Anabolic Steroids & Kidney

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.
Health to Paul. Keep us updated please.
 
Just a reminder that what we do has consequences, and we need to be aware of that.

And in saying that (which I totally agree with) there may be preventable steps that can be taken:
such as drinking a plethora of water each day (I am close to a gallon).
Keep caffeine intake moderate to low.
Take herbal supplements that may have beneficial affects for kidney and liver health.
Eat wholesome fresh foods. Not canned, boxed, vacuumed sealed.
Stay away from High Fructose Corn Syrup and most sweeteners.
Take breaks off BB supplements such as creatine.
Most importantly, take breaks from the juice.
And even try lower dosages. If you are not at a competition level in any sport, why take astronomical levels of juice that will take it's toll down the road?

I am glad to hear things are clearing up for you Paul and thanks for sharing. It's a reminder to all us and the Cold Hard Facts of what we are doing and hopefully will keep us all on our toes!
 
I wondered about this myself. I do not drink sodas but I've had a diet coke or two/day for years, as well as a coffee maybe 1-2x/day. Throw in the occasional energy drink and I often wonder how much this can further dehydrate me. Less caffeine and more water is what I need myself
Yep I never knew this until now. If I drink a beer or Diet Coke I try to follow it with a glass of water. I think you'll live longer if you do.
 
suPAR – a new marker for “chronic kidney disease”
http://www.nejm.org/doi/full/10.1056/NEJMoa1506362

You thought you were healthy until someone measured your imaginary glomerular filtration rate (eGFR).

Then you were told you had grade 2 chronic kidney disease.


You obediently turned up for a repeat creatinine measurement after a year.

This time they decided to measure your plasma level of soluble urokinase-type plasminogen activator receptor (suPAR) as well, because they had read this study in the NEJM.

“In 1335 participants with a baseline eGFR of at least 60 ml per minute per 1.73 m2, the risk of progression to chronic kidney disease in the highest quartile of suPAR levels was 3.13 times as high (95% confidence interval, 2.11 to 4.65) as that in the lowest quartile.”

“Progression to CKD” was defined as moving to an eGFR below 60.

There was no attempt to link suPAR with any patient meaningful endpoint.

So my questions would be: in what way could this test provide information that makes any difference to anyone’s outlook or management?

Is it even ethical to do tests which leave doctors unable to explain their meaning to individuals? http://blogs.bmj.com/bmj/2015/11/09/richard-lehmans-journal-review-9-november-2015/
 
Alkhunaizi AM, ElTigani MA, Rabah RS, Nasr SH. Acute bile nephropathy secondary to anabolic steroids. Clin Nephrol. http://www.dustri.com/nc/article-response-page.html?artId=13913&doi=

Renal dysfunction in cholestatic liver disease is multifactorial. Acute kidney injury may develop secondary to renal vasoconstriction in the setting of peripheral vasodilation and relative hypovolemia, tubular obstruction by bile casts, and direct tubular toxicity from bile. Anabolic steroids are frequently used by athletes to boost endurance and increase muscle mass. These agents are a recently recognized cause of hepatotoxicity and jaundice and may lead to acute kidney injury. To increase awareness about this growing problem and to characterize the pathology of acute kidney injury in this setting, we report on a young male who developed acute kidney injury in the setting of severe cholestatic jaundice related to ingestion of anabolic steroids used for bodybuilding. Kidney biopsy showed bile casts within distal tubular lumina, filamentous bile inclusions within tubular cells, and signs of acute tubular injury. This report supports the recently re-emerged concept of bile nephropathy cholemic ephrosis.
 
Alkhunaizi AM, ElTigani MA, Rabah RS, Nasr SH. Acute bile nephropathy secondary to anabolic steroids. Clin Nephrol. http://www.dustri.com/nc/article-response-page.html?artId=13913&doi=

Renal dysfunction in cholestatic liver disease is multifactorial. Acute kidney injury may develop secondary to renal vasoconstriction in the setting of peripheral vasodilation and relative hypovolemia, tubular obstruction by bile casts, and direct tubular toxicity from bile. Anabolic steroids are frequently used by athletes to boost endurance and increase muscle mass. These agents are a recently recognized cause of hepatotoxicity and jaundice and may lead to acute kidney injury. To increase awareness about this growing problem and to characterize the pathology of acute kidney injury in this setting, we report on a young male who developed acute kidney injury in the setting of severe cholestatic jaundice related to ingestion of anabolic steroids used for bodybuilding. Kidney biopsy showed bile casts within distal tubular lumina, filamentous bile inclusions within tubular cells, and signs of acute tubular injury. This report supports the recently re-emerged concept of bile nephropathy cholemic ephrosis.
That doesn't sound good
 
I know , Ive been fighting the BP too , on 25mg Metoprolol w/5mg Amlodipine . The doc added the amlodipine to enlarge the blood vessels , the metoprolol slows down the heart just slightly so it doesnt work as hard (where it should be) went from 150/80 to 130/75 .
My dad also uses this combo and its pretty popular , maybe ask your doc about it ...
just curious. can metoprolol be used ON cycle? my bp has slightly increased not too mch but its up to 142/60 then goes down to 134/60 etc
 
@Michael Scally MD does it say anything about what kind of doses of anabolics these subjects where taking? I think I've read that at about 10 mg per day of winstrol or dianabol there shouldnt be too much toxicity, but on these forums you usually see people advising 50 mg a day as a beginner's dose.
 
Acute Bile Nephropathy Secondary To Anabolic Steroids

Renal dysfunction in cholestatic liver disease is multifactorial. Acute kidney injury may develop secondary to renal vasoconstriction in the setting of peripheral vasodilation and relative hypovolemia, tubular obstruction by bile casts, and direct tubular toxicity from bile.

Anabolic steroids are frequently used by athletes to boost endurance and increase muscle mass. These agents are a recently recognized cause of hepatotoxicity and jaundice and may lead to acute kidney injury.

To increase awareness about this growing problem and to characterize the pathology of acute kidney injury in this setting, we report on a young male who developed acute kidney injury in the setting of severe cholestatic jaundice related to ingestion of anabolic steroids used for bodybuilding.

Kidney biopsy showed bile casts within distal tubular lumina, filamentous bile inclusions within tubular cells, and signs of acute tubular injury. This report supports the recently re-emerged concept of bile nephropathy cholemic nephrosis.

Alkhunaizi AM, ElTigani MA, Rabah RS, Nasr SH. Acute bile nephropathy secondary to anabolic steroids. Clin Nephrol 2016;85(2):121-6. Dustri Online Services
 
[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.

I have read a few articles showing testosterone was protective of the kidneys in the cas of IgA nephropathy.
That is if you manage well the blood pressure.
And I mean bioidentical testosterone only, not derived AAS.

I found no proper study about this protective effect, have you?
 
[OA] The Cost of Seeking an Edge: Recurrent Renal Infarction in Setting of Recreational Use of Anabolic Steroids

Highlights
  • Consideration of earlier CT study with contrast.
  • Thorough history taking including gym supplements.
  • The use of NOACs.
  • The need for further understanding of how anabolic steroids affect coagulation.
  • Educating patients using anabolic steroids regarding the risks of continued use.
INTRODUCTION: Anabolic-androgenic steroid (AAS) use and testosterone therapy have been well established risk factors for the creation of a pro-thrombotic state, and to precipitate formation of thromboemboli in individuals already predisposed to thrombosis.

CASE REPORT: Here, we present the case of an amateur bodybuilder, with a negative thrombophilia workup, who experienced primary renal infarction while using the AAS trenbolone acetate and testosterone, as well as a subsequent renal infarction while anticoagulated with apixaban.

DISCUSSION: The development of subsequent infarctions in an anticoagulated patient with discontinued recreational steroid use poses a unique situation and challenges the current understanding of a thrombophilic state associated with steroids. The lifetime prevalence of anabolic steroid use is estimated to be 1% in the male population in the United States which is significant.

CONCLUSION: Further understanding and recommendations of appropriate anticoagulant should be further elucidated to appropriately medically manage patients from this confounding social and medical history.

Colburn S, Childers WK, Chacon A, Swailes A, Ahmed FM, Sahi R. The cost of seeking an edge: Recurrent renal infarction in setting of recreational use of anabolic steroids. Ann Med Surg (Lond) 2017;14:25-8. http://www.annalsjournal.com/article/S2049-0801(17)30016-X/fulltext
 
I heard that anavar in giant dose is hard in the kidneys.
But,anyway,test e/cyp/sustanon/undecanoate are hard on the kidneys too?
Thanks in advance doc
 
Nanavati A, Herlitz LC. Tubulointerstitial Injury and Drugs of Abuse. Adv Chronic Kidney Dis 2017;24(2):80-5. http://www.ackdjournal.org/article/S1548-5595(16)30078-7/abstract

Drug abuse is widespread in many populations, and patients abusing illicit substances are at a significantly increased risk of kidney injury. The tubulointerstitial compartment is a common target of these nephrotoxic agents.

This review will cover some of the common illicit drugs and will focus on the tubulointerstitial injuries seen in the setting of drug abuse.

Agents addressed in this review are synthetic cannabinoids, "bath salts," ecstasy, anabolic steroids, inhaled solvents, heroin, and cocaine.

The most frequent biopsy findings are those of acute tubular necrosis and acute interstitial nephritis. Unfortunately, histology is often unable to sufficiently narrow the differential diagnosis and point to a single likely cause.

A high suspicion for drug abuse as a potential cause of kidney injury is needed to identify the patients for whom this is the cause of their kidney failure. Toxicology screens are often of little use in identifying patients using emerging drugs of abuse.


 

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Is high amount Testosterone (min 300mg/week) directly toxic to the kidneys, or only indirectly due to it's effect on increasing blood pressure and blood-thickening effect?
 
I think the answer is yes, there are other modes of action besides blood pressure and high rbc that effect the kidneys
 
No what?

I asked one question and its alternative in the same sentence so your answer is not understandable as such
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.
 
Also donate blood every 90 days. This will lower yiur red blood cell count and help with the "thickening". It also helps
me with my blood pressure.
 
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