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In this thread, I will address the question of whether AAS abuse leads to kidney damage. Furthermore, I will examine through which mechanisms this happens, and speculate what preventative measures bodybuilders could take.
Let's start by reviewing the (case) studies on AAS and kidney disease in humans. There is surprisingly little information on the relationship between AAS abuse and kidney damage, with case studies popping up only recently.
1) Herlitz et al. (2010)
The first thing to note is that with these case studies, we cannot prove that the AAS abuse is the cause for the kidney disease. It could be that other (genetic and lifestyle factors) caused the kidney damage. After all, there are tens of thousands of bodybuilders in the US who are on similar cycles as the study subjects and don't develop symptoms severe enough to seek medical attention. That being said, these case studies do strongly suggest that the AAS abuse played a causal role, based on the changes over time observed for each individual.
Take for example the following chart detailing the creatinine and proteinuria levels of a patient. Upon cessation of AAS use (and supplements and training), both parameters improved quickly and dramatically, only to increase again once the patient resumed his regimen. Unless you suspect the training and supplements to be the culprit (which is very unlikely), you can with high confidence conclude that the AAS caused the kidney damage as measured by worse kidney filtration and leaking of protein (both are imperfect measures in bodybuilders, but the trends are clear).
All patients in this study were diagnosed with secondary Focal segmental glomerulosclerosis (FSGS) caused by a combination of high lean mass and AAS abuse.
However, the patients' clinical features and biopsy results were different than typically observed in FSGS: the degree of proteinuria was higher, there was higher levels of global (in addition to the segmental) glomerulosclerosis, more of the glomeruli were affected, and there was much more interstitial scarring. So overall more severe and characteristically unique presentation of AAS induced FSGS.
Despite this, only one out of 8 patients with follow-up developed into full blown kidney failure. The remaining 7 patients' kidney function stabilized upon ceasing AAS abuse and lowering their lean mass (plus some ACEi/ARB treatment).
2) Gollasch et al. (2018)
This guy wasn't as lucky, his FSGS was too advanced and his kidney function did not recover.
There's a couple of take away points from this study. First, the authors argue that his FSGS developed over years until the damage was too much to recover from. So a lesson is to continuously monitor your kidney function to if necessary pull the plug in time. Second, the authors point to the importance of genetic factors. They identify a number of risk factors in the patient's DNA that could predispose him to developing FSGS. So the reason why AAS abuse leads to FSGS in some bodybuilders but not others may come down to genetic factors. Basically, your genes determine how much AAS your organs can take before failing. However, we don't know our DNA and whether we have those (poorly understood) risk factors. Again, the lesson is to do regular check ups, given that you could be one of the people who are predisposed.
Next, the kidney biopsy revealed signs of long standing hypertension. Upon admission, the patient's BP was 146/90. This is despite the fact that he was on prescribed Telmisartan and a diuretic at the time! This is another important lesson, you have to adjust your BP meds and dosages based on your BMI and based on the AAS (dosage) you are currently taking. Furthermore, just an ARB or ACEi may be insufficient to adequately control blood pressure. Especially when on a highly androgenic drug regimen, you need to also take care of the neurohormonal pathway via beta blockers.
The authors conclude that the combination of high lean mass, PED abuse, genetic factors, and hypertension lead to the kidney failure.
3) Garcia et al. (2017)
Another case study that drives home the point of how important blood pressure management is when on AAS. As we will discuss later, increases in blood pressure are one of the channels through which AAS use damages the kidneys. The case study only focuses on the short term management of the hypertensive crisis, but it is reasonable to assume that the untreated hypertension and AAS abuse over years lead to kindney failure which then pushed him into hypertensive crisis.
4) El-Reshaid et al. (2018)
Another very recent study that is suggestive about the development of different types of renal damage over time when abusing AAS. Only 8 of the 22 patients had developed FSGS, and those that did had a longer exposure to AAS. Interstitial fibrosis and other forms of renal damage are associated with shorter AAS exposure and have a better prognosis. This is neatly in line with Gollasch et al. (2018) who suspect that their patient's FSGS developed over many years rather than being acute onset. Also interesting is the presence of nephrocalcinosis in 2 patients. Possibly related to excess Vitamin D and calcium intake? In any case, don't overdose on VitD and do take sufficient VitK2 with it to be safe.
In the next part, I'm gonna review the animal studies available. But based on the human studies alone, one should conclude that yes, AAS leads to kidney damage, with the extent depending on genetic predisposition, the steroids used, dosages, blood pressure control, (lean) body mass, hydration, etc.
Let's start by reviewing the (case) studies on AAS and kidney disease in humans. There is surprisingly little information on the relationship between AAS abuse and kidney damage, with case studies popping up only recently.
1) Herlitz et al. (2010)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799287/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.
The first thing to note is that with these case studies, we cannot prove that the AAS abuse is the cause for the kidney disease. It could be that other (genetic and lifestyle factors) caused the kidney damage. After all, there are tens of thousands of bodybuilders in the US who are on similar cycles as the study subjects and don't develop symptoms severe enough to seek medical attention. That being said, these case studies do strongly suggest that the AAS abuse played a causal role, based on the changes over time observed for each individual.
Take for example the following chart detailing the creatinine and proteinuria levels of a patient. Upon cessation of AAS use (and supplements and training), both parameters improved quickly and dramatically, only to increase again once the patient resumed his regimen. Unless you suspect the training and supplements to be the culprit (which is very unlikely), you can with high confidence conclude that the AAS caused the kidney damage as measured by worse kidney filtration and leaking of protein (both are imperfect measures in bodybuilders, but the trends are clear).
All patients in this study were diagnosed with secondary Focal segmental glomerulosclerosis (FSGS) caused by a combination of high lean mass and AAS abuse.
https://www.kidney.org/atoz/content/focalMany diseases and conditions can affect your kidney function by attacking and damaging the glomeruli, the tiny filtering units inside your kidney where blood is cleaned. These diseases and conditions are called glomerular diseases and can have many different causes. Focal Segmental glomerulosclerosis is a type of glomerular disease and describes scarring (sclerosis) in your kidney. The scarring of FSGS only takes place in small sections of each glomerulus (filter), and only a limited number of glomeruli are damaged at first.
However, the patients' clinical features and biopsy results were different than typically observed in FSGS: the degree of proteinuria was higher, there was higher levels of global (in addition to the segmental) glomerulosclerosis, more of the glomeruli were affected, and there was much more interstitial scarring. So overall more severe and characteristically unique presentation of AAS induced FSGS.
Despite this, only one out of 8 patients with follow-up developed into full blown kidney failure. The remaining 7 patients' kidney function stabilized upon ceasing AAS abuse and lowering their lean mass (plus some ACEi/ARB treatment).
2) Gollasch et al. (2018)
https://www.karger.com/Article/FullText/489087We present a 42-year-old man with a BMI of 32, who was referred because of proteinuria and decreased renal function. We were impressed by his markedly muscular physique. A renal biopsy was performed, which showed focal segmental glomerular sclerosis (FSGS). Is this patient merely an obese person with FSGS or is something else going on here?
[...]
The patient was a German professional bodybuilder who was not fat despite a BMI of 32 that classified him as an obese person (obesity class 2). He used progressive resistance exercise to develop his musculature from the age of 18–39 years. As part of his bodybuilding regimen, he consumed anabolic steroids, muscle growth-stimulating substances, and high-protein, low-fat diets. For more than 6 months until admission to our hospital, he resumed progressive resistance exercise and also regularly used anabolic androgenic steroids, including testosterone enanthate (depot 250 mg × 2/week, i.m.), recombinant growth hormone (somatotropin 2× 2 IU/day, i.m.), and boldenone 200 mg × 2/week, i.m. In addition, he administered trenbolone enanthate (TrENOL 100) 100 mg × 1/week, i.m. and methandienone (Metabolon) 10 mg × 3/day, p.o., and consumed a high-protein, low-fat diet: protein 1,326 kcal (42.8%), carbohydrate 1,615 kcal (52.1%), fat 160 kcal (5.1%), and vitamins, spread over 6 meals a day. Our patient reported intense training sessions within the past weeks.
This guy wasn't as lucky, his FSGS was too advanced and his kidney function did not recover.
There's a couple of take away points from this study. First, the authors argue that his FSGS developed over years until the damage was too much to recover from. So a lesson is to continuously monitor your kidney function to if necessary pull the plug in time. Second, the authors point to the importance of genetic factors. They identify a number of risk factors in the patient's DNA that could predispose him to developing FSGS. So the reason why AAS abuse leads to FSGS in some bodybuilders but not others may come down to genetic factors. Basically, your genes determine how much AAS your organs can take before failing. However, we don't know our DNA and whether we have those (poorly understood) risk factors. Again, the lesson is to do regular check ups, given that you could be one of the people who are predisposed.
Next, the kidney biopsy revealed signs of long standing hypertension. Upon admission, the patient's BP was 146/90. This is despite the fact that he was on prescribed Telmisartan and a diuretic at the time! This is another important lesson, you have to adjust your BP meds and dosages based on your BMI and based on the AAS (dosage) you are currently taking. Furthermore, just an ARB or ACEi may be insufficient to adequately control blood pressure. Especially when on a highly androgenic drug regimen, you need to also take care of the neurohormonal pathway via beta blockers.
The authors conclude that the combination of high lean mass, PED abuse, genetic factors, and hypertension lead to the kidney failure.
3) Garcia et al. (2017)
**broken link removed**We report the case of a 37-year-old male with hypertension known for the last 10 years, with no treatment, who regularly practised bodybuilding; took intramuscular anabolic steroids (testosterone and stanozolol), growth hormone and oral creatine; and followed a protein-rich diet. He visited the Emergency Department due to signs and symptoms of general malaise, nausea, headache and blurred vision that had lasted for one week. He was found to have high BP (250/180mmHg) and severe acute kidney failure. Complementary tests revealed anaemia and thrombocytopenia (haemoglobin 9.9g/dl, haematocrit 28.4%, platelets 91,000/mm3) as well as the above-mentioned kidney failure (urea 246mg/dl, creatinine 23.5mg/dl). An immunology study was negative (except for a slight decrease in C3 and C4 fraction), with proteinuria of 1.7g/24h and oligoalbuminuria of 491mg/l.
Another case study that drives home the point of how important blood pressure management is when on AAS. As we will discuss later, increases in blood pressure are one of the channels through which AAS use damages the kidneys. The case study only focuses on the short term management of the hypertensive crisis, but it is reasonable to assume that the untreated hypertension and AAS abuse over years lead to kindney failure which then pushed him into hypertensive crisis.
4) El-Reshaid et al. (2018)
https://www.ncbi.nlm.nih.gov/pubmed/29657200We report our experience of renal disease associated with bodybuilders who had been on high-protein diet, anabolic androgenic steroids (AASs), and growth hormone (GH) for years. A total of 22 adult males who volunteered information about use of high protein diet and AAS or GH were seen over a six-year period with renal disease. Kidney biopsy revealed focal segmental glomerulosclerosis (FSGS) in eight, nephroangiosclerosis in four, chronic interstitial nephritis in three, acute interstitial nephritis in two, nephrocalcinosis with chronic interstitial nephritis in two, and single patients with membranous glomerulopathy, crescentic glomerulopathy, and sclerosing glomerulonephritis. Patients with FSGS had a longer duration of exposure, late presentation, and worse prognosis. Those with interstitial disease had shorter exposure time and earlier presentation and had improved or stabilized after discontinuation of their practice. There is a need for health education for athletes and bodybuilders to inform them about the risks of renal disease involved with the use of high-protein diet, AAS, and GH.
Another very recent study that is suggestive about the development of different types of renal damage over time when abusing AAS. Only 8 of the 22 patients had developed FSGS, and those that did had a longer exposure to AAS. Interstitial fibrosis and other forms of renal damage are associated with shorter AAS exposure and have a better prognosis. This is neatly in line with Gollasch et al. (2018) who suspect that their patient's FSGS developed over many years rather than being acute onset. Also interesting is the presence of nephrocalcinosis in 2 patients. Possibly related to excess Vitamin D and calcium intake? In any case, don't overdose on VitD and do take sufficient VitK2 with it to be safe.
In the next part, I'm gonna review the animal studies available. But based on the human studies alone, one should conclude that yes, AAS leads to kidney damage, with the extent depending on genetic predisposition, the steroids used, dosages, blood pressure control, (lean) body mass, hydration, etc.