Written by DR. GEORGE TOULIATOS, MD
07 April 2020

 RENAL-ISSUES -FROM-AAS-ABUSE

Dr. Testosterone
By George Touliatos, MD

 

Renal Issues From AAS Abuse

 

The abuse of AAS adversely affects renal function through direct and indirect mechanisms. Firstly, AAS have a direct toxic effect on glomeruli and are associated with the development of focal segmental glomerulosclerosis and tubular necrosis. On the other hand, rhabdomyolysis, high protein/creatine intake, inadequate hydration, and high incidence of polydrug use are other factors that contribute to a rapid decline in renal function.

 

AAS metabolism burdens the kidneys through the process of glomerular filtration in the renal parenchyma. The creatinine serum level, which is a reliable indicator of renal function, increases (> 1.5mg/ dl), as well as urea (> 80 mg/ dl) and uric acid (> 7.5 mg/ dl). All these biochemical parameters are affected from several other non-renal factors (state of hydration, vegan diet) and their levels will not be raised above the normal range, until 60% of total kidney function is lost. So, the most reliable indicator of renal function is the measurement of creatinine clearance (GFR) at 24 hours.

 

Trenbolone is a highly toxic to kidneys. During a cycle with trenbolone, urine turns brownish with a characteristic heavy odor, responsible for kidney damage, as shown to cause focal segmental glomerulosclerosis (FSGS), tubular necrosis and acute renal failure (ARF).This is majorly due to the fact that it affects systemic blood pressure. As known, kidneys are regulating blood pressure through the renin-angiotensin system. This serious complication usually requires dialysis or renal transplantation.

 

Focal segmental glomerulosclerosis is a condition in which there is focal scarring of some glomeruli within the kidneys. It affects majorly the filtration process, leading to proteinuria, edema in the face and lower extremities, hypoalbuminemia, progressing to end-stage renal disease.

 

Clinically, the patient presents with edema in the face and lower extremities (proteinuria, hypoalbuminemia), hypertension, oliguria or even anuria (urine volume < 500ml/24h). In microscopic urinalysis proteinuria, microhematuria and cylinders are present. GFR falls, creatinine elevates and the kidney is unable to perform its normal excretory functions. This causes disruption of electrolyte regulation, leading to a further rise in potassium levels. Hyperkalemia might lead to heart arrhythmias, such as atrial fibrillation or ventricular tachycardia.

 

Numerous animal modelshave investigated the influence of sex hormones on the development of renal disease, and they generally show a protective role for estrogens, while androgens either are permissive or accelerate injury. Men are known to be at an overall increased risk for renal disease compared with women, and the prognosis in men is worse for various types of chronic kidney disease. The sources for these differences are under investigation, and there is mounting evidence that androgens may play a central role in both normal and diseased kidney function and that estrogens are protective.

In rare cases, abuse of AAS has been associated with the development of kidney tumors (nephroblastoma, adenocarcinoma).

Aside from AAS abuse, athletes have additional factors that could exert stress on renal function, such as high protein and creatine intake, excessive overtraining, elevated BMI (> 30), dehydration and polydrug use (for reducing side effects and boosting AAS effects).

Protein and creatine supplements with a high protein intake of > 300 grams per day increases the renal blood flow and glomerular filtration rate in an attempt to excrete the nitrogenous byproducts of its catabolism. Protein ingestion seems to cause an increase in renal blood flow and GFR by a variety of mechanisms. Although this is an appropriate adaptive response to the increase in nitrogenous waste that is the byproduct of protein metabolism, chronic hyperfiltration from a high-protein diet may accelerate progression to glomerulosclerosis and is also is associated with FSGS and acute tubular necrosis.

Creatine monohydrate with loading doses of 20 grams per day for 5 days and then maintenance doses of 5 grams per day are considered to be safe, always with proper hydration. Moreover, creatine consumption affects creatinine’s serum levels, since it is metabolized into it. Creatine is an ingredient of red meat; therefore its consumption will also increase creatine’s concentration. Protein consumption tends to be diuretic, in the absence of carbohydrates and in such cases ketosomes are detected in a biochemical analysis, leading to exhalation of ketones (rotten apple smell). During pre-contest preparation and glycogen depletion phase, high consumption of animal protein (> 3gr/kg) leads to ammoniaimia (skin and sweat get a characteristic heavy odor of ammonia). As known, ammonia is a waste product in the urea cycle, being toxic to the brain’s function (hepatic encephalopathy).

During intense overtraining, where rhabdomyolysis appears (serum CPK > 1000), damaged muscle fibers release myoglobin. This protein is toxic to the renal glomeruli and tubules and may lead to acute tubular necrosis and ARF. Kidney function impairment from rhabdomyolysis presents with a dark color of the urine, microscopic hematuria (pinkish, red color), proteinuria or presence of cylinders.

High protein consumption produces an acidic environment in the kidneys (pH < 5). That, along with calcium retention from nandrolone abuse, could be responsible for the formation of kidney stones.

Greater body mass (BMI > 30) leads to higher glomerular hyperfiltration, which in time leads to mechanical strain and scarring.When BMI is raised and overtraining occurs, rhabdomyolysis is more risky since more myoglobin is released into plasma.

 

Highly nephrotoxic AAS, such as trenbolone, should not be combined with other aggravating substances for the kidney, such as non-steroidal anti-inflammatory drugs or NSAIDs (diclofenac, nimesulide), antibiotics (aminoglycosides) and diuretics (furosemide). Because kidneys contribute to systemic blood pressure (renin-angiotensin system), abuse of CNS stimulants such as beta-agonists (clenbuterol) or ephedrine leads to vasoconstriction of renal vessels, chronic systemic hypertension, proximal and distal tubular necrosis and acceleration of renal failure. Diuretics also have a negative impact on renal function, particularly when their abuse is accompanied by water restriction.

 

Bodybuilders, usually exposed to forced muscle gain, diets high in protein and creatine and polydrug abuse should be considered a high-risk group in particular. Continuous renal function monitoring and early detection of kidney injury is very important for AAS users.

 

George Touliatos, MD is an author, lecturer, champion competitive bodybuilder and expert in medical prevention regarding PED use in sports. Dr. Touliatos specializes in medical biopathology and is the medical associate of Orthobiotiki.gr and Medihall.gr, Age Management and Preventive Clinics in Athens, Greece. Heis the author of four Greek books on bodybuilding, has extensively developed articles for www.anabolic.org and is the medical associate for the book Anabolics, 11th Edition (2017). Dr. Touliatos has been a columnist for the Greek editions of MuscleMag and Muscular Development magazines, and has participated in several seminars across Greece and Cyprus, making numerous TV and radio appearances, doing interviews in print and online. His personal website is

https://gtoul.com

 

 

 

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