Anabolic steroids and kidney failure
- Thread starter prozak
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crushershockey
New member
it doesn't matter what you take you can have kidney failure at any moment... there's things you can do to help it not happen but if it's gonna happen it's gonna happen
roccodart440
New member
DocJ said:
I would like to believe all of this. YOu got an evidence to make us all feel warm and fuzy doc? I'm not sure either way but my piss smells like hell these days. LOL. DOn't know why.
T
Thoms
Guest
As far as I am concerned, the kidney issue from Anabolic Androgenic Steroids (AAS) is a myth with the possible exception of the constant megadosages used by the pros, and even then the insane amounts of protein they consume are more likely to blame. As a recreational user I don't worry about it one second. Like DocJ said, it's more an internet myth than truth. Even if you run into issues, it's probably because you have a pre-existing condition.
mattd46612
New member
Most of the issues pros run into with kidneys and organs is because of dieuretics and not the gear. CEE, vitamins and stuff you eat can affect you rpiss. Try drinkin more water if your piss is so that bad.
DocJ
New member
Here's a study that should concern us:roccodart440 said:
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Kidney Int: 2004 Apr;65(4):1252-61.
Testosterone promotes apoptotic damage in human renal tubular cells.Verzola D, Gandolfo MT, Salvatore F, Villaggio B, Gianiorio F, Traverso P, Deferrari G, Garibotto G.
Nephrology Division, Department of Internal Medicine and Urology Division, University of Genoa, Genoa, Italy.
BACKGROUND: Apoptosis is a mode of cell death that participates in the kidney physiologic remodeling processes and is thought to contribute to cell loss and kidney structural damage in chronic renal diseases. Gender is one factor which contributes to accelerated nephron loss, with progression more rapid in men than in women in diabetic and nondiabetic chronic renal diseases. Mechanisms by which androgens may cause higher rate of progression of chronic renal diseases in men are poorly explored. METHODS: In this study, to investigate the role of androgens on apoptotic damage and its associated mechanisms, we examined the effects of testosterone (T) (0.1 nmol/L to 1 micromol/L) on apoptosis, and apoptosis-related proteins in a proximal human tubule cell line (HK-2 cells). Additional experiments were performed in primary cultures of proximal tubular epithelial cells (PTECs). Cells were grown to subconfluence in normal growth medium, and apoptotic damage was induced by serum deprivation for 24 to 48 hours. Cycloheximide, flutamide (a T-receptor antagonist), 17-beta estradiol, or caspase inhibitors were added to cultures that were successively processed for terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end-labeling (TUNEL) analysis, annexin V/propidium iodide staining, immunofluorescence, or immunoblots to identify effects and apoptotic pathways that could be modulating cell survival. RESULTS: Both morphologic analysis by annexin V/propidium iodide staining and TUNEL showed that physiologic T levels (1 to 10 nmol/L) induced a significant increase in apoptosis both in HK-2 cells and PTECs. In both types of cell lines pretreatment with the androgen receptor antagonist flutamide prevented the T-induced apoptosis. T-induced apoptosis was enhanced by treatment with cycloheximide and prevented by 17beta-estradiol. Fas, Fas ligand (FasL), and Fas-associating death domain containing protein (FADD) were clearly up-regulated within 48 hours of T treatment in HK-2 cells. Also, T significantly increased the expression of Bax protein (P < 0.01 vs. control) (an effect which was blocked by flutamide), and decreased the expression of Bcl-2. Western blot analysis showed that caspase-3 was activated. Moreover, cleavage into an 85-kD poly(ADP-ribose) polymerase-1 (PARP-1) terminal breakdown product was detectable. The changes in cellular morphology induced by T at 48 hours were no longer observed after the addition of caspase-8, caspase-9, and caspase-3 inhibitors to the culture medium. CONCLUSION: These results indicate that T increases the permissiveness of proximal tubule kidney cells to apoptotic effects by triggering an apoptotic pathway involving caspase activation, Fas up-regulation, and FasL expression, thus potentially interacting with mechanisms of cell loss which have been already shown to be activated in chronic renal diseases. This is consistent with a role for T in promoting renal injury in men.
PMID: 15086464 [PubMed - indexed for MEDLINE]
Here's one that should put your mind at ease:
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BMC Nephrol: 2002 Aug 14;3:6.
Sex steroids do not affect shigatoxin cytotoxicity on human renal tubular or glomerular cells.Hughes AK, Schmid DI, Kohan DE.
Division of Nephrology, University of Utah Health Sciences Center and Salt Lake Veterans Affairs Medical Center, Salt Lake City, UT, USA. alisa.highes@hsc.utah.edu
BACKGROUND: The greater susceptibility of children to renal injury in post-diarrheal hemolytic-uremic syndrome (HUS) may be related, at least in part, to heightened renal cell sensitivity to the cytotoxic effect of Shiga toxin (Stx), the putative mediator of kidney damage in HUS. We hypothesized that sexual maturation, which coincides with a falling incidence of HUS, may induce a relatively Stx-resistant state in the renal cells. METHODS: Cultured human glomerular endothelial (HGEN), human glomerular visceral epithelial (HGEC) and human proximal tubule (HPT) cells were exposed to Stx-1 after pre-incubation with progesterone, beta-estradiol or testosterone followed by determination of cytotoxicity. RESULTS: Under basal conditions, Stx-1 potently and dose-dependently killed HPT and HGEC, but had relatively little effect on HGEN. Pre-incubation for 1, 2 or 7 days with physiologic or pharmacologic concentrations of progesterone, beta-estradiol or testosterone had no effect on Stx-1 cytotoxicity dose-response on any cell type. In addition, no steroid altered Gb3 expression (Stx receptor) by any cell type at any time point. CONCLUSION: These data do not support the notion that hormonal changes associated with puberty induce an Stx-resistant state within kidney cells.
PMID: 12181081 [PubMed - indexed for MEDLINE]
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I could go on all day...for every study showing possible kidney damage caused by androgens, I can find at least 1-2 that says they didn't see any damage.
Micro
New member
My last cycle I was running Tren E and my Creatinine levels came back at 1.6 and the GFR test was 51. I was off Tren for about 3wks when I got this test done. My test results show kidney damage. I know one guy that say his doctor told him his kidneys are in bad shape because his GFR was 49. I'm going to my doctor this week to get it checked again.
Micro
Micro
High Readings
Do not forget that if your diet was where it shoulda been while "ON" then the high doses of proteins may and I did say May have had something to do with it. Alcohol also causes liver and kidney damage as well. Some of this damage will repair itself if it's not too bad. This is why time "OFF" is also as important. It allows the body to heal and grow. w/out knowing doses and length of duration of your cycle it is hard to say. But do not freak out. You are taking the common sense approach, if in doubt, check it out.Micro said:
running gun
Gear In Motion
Micro, did you have any symptoms before you were tested?
Micro
New member
running gun said:
No, I accually had an anxiety attack afew wks ago and they did some blood work at the hospital that is when it showed my GFR was low. Creatinine levels should be between 0.6-1.5, mine was 1.6 even though it's over 1.5 I wouldnt say it's that bad because bodybuilders are known to have higher creatinine levels and GFR should be greater then 60 mine was 51.96. RBC was 18.2 normal is 13.7-17.5 , my sister is anemic and her's is 8, Bun was 20 normal is 8-25. I'll get a CBC next wk and see were I'm at. I just order some Liv52 and UriCare for my liver and kidneys.
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