Bodybuilders and kidney damage

I'll post here an old article (2009) from "The New York Times"

After this article adding the studies mentioned. Don't know about you, but I find it damned interesting.

Many competitive bodybuilders take anabolic steroids to achieve their freakishly exaggerated physiques. That is no secret. But steroids can be only one part of an extreme regimen that can wreak havoc on the body.
Human growth hormone, supplements, painkillers and diuretics can also be used to create the “shrink-wrapped” muscles so prized in the aesthetic. And the high concentration of muscle mass puts stress on the body, as if the lifter were obese.

Lifting weights in the gym is “extremely healthy for you,” said Kenneth Wheeler, a former elite bodybuilder known as Flex. “But if you want to be a bodybuilder and compete at the highest level, it has nothing to do with health.” A relatively rare form of kidney disease forced Wheeler to retire in 2003 at age 37, and he needed a kidney transplant later that year.

Determining the extent of the damage that bodybuilders inflict on themselves is difficult, in part because there is little interest in financing studies on such an extreme group, and because bodybuilders are not always honest about what they take. That is why a case study published last month by a top kidney journal is generating interest in the nephrology and bodybuilding communities. It is among the first to assert a direct link between long-term steroid use and kidney disease.

The study began 10 years ago when a kidney pathologist at Columbia University Medical Center in New York noticed that a bodybuilder had an advanced form of kidney disease. Curious, she started looking for similar cases and eventually studied 10 men with serious kidney damage who acknowledged using steroids. Nine were bodybuilders and one was a competitive powerlifter with a similar training routine.

All 10 men in the case series, published in November by the Journal of the American Society of Nephrology, showed damage to the filters of the kidney. Nine had an irreversible disease known as focal segmental glomerulosclerosis — the same disease contracted by Wheeler — even though the men in the study did not have other apparent risk factors. Their disease was worse than in obese patients with a higher body-mass index, suggesting that steroids — combined with the other practices — might be harming the kidneys.

Among the study’s most persuasive details is the story of a man, 30 years old at the time, who damaged his kidneys after more than a decade of bodybuilding. The patient’s condition improved after he stopped using the drugs, discontinued his regimen and lost 80 pounds. But it worsened after the man, who became depressed, returned to bodybuilding and steroids.

“These patients are likely the tip of the iceberg,” said Vivette D. D’Agati, the lead researcher. “It’s a risk. A significant risk.”

Several experts not affiliated with the study said that while the claims were intriguing, the study’s value was limited because it focused only on intensive steroid users and because the bodybuilders’ layered training practices had to be taken into account. “I think it’s hard to be certain what’s causing their kidney disease,” said William Bremner, chairman of the Department of Medicine at the University of Washington and an endocrinologist who studies steroids.

D’Agati said, “It’s probably multiple factors that are converging in these patients, but the common entity in all of them is anabolic steroids.”

One participant in the study, Patrick Antonecchia (picture), 46, competed in powerlifting and strong man events for more than 25 years and said he used steroids, supplements and a high-protein diet to attain feats such as pulling a 40,000-pound truck. He ended his career and stopped using steroids about a year ago, and in February received a diagnosis of serious kidney damage. His doctors warned him not to use the drugs again. “They said: ‘Pat. Don’t. Because it comes back,’ ” he said.

Antonecchia has lost about 50 pounds and said he misses the attention his 290-pound frame attracted: “The toughest thing now is it was my identity for 25 years. Now, when people see me, they say, ‘What happened to you?’ ”

Jerry Brainum writes a column for Iron Man Magazine called Bodybuilding Pharmacology and said he welcomes more research on the subject. “I found it very alarming, quite frankly,” Brainum said.

Since the 1990s, at least eight accomplished bodybuilders have died at a young age, and in addition to Wheeler, another six were forced to stop competing because of serious illness, often involving kidney disease.
The main source of information for bodybuilders is word of mouth and experimentation, Brainum said. “These guys have no guidance, they talk among themselves, and they don’t even tell the truth to each other,” he said.

The risk-taking has been made worse by a trend toward ever larger physiques among the sport’s top competitors, some said. Jay Cutler, who won the 2009 Mr. Olympia contest, weighs almost 40 pounds more than Arnold Schwarzenegger did when he won the title in 1974, even though Cutler is five inches shorter.

“Each decade you have a guy that comes along that sets new standards and you say O.K., now I’m going to have to take it to the next level,” said Shahriar Kamali, a professional bodybuilder known as King.

The International Federation of Body Building and Fitness reserves the right to test for steroids and human growth hormone at the professional level, and testing is done on a random basis, said Bob Cicherillo, athlete representative for the federation, which is the main governing body for bodybuilding.

But several bodybuilders said the testing was nearly nonexistent, and Cicherillo said he could not provide specific figures on competitors who tested positive. In addition, the chairman of the organization’s medical commission, Robert M. Goldman, is a leading champion of the anti-aging effects of human growth hormone, a drug that is banned by most sports governing bodies.

James Manion, who runs the professional division of the federation, did not return several calls seeking comment.

Some bodybuilders expressed doubt that their practices were dangerous, pointing to former competitors who are still healthy in their 70s. They attributed the deaths of elite bodybuilders to the abuse of over-the-counter painkillers and diuretics, not steroids. The bodybuilding federation tests for diuretics at professional events, although competitors said they are still used.

Bodybuilders said that they were unfairly singled out as drug abusers when athletes in most other sports were also using performance-enhancing drugs. “Like anything else, it’s use and abuse,” Cicherillo said. “We’re the ones who are visual. We’re the ones who walk around, and you see us with the big muscles.”

Wheeler said he was convinced steroid use did not cause his kidney disease, although it might have made it worse.

The patient whose case was the centerpiece of the kidney study said he was most likely predisposed to develop the condition. “The drugs weren’t the reason I got sick,” said the man, who declined to be identified because his steroid use was illegal. After taking a year off from steroids and bodybuilding because of the kidney disease, the man, age 34, is returning to competition. His symptoms have worsened, a sacrifice he said he is willing to accept.

“It’s just really hard to walk away from it,” he said. “I know I can only do this until my early 40s, so I really want to give it my all now.”


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.

Index Case



The index case (patient 1) is a 30-yr-old white male professional bodybuilder who had no significant medical history and presented to a local hospital with lower extremity edema. The patient was on no prescription medications, but as part of his bodybuilding regimen, he regularly consumed a high-protein diet (>550 g/d) and dietary supplements including 10 g/d creatine monohydrate, 1000 mg/d branched-chain amino acids, 10 g/d glutamine, and multivitamins. For more than a decade, he regularly used anabolic androgenic steroids (AASs), including injectable testosterone, methyl-1-testosterone (taken orally), growth hormone, and insulin to augment his bodybuilding. At the time of biopsy, his steroid regimen consisted of growth hormone 4 IU 5 d/wk and testosterone 500 mg intramuscularly twice weekly. In addition, he took 75 mg of ephedrine and 600 mg of caffeine before each workout session.

Physical examination revealed a height of 71 inches (180 cm), a weight of 295 pounds (134 kg), and a body mass index (BMI) of 41.2 kg/m2 with an extremely muscular, highly toned physique. BP was 145/80 mmHg, and there was 2+ bilateral lower extremity edema. The patient was found to have a serum creatinine of 2.7 mg/dl, blood urea nitrogen of 24 mg/dl, serum albumin of 1.9 g/dl, total serum protein of 5.7 g/dl, serum cholesterol of 212 mg/dl, hematocrit of 45%, and white blood cell count of 10.3 × 109/L with a normal differential and platelet count of 254 × 109/L. Serum glucose and electrolytes including sodium, potassium, bicarbonate, chloride, and calcium were within normal limits. Serologic evaluation revealed a borderline positive ANA (titer 1:80 with a homogeneous pattern) with negative anti–double-stranded DNA antibody and negative viral serologies including HIV, hepatitis B surface and core antigens, and hepatitis C antibody. Serum complement levels including C3, C4, and CH50 were within normal limits. Urinalysis revealed 4+ protein, and microscopic examination showed fewer than five red blood cells per high-power field and no white blood cells or casts. Twenty-four-hour urine collection revealed proteinuria of 26.3 g/d and creatinine clearance (CrCl) of 91 ml/min. A renal biopsy was performed in August 2004 to determine the cause of the patient's nephrotic syndrome.

I won't post all the technical data, if someone is interested he can mail me for the PDF

Although his renal function and proteinuria had significantly improved, the patient reported symptoms of severe depression related to changes in body image. He perceived himself as being too “skinny and weak” and complained of decreased libido. He wanted to resume bodybuilding but agreed to a reduced exercise regimen without supplements or hormones. Two months after restarting his exercise regimen, his weight increased to 267 lbs, his serum creatinine was 1.4 mg/dl, 24-h urine protein was 395 mg/d, and CrCl was 200 ml/min. At his next office visit, the patient reported feeling well but was dissatisfied with the muscle mass that he was able to achieve without supplements and hormones. Against his nephrologist's advice, he resumed his high-protein diet as well as the dietary supplements, testosterone, and growth hormone but at lower levels than previously. Six weeks after restarting supplements and hormones, his serum creatinine increased to 2.3 mg/dl and proteinuria increased to 4.7 g/d. He was advised to stop using supplements and hormones, decrease his protein intake, and decrease his workout regimen. The patient failed to comply, and 3.5 yr after restarting bodybuilding with hormones and supplements, the patient weighed 296 lbs (BMI 41.3 kg/m2) with creatinine of 2.4 mg/dl and 24-h urine protein of 14.1 g/d.

The dramatic improvement in renal parameters (including complete remission of proteinuria) achieved by stopping AASs, decreasing exercise, losing weight, and renin-angiotensin system (RAS) blockade, without resorting to immunosuppressive therapy, followed by relapse of nephrotic-range proteinuria and worsening of renal function after resumption of a full bodybuilding regimen strongly supports a secondary form of FSGS. We propose that abuse of AASs causes a secondary form of FSGS both by increasing lean body mass and by potential direct toxic effects on glomeruli.