Steroids and kidney damage?

Discussion in 'Steroid Forum' started by akiravp82, Jun 9, 2011.

  1. #1

    akiravp82 Member

    Any proof of long term steroid usage (injectables) causing kidney problems? i know people say that the liver is forgiving and once its damaged it has alot of potential to recover but for the kidneys its not that easy and once the kidneys get damaged you cant reverse it, anyone got more info on this?
  2. #2

    Herbie5353 Junior Member

    Funny you should ask...

    Read my other post on "Bill Roberts need help w Muscle Shotdown"

    I have been using AAS for 10yrs plus on and off. A few pretty serious cycles when I was more driven and did bench press contests. I just had a scare while on AAS and HGH and do have both parents with kindey issues.

    Mine just came back with no issues and working properly both kidneys and liver.

    Thank god.

    Not sure of others but Bill Roberts may be able to help you.

    Take Care
    Jodyhighroller likes this.
  3. #3

    zkt Member

  4. #4
    Bill Roberts

    Bill Roberts Steroid Forum Leader

    Alternately, very high blood pressure is common among those genuinely abusing steroids long-term.

    If there is evidence of kidney damage from cycling -- genuinely allowing at least comparable time off to time on -- in the absence of other adverse factors such as hypertension, I don't know it. I don't think it is a big issue, if at all. But steroid abuse can cause an issue here.
    Last edited: Jun 9, 2011
  5. #5

    akiravp82 Member

    Hey bill how about for TRT with masteron longterm? lets say 120mg a week of test cyp and 250mg a week of masteron longterm do you think this would be an issue for kidney or even liver health?
  6. #6
    Bill Roberts

    Bill Roberts Steroid Forum Leader

    Fine for the liver; whether decades on end of this continually would be fine for the kidneys, I can't say. Going past say 300 mg/week IMO fits more into the category of a never-ending steroid cycle rather than HRT.

    It's definitely substantially beyond the amount of androgenic effect from even the top end of the normal range. Whether that is fine 24/7/365 for greatly extended periods, I don't know. It seems lik pushing it a bit to me if intended for truly longterm, but that is guesswork.
    Last edited: Jun 11, 2011
  7. #7

    akiravp82 Member

    Bill your help is very much appreciated thanks for all the help! :)
  8. #8
    Bill Roberts

    Bill Roberts Steroid Forum Leader

    You're very welcome!
  9. #9

    zkt Member

    I dont know of any long term studies concerning steroids and renal damage, but I havent looked either.
    I wanted to point out the possibility of kidney damage for those who already have some degree of renal impairment.
  10. #10
    Michael Scally MD

    Michael Scally MD Doctor of Medicine

    See (Focal Segmental Glomerulosclerosis):

    Also, the recent publication:

    AASs are commonly excreted in urine mainly as glucuronide conjugates, the formation of which is catalyzed by various uridine diphosphate-glucuronosyltransferase (UGT) enzymes. The UGTs 2B7, 2B15 and 2B17 are found to be the principal enzymes involved in glucuronidation of androgens and their metabolites in humans.

    Therefore, in this paper researchers hypothesize that the observed renal disorders among AAS users is connected to the genetic profiles of these users and functional polymorphic deletion of the UGT2B17 gene significantly increases the chance of developing kidney complications.

    Deshmukh N, Petroczi A, Barker J, Szekely AD, Hussain I, Naughton DP. Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids. Subst Abuse Treat Prev Policy 2010;5:7. SATPP | Full text | Potentially harmful advantage to athletes: a putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic androgenic steroids

    BACKGROUND AND OBJECTIVE: With prolonged use of anabolic androgenic steroids (AAS), occasional incidents of renal disorders have been observed. Independently, it has also been established that there are considerable inter-individual and inter-ethnic differences, in particular with reference to the uridine diphosphate-glucuronosyltransferase 2B17 (UGT2B17) gene, in metabolising these compounds. This report postulates the association of deletion polymorphism in the UGT2B17 gene with the occurrence of renal disorders on chronic exposure to AAS.

    PRESENTATION OF THE HYPOTHESIS: The major deactivation and elimination pathway of AASs is through glucuronide conjugation, chiefly catalyzed by the UGT2B17 enzyme, followed by excretion in urine. Excretion of steroids is affected in individuals with a deletion mutation in the UGT2B17 gene. We hypothesize that UGT2B17 deficient individuals are more vulnerable to developing renal disorders with prolonged use of AAS owing to increases in body mass index and possible direct toxic effects of steroids on the kidneys. Elevated serum levels of biologically active steroids due to inadequate elimination can lead to prolonged muscle build up. An increase in body mass index may cause renal injuries due to sustained elevated glomerular pressure and flow rate.

    TESTING THE HYPOTHESIS: In the absence of controlled clinical trials in humans, observational studies can be carried out. Real time PCR with allelic discrimination should be employed to examine the prevalence of different UGT2B17 genotypes in patients with impaired renal function and AAS abuse. In individuals with the UGT2B17 deletion polymorphism, blood tests, biofluid analyses, urinalysis, and hair analyses following the administration of an anabolic steroid can be used to determine the fate of the substance once in the body.

    IMPLICATIONS OF THE HYPOTHESIS: If the hypothesis is upheld, anabolic steroid users with a deletion mutation in the UGT2B17 gene may be exposed to an increased risk of developing renal disorders. In the current detecting - sanctioning anti-doping system, athletes motivated by the potential to evade detection owing to their unique genetic make-up could subject themselves to a serious health consequence. More research on AAS metabolism in the presence of UGT2B17 gene deletion is required. Benefit - harm evaluations in therapeutic use of anabolic steroids should also consider this potential link between UGT2B17 gene deletion polymorphism and renal disorders.

    Daher EF, Silva Junior GB, Queiroz AL, et al. Acute kidney injury due to anabolic steroid and vitamin supplement abuse: report of two cases and a literature review. Int Urol Nephrol 2009;41(3):717-23. Acute kidney injury due to anabolic steroid and vi... [Int Urol Nephrol. 2009] - PubMed result

    BACKGROUND: The use of anabolic steroids and vitamin supplements has reached alarming proportions in the last decades. Adverse effects have been documented and include virilization, feminization, adverse lipid profile, psychiatric disorders, cardiac and liver disease. Acute kidney injury (AKI) is not frequently described. The purpose of this study is to report two cases of AKI associated with anabolic steroid and vitamin supplement abuse.

    CASE REPORT: Two men, aged 21 and 30 years, presented to the Emergency Department with abdominal pain, nausea and vomiting. They reported the use of anabolic steroids and veterinary supplements with vitamins A, D and E. Laboratory tests showed AKI (serum urea 79 and 52 mg/dl, serum creatinine 3.9 and 1.9 mg/dl) and hypercalcemia (calcium 13.2 and 11 mEq/l). Kidney biopsies showed inflammatory interstitial nephritis and acute tubular necrosis. Treatment consisted of vigorous hydration with simultaneous use of furosemide and discontinuation of the vitamins and anabolic substances, and resulted in recovery of renal function.

    CONCLUSIONS: AKI is an important complication of anabolic steroid and vitamin supplement abuse. The exact pathophysiology of this type of AKI remains unclear. The main cause of renal dysfunction in these cases seems to be the vitamin D intoxication and drug-induced interstitial nephritis. It is mandatory to start early treatment for serious hypercalcemia, with vigorous venous hydration, diuretics and corticosteroids.
    Last edited: Jun 11, 2011
    Millard Baker likes this.
  11. #11

    akiravp82 Member

    Thanks for the article Dr.Scally!
  12. #12
    Dr JIM

    Dr JIM Member

    Oh an FYI, while "renal tubule" damage can and often is reversible, glomerular damage is nonreversible for all intents and purposes.

    That's an import distinction bc many nephrotoxins result in tubular injury rather than the glomeruli
  13. #13

    Demondosage Member

    All I can give you is my own experience from using anabolics for the better part of 15 years and my recent bloodwork. Recent bloodwork showed elevated levels of crealbumin, but creatinine was in normal range. Bun was also in normal range. This was taken right after a pretty good whack of winny. From everything I've researched BUN and creatinine levels are a more direct indicator of kidney failure/damage than crealbumin is, but it was enough to make me go get some cranberry extract and a kidney detox formula.

    To say it's not harmful over many years of use is just not something I can agree with. I've just heard of too many guys on dialysis and personally know a guy who is probably going to die soon if he doesn't get a kidney transplant. But I'm certainly no Doc, just my input on it
  14. #14
    Dr JIM

    Dr JIM Member

    What is "crealbumin"?
  15. #15
    I think that's the creatine that's bound to albumin. I always test free creatine levels myself.o_O:confused::eek:
    Dr JIM likes this.
  16. #16
    Dr JIM

    Dr JIM Member

    Perhaps but I've NEVER seen an assay for "crealbumin" nor have I noted such a result cited in the medical literature.

    To that end, I've no doubt using "crealbumin" (if such a test even exists) as a marker of renal dysfunction is certainly not evidence based.

    Which leads me to query whether this "test" is the epitome of bro science!
    CensoredBoardsSuck likes this.
  17. #17
    Dr JIM

    Dr JIM Member

    As an aside one of the reasons creatinine is such a relIable indicator of renal dysfunction is its overwhelming tendency to remain unbound to serum proteins during its transit to the kidney.

    Moreover once creatnine is filtered it will be excreted rather than resorbed, exclusive of intrinsic renal disease

    Overall this process would be significantly atered if protein binding was the primary mode of creatnine transport.

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