ORCID Profile
0000-0002-3610-5053
Current Organisations
Royal Melbourne Hospital Royal Park Campus
,
Royal Australasian College of Physicians
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Publisher: Springer Science and Business Media LLC
Date: 13-06-2018
DOI: 10.1038/S41598-018-27151-4
Abstract: People with biopsy-proven glomerulonephritis (GN) as their cause of end-stage kidney disease (ESKD) who undergo kidney transplantation incur significant risk of recurrent GN-related graft failure, but the risk in recipients with ESKD where GN was suspected but not biopsy proven (presumed/advanced GN) and when the cause of ESKD is unknown remains uncertain. Using the Australia and New Zealand Dialysis and Transplant registry, we examined the associations between primary kidney transplant recipients whose ESKD was attributed to: 1) commonly-recurring GN (i.e. IgA nephropathy, membranoproliferative GN, focal segmental glomerulosclerosis and membranous GN), 2) presumed/advanced GN, and 3) cause of ESKD unknown (uESKD) and GN-related graft failure using adjusted competing risk models. Of 5258 recipients followed for a median of 8 years, 3539 (67.3%) had commonly-recurring GN, 1195 (22.7%) presumed/advanced GN, and 524 (10.0%) uESKD. Compared to recipients with commonly-recurring GN, recipients with presumed/advanced GN or uESKD experienced a low incidence of GN-related graft failure ( %) and a lower hazard of GN-related graft failure (adjusted sub-distribution hazard ratio [HR] 0.28 [95%CI 0.15-0.54,p 0.001] and 0.20 [95%CI 0.06-0.64,p = 0.007], respectively). People with ESKD attributed to either presumed/advanced GN or unknown cause face a very low risk of graft failure secondary to GN recurrence after transplantation.
Publisher: Elsevier BV
Date: 2014
Publisher: Oxford University Press (OUP)
Date: 07-2012
DOI: 10.1093/NDT/GFS279
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.MOLIMM.2015.03.246
Abstract: Tremendous advances in our understanding of the thrombotic microangiopathies (TMAs) have revealed distinct disease mechanisms within this heterogeneous group of diseases. As a direct result of this knowledge, both children and adults with complement-mediated TMA now enjoy higher expectations for long-term health. In this update on atypical hemolytic uremic syndrome, we review the clinical characteristics the genetic and acquired drivers of disease the broad spectrum of environmental triggers and current diagnosis and treatment options. Many questions remain to be addressed if additional improvements in patient care and outcome are to be achieved in the coming decade.
Publisher: Oxford University Press (OUP)
Date: 17-10-2014
DOI: 10.1093/NDT/GFU317
Publisher: Wiley
Date: 06-2018
DOI: 10.1111/NEP.13234
Abstract: Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. While TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4-8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 activity (a disintegrin and metalloprotease thrombospondin, number 13). A sodium citrate plasma s le should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin-associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC-HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC-HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. While early confirmation of aHUS is often not possible, except in the minority of patients in whom autoantibodies against factor H are identified, genetic testing ultimately reveals a complement-related mutation in a significant proportion of aHUS cases. The presence of other TMA-associated conditions (e.g. infection, pregnancy ostpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.
Publisher: Oxford University Press (OUP)
Date: 10-03-2013
DOI: 10.1093/NDT/GFS430
Publisher: Elsevier BV
Date: 11-2013
Publisher: Elsevier BV
Date: 06-2020
Publisher: Oxford University Press (OUP)
Date: 21-07-2011
DOI: 10.1093/NDT/GFR394
Abstract: Glomerulonephritis occurs in 1% of Hodgkin's lymphoma patients. In the even rarer setting of rapidly progressive glomerulonephritis, lymphoma may go unrecognized. We describe a case of necrotizing glomerulonephritis in which treatment with cyclophosphamide and steroids led to resolution of lymphadenopathy. Two years later, recrudescent lymphadenopathy was shown to be Hodgkin's lymphoma, but renal disease did not recur.
Publisher: Informa UK Limited
Date: 07-2019
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 11-01-2007
Publisher: Wiley
Date: 02-2017
DOI: 10.1111/NEP.12939
Abstract: In C3 glomerulopathy, uncontrolled complement C3 activation via the alternative pathway results in glomerular C3 deposition and, in many cases, progressive renal failure. Despite advances in understanding of C3G pathogenesis over the last few years, there are no proven treatments. We describe a patient in whom C3 glomerulopathy was associated with renal impairment and elevated serum free kappa light chains. An initial response to corticosteroids was followed by relapse once steroids were weaned, prompting use of mycophenolate mofetil to maintain remission. We discuss some of the diagnostic and therapeutic issues surrounding C3G, including in the setting of monoclonal gammopathy.
Publisher: Elsevier BV
Date: 12-2015
DOI: 10.1038/KI.2015.233
Publisher: Wiley
Date: 24-03-2014
DOI: 10.1111/NEP.12217
Abstract: Antiphospholipid syndrome (APS) may occur in isolation or in association with systemic lupus erythematosus (SLE), with the potential to cause renal failure via several distinct pathologies. Renal transplantation in the presence of APS carries a risk of early graft loss from arterial or venous thrombosis, or thrombotic microangiopathy (TMA). Whilst perioperative anticoagulation reduces the risk of large vessel thrombosis, it may result in significant haemorrhage, and its efficacy in preventing post-transplant TMA is uncertain. Here, we report a patient with end-stage kidney disease (ESKD) due to lupus nephritis and APS, in whom allograft TMA developed soon after transplantation despite partial anticoagulation. TMA resolved with plasma exchange-based therapy albeit with some irreversible graft damage and renal impairment. We discuss the differential diagnosis of post-transplant TMA, and current treatment options.
Publisher: Wiley
Date: 06-2018
DOI: 10.1111/IMJ.13804
Abstract: Thrombotic microangiopathy (TMA) arises in a variety of clinical circumstances with the potential to cause significant dysfunction of the kidneys, brain, gastrointestinal tract and heart. TMA should be considered in all patients with thrombocytopenia and anaemia, with an immediate request to the haematology laboratory to look for red cell fragments on a blood film. Although TMA of any aetiology generally demands prompt treatment, this is especially so in thrombotic thrombocytopenic purpura (TTP) and atypical haemolytic uraemic syndrome (aHUS), where organ failure may be precipitous, irreversible and fatal. In all adults, urgent, empirical plasma exchange (PE) should be started within 4-8 h of presentation for a possible diagnosis of TTP, pending a result for ADAMTS13 (a disintegrin and metalloprotease thrombospondin, number 13) activity. A sodium citrate plasma s le should be collected for ADAMTS13 testing prior to any plasma therapy. In children, Shiga toxin-associated haemolytic uraemic syndrome due to infection with Escherichia coli (STEC-HUS) is the commonest cause of TMA, and is managed supportively. If TTP and STEC-HUS have been excluded, a diagnosis of aHUS should be considered, for which treatment is with the monoclonal complement C5 inhibitor, eculizumab. Although early confirmation of aHUS is often not possible, except in the minority of patients in whom auto-antibodies against factor H are identified, genetic testing ultimately reveals a complement-related mutation in a significant proportion of aHUS cases. The presence of other TMA-associated conditions (e.g. infection, pregnancy ostpartum and malignant hypertension) does not exclude TTP or aHUS as the underlying cause of TMA.
Publisher: Wiley
Date: 31-05-2020
DOI: 10.1111/NEP.13722
Publisher: Elsevier BV
Date: 04-2016
Publisher: Springer Science and Business Media LLC
Date: 23-07-2020
DOI: 10.1186/S12882-020-01941-3
Abstract: Cryoglobulins are cold-precipitable immunoglobulins that may cause systemic vasculitis including cryoglobulinaemic glomerulonephritis (CGN). Type 1 cryoglobulins consist of isolated monoclonal immunoglobulin (mIg), whereas mixed cryoglobulins are typically immune complexes comprising either monoclonal (type 2) or polyclonal (type 3) Ig with rheumatoid activity against polyclonal IgG. Only CGN related to type 1 cryoglobulins has been clearly associated with monoclonal gammopathy of undetermined significance (MGUS) using the conventional serum-, urine- or tissue-based methods of paraprotein detection. We present four patients with noninfectious mixed (type 2 or 3) CGN and MGUS. Two patients had type 2 cryoglobulinaemia, one had type 3 cryoglobulinaemia, and one lacked definitive typing of the serum cryoprecipitate. The serum monoclonal band was IgM-κ in all four cases. Treatments included corticosteroids, cyclophosphamide, plasma exchange, and rituximab. At median 3.5 years’ follow-up, no patient had developed a haematological malignancy or advanced chronic kidney disease. Other potential causes of mixed cryoglobulinaemia were also present in our cohort, notably primary Sjögren’s syndrome in three cases. Our study raises questions regarding the current designation of type 2 CGN as a monoclonal gammopathy of renal significance, and the role of clonally directed therapies for noninfectious mixed CGN outside the setting of haematological malignancy.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Start Date: 2011
End Date: 2014
Funder: Kidney Research UK
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