The Effects of Cyclosporine Versus Standard Care in Dogs With Naturally Occurring Glomerulonephritis

Vaden, Shelly L.; Breitschwerdt, Edward B.; Armstrong, Peter; Correa, María T.; Brown, Cathy A.; Polzin, David J.; Brace, James J.; DiBartola, Stephen P.; Barsanti, Jeanne A.; Crowell, Wayne A.; Jans, H; Dimski, Donna S.; Bartges, Joseph W.

doi:10.1111/j.1939-1676.1995.tb01077.x

Cited by 27 publications

(16 citation statements)

References 27 publications

(4 reference statements)

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“…Although cyclosporine A itself can also result in interstitial fibrosis, we noticed no effect of cyclosporine A on the interstitial area in either normal dogs or affected male dogs. This may be a reflection of the drug levels maintained in this study; these values have been shown to be safe for use in dogs (26). Similarly, the patients with Alport syndrome who received cyclosporine A were reported to show no evidence of toxicity on biopsy (21), although no morphometry was done.…”

Section: Discussionmentioning

confidence: 77%

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Cyclosporine A Slows the Progressive Renal Disease of Alport Syndrome (X-Linked Hereditary Nephritis)

Chen¹,

Jefferson²,

Harvey³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Alport syndrome refers to a hereditary disorder characterized by progressive renal disease and a multilaminar appearance to the glomerular basement membrane (GBM). In a small group of patients with Alport syndrome, cyclosporine A was reported to decrease proteinuria and maintain stable renal function over 7 to 10 yr of follow-up. The present study examined the effect of cyclosporine A on GBM structure and the progression to renal failure in a canine model of X-linked Alport syndrome. Affected male dogs and normal male dogs treated with cyclosporine A underwent serial renal biopsies. Body weight, serum concentrations of creatinine and albumin, and GFR were sequentially determined. Controls consisted of untreated dogs that developed end-stage renal failure by 8 mo of age. Renal biopsies were assessed for glomerulosclerosis and the percent of multilaminar GBM as measured by image analysis. Significant differences were found between treated and untreated affected dogs for weight, serum creatinine, and GFR. There was a significant delay in the progression of multilaminar change to the GBM, although treated affected dogs at termination had attained approximately 100% split GBM as did untreated affected dogs. A significant difference in the number of sclerotic glomeruli was also noted; treated dogs rarely developed obsolete glomeruli during the period studied. Interstitial fibrosis was not significantly affected by cyclosporine A treatment. These findings indicate that cyclosporine A is beneficial in slowing, but not stopping, the clinical and pathologic progression of Alport syndrome. At least part of this beneficial effect comes from a delayed deterioration of GBM structure, which in turn may be related to glomerular hemodynamics altered by cyclosporine A.

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Section: Discussionmentioning

confidence: 77%

“…This dose was adjusted to maintain trough concentrations (16 h after the last dose) between 100 and 400 ng/ml. By 6 mo of age, the desired trough concentrations were attained at the recommended daily dose rate of approximately 10 mg/kg (26). Cyclosporine A was administered throughout the duration of the study.…”

Section: Subjectsmentioning

confidence: 99%

Cyclosporine A Slows the Progressive Renal Disease of Alport Syndrome (X-Linked Hereditary Nephritis)

Chen¹,

Jefferson²,

Harvey³

et al. 2003

Journal of the American Society of Nephrology

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“…Uncommonly, cyclosporine may cause idiosyncratic hepatotoxicity, which does not seem to be dose‐dependent; gingival hyperplasia and hypertrichosis also have been reported occasionally . Nephrotoxicity is a potential problem in people receiving cyclosporine, but clinically relevant renal damage has not been documented in dogs at standard dosages …”

Section: Results and Recommendationsmentioning

confidence: 99%

ACVIM consensus statement on the treatment of immune‐mediated hemolytic anemia in dogs

Swann

Garden

Fellman

et al. 2019

Veterinary Internal Medicne

187

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Immune‐mediated hemolytic anemia (IMHA) causes severe anemia in dogs and is associated with considerable morbidity and mortality. Treatment with various immunosuppressive and antithrombotic drugs has been described anecdotally and in previous studies, but little consensus exists among veterinarians as to the optimal regimen to employ and maintain after diagnosis of the disease. To address this inconsistency and provide evidence‐based guidelines for treatment of IMHA in dogs, we identified and extracted data from studies published in the veterinary literature. We developed a novel tool for evaluation of evidence quality, using it to assess study design, diagnostic criteria, explanation of treatment regimens, and validity of statistical methods. In combination with our clinical experience and comparable guidelines for humans afflicted with autoimmune hemolytic anemia, we used the conclusions of this process to make a set of clinical recommendations regarding treatment of IMHA in dogs, which we refined subsequently by conducting several iterations of Delphi review. Additionally, we considered emerging treatments for IMHA in dogs and highlighted areas deserving of future research. Comments were solicited from several professional bodies to maximize clinical applicability before the recommendations were submitted for publication. The resulting document is intended to provide clinical guidelines for management of IMHA in dogs. These guidelines should be implemented pragmatically, with consideration of animal, owner, and veterinary factors that may vary among cases.

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“…The cyclosporine‐cyclophilin complex inhibits calcineurin, which is essential for the transcription of interleukin 2 and interleukin 2 activation of T lymphocytes . The effectiveness of cyclosporine in dogs with spontaneous glomerular disease has been evaluated in a randomized, controlled clinical trial, but was found to provide little apparent benefit . A limitation of this study was the lack of precise pathologic characterization of the tested glomerular diseases for evidence of active immune‐mediated injury potentially responsive to cyclosporine.…”

Section: Drug Options For Immunosuppressive Therapy Of Glomerular Dismentioning

confidence: 99%

Consensus Recommendations for Immunosuppressive Treatment of Dogs with Glomerular Disease Based on Established Pathology

Segev

Cowgill

Heiene

et al. 2013

Veterinary Internal Medicne

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The purpose of this report was to provide consensus recommendations for the use of immunosuppressive therapy in dogs with active glomerular diseases. Recommendations were developed based on comprehensive review of relevant literature on immunosuppressive therapy of glomerular disease in dogs and humans, contemporary expert opinion, and anecdotal experience in dogs with glomerular disease treated with immunosuppression. Recommendations were subsequently validated by a formal consensus methodology. The Study Group recommends empirical application of immunosuppressive therapy for dogs with severe, persistent, or progressive glomerular disease in which there is evidence of an active immunemediated pathogenesis on kidney biopsy and no identified contraindication to immunosuppressive therapy. The most compelling evidence supporting active immune-mediated mechanisms includes electron-dense deposits identified with transmission electron microscopic examination and unequivocal immunofluorescent staining in the glomeruli. For diseases associated with profound proteinuria, attendant hypoalbuminemia, nephrotic syndrome, or rapidly progressive azotemia, single drug or combination therapy consisting of rapidly acting immunosuppressive drugs is recommended. The Study Group recommends mycophenolate alone or in combination with prednisolone. To minimize the adverse effects, glucocorticoids should not be used as a sole treatment, and when used concurrently with mycophenolate, glucocorticoids should be tapered as quickly as possible. For stable or slowly progressive glomerular diseases, the Study Group recommends mycophenolate or chlorambucil alone or in combination with azathioprine on alternating days. Therapeutic effectiveness should be assessed serially by changes in proteinuria, renal function, and serum albumin concentration. In the absence of overt adverse effects, at least 8 weeks of the rapidly acting nonsteroidal drug therapy and 8-12 weeks of slowly acting drug therapy should be provided before altering or abandoning an immunosuppressive trial.

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The Effects of Cyclosporine Versus Standard Care in Dogs With Naturally Occurring Glomerulonephritis

Cited by 27 publications

References 27 publications

Cyclosporine A Slows the Progressive Renal Disease of Alport Syndrome (X-Linked Hereditary Nephritis)

Cyclosporine A Slows the Progressive Renal Disease of Alport Syndrome (X-Linked Hereditary Nephritis)

ACVIM consensus statement on the treatment of immune‐mediated hemolytic anemia in dogs

Consensus Recommendations for Immunosuppressive Treatment of Dogs with Glomerular Disease Based on Established Pathology

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