Penicillamine-lnduced Rapidly Progressive Glomerulonephritis in a Patient with Rheumatoid Arthritis

Almirall, Jaume; Alcorta, Iñaqui; Botey, A; Revert, L

doi:10.1159/000168636

Cited by 21 publications

(9 citation statements)

References 8 publications

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“…Interestingly, after WND patients have received penicillamine treatment, the chelator accumulates in the proximal tubules but not the glomeruli nor the distal tubules [21]. Glomerular dysfunction also occurs in patients suffering from rheumatoid arthritis who are treated with D -penicillamine [22]. Therefore, the majority of glomerular damage is likely due to penicillamine treatment rather than a consequence of disrupted copper transport.…”

Section: Discussionmentioning

confidence: 99%

Expression in Mouse Kidney of Membrane Copper Transporters Atp7a and Atp7b

Moore¹,

Cox²

2002

Nephron

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Copper is essential for activity of many enzymes, but is toxic in excess. Several copper proteins are required for copper homeostasis. ATP7A and ATP7B are genes encoding membrane copper transporters. ATP7A, defective in Menkes disease (MNK), is expressed in many tissues involved primarily in copper uptake from dietary sources. ATP7B, defective in Wilson disease (WND), is essential for copper excretion. Although MNK patients have a copper deficiency in most tissues, copper accumulates in proximal tubules in the kidney. WND patients also have copper accumulation in the proximal tubules. In some WND patients this copper accumulation may result in tubular dysfunction, resulting in the increased excretion of low molecular weight substances (e.g. amino acids and calcium). In mouse, we have demonstrated, by in situ hybridization, the expression pattern in the kidney of mouse orthologues, Atp7a and Atp7b, and have confirmed Atp7b expression by immunohistochemistry. Both Atp7a and Atp7b are expressed in glomeruli; however, Atp7b is also seen in the kidney medulla. This suggests that glomeruli are responsible for regulating copper levels in the filtrate. In WND patients, urinary copper levels are extremely high suggesting Atp7b in the loops of Henle may have a role in copper reabsorption.

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Section: Discussionmentioning

confidence: 99%

Expression in Mouse Kidney of Membrane Copper Transporters Atp7a and Atp7b

Moore¹,

Cox²

2002

Nephron

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“…In the present series of cases with crescents, there was a preponderance of rheumatoid arthritis as the primary disease. Various glomerular lesions have been known to be associated with rheumatoid arthritis or to have untoward reactions to drugs 18–21 . They include mesangial proliferative glomerulonephritis, membranoproliferative glomerulonephritis, membranous glomerulonephritis and focal glomerulosclerosis 22 .…”

Section: Discussionmentioning

confidence: 99%

Glomerular crescents in renal amyloidosis: An epiphenomenon or distinct pathology?

Nagata¹,

Shimokama

Harada

et al. 2001

Pathology International

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There have been several reports of cases of renal amyloidosis with glomerular crescents. However, it is not clear whether the association is fortuitous or pathogenic related. The present study analyzed 105 cases of renal amyloidosis (61 autopsy cases and 44 biopsy cases) and found glomerular crescents in 14 (13.3%) cases. Among the 14 cases with crescents, a female predominance was noted (male: female, 3: 11) and rheumatoid arthritis was the most common primary disease of amyloidosis. Immunohistochemical analysis demonstrated amyloid protein of AA type in 12 cases. According to the histologic classification, there were 11 cases of mesangial nodular type, which was almost exclusively accompanied by AA amyloid deposition. Of note, the incidence of crescents neither correlated with the extent of amyloid deposition nor the presence of nephrotic syndrome. By contrast, localization of amyloid deposition was closely related to crescent formation. Moreover, electron microscopic observation displayed rupture of the glomerular basement membrane at the site of amyloid deposition. Our results indicated that glomerular crescents were more frequently associated with renal amyloidosis than previously appreciated. Rupture of the fragile glomerular basement membrane by amyloid deposition, as revealed by immunostaining and electron microscopy, may be the mechanism of crescent formation. We suggest that glomerular crescents are a distinct pathology associated with renal amyloidosis, not fortuitous conditions.

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“…d ‐penicillamine and trientine are the major drugs used for WD treatment. Although d ‐penicillamine is a Cu chelator extensively used in humans, there are some studies showing a pancreatic islet autoantibody production and a glomerulonephritis induced by penicillamine. These deleterious effects of penicillamine might contribute to the absence of studies testing d ‐penicillamine for the treatment of DM.…”

Section: Cu Chelation Therapy For Treatment Of Diabetesmentioning

confidence: 99%

Dissecting copper homeostasis in diabetes mellitus

2017

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Diabetes Mellitus (DM) is characterized by elevated blood glucose levels (hyperglycemia). It can occur due to impaired secretion or action of the hormone insulin, which is produced by pancreatic beta-cells to promote the entry of glucose into the cells. It is known that hyperglycemia has an important role in the production of reactive oxygen species in all types of DM and that an imbalance of transition metal as Cu and Fe plays a pivotal role in stimulating the oxidative stress. Different levels of some transition metals, as Cu, Fe, Mn, and Zn has been reported comparing diabetic animal models with the control group. An increased Cu status is also described in diabetic patients. Homeostasis of Cu depends on distinct proteins, where Cu(I)-ATPases are important transmembrane proteins for acquisition, active transport, distribution and elimination of Cu ions. In this review we first provide an overview of the literature about the relationship between diabetes and copper, the modulation of Cu(I)-ATPases activity and protein expression in DM, to next discuss the alternative treatments for diabetes using Cu chelation. V C 2017 IUBMB Life, 69(4): [255][256][257][258][259][260][261][262] 2017

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Penicillamine-lnduced Rapidly Progressive Glomerulonephritis in a Patient with Rheumatoid Arthritis

Cited by 21 publications

References 8 publications

Expression in Mouse Kidney of Membrane Copper Transporters Atp7a and Atp7b

Expression in Mouse Kidney of Membrane Copper Transporters Atp7a and Atp7b

Glomerular crescents in renal amyloidosis: An epiphenomenon or distinct pathology?

Dissecting copper homeostasis in diabetes mellitus

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