Anti-Glomerular Basement Membrane Nephritis after Extracorporeal Shock Wave Lithotripsy

Iwamoto, Ichiro; Yonekawa, Shinsuke; Takeda, Takeshi; Sakaguchi, Mika; Ohno, Tomoyasu; Tanaka, Hiroyoshi; Higuchi, Hisashi; Imada, Akio; Horiuchi, Akiko; Umekawa, Tohru; Kitahara, Takashi

doi:10.1159/000013401

Cited by 11 publications

(8 citation statements)

References 17 publications

(16 reference statements)

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“…Eleven patients were found to participate in this study. For each of these patients, we retrospectively determined clinical features including age at diagnosis of hydronephrosis, sex, medical history of preexisting renal disease, especially membranous nephropathy, causes of hydronephrosis and the presence or absence of clinical risk factors for the development of anti-GBM antibodies such as smoking history, exposure to organic solvents, recent infection prior to the onset of renal impairment and enforcement of ESWL [ 4 , 5 , 6 , 7 , 10 ]. We also investigated their serum creatinine (sCr mg/dl), the degree of hematuria shown as the number of urinary red blood cells (RBCs) per high-power field (HPF), the deformity of urinary RBCs and RBC cast formation and titer of serum anti-GBM antibodies before and after treatment for hydronephrosis.…”

Section: Methodsmentioning

confidence: 99%

“…Considering the available evidence, it is hypothesized that a disruption of the stabilized NC1 hexamer and exposure of the cryptic antigen of the α3-chain to the host immune system are required for the development of anti-GBM antibodies [ 3 ]. Several studies have proposed causes for the modifications of intact NC1, namely smoking, infections, exposure to organic solvent and enforcement of extracorporeal shock wave lithotripsy (ESWL) [ 4 , 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

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A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

Takeuchi¹,

Takeuchi

Kamata³

2015

Case Rep Nephrol Dial

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Background: Anti-glomerular basement membrane (anti-GBM) antibody-mediated glomerulonephritis (anti-GBM GN) is an autoimmune disease with rapidly progressive glomerulonephritis. Based on a case report of anti-GBM GN following hydronephrosis, we hypothesized that hydronephrosis may act as a trigger for the development of anti-GBM antibodies. Patients and Methods: We evaluated 11 patients who were diagnosed with hydronephrosis. It was measured with serum anti-GBM antibody. These patients' medical histories as well as risk factors for the development of anti-GBM antibodies and causes of hydronephrosis were reviewed. Renal function and hematuria were also considered. The serum anti-GBM antibody was measured with enzyme-linked immunosorbent assays (ELISA) or chemiluminescent enzyme immunoassays (CLEIA). Histopathological findings of renal biopsy specimens were also evaluated. Results: No patient had a medical history of renal disease. Five patients had a history of smoking. Ten of the 11 patients had renal dysfunction as evidenced by serum creatinine levels of 0.85-13.8 mg/dl, while 8 patients had RBCs in their urinary sediment at the time of diagnosis for hydronephrosis. Two of the patients assessed by ELISA and CLEIA were positive for anti-GBM antibodies. In 1 of these 3 patients, anti-GBM antibodies and renal dysfunction improved upon treatment for hydronephrosis. Another of the 3 patients developed anti-GBM GN, but anti-GBM antibodies and renal dysfunction improved dramatically upon treatment. In the 3rd patient without improved hydronephrosis, anti-GBM antibodies and renal dysfunction remained unchanged. Conclusion: Our results provide insights into the development of anti-GBM antibodies in patients with ureteral obstruction and hydronephrosis.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

Takeuchi¹,

Takeuchi

Kamata³

2015

Case Rep Nephrol Dial

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“…Reported success rates for lithotripsy vary from 30 to 100%, depending on how patients are selected, how hard the stone is, and the type of lithotripter used [39,40]. Complications of lithotripsy are rare [41], although there have been unusual case reports of post-treatment anti-GBM antibody-positive glomerulonephritis [42,43], and even a later increase in the incidence of hypertension and diabetes [44]. A stone in a calyceal diverticulum, or a dependent lower pole calyx, can break up, but may not pass.…”

Section: Surgical Managementmentioning

confidence: 99%

An Update and Practical Guide to Renal Stone Management

et al. 2010

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Renal stone disease covers kidney and lower urinary tract stones caused by a variety of conditions, including metabolic and inherited disorders, and anatomical defects with or without chronic urinary infection. Most cases are idiopathic, in which there is undoubtedly a genetic predisposition, but where environmental and lifestyle factors play an important role. Indeed, it is becoming apparent that renal stone disease is often part of a larger ‘metabolic picture’ commonly associated with type 2 diabetes, obesity, dyslipidaemia, and hypertension. Renal stone disease is a growing problem in the UK (and other developed and developing populations) with a cross-sectional prevalence of ∼1.2%. This means that there are currently ∼720,000 individuals with a history of kidney stones in the UK. Almost 40% of first-time stone formers will form a second stone within 3 years of the first episode if no prophylactic measures are instituted to prevent stone recurrence, since removal or disintegration of the first stone does not treat the underlying cause of stones in the majority of patients. The age of onset is getting younger and the sex ratio (until recently more men than women) is becoming almost even. Metabolic screening remains an important part of investigating renal stone disease, but to the disappointment and frustration of many doctors, medical treatment is still essentially pragmatic, except perhaps in cystinuria, and to a limited extent in primary hyperoxaluria (if pyridoxine-sensitive); although newer treatments may be emerging. This review summarizes current thinking and provides a practical basis for the management of renal stone disease.

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“…Die im Vergleich zu der obligatorisch vorliegenden Nierenbeteiligung weniger häu-fig vorkommende pulmonale Manifestation wird auf eine geringere Zugänglichkeit der alveolären Epitope für die zirkulierenden Antikörper zurückgeführt [6]. Dies erklärt auch, warum Schäden der pulmonalen Endothelien -verursacht durch Rauchen, kohlenwasserstoffhaltige Dämpfe, respiratorische Infektionen oder eine kardiale Stauung -eine Lungenbeteiligung der Erkrankung auslösen können [6].Aber auch für die Nephritis sind Triggerfaktoren wie Lithotripsien [14] oder Ureterobstruktionen [15] beschrieben worden.…”

Section: Anti-gbm-nephritis Und Goodpasture-syndromunclassified

Rasch progrediente Glomerulonephritiden

Birck

Woude

2002

Internist

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Rapidly progressive glomerulonephritides (RPGN) belong to a heterogeneous group of inflammatory kidney diseases which are commonly associated with systemic vasculitic syndromes. Renal histology is characterized by necrotizing lesions within the glomerual tuft and extracapillary proliferation, in most cases leading rapidly to renal failure. The etiology and pathogenesis are only partly elucidated. Since irreversible renal scaring develops within days to weeks, RPGN represent a nephrological emergency necessitating urgent diagnostic evaluation and rapid institution of effective therapy. New onset nephritic sediment combined with concomitantly deteriorating excretory renal function should lead to immediate nephrological consultation. Autoimmune serology and particularly renal biopsy are of the utmost importance for rapid diagnosis. Most forms of RPGN are treated with immunosuppressive regimens which generally consist of high dose steroids in combination with the alkylating agent cyclophosphamide. Some forms also require the use of plasma exchange therapy. Rapid diagnosis and early therapy improves both renal and overall outcome in the affected patients.

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Anti-Glomerular Basement Membrane Nephritis after Extracorporeal Shock Wave Lithotripsy

Cited by 11 publications

References 17 publications

A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

A Possible Clue for the Production of Anti-Glomerular Basement Membrane Antibody Associated with Ureteral Obstruction and Hydronephrosis

An Update and Practical Guide to Renal Stone Management

Rasch progrediente Glomerulonephritiden

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