Anabolic Steroids & Kidney

[Deleted member 59947]

Sorry your right but that answer is extremely complicated. I was born with an already diminished kidney function and have to see a dr every 3 months for the rest of my life. I don't know everything about kidney function but I have learned quite a bit over the years. My Dr stil allows me to take prescribed tedtastorone Cypionate at 250 mg per week. He is a urologist and very knowledge. Your body is already used to processing testastorne and is ready to handle it kidneys and liver included. My bloods come in around 1000-1500 regularly. That is an acceptable range. A range some males produce naturally in their teens and early 20s. Your body will see this as somewhat normal even as you get older and is ready to process it. Hormones like tren, anadrol, dianabol used a high levels for prolonged periods will tax your kidneys and liver. Yiur liver can regenerate but yiur kidneys cannot. Once your wear out or destroy the "peticuli" within your kidney they are gone and can't come back. You can see if this is occurring if your dr finds excessive protein in yiur urine. This means your kidneys are processing your protein and you may have CKD. Most bodybuilder worry a lot about their liver when it's really the kidney that's at risk. Stay hydrated a gallon of water a day. Limit your tren and anadrol cycles to 6 weeks with PCT afterwards. Don't use Advil and high protein diets tax the kidneys and over stress them. You'd be surprised to know that you don't need 40 grams of protein in each meal. Once your kidney function is diminished it cannot return to normal. Hope this helps.

I guess you meant "glomeruli", don't know what are "peticuli".

What are you seeing that urologist every 3 months for?

Either your kidney function is diminished to the point you need dialysis, or you can get by with blood works twice a year otherwise.

What does that doctor do to you "every 3 months" apart from checking your blood and being helpless with your condition than can't get better and can't be cured?

 

[Bjorn Turock]

It is extremely important to remember that if you are on a high-intensity training regimen and a high protein diet the "eGFR" test is completely useless. It is a complete guess at what your kidney function may be if your protein intake and muscle breakdown (how much/often you lift) are fitting within the averages of the population.

 

[Deleted member 59947]

It is extremely important to remember that if you are on a high-intensity training regimen and a high protein diet the "eGFR" test is completely useless. It is a complete guess at what your kidney function may be if your protein intake and muscle breakdown (how much/often you lift) are fitting within the averages of the population.

If your point is to say eGFR measure is skewed, yes. Is it useless? No.
Because having the stress of high protein intake and high muscle breakdown IS a degrading factor for your kidneys, so the diminished eGFR does tell you that you will need dialysis 10/20 years down the road

 

[Bjorn Turock]

My point is the eGFR is completely hypothetical. And Goingstronger, I'm sorry but you are wrong. I have had elevated creatinine labs since I was 16, thus eGFR was always low (60-80). When my actual GFR was tested via iohexal clearance my GFR was 161.

every nephrologist I worked with said the eGFR was completely meaningless.

I would strongly encourage everyone with concerns about CKD to focus on blood pressure control as a primary measure of fitness.

 

[Michael Scally MD]

[Rats] Nandrolone Administration with Or Without Strenuous Exercise Promotes Overexpression of Nephrin And Podocin Genes and Induces Structural and Functional Alterations in The Kidneys

Highlights
· Nandrolone treatment with or without training increased 8-OHdG as a DNA damage marker.
· Nandrolone treatment with or without training increased nephrin and podocin gene expression.
· Nandrolone treatment with or without training led to kidney function alteration.

[Thirty-two male wistar rats aged 4 months with an initial body weight of 220±10 g were randomly divided into four groups (eight in each group) namely control, nandrolone, nandrolone with strenuous exercise, and strenuous exercise groups. Nandrolone group received 10 mg of nandrolone decanoate per body weight by a single injection in the femoral muscle, three times per week (Saturdays, Mondays, and Wednesdays) for six weeks.]

Among the various adverse effects of nandrolone administration with or without strenuous exercise, kidney abnormalities, where there are associations between nandrolone decanoate consumption, have not been well defined yet.

The aim of this study was to investigate the effect of nandrolone decanoate intake with or without strenuous exercise on nephrin and podocin gene expressions, cystatin C, oxidative DNA damage, and histological changes in the kidneys of rats.

Thirty-two male wistar rats were assigned into four groups, namely control, nandrolone, nandrolone with strenuous exercise, and strenuous exercise groups.

After six weeks of treatment, the results revealed a significant increase in the nephrin and podocin gene expression, plasma cystatin C, and the amount of 8-OHdG in the kidney tissue; as well as a decrease in creatinine clearance in nandrolone and nandrolone with strenuous exercise groups compared to the control group. Moreover, compared to the control group, the nandrolone and the nandrolone with strenuous exercise groups, showed histological changes such as fibrosis and kidney tissue cells proliferation.

These findings indicate that nandrolone induces kidney abnormalities, which may in part be associated with overexpression of nephrin and podocin genes mediated by oxidative stress, which was manifested in increased 8-OHdG in kidney tissue.

Tofighi A, Ahmadi S, Seyyedi SM, Shirpoor A, Kheradmand F, Gharalari FH. Nandrolone administration with or without strenuous exercise promotes overexpression of nephrin and podocin genes and induces structural and functional alterations in the kidneys of rats. Toxicol Lett. http://www.sciencedirect.com/science/article/pii/S0378427417314388

 

[Michael Scally MD]

Kantarci UH, Punduk Z, Senarslan O, Dirik A. Evaluation of anabolic steroid induced renal damage with sonography in bodybuilders. J Sports Med Phys Fitness. https://www.minervamedica.it/en/jou...-fitness/article.php?cod=R40Y9999N00A17111701

BACKGROUND: The aim of this study was to investigate the effect of anabolic steroids on kidneys in bodybuilders.

METHODS: Twenty two bodybuilders were included in the study. Participants were divided into three groups according to the scheme of steroid usage: Group 1 (n=8, intramuscular 500 mg testosterone enanthate, intramuscular 400 mg nandrolone decanoate and oral 40 mg methandrostenolone for 12 weeks), Group 2 (n=7, intramuscular 500 mg testosterone enanthate, intramuscular 300 mg nandrolone decanoate and intramuscular 300 mg boldenone undecylenate for 16 weeks) and Group 3 (n=7, no steroid intake). Blood urea nitrogen (BUN), creatinine (Cr), urine microalbumin and electrolyte levels were measured. Renal volume, cortical thickness and echogenicity were obtained in ultrasonographic scans.

RESULTS: Renal volume, cortical thickness, echogenicity and protein intake value were significantly higher in group 2 than group 1 and 3. Plasma levels of BUN and Cr in group 2 were significantly higher than other groups (p < 0.001). Urine microalbumin and electrolyte levels were normal in all groups.

CONCLUSIONS: The results of this study indicate that high protein intake, steroid usage, particularly the schemes, including boldenone undecylenate increases cortical echogenicity, thickness of renal parenchyma and renal volume in bodybuilders.

 

[Michael Scally MD]

Is Testosterone Detrimental to Renal Function?

Male gender is associated with a higher morbidity and mortality in both children and adolescents with chronic kidney disease (CKD). Testosterone has been implicated in the difference of progression of CKD, by gender. Children with renal dysplasia often reach end-stage kidney disease during puberty. There is evidence for a significantly steeper deterioration of renal function during puberty, independent of changes in body composition.

In adults, there is also evidence for gender disparity of progression of CKD,5 with a higher rate of end-stage kidney disease in men. The direct influence of testosterone upon renal function, and in particular renal hemodynamics, has not been established in humans.

We recently had the opportunity to observe substantial worsening of renal function in a 14-year-old boy with hypergonadotropic hypogonadism who had repeatedly exhibited reduction in renal function following administration of testosterone. We used a novel computed tomography (CT) perfusion imaging technique. This was combined with a state-of-the-art 256-slice CT scanner, to provide whole organ coverage without the challenges of image registration associated with the limited scan slice thickness of commonly available instruments.

This allowed an in vivo assessment of renal blood flow, patterns of renal perfusion, and other functional parameters of the kidneys in previously unobtainable detail. Our method has not been published, but the principles of measuring renal blood flow and blood volume are comparable to those presented by Ehling et al.

...

We present a case of acute testosterone-induced deterioration of renal function in a 14-year-old boy with Townes Brock syndrome and hypergonadotropic hypogonadism. Further reduction of renal function after subsequent reintroduction of testosterone was associated with the same response, inferring an association.

The pathophysiology of this effect appears to be attributable to testosterone-mediated changes in intrarenal hemodynamic parameters. This was confirmed on direct dynamic imaging and strongly supported by the observed reduction in proteinuria.

The key questions raised by this potentially highly instructive case are,
Why did this happen? and,
Why was it reversible?

Filler G, Ramsaroop A, Stein R, et al. Is Testosterone Detrimental to Renal Function? Kidney international reports 2016;1:306-10. Is Testosterone Detrimental to Renal Function?

 

[Michael Scally MD]

Merino García E, Borrego Utiel FJ, Martínez Arcos MÁ, Borrego Hinojosa J, Pérez del Barrio MP. Kidney damage due to the use of anabolic androgenic steroids and practice of bodybuilding. Nefrología (English Edition). Kidney damage due to the use of anabolic androgenic steroids and practice of bodybuilding - ScienceDirect

Dear Editor,

We report the case of a patient, male with acute kidney failure and haemolytic anaemia in the context of secondary malignant hypertension (HTN) and anabolic steroid user.

…

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 (250/180 mmHg) and severe acute kidney failure. Complementary tests revealed anaemia and thrombocytopenia (haemoglobin 9.9 g/dl, haematocrit 28.4%, platelets 91,000/mm3) as well as the above-mentioned kidney failure (urea 246 mg/dl, creatinine 23.5 mg/dl). An immunology study was negative (except for a slight decrease in C3 and C4 fraction), with proteinuria of 1.7 g/24 h and oligoalbuminuria of 491 mg/l. A peripheral blood smear showed real thrombocytopenia and schistocytes (2.1%). Venous blood gases were normal and potassium levels were at the lower limit of normal (this was likely an effect of the anabolic steroids).

Given his haemolytic anaemia with mild thrombocytopenia and schistocytes on smear testing, the patient was thought to have microangiopathic haemolytic anaemia. A brain CT scan was performed (to rule out brain damage secondary to HTN). The scan showed a punctiform image in the caudate nucleus that was not suggestive of acute haemorrhagic lesion.

…

Treatment of malignant HTN should be started immediately. Initially, it may be necessary to use parenteral drugs (labetalol, sodium nitroprusside) combined with oral drugs (ACE inhibitors/angiotensin II receptor antagonists, vasodilators such as calcium antagonists and other more powerful agents such as minoxidil plus beta-blockers and loop diuretics). Approximately 20% of cases require dialysis techniques.

In our case, poor management of long-standing HTN, together with anabolic steroid use and intense anaerobic exercise, precipitated the development of malignant HTN. This disease requires immediate therapeutic action to prevent many complications leading to death in 25% of cases in 5 years, despite hypotensive treatment.

 

[GDL]

I wish some of the acronyms were explained so I understood what the hell was being told.

What is HTN

 

[hurricane]

[POSTULATE] Collapsing Glomerulopathy Following Anabolic Steroid Use with Underlying Primary IgA Nephropathy

A 16-year-old boy presented with history of vomiting and headache of 15 days duration. On evaluation, he was found to have blood pressure of 160/80 mmHg. He had a history of consumption of anabolic steroids (dexona + dianabol [methandrostenolone] combination) for general body development for a duration of 3 months.

Laboratory studies revealed a serum creatinine of 2.27 mg/dl, urine protein to creatinine ratio of 6, proteinuria of 4.7 g in 24 h. Urine microscopy showed 10-12 white blood cells and 5-40 red blood cells per high power field. His liver function tests (LFT) were normal. There was no jaundice or evidence of cholestasis. Tests for antibodies to HIV, hepatitis B and C viruses were negative. There was no biochemical evidence of a TMA. Ultrasound examination of both kidneys revealed Grade II renal parenchymal changes.

The present case describes short-term anabolic steroid abuse and development of CG in a young patient from a low risk population with underlying primary IgAN.

The diagnosis of primary IgAN was based on LM, IF and electron microscopy (EM) studies. EM demonstrated presence of paramesangial electron-dense deposits with GBM thinning and splitting, which are additional ultrastructural findings supportive of a primary rather than secondary IgAN.

Normal LFT also made IgAN secondary to drug-induced hepatic dysfunction unlikely. The onset of CG followed intake of anabolic steroids and despite high prevalence of IgAN in this population, there is no previous documentation of concurrent CG and IgAN from India. There was no biochemical or histological evidence of thrombotic microangiopathy (TMA) or severe ischemic changes or other viral infections to suggest possible etiologies of CG.

Although all patients with IgAN exposed to anabolic steroids do not develop CG, the temporal sequence of events in our case, as described above, helps identify anabolic steroids as a co-factor precipitating CG in this patient.

Matthai SM, Basu G, Varughese S, Pulimood AB, Veerasamy T, et al. Collapsing glomerulopathy following anabolic steroid use in a 16-year-old boy with IgA nephropathy. Indian J Nephrol. 2015;25(2):99-102. Collapsing glomerulopathy following anabolic steroid use in a 16-year-old boy with IgA nephropathy Matthai S M, Basu G, Varughese S, Pulimood A B, Veerasamy T, Korula A - Indian J Nephrol

Collapsing glomerulopathy (CG) is a proliferative podocytopathy, increasingly recognized in a variety of disease conditions.

We report a case of CG in a 16-year-old boy with IgA nephropathy (IgAN) who presented with acute kidney injury, marked proteinuria and hypertension following a short period of anabolic steroid use.

Although CG has been associated with long-term anabolic steroid use among body builders, there is no data on the effect of anabolic steroid use in persons with underlying renal disease like IgAN.

We POSTULATE that development of CG in our patient could be temporally linked to intake of body-building steroids along with a predisposing background renal disease of IgAN.

Valuable info Doc. This question just came up. I bumped it for a reason. So calm down jakoffs!

 

[MindlessWork]

Valuable info Doc. This question just came up. I bumped it for a reason. So calm down jakoffs!

I had my doc scare me about my kidney function when I had a physical and I happened to be on cycle last fall. Spent $300 on specialists for my peace of mind to show my doc I had no issues...also did not want to disclose my gear use to him even though he is a lifter like me.

I learned gear use does throw off kidney function a bit and hopefully no lasting effects now that I am off cycle. Going to my nephrologist one last time this week and getting labs done.

 

[Michael Scally MD]

I wish some of the acronyms were explained so I understood what the hell was being told.

What is HTN

Hypertension

 

[Michael Scally MD]

[OA] [WTF!] Complementary Bodybuilding: A Potential Risk For Permanent Kidney Disease

We 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.

El-Reshaid W, El-Reshaid K, Al-Bader S, Ramadan A, Madda JP. Complementary bodybuilding: A potential risk for permanent kidney disease. Saudi journal of kidney diseases and transplantation: an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia 2018;29:326-31. Complementary bodybuilding: A potential risk for permanent kidney disease El-Reshaid W, El-Reshaid K, Al-Bader S, Ramadan A, Madda JP - Saudi J Kidney Dis Transpl

 

[Michael Scally MD]

Testosterone Replacement Therapy Is Associated with Increased Incidence or Urolithiasis

INTRODUCTION AND OBJECTIVES - Hypogonadism is a highly prevalent condition among middle-aged and elderly men, with estimations that roughly a quarter of men of this age range are affected. While indications for testosterone replacement therapy (TRT) have broadened over the preceding decades, there has been coincident controversy regarding the risks, benefits, and appropriate indications for TRT use.

Though it has been suggested there may be an association between serum testosterone levels and incidence of urolithiasis, no study has analyzed the association between TRT and subsequent stone episodes. As a result, we set out to compare the incidence of urolithiasis in a cohort of men using TRT with a cohort of age and comorbidity-matched controls.

METHODS - We conducted a retrospective matched cohort study utilizing data sourced from the Military Health System Data Repository (MDR; a large military-based database that includes beneficiaries of the TRICARE program) of men aged 40-64 with a diagnosis of low testosterone who received continuous TRT between January 2006 and December 2010.

Exclusion criteria were TRICARE enrollment of less than one year, less than 180-day washout period, or oral testosterone use.

The primary endpoint was time to first diagnosis of urolithiasis (identified by a comprehensive list of diagnosis and procedure codes). We compared event-free survival (for urolithiasis) as a function of time and calculated two-year absolute risk of event.

RESULTS - There were 8126 pairs in our cohort. 82 stone-related events were observed at two years in the no TRT group versus 222 in the TRT group. Log rank comparisons showed this to be a statistically significant difference in events between the two groups (p<0.001).

CONCLUSIONS - In this retrospective matched cohort comparison, we have observed an increase in two-year absolute risk of stone events among those on TRT compared to those who have not undergone this hormonal therapy. These findings merit further investigation and consideration by clinicians when determining the risks and benefits of placing patients on TRT.

McClintock TR, Cole AP, Kwon NK, et al. Testosterone replacement therapy is associated with increased incidence or urolithiasis. Data presented in poster format at the American Urological Association 2018 annual meeting in San Francisco, May 18–21. Abstract MP13-19. https://www.jurology.com/article/S0022-5347(18)39801-X/fulltext

 

[RELENTLESS]

I don't know. My doc just told me this morning that there's is kidney damage. My bp has been all over the place. Resting heart rate was between 90-120.

If I can get some info, I will post it. Its covered by insurance, I don't want to tell them I juice. I already look suspicious, 220lbs cut. I have been hoping they wouldn't ask and what I would say if they do.

was pretty sick for 3 days before I was admitted. But bp has been screwed up for a year and a half. Hard to control it.

I went yesterday for full blood panel testing. Blood pressure was read 3 different times. Each time huge differences all high of course. Part of the problem is not having a damn cuff to fit my arm so they try the wrist then the forearm, then a thigh cuff around my arm....I asked, no offense but my arm is only 22 inches. What do you use on the 400 lb. fat women with 30 arms? It was ridiculous. So, at this point I don't know if my shit is high or not? I have been on bp meds for years. You would think with todays tech, they would have something to accurately check your bp with!

 

[Michael Scally MD]

[OA] Bile Cast Nephropathy: The Unknown Dangers of Online Shopping

Renal dysfunction in the setting of cholestatic liver disease is multifactorial but most often due to decreased kidney perfusion from intravascular volume depletion, acute tubular injury/necrosis, and hepatorenal syndrome. Drug-induced hepatotoxicity may be associated with a cholestatic injury pattern.

We report a case of a 56-year-old man with a diagnosis of bile cast nephropathy, as a complication of drug-induced severe hyperbilirubinemia due to the abuse of intramuscular anabolic steroids bought on the internet to increase muscular mass for bodybuilding training.

Kidney biopsy showed the histological pattern of diffuse potentially reversible tubular damage with intratubular bile casts obstructing the renal tubules. The patient developed acute kidney injury and needed dialysis treatment for 4 weeks until renal function recovered.

The severity of the kidney injury and the requirement of hemodialysis observed in our patient are unique and have not been previously described. As full recovery of renal function is suspected with decreasing bilirubin levels, early recognition and treatment of the underlying disease is essential.

Fisler A, Breidthardt T, Schmidlin N, et al. Bile Cast Nephropathy: The Unknown Dangers of Online Shopping. Case reports in nephrology and dialysis 2018;8:98-102. Bile Cast Nephropathy: The Unknown Dangers of Online Shopping

 

[Michael Scally MD]

Rapid Recovery of Hypogonadism in Male Patients with End Stage Renal Disease After Renal Transplantation

PURPOSE: End stage renal disease (ESRD) in male patients is associated with a high prevalence of hypogonadism. After renal transplantation (RTx) an improvement in gonadal function is often observed. However, the time course of changes in pituitary-gonadal axis after RTx and the influence of renal function, age and anthropometric parameters are not well characterized. We prospectively evaluated pituitary-gonadal axis in male patients with ESRD before and after RTx for up to 1 year.

METHODS: Ninety-seven male patients with ESRD were consecutively investigated on day of surgery and 1, 3, 6, and 12 months after RTx. Time course of changes in sex hormones (total testosterone ((TT)), calculated free testosterone ((cfT)), estradiol (E2), LH, FSH and prolactin), and interdependence with renal function, age, anthropometric factors, cause of ERDS, time on dialysis, and transplant associated factors were analyzed.

RESULTS: Hypogonadism (TT < 8 nmol/l) was present in 40% of pts prior to RTX and in only 18% at 1 year after RTX. Recovery from hypogonadism was significantly higher in pts < 50 years and occurred within 3 months. RTx resulted in a decrease in E2/T ratio starting at 1 month and suggesting a shift from estrogen to testosterone production.

BMI and waist circumference had the similar impact on T levels after successful RTx compared to patients without renal disease. No specific impact on recovery of hypogonadism was found for time on dialysis prior to RTx and living or cadaver transplantation.

CONCLUSIONS: Successful RTx is associated with a rapid recovery from hypogonadism within 3 months preceeded by improvement in renal function particularly in patients younger than 50 years.

Reinhardt W, Kubber H, Dolff S, Benson S, Fuhrer D, Tan S. Rapid recovery of hypogonadism in male patients with end stage renal disease after renal transplantation. Endocrine 2018;60:159-66. https://link.springer.com/article/10.1007/s12020-018-1543-2

 

[Michael Scally MD]

[OA] Tarashande Foumani A, Elyasi F. Oxymetholone-Induced Acute Renal Failure: A Case Report. Caspian journal of internal medicine 2018;9:410-2. Oxymetholone-Induced Acute Renal Failure: A Case Report

Background: The prevalence of using anabolic steroids such as oxymetholone is increasing. This highlights the need for closely monitoring side effects of this drug. Acute renal failure (ARF) has been reported as a complication of rhabdomyolysis in anabolic steroids users.

Case presentation: We present one 33-year-old man complaining of decreased urine volume, urine color change, and lower abdominal pain. He is engaged with a rare side effect of oxymetholone abuse. During assessments of potential medical issues associated with the intake of anabolic steroids, known side effects are known to be transient, but the need for appropriate interventions remains essential.

Conclusions: Rhabdomyolysis due to drug use and the consequent acute kidney injury are among the lethal risks associated with anabolic steroid abuse. In most cases, the symptoms are extensive and often misleading. Therefore, detailed history taking, physical scrutiny, paraclinical testing, and early diagnosis are crucial for rhabdomyolysis patients.

 

[Old]

complication of rhabdomyolysis

Why would a BB suffer rhabdomyolysis?

• Excess exercise?
• Amphetamine or other weight-loss drug (author states 'due to drug use' though presumably referring to oxymetholone)?
• Poor hydration?

These are not unique to AAS though perhaps the steroids are an additional stress factor.

 

[Michael Scally MD]

[OA] [Italian] Flachi M, Menghi V, Moschella MR, et al. [FSGS collapsing variant during anabolic steroid abuse: Case Report]. Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia 2018;35. GSFS variante collapsing in corso di abuso di steroidi anabolizzanti: case report - GIN

Anabolic Androgenic Steroids (AAS) is an hormone family whose use has considerably increased among body-builders during the last decades. The AAS abuse, especially associated with other drugs or nutritional supplements and protein loads, may cause a variety of pathologies to several organs with a mechanism related to dosage, timing and substance.

The kidney is the main metabolizer of these drugs and it can be acutely or chronically damaged with ESKD. The literature reports some cases of Focal Segmental Glomerulosclerosis (FSGS) in body-builders who abused of AAS. However, the link is not well understood and limited to some case-studies.

In this paper, we report the case of a young body-builder who developed a FSGS collapsing variant with ESKD after prolonged abuse of AAS and a strongly hyperproteic diet and other dietary supplements. The patient underwent a genetic test because of the rapid and irreversibile onset of ESKD. The test showed a gene mutation of ACTN4, predisposing and causal of some genetic forms of FSGS. It was a very complex case, caused by several factors.

The mutant protein of ACTN4 gene makes most vulnerable the cytoskeleton of the podocytes to external disturbances. That would explain why in those patients where the mutation has occurred, only those patients subject to "unfavorable environmental conditions", like the abuse of AAS, can develop a disease.