Abstract
Proliferative glomerulonephritis with monoclonal immune deposits (PGNMID) is a newly described entity characterised by monoclonal IgG deposits consisting of single light chain isotype and single heavy chain subtype (IgG1-4) in the kidneys. We are presenting two cases of patients who presented with acute kidney injury and worsening proteinuria. Kidney biopsy showed membranoproliferative pattern. Special staining for subclass of IgG showed monoclonal IgG3-kappa (case 1) and IgG1-kappa deposits (case 2) suggestive of PGNMID. Workup for underlying infection, malignancy, monoclonal gammopathy was negative. Since pathogenesis of PGNMID involves clonal proliferation of B-cells, we treated both patients with rituximab along with steroids that led to improvement of proteinuria and renal function. We also reviewed current literature to assess efficacy of rituximab in treatment of PGNMID. However, a larger pool of patients and a longer follow-up period is required to establish a role of rituximab and steroids in the treatment of this disease entity.
Keywords: acute renal failure, nephrotic syndrome
Background
Proliferative glomerulonephritis with monoclonal IgG deposits (PGNMID) is a relatively new disease thought to be part of the dysproteinaemia-related diseases or monoclonal gammopathy of renal significance.1 2 It does not fall into previously identified disease processes such as fibrillar or immunotactoid glomerulonephritis, light and heavy chain deposition disease or type I cryoglobulinaemia. The incidence of PGNMID in the native kidneys is about 0.17%. Clinically, patients develop proteinuria, microscopic haematuria and renal insufficiency. So far, there is no consensus regarding the treatment of this disease. Patients have been either treated conservatively with renin–angiotensin system (RAS) inhibition alone or with immunomodulatory therapy including steroids, cyclophosphamide, cyclosporine, mycophenolate, bortezomib or rituximab with variable success rates.
We present two cases of PGNMID in native kidneys which were treated with rituximab and steroids combination therapy with improvement in renal function and proteinuria. We also reviewed current literature on the efficacy of rituximab in patients with PGNMID in native and transplant kidneys.
Case presentation
Case 1
A 49-year-old man with history of type 2 diabetes mellitus, recently treated with levofloxacin for 3 weeks for prostatitis, presented with decreased urine output and worsening lower extremity oedema. He was found to have acute kidney injury (AKI) with a serum creatinine (Cr) of 2.7 mg/dL (baseline Cr 1.1 mg/dL) and proteinuria of 500 mg/day that progressively got worsened to 4.6 g/day. His kidney biopsy showed 19 non-obsolescent glomeruli and one obsolescent glomerulus, minimal interstitial fibrosis and tubular atrophy, mesangial endocapillary proliferation with basement membrane reduplication on light microscopy (LM), mesangial and subendothelial immune deposits on electron microscopy (EM) and positivity for IgG3 kappa, C3 and C1q on immunofluorescence (IF) (figure 1). This was consistent with PGNMID with membranoproliferative glomerulonephritis (MPGN) pattern.
Figure 1.
Case 1: Membranoproliferative pattern. (A) Light photomicrograph—there is global hypercellularity with occlusion of capillary loops. Basement membranes show duplication (black arrows). Some capillary loops contain leucocytes (blue arrows) (Periodic Acid-Schiff) ×400. (B) Immunofluorescence positive for IgG ×400. (C) Immunofluorescence for kappa light chains staining is positive ×400. (D) Electron microscopy—prominent subendothelial electron dense deposits (white arrow). The glomerular basement membrane is duplicated (blue arrows).
Case 2
A 34-year-old man with progressive chronic kidney disease (CKD) with baseline serum Cr of 1.6–1.8 mg/dL presented with gross haematuria and proteinuria of 1.1 g/day. He underwent kidney biopsy that showed 22 non-obsolescent glomeruli, mild interstitial fibrosis and tubular atrophy, diffuse immune mediated endocapillary proliferative and MPGN. His IF was positive for monoclonal IgG1-kappa deposits consistent with PGNMID (figure 2). He was started on RAS-inhibition. The patient was lost to follow-up and presented 9 months later with serum Cr of 6.7 mg/dL, uncontrolled hypertension and worsening leg swelling. The patient also had worsening proteinuria of 25 g/day.
Figure 2.
Case 2: (A) Light photomicrograph—membranoproliferative pattern of global hypercellularity with occlusion of capillary loops. There is duplication of glomerular basement membranes (black arrows). Some capillary loops contain leucocytes (blue arrow). (B) Immunofluorescence for kappa light chains. Capillary loops show curvilinear subendothelial deposits (white arrow). Mesangial deposits are also present (blue arrow) ×400. (C) Immunofluorescence for lambda light chains staining is completely negative, indicating monoclonality for kappa light chains ×400. (D) Electron microscopy—prominent subendothelial electron dense deposits (white arrow). The glomerular basement membrane is duplicated (blue arrows).
Investigations
Case 1
The patient’s serological workup showed antinuclear antibodies (ANA) positive 1:80, anti-dsDNA negative, antineutrophil cytoplasmic antibodies (ANCA) panel negative, antiglomerular basement membrane (GBM) negative. Complement C3 was low, cryoglobulin negative, hepatitis panel negative, HIV non-reactive. Free light chain ratio was normal. Serum protein electrophoresis (SPEP), serum immune electrophoresis (SIFE), urine protein electrophoresis (UPEP) did not suggest monoclonal gammopathy. His Bone marrow biopsy was negative. Workup for underlying malignancy was negative as well.
Case 2
The patient was found to have low C3 of 80, normal C4, ANA 1:40, ANCA panel negative, anti-GBM negative. Workup for underlying infection, malignancy was negative. SPEP, SIFE, urine free light chain ratio and 24-hour UPEP did not show monoclonal gammopathy. His serum free light ratio was slightly elevated at 1.79 (normal 0.26–1.65). He was evaluated by haematology and determined that he did not need any additional testing such as bone marrow biopsy as felt no evidence of lymphoproliferative disorder. He was recommended to get yearly SIFE.
Differential diagnosis
Case 1
Given recent treatment with levofloxacin, acute interstitial nephritis (AIN) causing AKI was a possibility, but we usually do not have massive proteinuria with AIN. He had prostatitis 4 weeks prior to presentation, therefore, postinfectious glomerulonephritis with a low C3 was also one of our differentials.
Case 2
The patient already had biopsy-proven diagnosis of PGNMID. He was evaluated by haematology and deemed to have no evidence of plasma cell dyscrasia or lymphoproliferative disorder. Mild elevation in serum free light chain ratio was attributed to underlying renal dysfunction.
Treatment
Case 1
Despite RAS-inhibition, his serum Cr worsened to 4.6 mg/dL, and proteinuria progressed to 6 g/day over the next 2 weeks. He was started on high-dose prednisone 1 mg/kg/day and was administered two doses of rituximab (1 g intravenous, 2 weeks apart) subsequently with a steroid taper as shown in figure 3.
Figure 3.
Trend of proteinuria and serum creatinine (S. creatinine) in case 1. For proteinuria, along y-axis, units are in g/day. For creatinine along y-axis, units are in mg/dL.
Case 2
The patient was treated with pulse dose of steroids with 1 g methylprednisolone intravenous for 3 days followed by prednisone 1 mg/kg/day with a steroid taper over the next 4 months as shown in figure 4. In addition, two doses of rituximab (1 g intravenous, 2 weeks apart) were administered.
Figure 4.
Trend of proteinuria and serum creatinine (S. creatinine) in case 2. For proteinuria, along y-axis, units are in g/day. For creatinine along y-axis, units are in mg/dL.
Outcome and follow-up
Case 1
The patient’s serum Cr and proteinuria trended down as shown in the figure 3.
On follow-up at 24 months, his renal function is stable at 1.2 mg/dL and his proteinuria has improved to 180 mg/day. He did have an episode of shingles in the right leg 4 months after the treatment with rituximab which was treated with Valtrex and resolved without any complications. No other major adverse events were noted with immunosuppressive treatment.
Case 2
The patient’s serum Cr and proteinuria trended down as shown in figure 4. On follow-up at 12 months, his renal function was stable at 2.0–2.5 mg/dL (prior baseline Cr was 1.6–1.8 mg/dL) and his proteinuria has improved to 1.5–2 g/day. There were no major adverse events in this patient after receiving rituximab and steroids.
Discussion
PGNMID is a rare entity described first by Nasr et al 1 when they observed cases of glomerulonephritis associated with monoclonal IgG deposition. They then described the diagnostic criterion which included: (1) endocapillary proliferative, membranoproliferative or membranous features with positive staining of glomerular IgG deposits restricted to a single IgG subclass (IgG1-4) and a single light chain isotype (kappa or lambda), (2) the presence of granular deposits by EM and (3) the absence of clinical and laboratory evidence of cryoglobulinaemia.
Nasr et al 2 published a review of 37 cases of PGNMID. They noted that this disease seems to be more prevalent in white women mostly older than 50 years. Both of our patients were Caucasian men and younger in age. The most common presentation was presence of lower extremity oedema, AKI, microscopic haematuria and proteinuria. There were a very few percentage of patients who had M-spike in urine or serum.2 3 It does not seem to be a premyelomatous condition, except for a recent case report in the patient with multiple myeloma4 and a few cases reported with other haematological malignancies such as chronic lymphocytic leukaemia (CLL),5 lymphoma.3 6 Our first patient had an episode of prostatitis prior to presentation and there have been other reports of association of PGNMID with infectious causes like upper respiratory tract infection, HIV, parvovirus B19 and hepatitis C infections.2 7 8 Most cases of postinfectious glomerulonephritis have polyclonal IgG and C3 positivity on IF and it is not limited to one subclass of IgG. There have also been some reports of PGNMID in patients with autoimmune disease like Sjögren’s syndrome,9 autoimmune haemolytic anaemia.2 10 Extensive workup in our patients did not reveal any other underlying disease processes.
The most common histological pattern seen in PGNMID is MPGN, followed by endocapillary proliferative glomerulonephritis and a small number of cases of membranous glomerulonephritis. Fujiwara et al speculated that the prognosis may depend on predominance of histological pattern on LM10 They noted poor renal outcomes in patients with MPGN pattern despite use of immunomodulatory therapy. They also noticed favourable response to steroids in patients with membranous features or pure mesangial proliferation.11–13 Based on IF, IgG is the only immunoglobulin deposited out of which IgG3 subclass is the predominant type in most patients. IgG3 subtype correlates with the absence of M-spike while the IgG1 stain seems to be more common in patients with paraproteinaemia and CLL.2 5 Guiard et al also noted that IgG3 deposits were more associated with MPGN pattern and IgG1 deposits were associated more commonly with membranous pattern.3 Interestingly, both of our patients had MPGN pattern but first patient had IgG3-kappa deposits and second patient had IgG1-kappa deposits.
Pathogenesis of PGNMID presumably involves glomerular injury secondary to either intrinsic or extrinsic antigen that stimulates hypersecretion of monoclonal IgG by clonal proliferation of B cells. IgG3 subtype has the highest molecular weight, is positively charged and has a high affinity to the negatively charged GBM. It is capable of self-aggregation and gets deposited in the glomerulus.2 7 Rituximab is a monoclonal antibody to CD20 that results in the depletion of B lymphocytes, and hence, targeted immunosuppression may help limit glomerular injury. We had used high-dose steroids that induced at least a partial response. Given the nature of the disease, we started rituximab following which steroids were able to be rapidly tapered with good sustained response.
We have reviewed literature and compiled the cases treated with rituximab to assess efficacy in patients with PGNMID (table 1). Nasr et al reported two patients treated with rituximab alone which had partial remission and two other patients treated with rituximab along with other agents who had persistent renal disease.2 Bhat et al have reported a case series of three patients, in which one of the patients with PGNMID was treated with RAS inhibition and two dosages of rituximab 1 g separated by 2 weeks with improvement in urine protein excretion from 3 g/day to 1 g/day.6 Another patient in this study had immunotactoid GN with IgG1-k deposits who initially responded to steroids and rituximab but eventually had recurrence of CLL and progressed to end-stage renal disease (ESRD). There had also been reports of two patients with PGNMID secondary to CLL. Both of these patients had IgG1 deposits. They were treated with cyclophosphamide in one case and fludarabine in other case, in addition to rituximab with significant improvement in renal disease and CLL.5 A separate observational study done by Guiard et al included 26 patients with monoclonal IgG deposits of either MPGN or membranous type. They did not have EM findings in 46% of the patients and thus could not differentiate between immunotactoid GN which have microtubular deposits versus PGNMID which have non-organised deposits. Out of these 26 patients, seven patients were treated with rituximab along with other immunomodulatory therapy and five of them achieved complete remission and two had partial response.3
Table 1.
Rituximab (RTX) in patients with proliferative glomerulonephritis with monoclonal immune deposits (native kidneys)
| Reference nos | 2 | 2 | 2 | 6 | 5 | 5 |
| No of patients | 1 | 1 | 2 | 1 | 1 | 1 |
| Native/transplant | N | N | N | N | N | N |
| Proteinuria (g) | 17 | 3 | – | 3 | 6.9 | 4.7 |
| Creatinine at time of treatment (mg/dL) | 2.7 | 0.7 | – | 0.6 | 4.1 | 2.04 |
| Immunofluorescence (IF) deposits | Not known. | Not known. | Not known. | IgG lambda. | IgG-1 kappa. | IgG-1 lambda. |
| Glomerular lesion | Not known. | Not known. | Not known. | Membranoproliferative glomerulonephritis (MPGN) and segmental membranous. | Endocapillary proliferation. | Endocapillary proliferation. |
| Associated illness | Not known. | Not known. | Not known. | Not known. | Chronic lymphocytic leukaemia (CLL). | CLL. |
| RTX dose | Not known. | Not known. | Not known. | 1000 mg for 2 doses 2 weeks apart. | 375/m2 weekly for 6 doses. | 875/m2 every 4 weeks for 6 months. |
| Other treatment | Not known. | Not known. | Cyclophosphamide ±Mycophenolate mofetil. |
ACE inhibitor. | Cyclophosphamide. | Fludarabine. |
| Outcomes | Partial remission. | Partial remission. | Persistent renal disease. | Proteinuria decreased to 1 g at 18 months follow-up. | Creatinine decreased to 1.78 and proteinuria decreased to 128 mg/mmol. | Creatinine improved to 1.67 and proteinuria decreased to 150 mg. |
| References nos | 3 | 3 | 3 | 3 | 3 | 6 |
| No of patients | 2 | 1 | 1 | 1 | 1 | 1 |
| Native/transplant | N | N | N | N | N | N |
| Proteinuria (g) | Not known. | Not known. | Not known. | Not known. | Not known. | 10.5 |
| Creatinine at time of treatment | Not known. | Not known. | Not known. | Not known. | Not known. | 4.1 |
| IF deposits | IgG 2 kappa and IgG 3 kappa. | IgG 3 kappa. | IgG 3 kappa. | IgG kappa. | IgG kappa. | IgG lambda. |
| Glomerular lesion | Membranous. | MPGN. | MPGN. | MPGN. | MPGN. | MPGN. |
| Associated illness | – | Non Hodgkins Lymphoma. | – | – | – | Infiltrative B cell lymphoma |
| RTX dose | Not known. | Not known. | Not known. | Not known. | Not known | Not known. |
| Other treatment | – | Cyclosporine. | – | Cyclosporine, corticosteroids, Azathioprine- Relapsed in 36 months. | corticosteroids relapsed in 24 months. | ACE inhibitor and Angiotensin Receptor Blocker. |
| Outcomes | One patient had complete remission and the other had partial remission. | Complete remission. | Complete remission. | Complete remission after treatment of relapse with RTX. | Complete remission after treatment of relapse with RTX. | After initial improvement in proteinuria to 2.3 g patient eventually progressed to end-stage renal disease. |
PGNMID has also been reported in kidney transplant population.7 14 15 It can recur or present as de novo disease post-transplant. Few cases are reported in literature with favourable response to treatment with rituximab in transplant population (table 2).
Table 2.
Rituximab (RTX) in patients with kidney transplant with proliferative glomerulonephritis with monoclonal immune deposits
| Reference nos | 14 | 14 | 7 | 7 | 7 |
| No of patients | 1 | 1 | 1 | 1 | 1 |
| Native/transplant | T | T | T | T | T |
| Proteinuria (g) | 4.5 | 1.5 | 7.4 | 5.8 | 0.061 |
| Creatinine (Cr) at time of treatment | 1.6 | 2.25 | 3.7 | 4.8 | 1.2 |
| Immunofluorescence deposits | Ig-G-1 kappa. | Ig-G-3 Kappa. | IgG kappa. | IgG 3 lambda. | IgG 3 kappa. |
| GN type | Mesangial and focal endocapillary proliferation. | Focal endocapillary proliferative glomerulonephritis (GN). | Mesangial proliferative GN with mild membranoproliferative future. | Mesangial proliferative GN with mild membranoproliferative features. | |
| Associated illness | Not known. | Not known. | – | – | – |
| RTX dose | 375/m2 every 2 weeks for 2 dose. | 375/m2 every 2 weeks for 2 dose. | Not known. | Not known. | Not known. |
| Other treatment | ACE inhibitor and steroids. | Not known. | Prednisone for 8 months, lisinopril for 6 months. | Plasma exchange x4, prednisone. | Prednisone. |
| Outcomes | Cr improved to 1.1 and proteinuria improved to 0.5–0.8 mg/dL. | Cr improved to 1.5 and proteinuria improved to 1.5–2 mg/dL. | Final serum cr 1.1 and 24-hour urine protein 0.390. | Final serum Cr 1.3 and 24-hour urine protein 0.690. | Final serum Cr 2.3 and 24-hour urine protein 0.059. |
RAS blockade also seems to play an important role in the management of these patients. Nine patients were treated with RAS blockade alone in the study by Nasr et al. Two patients had complete remission and two patients had partial remission, four patients showed no improvement and one progressed to ESRD.2 In 2012, Komatsuda et al described a case of PGNMID with monoclonal lambda light chain deposits which was conservatively treated with RAS blockade and had stable renal functions at 1-year follow-up.16 Our second patient was conservatively managed with RAS inhibition initially, but had worsening of renal function and developed heavy proteinuria 9 months later, requiring additional immunosuppression with rituximab and steroids.
Other treatment modalities that have been used so far are steroids and bortezomib. Fujiwara et al reported a case of a 25-year-old woman who developed crescentic GN superimposed on PGNMID while she was pregnant. She was treated with prednisolone 20 mg/day and responded well. She delivered a healthy infant and her renal function also improved.10 Komatsuda et al also described a case of PGNMID with pure mesangial proliferative features and IgG3 lambda deposits, treated with prednisone 30 mg daily that responded well with resolution of proteinuria.12 Recently in 2017, Noto et al reported a case of PGNMID associated with multiple myeloma with IgG1 kappa deposits treated with bortezomib and dexamethasone leading to reduction in proteinuria and resolution of active lesions on the follow-up biopsy at 8 months.4 However, Al-Rabadi et al found no response to three cycles of bortezomib therapy on a patient with PGNMID in renal allograft. They also described a patient with PGNMID treated with bortezomib who did not respond and developed ESRD. He then underwent renal transplant and his disease recurred in renal allograft. The patient refused any further therapy and was restarted on dialysis 9 months post-transplant.17
In conclusion, based on the review of current data, it appears that rituximab and steroids could be a reasonable and safe option for treatment in patients with PGNMID. However, there is need for further studies to determine the appropriate dosing regimen. We also need to look into long-term outcomes in terms of progression to CKD or ESRD, as well as relevance of repeat dosing in the patients with partial remission or relapse. Another area to focus on will be titrating rituximab to circulating CD20 B cell count and also potentially monitoring closely for relapse when CD20 count recovers.
Learning points.
Patients with idiopathic membranoproliferative glomerulonephritis or membranous pattern on biopsy with IgG positive and single light chain isotype on immunofluorescence should be evaluated for subclass of IgG for possibility of diagnosis of the proliferative glomerulonephritis with monoclonal immune deposits (PGNMID).
In our experience, rituximab along with steroids seems to be an effective regimen in patients with PGNMID.
More extensive studies are needed, specially to establish the standard of care and dosing regimen in this patient population.
Footnotes
Contributors: All authors listed on the manuscript have contributed sufficiently to the project to be included as authors. The case was initially seen by the nephrology fellow DM. BC was the attending on the patient 2. She helped with the review of current management strategies. SA was the attending for patient 1. SA suggested to write up these rare cases and has mentored the write up, assisted the fellow in formatting the tables, figures and the final draft of the case report. SA and DM have conducted review of literature for assessing efficacy of rituximab in native and transplant kidneys with PGNMID. MB is the pathologist who assisted in obtaining the biopsy slides and helped in reviewing the manuscript as well. Final approval of the version to be published was done by all the authors: DM, BC, MB and SA.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Patient consent: Obtained.
Provenance and peer review: Not commissioned; externally peer reviewed.
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