Glomerulonephritis Human

A number of studies in humans show that PUFAs can generate significant immunomodulatory effects. Generally, these studies have utilized considerably lower amounts of fish oil to treat subjects than found in most animal studies. Numerous clinical trials have examined the effects of fish oil on rheumatoid arthritis and many have reported statistically significant benefits such as decreased morning stiffness and numbers of tender joints [57]. Several other studies have reported that PUFAs can provide therapeutic benefits for patients with IgA nephropathy, the most common primary human glomerulonephritis... 

Complement is involved not only in attacking foreign cells but in inflammation. Unfortunately, this is sometimes accompanied by serious problems. Human diseases in which complement is thought to be involved include glomerulonephritis, rheumatoid arthritis, myasthenia gravis, and lupus erythematosus. 

Various experimental procedures were described as models for glomerulonephritis in human beings. Most of them were developed in rats and rabbits. They involve the reactions of antibodies against renal components, such as Masugi nephritis (Masugi and Sato 1934), Heymann nephritis (Heymann 1959), nephrotoxic serum nephritis (Unanue and Dixon 1967), crescentic type anti-glomerular membrane nephritis (Nagoe et al. 1994, 1998), anti-Thyl nephritis (Chen etal. 1999). 

Moreover, MRL Mpf lpr/lpr (MRL/lpr)-mice were described which spontaneously develop a severe disease with many symptoms very similar to human systemic lupus erythematodes, i.e. hypergammaglobulinemia, and glomerulonephritis (Theofilopoulos and Dixon 1981). 

Thaiss et al. (1989) evaluated the effect of the immunosuppressant cyclosporin A on an active model of in situ immune complex glomerulonephritis. Wistar rats were preimmunized with human IgG and 2weeks after the last antigen injection, the left kidney was perfused with cationized human IgG in order to induce unilateral in situ immune complex glomerulonephritis. 

In the kidney, clusterin is a component of immune deposits and its expression is increased after ischemia or obstruction. In gentamicin-treated rats, an increase in urinary clusterin protein may provide an early sign of nephrotoxicity [336]. In rats with unilatertral ureteral obstruction, clusterin mRNA and clusterin-beta have been detected in the kidney along with clusterin-alpha in the urine [337]. A central role for glomerular clusterin as a modulator of inflammation that potentially influences the chnical outcome in human membranous glomerulonephritis has been described [338]. 

Segawa C, WadaT,Takaeda M, Eurulchl K, Matsuda I, HIsada Y, Ohta S,Takasawa K,Takeda S, Kobayashi K, Yokoyama H. 1997./n s/ fu expression and soluble form of P-selectIn In human glomerulonephritis. Kidney Int 1997 52 1054-1063. 

Takaeda M, Yokoyama H, Segawa-Takaeda C, Wada T, Kobayashi K. 2002. High endothelial venule-llke vessels In the Interstitial lesions of human glomerulonephritis. Am J Nephrol. 22 48-57. 

Roy-Chaudhury P, Wu B, King G, Campbell M, Macleod AM, Flaites NE, Simpson JG, Power DA. Adhesion molecule interactions in human glomerulonephritis importance of the tubulointerstitium. Kidney Int. 1996 49 127-34. 

Lerner RA, Glassock RJ, Dixon FJ. The role of anti-glomerular basement membrane antibody in the pathogenesis of human glomerulonephritis. J Exp Med. 1967 126 989-1004. 

Other manifestations of mTOR inhibitor renal effects are delayed recovery from ischemic renal injury. In rats not on cyclosporine, siroiimus impairs recovery from acute renal ischemia [785]. Human series describe delayed recovery from post-transplant ischemic injury, and worsening function in glomerulonephritis in the presence of siroiimus [786-787]. Few studies have tested TAC and everoiimus for similar changes [788]. 

Turpentine is a skin, eye, mucous membrane, and upper respiratory tract irritant in humans. It may also cause skin sensitization and adverse effects to CNS, gastrointestinal, and urinary tract. The lowest estimated oral dose reported to be lethal in humans is 441 mg kg Exposure to a 75 ppm concentration for 3-5 min irritates the nose and throat, and exposure to a 175 ppm concentration irritates the eyes and may be considered intolerable by human volunteers. Ingestion of turpentine causes a burning pain in the mouth and throat, nausea, vomiting, diarrhea, abdominal pain, excitement, ataxia, confusion, stupor, seizures, fever, and tachycardia and may cause death due to respiratory failure. Toxic glomerulonephritis and bladder irritation, with hematuria, albuminuria, oliguria, and dysuria, have been associated with overexposure to the vapor of turpentine in the past however, the more purified form... 

Thirteen different hydrocarbons, including aliphatics, aromatics, carbon tetrachloride, trichloroethylene, and other halogenated aliphatics, have been shown to cause glomerulonephritis (an inflammation of the kidney that can lead to loss of kidney function and hypertension) in laboratory animals and humans (see and references contained therein). 

Munger KA, Montero A, Fukunaga M, Uda S, Yura T, Imai E, Kaneda Y, Valdivielso JM, Badr KF (1999) Transfection of rat kidney with human 15-lipoxygenase suppresses inflammation and preserves function in experimental glomerulonephritis. Proc Natl Acad Sci USA 96 13375-13380... 

Hg is one of the few chemicals which is able to induce loss of tolerance to self-antigens in animals. This effect is human leukocyte antigen (HLA) dependent and has been demonstrated in genetically susceptible strains of rats and mice. Brown-Norway rats injected with Hg chloride (HgCl2) produce antilaminin antibodies, which attack the kidneys, causing an autoimmime glomerulonephritis (Dmet et al. 1994). The... 

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