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If you remember from past posts, after a life insurance exam found protein in my urine, I went for a biopsy and was diagnosed with FSGS (focal segmental glomerularsclerosis), a condition where there is scarring of the renal glomerus which allows protein to leak into the urine. Recently this condition has been tentatively linked to steroid use (see article below).
For treatment I have been prescribed an ACE inhibitor as I only have a mild form and I get regular screening to measure the amount of protein in the urine. 6 months ago, I was on a relatively high dose test and masteron cycle and my protein content was around 500mg. 2 months ago, I was off-cycle for several weeks and my protein content was 400mg. After that test, I started a test e/tren e cycle and a week ago, my test showed 1700mg of protein (over 400% increase). Based on my analysis of my lifestyle and supplementation, I can come to no other conclusion that that it is the tren which is responsible for the increase.
Development of Focal Segmental Glomerulosclerosis after Anabolic Steroid Abuse
Leal C. Herlitz*, Glen S. Markowitz*, Alton B. Farris, Joshua A. Schwimmer,, Michael B. Stokes*, Cheryl Kunis, Robert B. Colvin and Vivette D. D’Agati*
* Departments of Pathology and
Medicine, Columbia University, College of Physicians and Surgeons, New York, New York;
Department of Medicine, Lenox Hill Hospital, New York, New York; and
Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
Correspondence: Dr. Vivette D. D’Agati, Columbia University College of Physicians and Surgeons, Department of Pathology, VC14-224, 630 West 168th Street, New York, NY 10032. Phone: 212-305-7460; Fax: 212-342-5380; E-mail: [email protected]
Received for publication April 28, 2009. Accepted for publication September 17, 2009.
Anabolic steroid abuse adversely affects the endocrine system, blood lipids, and the liver, but renal injury has not been described. We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of 10 bodybuilders (six white and four Hispanic; mean body mass index 34.7) after long-term abuse of anabolic steroids. The clinical presentation included proteinuria (mean 10.1 g/d; range 1.3 to 26.3 g/d) and renal insufficiency (mean serum creatinine 3.0 mg/dl; range 1.3 to 7.8 mg/dl); three (30%) patients presented with nephrotic syndrome. Renal biopsy revealed FSGS in nine patients, four of whom also had glomerulomegaly, and glomerulomegaly alone in one patient. Three biopsies revealed collapsing lesions of FSGS, four had perihilar lesions, and seven showed 40% tubular atrophy and interstitial fibrosis. Among eight patients with mean follow-up of 2.2 yr, one progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received corticosteroids. All seven patients discontinued anabolic steroids, leading to weight loss, stabilization or improvement in serum creatinine, and a reduction in proteinuria. One patient resumed anabolic steroid abuse and suffered relapse of proteinuria and renal insufficiency. We hypothesize that secondary FSGS results from a combination of postadaptive glomerular changes driven by increased lean body mass and potential direct nephrotoxic effects of anabolic steroids. Because of the expected rise in serum creatinine as a result of increased muscle mass in bodybuilders, this complication is likely underrecognized.
For treatment I have been prescribed an ACE inhibitor as I only have a mild form and I get regular screening to measure the amount of protein in the urine. 6 months ago, I was on a relatively high dose test and masteron cycle and my protein content was around 500mg. 2 months ago, I was off-cycle for several weeks and my protein content was 400mg. After that test, I started a test e/tren e cycle and a week ago, my test showed 1700mg of protein (over 400% increase). Based on my analysis of my lifestyle and supplementation, I can come to no other conclusion that that it is the tren which is responsible for the increase.
Development of Focal Segmental Glomerulosclerosis after Anabolic Steroid Abuse
Leal C. Herlitz*, Glen S. Markowitz*, Alton B. Farris, Joshua A. Schwimmer,, Michael B. Stokes*, Cheryl Kunis, Robert B. Colvin and Vivette D. D’Agati*
* Departments of Pathology and
Medicine, Columbia University, College of Physicians and Surgeons, New York, New York;
Department of Medicine, Lenox Hill Hospital, New York, New York; and
Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
Correspondence: Dr. Vivette D. D’Agati, Columbia University College of Physicians and Surgeons, Department of Pathology, VC14-224, 630 West 168th Street, New York, NY 10032. Phone: 212-305-7460; Fax: 212-342-5380; E-mail: [email protected]
Received for publication April 28, 2009. Accepted for publication September 17, 2009.
Anabolic steroid abuse adversely affects the endocrine system, blood lipids, and the liver, but renal injury has not been described. We identified an association of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of 10 bodybuilders (six white and four Hispanic; mean body mass index 34.7) after long-term abuse of anabolic steroids. The clinical presentation included proteinuria (mean 10.1 g/d; range 1.3 to 26.3 g/d) and renal insufficiency (mean serum creatinine 3.0 mg/dl; range 1.3 to 7.8 mg/dl); three (30%) patients presented with nephrotic syndrome. Renal biopsy revealed FSGS in nine patients, four of whom also had glomerulomegaly, and glomerulomegaly alone in one patient. Three biopsies revealed collapsing lesions of FSGS, four had perihilar lesions, and seven showed 40% tubular atrophy and interstitial fibrosis. Among eight patients with mean follow-up of 2.2 yr, one progressed to ESRD, the other seven received renin-angiotensin system blockade, and one also received corticosteroids. All seven patients discontinued anabolic steroids, leading to weight loss, stabilization or improvement in serum creatinine, and a reduction in proteinuria. One patient resumed anabolic steroid abuse and suffered relapse of proteinuria and renal insufficiency. We hypothesize that secondary FSGS results from a combination of postadaptive glomerular changes driven by increased lean body mass and potential direct nephrotoxic effects of anabolic steroids. Because of the expected rise in serum creatinine as a result of increased muscle mass in bodybuilders, this complication is likely underrecognized.