tren and kidneys

[gtbro1]

good Post RDW

[Van_Bilderass]

I don't believe it's as bad on the kidneys as some seem to think, however, 6 months of 150mg/day for 6 months is not wise in my opinion.  The problem with  many of the studies is that they focus on direct acting problems (or lack there of) of the kidneys and renal system.  Tren doesn't seem to have any significant direct effects, however when combined with high levels of potassium the kidneys have greater trouble maintaining pH balance in the blood.  I think this is why some people seem to have problems and others don't.  Those who take potassium suppliments in order to hold more water in the muscle and get a hypertrophic look when in the gym or whevever else put themselves are higher risk for hyperkalaemia and metabolic acidosis.  Under normal use I doubt anyone will encounter this, but again, 6 months @ 150mg... that is just asking for trouble.  Too much of anything is bad, as a general rule for all things, aim for 80/20 rule.  That is that with 20% of the effort/risk you get 80% of the reward.  To go further you must climb and exponential hill and the risk-reward factor becomes underwhelming.  For those of you that know what I mean about the 80/20 rule, it fits quite well with most things in life if you apply it.  If you don't know what I'm talking about, there is a time constant in physics and engineering for frequency response linear time-invariant systems (It's really 1/5 or 20% time step to equal 63.3% production, but people call it the 80/20 rule), worth reading up as it applies to litterally most things in life.  Anyway, as usualy I have veered from the original path and am now rambling...

Could you explain the connection between tren specifically and high potassium levels? If tren is bad for the kidneys, what is the mechanism?

I know some use Potassium Citrate for the alkalizing effects. What do you think about that? It's the preferable alkalizing agent for many athletes from what I've seen.

Here's a proposed mechanism whereby androgens could be harmful to the kidneys. The bad news is that this happens with testosterone.

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

[RDW]

First off, Apoptosis is a normal part of cellular proliferation. Apoptosis is a PCD (Programmed Cell Death) and actually helps prevent uncontrolled cellular proliferation which leads to cancer.  By killing off the old cellular (and possibly mutated) construction it allows for new healthy cells.  Testosterone speeds up this process as stated in your article by

increasing the permissiveness of proximal tubule kidney cells to apoptotic effects by triggering an apoptotic pathway involving caspase activation

.  The caspase enzymes clear out the proteins in the existing cells and is essential to apoptosis.  In moderation testosterone actually helps keep the cellular structure new and healthy, however, as is the case with all things, too much of this is litterally "overkill".

As far as Tren goes, trenbolone and 17epi-trenbolone are both excreted as conjugates that can be hydrolyzed.  Hydrolysis involves refluxing the esters of carboxylic acid with an aqueous base such as NaOH or KOH (Potassium Hydroxide) binding it's hydroxyl group and leaving the potassium.  The more potassium available in conjunction with tren the more this process can occur, this can result in hyperkalaemia.  The risk factor is low under normal potassium intake levels, I am talking about extreme cases of those who take 1000mg of Potassium capsules continually to maintain a hypertrophic look (not those who are trying to maintain electrolyte levels).  That's why in my first post I said I don't see a real problem with Tren and the kidneys, however if there is one, it is likely due to this.  If this occurs, however, your primary concern should be the arrhythmia it will likely cause.

[Fulgorre]

I doubt it blowing out anyone kidneys. 

[Vet]

First off, Apoptosis is a normal part of cellular proliferation. Apoptosis is a PCD (Programmed Cell Death) and actually helps prevent uncontrolled cellular proliferation which leads to cancer.  By killing off the old cellular (and possibly mutated) construction it allows for new healthy cells.  Testosterone speeds up this process as stated in your article by .  The caspase enzymes clear out the proteins in the existing cells and is essential to apoptosis.  In moderation testosterone actually helps keep the cellular structure new and healthy, however, as is the case with all things, too much of this is litterally "overkill".

As far as Tren goes, trenbolone and 17epi-trenbolone are both excreted as conjugates that can be hydrolyzed.  Hydrolysis involves refluxing the esters of carboxylic acid with an aqueous base such as NaOH or KOH (Potassium Hydroxide) binding it's hydroxyl group and leaving the potassium.  The more potassium available in conjunction with tren the more this process can occur, this can result in hyperkalaemia.  The risk factor is low under normal potassium intake levels, I am talking about extreme cases of those who take 1000mg of Potassium capsules continually to maintain a hypertrophic look (not those who are trying to maintain electrolyte levels).  That's why in my first post I said I don't see a real problem with Tren and the kidneys, however if there is one, it is likely due to this.  If this occurs, however, your primary concern should be the arrhythmia it will likely cause.

The arrythmia from 1000 mg of Potassium orally for repeated doses is going to kill you long before the kidneys shut down.  That said, the potassium idea is an interesting one, but it seems to go against the current ideas in emergency and critical care medicine that Sodium is the real culprit when considering the kidneys abilities to handle electrolytes.   Remember, potassium is a passive/cotransportation process in the renal tubules but Sodium is an active transport process.  Potassium is the primary cation in the cells of the body, while sodium is in the plasma.  This means that excessive potassium does have a place to go (intracellularly) and is readily excreted from the body via the urine.  This means that diets high in sodium, or substances that force the body to retain sodium can place an increased stress on the cells of the renal tubule via the increased active transport.  This can then lead to problems in predisposed individuals. 

If you combine the Sodium idea with activation of the Renin-Angiotensin-Aldosterone system which anabolic steroids all cause, and consider the fact that these all contribute to hypertension combined wiht the well known fact that glomerular hypertension will "fry" the kidneys, you've got an academic, but reasonable explanation for the reports of Tren possibly causing kidney disease.   It really boils down to Tren causes hypertension---profound hypertension in some people---and they fry their kidneys secondarily to the high blood pressure.

The thing that gets me is that Tren is used in thousands of cattle across the country----animals that are implanted and then butchered.   No where have I seen a report of implants being associated with renal disease in cattle.  Considering the current steroid witch hunts, if there was going to be even the slightest possibility of this type of substantiated claim being made, you'd think it'd show up in the veterinary literature.  To the best of my knowledge, it hasn't. 

[dr_para24]

make your own.

How you make it?

[Fulgorre]

How you make it?

I'm not going to link a step by step guide for you bro.  And there is no reason to make it, imo, since UG has pure tren. Well, it is a little pricey.

You take these finaplex pellets and crush them, then filter them to get rid of the estradiol, then add oil.  I've never made it so forgive me, but that is the very basic way.  They get the filters and all the supplies from laboratory research companies... which is probably legal.

The pellets are put into cattle ear 63 days before they are slaughtered so they can feed them less, yet increase the amount of meat which is going to be sold to the public.  Both the trenbolone and the estradiol make the cattle grow.  Wikipedia explains it.

[Van_Bilderass]

The arrythmia from 1000 mg of Potassium orally for repeated doses is going to kill you long before the kidneys shut down.  

Is there any danger in taking lots of potassium if not taking diuretics or if you have no other health problems? Like I mentioned earlier some athletes use potassium citrate in multigram dosages before exercise as a buffering agent. One Doc out of Germany, one Torsten Albers, who works with bodybuilders and other athletes advocated this as well.

[Vet]

Is there any danger in taking lots of potassium if not taking diuretics or if you have no other health problems? Like I mentioned earlier some athletes use potassium citrate in multigram dosages before exercise as a buffering agent. One Doc out of Germany, one Torsten Albers, who works with bodybuilders and other athletes advocated this as well.

Increased potassium may be caused by increased intake, reduced renal excretion, or a shift of potassium from the cells to the extracellular space. The ability of the kidneys to excrete potassium is very efficient.  Usually hyperkalemia from excessive "intake" is iatrogenic and related to potassium being added to intravenous fluids in excessive amounts or administered too rapidly while renal disease is the most commonly identified cause of elevated potassium levels.  Angiotensin-converting enzyme inhibitors and potassium-sparing diuretics can also cause decreased renal excretion of potassium. Also, drugs such as β-adrenergic blocking agents can result in translocation of potassium from the intracellular space to the serum.

The things that have to be considered are health status of the athlete, dietary intake, amount of supplemental potassium being taken, renal status of the athlete, and most importantly, any other drugs the athlete may be taking.   Those all need to be carefully thought out before dosing with megadoses of potassium, even oral potassium, and especially with any other form (ie IV). 

IV KCL is a means of euthanasia.  Its also used as a part of the drug cocktail used for execution of death row inmates.  Keep that in mind.