Is Testosterone Bad for Your Kidneys?

Testosterone does place measurable stress on the kidneys through several biological pathways, but calling it flatly “bad” oversimplifies the picture. At normal physiological levels, testosterone promotes higher blood pressure within the kidney’s filtering units and activates hormonal systems linked to salt retention and tissue scarring. At supraphysiological doses, particularly through anabolic steroid abuse, the damage can be severe and lasting. Yet in men who are testosterone-deficient, restoring levels to normal may actually protect the kidneys. The answer depends less on whether testosterone is present and more on how much, in what form, and in whom.

How Testosterone Stresses the Kidneys

The kidneys filter blood through tiny structures called glomeruli, and testosterone influences how hard those structures work. In animal models, testosterone activates the renin-angiotensin system, the hormonal cascade that regulates blood pressure and fluid balance. When researchers gave salt-loaded rats testosterone after castration, their blood pressure climbed, protein leaked into the urine, and their kidneys showed scarring. The hormone appeared to ramp up the production of angiotensinogen within the kidney itself, driving a local cycle of high pressure and tissue injury.¹ Earlier work proposed that testosterone boosts sodium reabsorption in the kidney’s tubules, which in turn triggers a feedback loop that widens the vessel feeding the glomerulus, letting too much pressure through.²

This pattern shows up in humans too. A study of men and postmenopausal women with type 2 diabetes found that men had higher glomerular filtration rates and a trend toward higher pressure inside the glomerulus compared with women, even after adjusting for blood pressure, blood sugar, and body size. The researchers attributed this to greater dilation of the vessel feeding the glomerulus, consistent with the idea that testosterone pushes the kidney toward hyperfiltration.³ Hyperfiltration sounds like it should be a good thing, since it means the kidneys are filtering more, but it wears glomeruli out faster over time, much like running an engine perpetually in the red zone.

There is also a protein-level dimension. Research tracking thousands of circulating proteins found that many kidney-protective molecules were positively associated with estradiol and negatively associated with testosterone. These included proteins involved in maintaining blood vessel health, reducing inflammation, and preserving kidney tissue structure.⁴ In other words, estrogen and testosterone pull the kidney’s protective machinery in opposite directions.

Separately, castration in diabetic male rats significantly reduced albumin leaking into the urine and lowered kidney weight, while the same procedure in females had no protective effect, reinforcing that testosterone specifically drives kidney stress in males.⁵

Why Men Lose Kidney Function Faster

Chronic kidney disease progresses more quickly in men than in women, and testosterone is one of the likely reasons. A large analysis adjusting for demographics, existing kidney function, other health conditions, social factors, and medications found that male sex was associated with roughly a 28% higher risk of kidney failure and a 29% higher risk of death compared with female sex.⁶ That gap persists even when you account for the fact that men tend to have higher blood pressure, more diabetes, and other conventional risk factors. The biological mechanisms described above, the glomerular hyperfiltration, the renin-angiotensin activation, and the suppression of protective proteins, offer a plausible explanation for why male kidneys seem to take more punishment from the same diseases.

Interestingly, this male disadvantage appears to have something to do with testosterone rather than simply with being biologically male. A study of young men with a condition that prevents the body from producing normal amounts of testosterone (hypogonadotropic hypogonadism) found that their kidneys were actually hyperfiltering more than those of healthy controls. Hyperfiltration correlated positively with the hypogonadal condition, and the elevated filtration rates existed independently of body weight or age.⁷ That finding complicates the story: even low testosterone doesn’t necessarily spare the kidney from abnormal filtration dynamics, suggesting the relationship between the hormone and kidney hemodynamics is not a straight line.

Anabolic Steroids and Severe Kidney Damage

If the effects of normal testosterone on the kidney are a slow push, anabolic steroid abuse is a shove off a cliff. The doses bodybuilders and athletes use can be ten or more times what the body produces naturally, and the kidney consequences match that excess. A landmark study identified severe focal segmental glomerulosclerosis, a form of scarring in the kidney’s filtering units, in a cohort of ten bodybuilders who had used anabolic steroids long-term. Biopsies showed FSGS in nine of them, with several also displaying abnormally enlarged glomeruli.⁸ That study was described as the first to link anabolic steroid abuse to serious kidney damage, and it prompted further attention from the nephrology community.⁹ Subsequent reviews confirmed that anabolic steroids are emerging as toxins to podocytes, the specialized cells that form the kidney’s filtration barrier.¹⁰

Animal experiments fill in the cellular detail. Mice given the anabolic steroid nandrolone over an extended period developed dose-related oxidative damage in their kidneys, with rising levels of a marker for cell membrane destruction and declining activity of the enzymes that normally neutralize damaging free radicals. The kidney tissue showed significant scarring and signs of inflammatory signaling.¹¹ Rats given anabolic steroids showed similar oxidative damage along with loss of kidney cell membrane integrity.¹²

Beyond the direct scarring and oxidative damage, anabolic steroids can wreck kidneys through indirect routes. Liver damage from oral steroids can cause a backup of bile acids into the bloodstream, and those bile acids are toxic to the kidney’s tubular cells. Separately, the combination of massive muscle mass, intense exercise, and intramuscular steroid injections raises the risk of rhabdomyolysis, where muscle fibers break down and flood the bloodstream with proteins that obstruct and poison kidney tubules.¹³ These indirect mechanisms mean that even a steroid user who avoids direct glomerular scarring can still end up with acute kidney injury through liver complications or muscle breakdown.

The Creatinine Problem

One of the trickiest aspects of evaluating testosterone’s effect on the kidneys is that our most common kidney function test, serum creatinine, is deeply confounded by the hormone. Creatinine is a waste product of muscle metabolism. More muscle means more creatinine in the blood, regardless of how well the kidneys are working. Since testosterone builds muscle, anything that raises testosterone, whether replacement therapy, anabolic steroids, or gender-affirming hormone therapy, will push creatinine up and make estimated kidney function look worse on paper even if the kidneys are fine.

This has been observed clearly in transgender men starting testosterone therapy. A systematic review and meta-analysis found that serum creatinine rose by about 0.15 mg/dL at twelve months in transgender men, while no study reported corresponding changes in cystatin C or directly measured filtration rates.¹⁴ A later study of transgender veterans confirmed this: creatinine climbed as early as three months after starting testosterone and stabilized by twelve months, while estimated filtration rates dropped accordingly.¹⁵ A meta-analysis focused specifically on this population found that estimated filtration rates showed a transient dip during the first year and then stabilized, while blood urea nitrogen, another kidney marker that is less influenced by muscle mass, did not change at all. The authors concluded the pattern was most likely attributable to increased creatinine production from testosterone-driven muscle gains rather than actual kidney damage.¹⁶

This matters practically. A clinician looking at creatinine-based estimated GFR in someone on testosterone therapy might flag declining kidney function when nothing is actually wrong. One paper examining this issue directly noted that prior research linking testosterone to kidney function decline relied on creatinine-based estimates, which may be biased by the association between testosterone and muscle mass.¹⁷ A study of men with testosterone-induced muscle enlargement explored whether cystatin C, a kidney marker less affected by muscle mass, could serve as a better alternative. In men with normal body weight, there was no meaningful correlation between creatinine and cystatin C, but the two markers tracked more closely as body fat percentage rose.¹⁸ For anyone on testosterone in any form, the practical takeaway is that cystatin C or directly measured GFR gives a more honest picture of kidney health than creatinine alone.

Testosterone Replacement Therapy in People with Kidney Problems

Low testosterone is extremely common in men with chronic kidney disease, with estimates ranging well above half of dialysis patients. For these men, the question is not whether testosterone hurts the kidneys but whether restoring it is safe and whether it might help. A study of TRT in chronic kidney disease patients found it effective at correcting clinical signs of low testosterone without significant risk of fluid overload or concerning prostate marker changes.¹⁹

A larger study looked at men who had both diabetes and low testosterone, a combination that puts the kidneys at particular risk. Compared with untreated men, those who received testosterone therapy had a significantly lower risk of acute kidney injury and kidney failure requiring dialysis or transplant.²⁰ That finding runs directly counter to what the animal studies and mechanistic work might predict. The likely explanation is that testosterone deficiency itself carries metabolic consequences, including worsened insulin resistance, increased fat mass, and greater systemic inflammation, that are also bad for kidneys. Correcting the deficiency may address those problems enough to outweigh the direct hemodynamic stress testosterone places on glomeruli.

The large TRAVERSE cardiovascular safety trial, which primarily tested whether TRT raised the risk of heart attacks and strokes, recorded acute kidney injury as a secondary safety signal. AKI was numerically more frequent in the testosterone arm than the placebo arm, but the difference did not reach statistical significance within the trial.²¹ The most consistent adverse effect by far was erythrocytosis, an overproduction of red blood cells, which was dramatically more common in men receiving testosterone. Whether that signal for kidney injury will become meaningful in longer or larger studies remains to be seen, but for now it sits in the “worth monitoring” category rather than the “established harm” category.

What Happens When You Strip Testosterone Away

If testosterone harms the kidneys, you might expect that eliminating it would protect them. Prostate cancer patients undergoing androgen deprivation therapy provide a natural experiment, and the results are surprisingly counterintuitive. An early population-based study found that men currently on any form of androgen deprivation therapy had roughly two and a half times the odds of acute kidney injury compared with men who had never used it.²² A meta-analysis including over 72,000 patients confirmed a significant association between androgen deprivation therapy and AKI, with the risk driven mainly by the drugs used rather than by testosterone suppression per se. Surgical castration, which removes testosterone completely, was not associated with increased AKI, while drug-based approaches were.²³

That distinction matters a great deal. It suggests the kidney risk from androgen deprivation therapy has more to do with the pharmacology of the drugs, particularly GnRH agonists and combination regimens, than with low testosterone itself. A newer analysis from the RADICAL-PC study muddied the waters further by finding no significant difference in the rate of kidney function decline between men on androgen deprivation therapy and those not on it. When analyzed as a time-varying factor, men using the therapy actually experienced less GFR decline than those without it. Baseline use was linked to more AKI in a simple analysis, but that association disappeared after adjusting for other health factors.²⁴ The researchers concluded that androgen deprivation therapy was not independently linked to kidney function decline or AKI, directly challenging the earlier literature. The bottom line on testosterone removal: it does not clearly help the kidneys, and the drugs used to achieve it may carry their own risks.

Testosterone and Kidney Stones

There is a separate and less-discussed way testosterone affects the kidneys: it promotes kidney stone formation. Men develop calcium oxalate stones significantly more often than women, and testosterone’s interaction with the androgen receptor appears to be a reason. Researchers used genetically modified mice to selectively knock out the androgen receptor in different tissues and found that removing it from the liver reduced the production of oxalate, one of the key ingredients in the most common type of kidney stone. Removing it from kidney cells directly reduced crystal formation within the kidney itself.²⁵ The androgen receptor was found to increase expression of an enzyme in the liver responsible for making oxalate and a separate enzyme in the kidney that generates oxidative stress, damaging the lining of kidney tubules and creating conditions favorable for crystals to form and stick. When the researchers used a compound that degrades the androgen receptor, stone formation dropped in both lab dishes and live animals. This line of research is still largely preclinical, but it offers a biological explanation for the well-known sex difference in kidney stone rates and raises the possibility that androgen receptor–targeted therapies could one day prevent stones.

Elevated Testosterone in Women with PCOS

Polycystic ovary syndrome offers another window into testosterone’s kidney effects, this time in women. PCOS is characterized by elevated androgens, and researchers have wondered whether that excess testosterone damages the kidneys. A study measuring markers of tubular injury in women with PCOS found that serum testosterone had a significantly positive correlation with all tubular proteinuria markers tested, suggesting testosterone plays a role in damaging the cells lining the kidney’s tubules.²⁶ Uric acid levels are also consistently higher in women with PCOS. However, a systematic review and meta-analysis found that standard measures of overall kidney function, creatinine and estimated filtration rate, were statistically similar between women with and without PCOS.²⁷ The picture in PCOS is one of early, subtle tubular damage that has not yet progressed to measurable loss of overall filtration, at least in the relatively young women studied so far. Whether those early signals eventually lead to clinical kidney disease with age remains an open question, and it is one more reason for women with PCOS to have their kidney health monitored over time.