Pathogenesis of Renal Disease in Monoclonal Gammopathies: Current Concepts

Beaufils, M.; Morel-Marogér, L

doi:10.1159/000181210

Cited by 37 publications

(17 citation statements)

References 15 publications

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“…Monoclonal components could have various antibody activities leading to the formation of circulating immune complex [11]. Evidence for the pathogenic role is shown through a case of WM with immune complex-mediated glomerulonephritis [12].…”

Section: Discussionmentioning

confidence: 99%

Nephrotic Syndrome due to Immunologically Mediated Hypocomplementic Glomerulonephritis in a Patient of Waldenström’s Macroglobulinemia

Haraguchi¹,

Tomiyoshi²,

Aoki³

et al. 2002

Nephron

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A 72-year-old man was diagnosed as having nephritic syndrome complicated by Waldenström’s macroglobulinemia (WM). A monoclonal IgM lamda protein and decreased serum complements were observed. The renal biopsy disclosed the capillary occluded by thrombi which was stained with IgG, IgA, IgM, C4, lamda light chain and slight kappa light chain in a granular pattern. Electron dense deposits were noted in the subendothelial spaces. An unusual case of WM who developed nephrotic syndrome due to immunologically mediated hypocomplementic glomerulonephritis is described.

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Section: Discussionmentioning

confidence: 99%

Nephrotic Syndrome due to Immunologically Mediated Hypocomplementic Glomerulonephritis in a Patient of Waldenström’s Macroglobulinemia

Haraguchi¹,

Tomiyoshi²,

Aoki³

et al. 2002

Nephron

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“…The fact that decrease of blood glucose may lead to a decrease in blood viscosity and to an increase in oxygen delivery to tissues [109] could be of paramount importance since hyperviscosity and/or hypoxia may act as triggering mechanisms for the development of capillary proliferation in the retina [101,114]. It has recently been pointed out that renal and retinal diabetic-like lesions have been observed in other diseases with hypoxia and/or hyperviscosity [101,107,114,115]. Strict control of blood glucose also normalises growth hormone secretion which may play a permissive role in the development of diabetic microangiopathy [116].…”

Section: Functional Microangiopathy Organ Size and Blood Compositionmentioning

confidence: 99%

Relation of diabetic control to development of microvascular complications

Tchobroutsky

1978

Diabetologia

400

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Summary. This review seeks to supply the arguments which support or deny the relationship between the quality of control of blood glucose levels and the course of diabetic microangiopathy. The ideal study is impossible to do in man but most prospective studies suggest that the better the control the slower the rate of progression and severity of lesions. "Scientific" but indirect arguments from biochemical, enzymatic and functional studies have shown that insulin and/or blood glucose control reverse some early diabetic changes that are probably related to the late events. Recent studies suggest that observations on animals that have shown the beneficial effect of treatment are relevant to the problem of diabetic microvascular lesions in man. Heredity influences the development of diabetic microangiopathy in diabetics but retinal and/or glomerular lesions -which are definitely not pathognomonic for diabetes -do not appear in the absence of hyperglycaemia. Muscle capillary basement membrane thickening that seems not to be a specific abnormality was not observed by several investigators in recently diagnosed diabetics. Therefore most of the arguments that have been given to support the point of view that tight control is not justified may be rejected. The opinion of the author is that strict control of diabetes is worthwile in patients with long life expectancy and no psychological, social or cultural handicaps.

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“…This entity is known to show glomerular capillary luminal IgM thrombi [19]. Avasthi et al [20] described 1 subject with proliferative glomerulonephritis probably induced by monoclonal IgM.…”

Section: Discussionmentioning

confidence: 99%

IgM Monoclonal Gammopathy Accompanied by Nodular Glomerulosclerosis, Urine-Concentrating Defect, and Hyporeninemic Hypoaldosteronism

et al. 1985

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A 54-year-old male had monoclonal IgM-kappa light chains in the serum and free monoclonal kappa light chains in the urine. Renal biopsy revealed nodular glomerulosclerosis associated with the accumulation of kappa light chains. Isolated microscopic hematuria was present for over 1 year. He also showed a defect in urine concentration for which the light chains deposited along the basement membrane in the inner medullary tubules were judged to be responsible. When the glomerular filtration rate fell to 30 ml/min, the syndrome of mild renal failure, decreased potassium excretion, and hyporeninemic hypoaldosteronism developed, suggesting that kappa light chain nephropathy is a cause of this syndrome. Chemotherapy appeared to have some beneficial effects in maintaining renal function.

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Pathogenesis of Renal Disease in Monoclonal Gammopathies: Current Concepts

Cited by 37 publications

References 15 publications

Nephrotic Syndrome due to Immunologically Mediated Hypocomplementic Glomerulonephritis in a Patient of Waldenström’s Macroglobulinemia

Nephrotic Syndrome due to Immunologically Mediated Hypocomplementic Glomerulonephritis in a Patient of Waldenström’s Macroglobulinemia

Relation of diabetic control to development of microvascular complications

IgM Monoclonal Gammopathy Accompanied by Nodular Glomerulosclerosis, Urine-Concentrating Defect, and Hyporeninemic Hypoaldosteronism

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