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We thank Singh et al.1Singh G. Bhardwaj S. Singh L. et al.Proliferative glomerulonephritis with monotypic IgA-kappa deposits in a 10-year-old.Kidney Int. 2017; 92: 765-766Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar for their interesting case. In this child, pathological findings were distinct from IgA nephropathy, with membranoproliferative pattern of glomerular lesions and kappa light chain restriction of IgA deposits contrasting with the usual lambda light chain predominance of polyclonal IgA deposits.2Chen N. Nusbaum P. Halbwachs-Mecarelli L. et al.Light-chain composition of serum IgA1 and in vitro IgA1 production in IgA nephropathy.Nephrol Dial Transplant. 1991; 6: 846-850Crossref PubMed Scopus (19) Google Scholar This case confirms that early age does not rule out monoclonal gammopathy of renal significance. Because various monoclonal gammopathy of renal significance types (mostly proliferative glomerulonephritis with monoclonal IgG deposits and AL amyloidosis)3Abeykoon J.P. Paludo J. Dispenzieri A. et al.Outcome of very young (≤ 40 years) patients with immunoglobulin light chain (AL) amyloidosis.Amyloid. 2017; 24: 50-51Crossref PubMed Scopus (2) Google Scholar, 4Nasr S.H. Satoskar A. Markowitz G.S. et al.Proliferative glomerulonephritis with monoclonal IgG deposits.J Am Soc Nephrol. 2009; 20: 2055-2064Crossref PubMed Scopus (280) Google Scholar were described in young adults, immunofluorescence studies of the kidney biopsy should systematically incorporate light chain–specific antibodies. In patients with monotypic deposits, ultrastructural diagnostic confirmation is required, because outcomes and management vary with each entity.4Nasr S.H. Satoskar A. Markowitz G.S. et al.Proliferative glomerulonephritis with monoclonal IgG deposits.J Am Soc Nephrol. 2009; 20: 2055-2064Crossref PubMed Scopus (280) Google Scholar As reported by Singh et al., monotypic Ig deposits may be the sole apparent manifestation of an underlying small clonal disorder. Indeed, hematologic workup was negative in two-thirds of patients in a series of IgA-proliferative glomerulonephritis with monoclonal IgG deposits and IgG-proliferative glomerulonephritis with monoclonal IgG deposits.2Chen N. Nusbaum P. Halbwachs-Mecarelli L. et al.Light-chain composition of serum IgA1 and in vitro IgA1 production in IgA nephropathy.Nephrol Dial Transplant. 1991; 6: 846-850Crossref PubMed Scopus (19) Google Scholar Identifying the lymphocytic or plasmacytic origin of the pathogenic clone is crucial for treatment decision. When routine explorations are negative (usually in the absence of detectable monoclonal gammopathy), other investigations should be considered, such as flow cytometry or molecular studies of bone marrow and peripheral blood lymphocytes, or imaging techniques to detect lymph nodes. Finally, because monoclonal gammopathy of renal significance renal lesions may precede by several years development of an overt hematological disease, prolonged surveillance is mandatory. Proliferative glomerulonephritis with monotypic IgA-kappa deposits in a 10-year-oldKidney InternationalVol. 92Issue 3PreviewWe read with great interest the series of cases on glomerular diseases related to monotypic IgA deposits by Vignon et al.1 We recently came across a 10-year-old boy presenting with nephrotic syndrome and a membranoproliferative glomerulonephritis demonstrating monotypic IgA (IgA-kappa) deposits (both on frozen and paraffin immunofluorescence) with mesangial and subendothelial electron dense deposits (Figure 1). The serum C3 was 83, 32, and 110 mg/dl during the course (range, 70–240 mg/dl). In significant past history, on evaluation of cough an echocardiogram revealed a large ostium secundum atrial septal defect with left to right shunt, mild tricuspid regurgitation, and mild pulmonary arterial hypertension. Full-Text PDF Open Archive