TLR AGONISTS EXCERBATE ACUTE KIDNEY INJURY MIMICKING AHUS IN A CFH MUTANT MOUSE WITH A KNOWN HUMAN MUTATION

V SHEN1, G ZHANG1, M HU2, J ZHOU1, S ROBINSON1, H MCCARTHY1, Y WANG2, Q CAO2, G ZHENG2, N ROGERS2, T BARBOUR3, I ALEXANDER4, D HARRIS2, S ALEXANDER1, Y WANG1
1Centre for Kidney Research, The Children’s Hospital at Westmead, Sydney, Australia, 2Centre for Transplant and Renal Research, University of Sydney at Westmead Hospital, Sydney, Australia, 3Department of Nephrology, Royal Melbourne Hospital, Melbourne, Australia, 4Gene Therapy Research Unit, The Children’s Hospital at Westmead, Sydney, Australia

Aim: To evaluate whether TLR4 and TLR7 agonists induce acute kidney injury in CFH mutant mice.
Background: Atypical haemolytic uremic syndrome (aHUS) is associated with mutations in the complement alternative pathway, most commonly complement factor H (CFH), a negative regulator of C3 activation. Mice carrying CFH mutations associated with functionally impaired CFH protein in human aHUS have been generated by ENU mutagenesis. The role of infection in triggering disease in these mice was tested by treatment with lipopolysaccharide (LPS, TLR4 agonist) and Imiquimod (IMQ, TLR7 agonist).
Methods: For LPS, a single low dose (4mg/kg) was administrated intraperitoneally to homozygous, heterozygous and wild type (WT) mice. For IMQ, 25μg was administered on alternate days for 3 weeks in the corresponding groups. After treatment, kidney function, histology and C3 immunofluorescence were assessed. Serum and liver CFH levels were measured using western blot.
Results: Homozygous mice showed spontaneous deposition of glomerular C3 and had minimal serum concentrations of CFH compared to WT and heterozygous mice. Following LPS treatment, homozygous mice showed significantly higher levels of proteinuria (3.1±0.2mg/16h) and serum creatinine (28.3±3umol/L) compared to heterozygous (1.3±0.4mg/16h, 20.3±2umol/L, p<0.01 and p<0.05 respectively) and WT mice (1.2±0.2mg/16h, 17.6±1.6umol/L, p<0.01 and p<0.05 respectively). IMQ treatment also had a worse effect on renal function in homozygous mice. LPS or IMQ treated homozygous mice exhibited significantly more glomerulosclerosis, tubular damage and interstitial inflammation than heterozygous and WT mice (p<0.01).
Conclusions: Mice homozygous for the aHUS-associated CFH mutation develop glomerular C3 deposition and are sensitive to LPS or IMQ, developing acute kidney injury and renal histological damage. This suggests a significant role for infection in triggering aHUS in susceptible individuals.


Biography:
Victor completed his Bachelor of Medical Science studies at the University of Sydney, majoring in immunobiology and physiology. He is currently studying his Honours year at the Centre for Kidney Research, The Children’s Hospital at Westmead under the supervision of Prof Stephen Alexander and Dr Yuan Min Wang. His area of interest involves hematology and role of complement regulators in glomerular injuries.

 

TARGETING CD103+ DENDRITIC CELLS USING FLT3 INHIBITORS FOR TREATMENT OF KIDNEY DISEASE; RELEVANCE TO HUMAN KIDNEY DISEASE.

T CHEN1,2,3, Q CAO1,2, R WANG1,2, P RAO1,2, G ZHENG1,2, V LEE1,2,3, N ROGERS1,2,3, M PATEL1,3, CH P’NG1,3, H YU2, S ALEXANDER4, Y WANG1,2, D HARRIS1,2,3
1University of Sydney, Westmead, Australia, 2The Westmead Institute for Medical Research, Westmead, Australia, 3Westmead Hospital, Westmead, Australia, 4Children’s Hospital at Westmead, Westmead, Australia

Aim: 1- To examine CD141+ dendritic cells (DCs; human homologue of CD103+ DCs) in human kidney diseases.
2- To explore the role of CD103+ DCs and therapeutic potential of targeting CD103+ DCs by repurposing Flt3 inhibitors in experimental kidney diseases
Background: Whereas CD103+ DCs were previously considered to be a minor DC subset in kidney disease, we and others have proven that they have a major role. Flt3 is a receptor specifically expressed on tissue CD103+ DCs. Flt 3 inhibitors are currently used for cancer treatment.
Methods: A human study included 294 kidney biopsies from 01/07/2016 to 01/04/2017. For animal experiments, we used murine Adriamycin Nephropathy (AN), anti-GBM disease and ischaemia reperfusion injury (IRI).
Results: In humans, the number and proportion of CD141+ DCs were significantly increased in proliferative glomerulonephritis and acute tubular necrosis (ATN). CD141+ DCs were found mainly in tubulointerstitium, except in lupus nephritis where they were also present in glomeruli. CD141+ DC numbers correlated with increasing severity of ATN (P<0.001) as well as fibrosis in IgA nephropathy (P=0.025), but not diabetic nephropathy. In murine AN, anti-GBM disease and IRI, the number and proportion of kidney CD103+ DCs were significantly increased. In AN, CD103+ DCs played a pathogenic role through activation of CD8+ T cells. Treatment with a Flt3 inhibitor specifically depleted CD103+ DCs and significantly reduced renal injury. The effect of Flt3 inhibition is currently being studied in anti-GBM disease and IRI.
Conclusions: Kidney CD103+ DC numbers correlate with severity of human kidney disease. Targeting CD103+DCs with Flt3 inhibitors effectively reduces renal injury in experimental kidney disease, suggesting a novel therapeutic strategy with accelerated translational potential through drug repurposing.


Biography:
Dr Titi Chen is a nephrology fellow and NHMRC postgraduate scholar. She has a passion for research and is currently completing her PhD through the University of Sydney.

NONINFECTIOUS CRYOGLOBULINAEMIC GLOMERULONEPHRITIS AND MONOCLONAL GAMMOPATHY: A CASE SERIES

A FLAVELL1, S HOLT1,R FULLINFAW2, M FINLAY3,T BARBOUR1
1Department of Nephrology, Royal Melbourne Hospital,, Australia, 2Department of Chemical Pathology, Royal Melbourne Hospital,, Australia, 3Department of Anatomical Pathology, Royal Melbourne Hospital, Australia

Aim: To assess coincident monoclonal gammopathy (MG) in patients with noninfectious cryoglobulinaemic glomerulonephritis (CGN).
Background: Increasing recognition that monoclonal immunoglobulin (mIg) including free light chain (LC) causes certain types of glomerulonephritis has led to the term monoclonal gammopathy of renal significance (MGRS). MGRS implies a need for clonally directed therapy where this would otherwise be considered unnecessary (i.e. for monoclonal gammopathy of unknown significance). MGRS is exemplified by (Brouet) type I CGN, in which the cryoglobulin is composed of mIg. By contrast, mixed CGN (type II/III, polyclonal immunoglobulin with or without mIg) is not specifically associated with MG.
Methods: A single-centre, retrospective review of clinical and pathological data from 2002 onwards for noninfectious CGN with accompanying MG excluding myeloma, Waldenstrom’s macroglobulinaemia and lymphoma.
Results: 5 cases included 3 with membranoproliferative glomerulonephritis, 2 with crescents, 4 with intracapillary hyaline microthrombi and 1 with necrotising arteritis; 0/2 assessed by immunoperoxidase showed LC restriction; 0/3 assessed by electron microscopy showed organised deposits. MG (median 2g/L) included 2 IgG-lambda, 1 IgM-kappa, 2 faint/untyped, with 1/5 Bence Jones positive. Cryoglobulinaemia (median 0.4g/L) was type II or III in all cases (no type I). 4/5 had rheumatoid factor positivity and 3/5 had low complements. 2 patients had primary Sjögrens syndrome, 1 subsequently undergoing surgery for cholangiocarcinoma, with no other systemic illnesses identified.
Conclusions: In patients with noninfectious CGN, coincident MG necessitates testing and surveillance for malignant B cell disorders. Where these are excluded, the renal lesion may in fact be unrelated to the MG, as (cautiously) appears to be the case in our small series. Here, renal immunostaining for LC restriction and careful typing of the cryoglobulin provide valuable information.


Biography:
Advanced Trainee in Nephrology

DOUBLE SEROPOSITIVE ANTI-GBM AND ANCA DISEASE WITH MULTIPLE RELAPSES: A CASE FOR MAINTENANCE IMMUNOSUPPRESSION

S SO1,2, B BOSE1,3, K SOL1,3, N WONG1
1Department of Renal Medicine, Nepean Hospital, Kingswood, Australia, 2Department of Renal Medicine, Westmead Hospital, Westmead, Australia, 3University of Sydney, Nepean Clinical School, Kingswood, Australia

Background: Double-seropositive antineutrophilic cytoplasmic antibody (ANCA) and anti-glomerular basement membrane (GBM) disease is increasingly recognised, and is characterised by shared features of both conditions. We report a case of relapsing ANCA-associated disease, with subsequent development of anti-GBM antibody and historic biopsy features consistent with anti-GBM disease.
Case: A 48-year-old man with known granulomatous polyangiitis (GPA) presented with haemoptysis, acute kidney injury, and fever. An initial diagnosis of “Goodpasture’s Syndrome” had been made at 18-years-old, on presentation with haemoptysis, arthritis and haematuria. Anti-GBM antibody serology was negative at the time and ANCA result unavailable. Retrospective renal biopsy review revealed crescentic necrotizing glomerulonephritis with linear immunoglobulin G staining of the GBM. Over 20 years, he had three relapses characterized by haemoptysis and subsequent investigations revealed positive ANCAs directed against proteinase-3 (PR3) at >100 U/L, leading to a diagnosis of GPA. All relapses responded to immunosuppression escalation followed by maintenance cyclophosphamide and prednisolone, until full immunosuppression withdrawal three years prior to current presentation. His cumulative cyclophosphamide dose exceeded recommended lifetime maximum.  He is a lifelong non-smoker. On current presentation, chest X-ray demonstrated bilateral nodular opacities with right upper lobe consolidation and Legionella pneumophila infection was confirmed serologically. He demonstrated new positive serology for anti-GBM antibody and persistent anti-PR3 positivity. Remission was induced with plasmapheresis, steroids, and low-dose intravenous cyclophosphamide, with subsequent clinical improvement and concurrent reduction in anti-GBM levels but persistence of anti-PR3 levels.
Conclusions: Although anti-GBM disease is classically a ‘one-hit’ disease, double positivity for ANCA likely infers a multirelapsing course and high initial mortality. This case is meaningful for understanding the pathophysiology of double-positive disease and highlight the considerations of long term immunosuppression.


Biography:
Dr So is a second-year renal advanced trainee in the Western Sydney renal network.

A CASE OF ADULT ONSET CRESCENTIC HENOCH-SCHÖNLEIN PURPURA NEPHRITIS (HSPN) WITH MASSIVE PROTEINURIA AND SEVERE RENAL INSUFFICIENCY

K ABDUL RAZAK1,3, T HAN1,2,Z THET1,2
1Department Of Nephrology, Rockhampton Base Hospital, Rockhampton, Australia, 2Rural Clinical School, University of Queensland, Rockhampton, Australia, 3School of Medicine, Griffith University, Gold Coast, Australia

Background: The clinical presentation of HSPN in adults is severe with relatively poor outcome. As HSPN primarily affects children, evidence on the treatment of HSPN in adults is quite limited. We report a case of severe HSPN with acute kidney injury and proteinuria that was treated successfully.
Case report: 53 year old obese female, with a history of type 2 diabetes mellitus and hypertension presented with nonblanching purpuric vasculitic rash on anterior abdominal wall and posterior surface of both arms. Vasculitis was associated with nephrotic range proteinuria (30g/day), microscopic hematuria and acute kidney injury with eGFR 43ml/min/1.73m2, creatinine 123µmol/L, urea 8.0 mmol/L and albumin 30g/L on admission that later declined to eGFR 20ml/min/1.73m2 and creatinine 231µmol/L during the hospital stay. There was no arthralgia, gastrointestinal symptoms or macroscopic hematuria. She was treated with oral prednisolone after skin biopsy report of florid small vessel or leukocytoclastic vasculitis, negative for immunofluorescence staining. Vasculitis screenings were negative for ANA, anti-dsDNA, anti-GBM, ANCA, hepatitis B, hepatitis C and serum C3 and C4 levels. Renal biopsy reported crescentic glomerular nephritis containing 93% cellular crescents and IgA deposits following which oral cyclophosphamide was initiated. Skin rashes subsided and renal disease improved to eGFR 61ml/min/1.73m2 and creatinine 93µmol/L but proteinuria persisted at 11g/day. Cyclophosphamide was switched to cyclosporin after 6 months of treatment and oral steroid tapered. A few months after initiation of cyclosporine, proteinuria improved persistently at <1g/day.
Conclusion: This case highlights the severity of renal involvement in adult-onset HSPN. Aggressive treatment is required when severe crescentic nephritis and nephrotic syndrome are observed simultaneously at presentation in adult HSPN and the treatment can alter the course of renal disease.


Biography:
Specialist Physician, Rockhampton Base Hospital, Queensland, Senior Lecturer, Rural Clinical School, Rockhampton, Queensland

A UNIQUE CASE OF ANTINEUTROPHIL CYTOPLASMIC ANTIBODY ASSOCIATED CRESCENTIC GLOMERULONEPHRITIS WITH MEMBRANOUS NEPHROPATHY IN A PATIENT WITH HASHIMOTO’S THYROIDITIS

T SOE1, S CHERIAN1,2, B PAWAR1, D FERNANDES1, S NAYAR1, P GEORGE1, S THOMAS1
1Department of Nephrology, Alice Springs Hospital, Alice Springs, Australia, 2Department of Nephrology, Royal Darwin Hospital, Darwin, Australia

Background: It has been known that there is an association between renal glomerular diseases and autoimmune thyroiditis. However, the coexistence of antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis and membranous nephropathy (MN) in such patients is rare.
Case report: A 61-year-old Caucasian man presented with microscopic haematuria and new onset renal impairment, which was preceded by a flu like illness. His past medical history included Hashimoto’s thyroiditis, renal calculi, hypertension and obesity. At presentation, his serum creatinine was 151 micromol/L and urine albumin creatinine ratio (ACR) was 200 mg/mmol. Serum ANCA was positive and myeloperoxidase titre was >80 AI (ref: <1 AI). Other glomerulonephritis serology including anti-glomerular basement membrane antibody and anti-dsDNA were negative. Thyroid stimulating hormone was 13.9 mU/L, with anti-thyroperoxidase antibody of 225 IU/mL and antithyroglobulin of 660kU/L. Renal biopsy showed focal segmental necrotising crescentic lesions in 36% of the glomeruli with minimal scarring in 10% of the interstitium. Immunofluorescence was strongly positive for granular pattern distribution of IgG. There were epimembranous deposits correlating with stage 1 membranous nephropathy in electron microscopy. Circulating anti-phospholipase A2 receptor (PLA2R) antibody and PLA2R staining on renal biopsy were negative. Malignancy as a secondary cause of MN was excluded by negative CT chest, abdomen and gastrointestinal endoscopy. He received induction therapy with methylprednisolone for 3 days followed by oral prednisolone and Rituximab 375mg/m2 weekly for 4 weeks. At the end of five months, his serum creatinine was 136 micromol/L. Urinalysis showed no haematuria and urine ACR was 56.4 mg/mmol.
Conclusion: To our knowledge, this is the first reported case of ANCA vasculitis with MN associated with Hashimoto’s thyroiditis, which was successfully treated with combination of steroid and Rituximab therapy.


Biography:
Thwe is a nephrology advanced trainee currently working at Fiona Stanley Hospital. This presentation is for the case which she encountered during her time at Alice Springs Hospital. She has the interest in autoimmune related glomerulonephritis.

ANTIBODY NEGATIVE ANTI-GLOMERULAR BASEMENT MEMBRANE DISEASE

K HEPBURN1,2,  E MILLAR2,3, J  KELLY1,2, I KATZ1,2
1Department of Renal Medicine, St George Hospital, Kogarah, Australia, 2St George Clinical School UNSW, St George Hospital, Kogarah, Australia, 3Department of Anatomical Histopathology, St George Hospital, Kogarah, Australia

Background: Anti-Glomerular basement membrane (anti-GBM) disease is a rare glomerulonephritis where IgG autoantibodies cause destruction of the glomerular basement membrane and a rapidly progressive GN. Atypical anti-GBM disease, a rare variant with undetectable serum anti-GBM antibodies, differing histopathology, and possibly a subacute course, has been reported in a limited number of case reports and series.
Case Report: A 23-year-old male was referred by his GP, with unexpected renal impairment with creatinine of 220µmol/L and eGFR 35ml/min/1.73m2, nephrotic range proteinuria (6.5g/24hr), hypoalbuminaemia (albumin 29) and elevated cholesterol of 10mmol/L. He was asymptomatic with no peripheral oedema, and no significant background medical history, except a 2-pack-year smoking history. Autoimmune screen, ANCA, IEPG, Hepatitis B, C and HIV were negative. Renal biopsy showed strongly positive linear IgG on immunofluorescence indicating anti-GBM disease, with advanced chronic nodular mesangial sclerosing proliferative glomerulonephritis, with occasional crescents and moderate interstitial fibrosis in keeping with “atypical” anti-GBM glomerulonephritis. Electron microscopy confirmed the diagnosis of anti-GBM disease, also noting mesangial expansion and ischaemic wrinkling of glomerular basement membranes. Serum IgG Anti-GBM antibodies using fluorescence enzyme immunoassay were negative. He received pulsed and oral steroids, IV cyclophosphamide and plasmapheresis. Unfortunately, the patient’s renal function did not improve. His current creatinine is 264umol/L and eGFR 28ml/min/1.73m2. His anti-GBM antibodies remain negative.
Conclusions: Atypical anti-GBM disease is characterised by undetectable serum anti-GBM antibodies and can have a range of histopathological features including focal crescents, nodular glomerulosclerosis, proliferative glomerulonephritis, and glomerular microangiopathy. Our case adds to the literature on this rare entity, highlighting that negative anti-GBM antibodies may not always exclude anti-GBM disease and that renal biopsy remains essential to diagnosis.


Biography:
Dr Kirsten Hepburn is a second year Nephrology Advanced Trainee in the East Coast Renal Network, NSW. Her other degrees include BSc (Psych) and MPH.

 

IMMUNOTACTOID/FIBRILLARY GLOMERULOPATHY MASQUERADING AS C3 GLOMERULOPATHY: A CASE REPORT

A STEINBERG1,  F CHOW1, S HOLT1, A TUCKFIELD2, M FINLAY3, T BARBOUR1
1Department of Nephrology, Royal Melbourne Hospital, Parkville, Australia, 2Department of Haematology, Peter MacCallum Cancer Centre, Parkville, Australia, 3Department of Anatomical Pathology, Royal Melbourne Hospital , Parkville, Australia

Background: C3 glomerulopathy (C3G) is characterised by predominant glomerular C3 staining, with amorphous dense deposits on electron microscopy (EM). Monoclonal gammopathy is sometimes present, including rare cases in which monoclonal immunoglobulin (Ig) or free light chain (FLC) has been shown to trigger complement activation via the alternative pathway (AP). By contrast, immunotactoid/fibrillary implies organised glomerular deposits (fibrils/tubules) on EM, with immune reactivity for IgG (with or without C3). The IgG in immunotactoid is frequently monotypic, and this lesion is strongly associated with malignant B cell disorders (myeloma, lymphoma, chronic lymphocytic leukaemia).
Case Report: A 42-year old, previously well Caucasian man presented with nephrotic syndrome (protein to creatinine ratio 587mg/mmol; serum albumin 26g/L), active urine sediment (erythrocytes 169×106/L; leukocytes 347×106/L) and mild renal impairment (creatinine 110umol/L). ANA, ENAs, dsDNA, ANCAs, cryoglobulins, RF, viral hepatitis serology, C3, C4, CH100 and C3 nephritic factor were negative (FH autoantibody was not sent). Kappa FLCs were markedly elevated in serum (2.4g/L; ratio to lambda 275) and urine. Renal biopsy showed a membranoproliferative pattern, Congo red negative, with moderate granular mesangial and capillary loop staining for C3c and fibrin (negative IgG, IgA, IgM and C1q; insufficient tissue for kappa and lambda). EM revealed long fibrils (diameter 60-80nm without definite tubular structure) arranged in bundles throughout the mesangium and subepithelial space (also subendothelial and intramembranous). Bone marrow biopsy showing 20% aberrant plasma cells led to autologous stem cell transplantation. The renal clinical abnormalities promptly resolved (U/PCR 7mg/mmol), with myeloma in remission at 2 years.
Conclusions: We speculate that the fibrils contained monoclonal kappa FLC precipitates, triggering local AP activation and giving the novel appearance on immune staining (but not EM) of C3G.


Biography:
Adam is a second-year advanced trainee in nephrology based at the Royal Melbourne Hospital.

A CASE OF ACUTE KIDNEY INJURY ASSOCIATED WITH MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS IN THE SETTING OF CRYOGLOBULINAEMIA AND B-CELL LYMPHOPROLIFERATIVE DISORDER.

V HERON1, S WILKINSON1, P DAVIES1,  A YOUNG1, S GOVINDARAJULU1, S VENUTHURUPALLI1
1Renal Service, Darling Downs Hospital And Health Service, Toowoomba, Australia

Background: Lymphoproliferative disorders uncommonly present with glomerulonephritis and acute kidney injury. Very few cases were reported in the literature and the recovery of renal disease is linked to recovery of the lymphoma. Membranoproliferative glomerulonephritis is the most common reported histological lesion especially with cryoglobulinemia.
Case report: A 72-year-old gentleman presented with acute kidney injury (AKI) and haemoproteinuria. He had a background history of carcinoma of prostate in 2009 and of larynx in 2015; both are in remission. On admission his creatinine was 316 µmol/L, with normal renal function a month before (creatinine 70 µmol/L). His renal function worsened during his stay, requiring acute dialysis. Given the finding of AKI with nephritic syndrome he was treated with empirical high dose intravenous methylprednisolone. His vasculitis work-up was negative, however kappa IgM monoclonal paraprotein levels were elevated on serum immunofixation. Serum cryoglobulins were reported positive. Kidney biopsy revealed histological changes consistent with membranoproliferative glomerulonephritis (MPGN) with kappa IgM light chain deposition. The perinephric renal tissue showed lymphocytic infiltration of monoclonal origin. Bone marrow confirmed a B-cell lymphoproliferative disorder. He received a single dose of rituximab as well. During hospitalisation his renal function recovered sufficiently and no longer required ongoing dialysis. He is scheduled for chemotherapy consisting of bendamustine and rituximab.
Conclusions: This is an uncommon case of AKI due to B-cell lymphoproliferative disorder with positive cryoglobulins and histological features consistent with MPGN. Early recognition and diagnosis with appropriate treatment helps in renal recovery as seen in our case. His long-term renal function depends on response to chemotherapy and any future relapses.


Biography:
Vanessa Heron is an advanced trainee in nephrology currently working at Toowoomba Hospital, Queensland.

A CASE OF MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS IN CHRONIC LYMPHOCYTIC LEUKEMIA

Z THET1,2, T HAN1,2, C HAN1,D JAMA3, M WIN3
1Department of Nephrology, Central Queensland Hospital and Health Service, Rockhampton, Australia, 2University of Queensland, Rural Clinical School, Rockhampton, Australia, 3Department of Haematology, Central Queensland Hospital and Health Service, Rockhampton, Australia

Background: Extramedullary/extranodal manifestations of chronic lymphocytic leukemia(CLL) are rare and they can occur with or without the presence of systemic CLL. Renal biopsies are rarely performed in patients with CLL and little is known about the mechanisms causing renal pathology in CLL. There is no standard of care in such patients.
Case Report: A 78 year old female was diagnosed with Binet Stage B CLL with trisomy 21 and IgM paraproteinaemia more than a decade ago. She had been on watchful waiting without any treatment for her CLL. In 2016, her eGFR declined gradually to 26ml/min/1.73m2. Urine examination showed microscopic glomerular haematuria and proteinuria (8g/day). Renal ultrasound, complement results, screening tests for infections, autoimmune diseases and cryoglobulinemia were normal. Renal Biopsy showed acute membranoproliferative glomerulonephritis (MPGN) with mixed lymphocytic infiltrate of aberrant B cells and reactive lymphocytes with no cytological atypia. There is clumpy focal staining for IgG, IgM, C3, C1q and light chains (lambda>kappa) in the glomeruli.  The RCVP (Rituximab, Cyclophosphamide, Vincristine, Prednisolone) chemotherapy regimen was given for 6 cycles with omission of Vincristine in the last 2 cycles. Restaging marrow post treatment showed good partial response. Subsequently, her renal function was normalised to baseline (eGFR 62ml/min/1.73m2) with resolution of proteinuria. Bone marrow examination repeated 2 months after her chemotherapy showed good partial response.
Conclusion: Deposition of monoclonal immunoglobulins especially IgM secreted by leukemia B cells may cause MPGN. Kidney biopsy can provide important information for diagnosis and therapeutic guidance. Renal dysfunction due to CLL can be reversed by treating the underlying CLL.


Biography:
Dr Zaw Thet is a full time Nephrologist from Central QLD Renal Service. He is also a Director of Physician Education and a member of Central QLD Clinical Senate. He is a leading investigator of local and state research projects.

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