnosis of recurrent or de novo pgnmid ( months)9861321321158proteinuria ( mg / mmol)4001002087050150hematuria1 + 3 + 2 + 2 + 2 + 1+serum complementnormalnormalnormalnormalnormalnormalcryoglobulinnegativenegativenegativen / an / an / ahepatitis bnegativenegativenegativenegativenegativenegativehepatitis cnegativenegativenegativenegativenegativenegativehivnon - reactivenon - reactivenon - reactivenon - reactivenon - reactivenon - reactivemonoclonal protein spikenegativenegativenegativenegativenegativenegativepattern of injuryec on both biopsies with a crescent on the second biopsynative biopsy : 1st  atn2nd  ectransplant biopsy : mpmpmpgn - likempmpgn - likenumber of glomeruli sclerosednone on first , 3 of 20 on second13/364 of 101 of 91 of 275 of 8interstitial fibrosisnone on first and 15% on second50%15%1 + 3 + 3+igg subtype kappa or lambdaigg3-kappanative : igg lambda ( subtype not available)2nd transplant : igg3-lambdaigg3-kappaigg3-kappa , mild lambdaigg3-kappaigg1-kappaelectron microscopy depositsedm , eds on both biopsiesnative biopsy : eds , edmtransplant biopsy : edmedm , edsmpgn - likempmpgn - likebone marrow biopsypositive stain for plasma cells for cd138 5% cellularity ; no staining for kappa and lambda light chain by in situ hybridizationpositive stain for plasma cells for cd138 < 5% cellularity ; no staining for kappa and lambda light chain by in situ hybridization ( pre - transplant)not done due to stability of kidney functionnonenonenonetreatmentbortezomib 3 doses , dexamethasone 3 dosespatient opted for noneno changeno changechange to mmf and prednisoneno changeoutcome after allograft biopsy : scr ( mol / l)149 , proteinuria 600 mg / mmolremains on is as aboveend - stage kidney disease114proteinuria 10 mg / mmolremains on is as abovefatal mi after 20 months of kidney biopsydied with cryptococcal meningitis 15 months after biopsyend - stage kidney diseasefollow - up ( months ) after biopsy17336201520patient # 7 # 8 # 9 # 10 # 11 # 12 age245560743866race / sexcaucasian / femalecaucasian / malecaucasian / femalecaucasian / femalecaucasian / femalecaucasian / femalecause of eskddiabetic nephropathypgnmidpgnmidpgnmidpgnmidpgnmidtransplant typesimultaneous kidney 
pancreasunrelated living donordeceased donorunrelated living donorunrelated living donordeceased donorisfk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmffk506 , prednisone , mmf stopped at 1 monthbaseline scr ( mol / l)15816710612379.260.7scr at biopsy ( mol / l)290246326422106176time from transplant to diagnosis of recurrent or de novo pgnmid ( months)4312221564318proteinuria ( mg / mmol)170807405806330hematuria3+yesyesyesno3+serum complementnormalnormallow c3 and c4low c3 and c4normaln / acryoglobulinn / anegativenegativenegativenot donenegativehepatitis bnegativenegativenegativenegativenegativenegativehepatitis cnegativenegativenegativenegativenegativenegativehivnon - reactivenon - reactivenon - reactivenon - reactivenon - reactiven / amonoclonal protein spikenegativenegativenegativenegativenegativepattern of injurympgn - likefirst two biopsies showed mp , third showed diffuse ec and fourth showed focal proliferativediffuse ec on both with diffuse on first and focal on second biopsyfirst biopsy showed diffuse ec and exudative gn , next two biopsies with mpminimal to mild mpec with crescentsnumber of glomeruli sclerosed8 of 133/37 sclerosed , 16/27 crescentsinterstitial fibrosis2+mildmildmild then moderatemild then moderateigg subtype kappa or lambdaigg3-kappaigg3-kappaigg3-kappaigg3-lambdaigg3-kappakappa ( subtype not available)electron microscopy depositsmpgn - likefirst two biopsies showed edm , and edm and eds on last twoedm , edsfirst and third showed eds and second showed edm and edsedm in first two biopsies and edm and eds in others ; third and fifth biopsies showed banff 1aedm and parietal depositsbone marrow biopsynonenonenonenonenonenonetreatmentno changeprednisone , oral cyclophosphamide for 6 monthsmethylprednisolone with prednisone , rituximab 2 doses , lisinoprilmethylprednisolone with prednisone , rituximab 1 dose , with plasmapheresis 4 and hd 3methylprednisolone for acr , rituximab 2 dosesplasmapheresis , ivig 0.5 g / kg / day with methylprednisolone total 850 mg , mmf 1.5 g / dayoutcome after allograft biopsy : scr ( mol / l)29020296.811420296.8 , transplant nephrectomy in the setting of sepsis 6 months post - treatment with biopsy showing resolution of disease despite nephrectomy , disappearance of ec and cellular crescents , if staining remained kappafollow - up ( months ) after biopsyshort151183636mpgn , membranoproliferative glomerulonephritis ; pgnmid , proliferative glomerulonephritis and monoclonal immunoglobulin deposits ; mp , mesangial proliferative ; ep , endothelial proliferative ; ec , endocapillary proliferative ; scr , serum creatinine ; mmf , mycophenolate mofetil ; edm , electron - dense mesangial deposits ; eds , electron - dense subendothelial deposits ; fk506 , prograf / tacrolimus . 

the increase in cells includes increased mononuclear elements within the expanded mesangial areas and many mononuclear inflammatory cells within the glomerular capillary lumens . as a result , the capillary tufts have a distinctly lobulated appearance .
3.the peripheral capillary walls are distorted and thickened , often with the formation of double contours or basement membranes with a chain - like appearance .
5.kappa light chains stain strongly positive ( 3+/4 + ) along the peripheral capillary walls and mesangial areas .
6.if staining for the igg subtypes shows intense glomerular positivity for ( c ) igg3 with negative staining for ( a ) , igg1 ( b ) igg2 and ( d ) igg3 . 

7.glomerular capillaries are greatly distorted and thickened by the presence of numerous , sometimes large and/or confluent subendothelial electron - dense deposits .
the electron - dense deposits have a variegated (  two - toned ) appearance and are finely granular , but they do not show organized substructures . magnification 12 000 , electron micrograph . clinical data of post  kidney transplant recipients with pgnmid mpgn , membranoproliferative glomerulonephritis ; pgnmid , proliferative glomerulonephritis and monoclonal immunoglobulin deposits ; mp , mesangial proliferative ; ep , endothelial proliferative ; ec , endocapillary proliferative ; scr , serum creatinine ; mmf , mycophenolate mofetil ; edm , electron - dense mesangial deposits ; eds , electron - dense subendothelial deposits ; fk506 , prograf / tacrolimus .
the increase in cells includes increased mononuclear elements within the expanded mesangial areas and many mononuclear inflammatory cells within the glomerular capillary lumens . as a result ,
the peripheral capillary walls are distorted and thickened , often with the formation of double contours or basement membranes with a chain - like appearance .
kappa light chains stain strongly positive ( 3+/4 + ) along the peripheral capillary walls and mesangial areas .
if staining for the igg subtypes shows intense glomerular positivity for ( c ) igg3 with negative staining for ( a ) , igg1 ( b ) igg2 and ( d ) igg3 .
glomerular capillaries are greatly distorted and thickened by the presence of numerous , sometimes large and/or confluent subendothelial electron - dense deposits .
the electron - dense deposits have a variegated (  two - toned ) appearance and are finely granular , but they do not show organized substructures . magnification 12 000 , electron micrograph .
a 74-year - old caucasian male developed eskd secondary to pgnmid seen on a native biopsy on september 2009 .
he received bortezomib and dexamethasone ; however , he developed eskd requiring hemodialysis ( hd ) after three doses .
he received a diseased donor transplant ( ddt ) in may 2013 , with his course complicated by biopsy - proven acute tubular injury .
mol / l until 6 months post - transplant , at which time his scr was  530
if from his biopsy showed positivity for igg3 , c3 , c1q and lambda light chains .
kappa was negative , as were peritubular capillaries for c4d ( see table  1 ) .
his kidney disease progressed and he declined therapy and restarted hd 9-month post - transplantation .
a 40-year - old hispanic female received a ddt in june 2001 after developing eskd . in 1995 , she had biopsy - proven type 1 mpgn .
there were no if data for reevaluation . in june 2012 , she had hematuria and her scr was 114 mol / l , up from her baseline scr of 97
her allograft biopsy showed a mesangioproliferative pattern of injury by light microscopy ( see table  1 ) . if revealed mesangial deposits restricted to igg3-kappa .
pgnmid , a novel type that does not conform to any subtypes , was described initially in 2004   followed by the largest series of 37 cases in 2009 .
histologic patterns by light microscopy were mostly membranoproliferative with a lobular nodular pattern of injury followed by an endocapillary proliferative pattern .
em revealed granular , nonorganized deposits mostly in the mesangium and subendothelium . if demonstrated granular glomerular deposits that stained for a single light - chain isotype and a single heavy - chain subtype , most commonly igg3-kappa [ 7 , 10 ] .
more than 40 additional cases were identified by other groups [ 6 , 1119 ] .
recently , recurrent pgnmid after kidney transplantation has been reported as case reports or small series of one to four patients [ 68 ] . the recurrent disease manifested clinically as allograft dysfunction , hematuria and proteinuria .
of the patients reported ( see table  1 ) , the average age was 57 years .
disease recurrence can range from an average of 3.8 months in some series   up to 2 years after kidney transplantation [ 5 , 7 ] .
the risk of recurrence is difficult to estimate based on the small number of patients and the absence of protocol biopsies in most cases .
moreover , the immunosuppressive treatment may have an impact on disease course that may be difficult to isolate .
disease recurrence can have a variable outcome , with some patients having persistent renal impairment and some progressing to end - stage renal disease .
pgnmid is often missed or underdiagnosed , with diagnoses of mpgn or even light- and heavy - chain deposition disease ( lhcdd ) . some cases like case 1 and case 3
were originally diagnosed as mpgn type 1 before this entity was well established . in many instances , if and em were not available , nor was staining for light chains .
pgnmid and lhcdd are similar in many aspects , however , the pathogenesis is different .
lhcdd results from the deposition of heavy and light chains in the glomerular and tubular basement membrane , as opposed to pgnmid , where the deposits are intact monoclonal immunoglobulin affecting only the glomeruli .
pgnmid is characterized by granular edds , in contrast to lhcdd , where those are mostly powdery deposits .
igg3 was the igg isoform identified most often in prior studies to be deposited in the glomeruli despite comprising only 8% of the total immunoglobulin in the serum [ 6 , 7 ] .
limitation to igg3 in our three cases confirms the specific predilection for igg3 to precipitate and self - aggregate in the glomeruli given its properties of high molecular weight , positive charge and complement activation capacity .
monoclonal gammopathy of renal significance is an increasingly recognized entity in patients who are found to have monoclonal protein with renal involvement .
patients who do not fulfill the criteria for multiple myeloma have traditionally been labeled as monoclonal gammopathy of undetermined significance given the limited diagnostic schema , and consequently no therapy has been offered .
however , it is more established now that addressing this clonal proliferation may preserve the kidneys and potentially prevent disease recurrence .
nevertheless , a thorough workup is strongly recommended as it may impact the therapeutic plan .
one patient with polycystic kidney disease was diagnosed with pgnmid 13 years after kidney transplantation . another patient had diabetes nephropathy leading to eskd and developed de novo pgnmid 3 years after transplantation . while having different primary pathology supports that allograft disease is de novo , late occurrence does not exclude recurrence , as kidney transplant recipients may have a different disease course and disease activity due to immunosuppressive drugs .
based on a pathogenesis hypothesis , it would seem rational to treat with immunomodulating therapy .
bortezomib was tried in one patient with native disease in one series , however , not in any transplant patients .
given the role of monoclonal ig in the disease pathogenesis , bortezomib was tried in two of our patients , one with disease in the native kidney prior to transplant ( case 2 ) and one with disease recurrence following transplant ( case 1 ) , with no favorable response .
pgnmid is becoming a more recognized entity , with more patients being evaluated for renal transplant .
evaluating these patients for transplant eligibility may be challenging in the absence of distinct data of remission given that most patients have normal bone marrow biopsy and no monoclonal band on serum and urine testing .
more long - term studies will be needed to further investigate disease course and response to therapy .
 glomerulopathy due to dysproteinemia can have a wide spectrum of pathologic and clinical features based on specific characteristics of the abnormal protein and the response induced within the parenchymal tissue . 
 monoclonal immunoglobulin g ( igg ) deposition can manifest as a different glomerular disease . 
 proliferative glomerulonephritis ( gn ) with monoclonal igg deposits ( pgnmid ) is a unique entity mimicking immune complex gn that does not conform to any of those subtypes . 
 igg monoclonal granular deposition in the glomeruli with a pattern similar to immune complex disease suggested by c3 and c1q deposition should prompt consideration of pgnmid . literature is scarce in terms of recurrence of disease in renal allografts . in this article 
 we present the clinical  
 pathologic features of three cases of pgnmid in the renal allograft showing the variable course and manifestation of the disease . 
Background
Case 1
Case 2
Case 3
Discussion
Conclusion
Conflict of interest statement