Occupational Solvent Exposure and Glomerulonephritis

Daniell, William

doi:10.1001/jama.1988.03720150056037

Cited by 44 publications

(5 citation statements)

References 42 publications

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“…Patients with organic solvents related nephrosis have been reported [1]–[3]. All patients manifest typical nephrosis with severe edema, massive non-alternative proteinuria, hypoalbuminemia and hypercholesterolemia.…”

Section: Introductionmentioning

confidence: 99%

Mixed Organic Solvents Induce Renal Injury in Rats

Qin

et al. 2012

PLoS ONE

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To investigate the injury effects of organic solvents on kidney, an animal model of Sprague-Dawley (SD) rats treated with mixed organic solvents via inhalation was generated and characterized. The mixed organic solvents consisted of gasoline, dimethylbenzene and formaldehyde (GDF) in the ratio of 2∶2:1, and were used at 12,000 PPM to treat the rats twice a day, each for 3 hours. Proteinuria appeared in the rats after exposure for 5–6 weeks. The incidences of proteinuria in male and female rats after exposure for 12 weeks were 43.8% (7/16) and 25% (4/16), respectively. Urinary N-Acetyl-β-(D)-Glucosaminidase (NAG) activity was increased significantly after exposure for 4 weeks. Histological examination revealed remarkable injuries in the proximal renal tubules, including tubular epithelial cell detachment, cloud swelling and vacuole formation in the proximal tubular cells, as well as proliferation of parietal epithelium and tubular reflux in glomeruli. Ultrastructural examination found that brush border and cytoplasm of tubular epithelial cell were dropped, that tubular epithelial cells were partially disintegrated, and that the mitochondria of tubular epithelial cells were degenerated and lost. In addition to tubular lesions, glomerular damages were also observed, including segmental foot process fusion and loss of foot process covering on glomerular basement membrane (GBM). Immunofluorescence staining indicated that the expression of nephrin and podocin were both decreased after exposure of GDF. In contrast, increased expression of desmin, a marker of podocyte injury, was found in some areas of a glomerulus. TUNEL staining showed that GDF induced apoptosis in tubular cells and glomerular cells. These studies demonstrate that GDF can induce both severe proximal tubular damage and podocyte injury in rats, and the tubular lesions appear earlier than that of glomeruli.

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Section: Introductionmentioning

confidence: 99%

Mixed Organic Solvents Induce Renal Injury in Rats

Qin

et al. 2012

PLoS ONE

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“…An Australian research 13 reported a prevalence of 36% of patients with anti-GBM disease have normal renal function. Other studies have found that 15%-35% [20][21][22][23][24] of patients with anti-GBM disease have normal renal function. All ve patients with normal renal function are alive, and the serum creatinine is less than 0.2 mmol/l in all (100%), hematuria persists in one (20%), and proteinuria > l g/day in two (40%).…”

Section: Rheumatol2015mentioning

confidence: 99%

Unusual cases of crescentic glomerulonephritis with normal renal function at diagnosis: a retrospective case series from a single center in Western China

Wu,

Zhang,

Wang

et al. 2024

Preprint

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Background. The aim of this study is to investigate the clinicopathologic characteristics, treatment and prognosis of crescentic glomerulonephritis (Crescentic GN) in patients with normal renal function at diagnosis, and compare to those with impaired renal function. Methods. We conducted a retrospective review of patients with renal biopsy proven Crescentic GN at our center and divided them into normal eGFR group (eGFR≥60 ml/min/1.73 m2) and low eGFR group (eGFR <60 ml/min/1.73 m2). Clinical and renal pathological findings at diagnosis and renal outcomes were compared between the two groups using t test, Wilcoxon rank sum test or Kruskal-Wallis H test. Comparison of cumulative renal survival rates for ESRD was done by Kaplan-Meier curves and the log-rank test. Results. From Jan 2010 to Dec 2021, 98 Crescentic GN patients with normal eGFR were included, in which clinicopathological diagnoses were LN(lupus nephritis) (60 cases, 66.77%), IgAN (IgA nephropathy) (9 cases, 10 %), HSPN (Henoch-Schnlein purpura nephritis) (4 cases, 15.6%) and AAV(ANCA-associated GN) (7 cases, 7.8%). Compared with the low eGFR group (n=300), the following characteristics were observed in the normal eGFR group: younger age (p<0.001), female predominance (p<0.001), longer time from onset to biopsy (p<0.001), lower hypertension rate (p<0.001), lower rate of oliguria(p<0.001), and anemia (p<0.001), lower levels of C3 (p<0.001), C4 (p<0.001) and Urine RBC (p<0.001), higher titers of ANA(p<0.001) and ds-DNA(p=0.002), lower positive rate of ANCA (<0.001) and GBM (p=0.02), less extra-renal involvement (p<0.05), lower proportions of crescents (56.3(51.8-62.7) vs 66.7 (56.3-81.3),p<0.001) and glomerular sclerosis(p<0.001), less severe tubulointerstitial lesion (p<0.001) and interstitial inflammation (p<0.001), higher degree of immune complex deposition of IgA, IgM, C3, C4 and C1q by Immunofluorescence. Normal eGFR group received lower frequency of intravenous methylprednisolone pulse therapy (71.2% vs 89%, p=0.044) and dialysis treatment (0% vs 53.7%, p<0.001). The 5- and 10-year cumulative renal survival rates from ESRD were 90.7% vs 45.5% and 58.3% vs 43.7%, respectively in normal and low eGFR group. Conclusion. Crescentic GN may present with normal renal function, which have poor renal outcomes and may benefit from intensive immunosuppressive treatment. This often occurs in patients with abnormal immunological indicators and systemic autoimmune disease. Shorter time from onset to biopsy may help better management and improve long-term outcomes in these cases. Renal biopsy remains the diagnostic gold standard when urinary abnormalities are present in nephritis.

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“…A higher level of autoantibodies are described after a wide variety of chemical exposures, including chlordane (Robinson 1996), solvents (Daniell, Couser, and Rosenstock 1988;Bombassei and Kaplan 1992), chlorinated solvents (Montoya 1990), PCBs/PBBs (Safran et al 1987), organochlorine, organophosphate and other pesticides (Street 1981), formaldehyde and aliphatic amines (Brooks et al 1985), silicone (Press et al 1992;, chlordane (Ziem and McTamney 1997), chlorpyrifos (Ziem and McTamney 1997), malathion (Ziem and McTamney 1997), and formaldehyde (Tarlo and Broder 1989). A greater number of chemical-speci c antibodies has been noted after exposure to building materials in remodeling (Thrasher et al 1989).…”

Section: Petrochemical-induced Injurymentioning

confidence: 99%

Profile of Patients with Chemical Injury and Sensitivity, Part II

Ziem¹

1999

Int J Toxicol

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Exposures which can induce multiple chemical sensitivity (MCS) involve symptomatic, usually repeated, exposures to pesticides, solvents, combustion products, remodeling, sick buildings, carbonless copy paper (occupational heavy use) and other irritants and petrochemicals. Accompanying toxic injury often involves the immune, endocrine and nervous systems as well as impairments in detoxication, energy and neurotransmitter metabolism, protein, mineral, and other nutrient de ciencies and gastrointestinal changes such as candida, parasites, reduced chymotrypsin (marker enzyme for reduced pancreatic enzyme function), gluten intolerance, and reduced Secretory IgA. Chronic cortisol elevation leading to adrenal insuf ciency if not corrected is common. Such elevation can lead to protein and mineral de ciencies with increased osteoporosis and reduced steroid precursors for normal estrogen and testosterone production. Detoxi cation changes often involve reduction in one or more Phase II pathways which causes excess free radical production. Impaired digestive enzymes can reduce breakdown of foods, with larger more antigenic molecules being absorbed and consequent food intolerances. Many of these conditions are treatable. There is extensive overlap of MCS with Chronic Fatigue Syndrome and Fibromyalgia which may be one condition in many cases. Current occupational exposure limits are not health based and thus may not prevent MCS and are totally inadequate to accommodate sensitive persons. Warning symptoms indicating increased risk for MCS onset include repeated headache, eye and respiratory irritation and fatigue. Eliminating exposures which cause repeated symptoms is a critical strategy for preventing sensitization and MCS. It also signi cantly reduces the degree of disability in persons with MCS, the single most important factor from the literature. Affected persons with disability can utilize the Americans With Disability Act to request reasonable accommodations for work, home (condo, apartment), and school.

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Occupational Solvent Exposure and Glomerulonephritis

Cited by 44 publications

References 42 publications

Mixed Organic Solvents Induce Renal Injury in Rats

Mixed Organic Solvents Induce Renal Injury in Rats

Unusual cases of crescentic glomerulonephritis with normal renal function at diagnosis: a retrospective case series from a single center in Western China

Profile of Patients with Chemical Injury and Sensitivity, Part II

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