Anabolic Steroids & Kidney

[Michael Scally MD]

[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. http://www.indianjnephrol.org/artic...=25;issue=2;spage=99;epage=102;aulast=Matthai

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.

 

[Oregongearhead]

On a related note , my creatinine levels just came back at 1.08 mg !! BUN was 14 . Im quite happy because my doc thought I might have some kidney disease because of past creatinine levels of 140 , 136 and 131 (125 is high range)

All I did was quit lifting weights for 2 weeks , no high protein diet and no steroids for 3 months.

 

[Michael Scally MD]

[Portugese] Nephrocalcinosis Associated With The Use Of Anabolic Steroid

The anabolic steroid have been used as a therapeutic tool in various clinical conditions. However, indiscriminate use associated with other nutritional supplements has generated serious adverse effects.

CASE REPORT: Male, 21 years old, admitted with nausea, fatigue, appetite loss, headache and hypertension. Blood tests showed Cr: 3.9 mg% U: 100 mg% and Total Calcium 14 mg/dl. Ultrasonography and renal biopsy were consistent with nephrocalcinosis. There has been gradual improvement in renal function and calcium levels after vigorous hydration and furosemide. However, after 1 year, renal calcium deposits persist, corticomedullary ratio reduced in ultrasound and stable creatinine of 1.4 mg/dl. Previous cases showed acute tubular necrosis and interstitial nephritis with little calcium deposits in the renal interstitium. In this case we found severe nephrocalcinosis associated with nephrosclerosis. Our objective is to report the occurrence of acute kidney Injury with nephrocalcinosis associated with use of anabolic steroid and provide a review of the matter.

Luchi WM, Ricarte RN, Roitman LF, Santos OD. [Nephrocalcinosis associated with the use of anabolic steroid]. J Bras Nefrol. 2015;37(1):135-40. http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002015000100135&lng=en&nrm=iso

 

[Michael Scally MD]

Robles-Diaz M, Medina-Caliz I, Lucena MI, Andrade RJ. Editorial: showing due DILIgence - the lessons from anabolic steroids; authors' reply. Aliment Pharmacol Ther. 2015;41(3):324. http://onlinelibrary.wiley.com/doi/10.1111/apt.13059/full


Neuberger J. Editorial: showing due DILI-gence - the lessons from anabolic steroids. Aliment Pharmacol Ther. 2015;41(3):321-3. http://onlinelibrary.wiley.com/doi/10.1111/apt.13048/full

 

[Michael Scally MD]

Asymptomatic Microhematuria
https://www.auanet.org/education/guidelines/asymptomatic-microhematuria.cfm

1. Asymptomatic microhematuria (AMH) is defined as three or greater red blood cells (RBC) per high powered field (HPF) on a properly collected urinary specimen in the absence of an obvious benign cause. A positive dipstick does not define AMH, and evaluation should be based solely on findings from microscopic examination of urinary sediment and not on a dipstick reading. A positive dipstick reading merits microscopic examination to confirm or refute the diagnosis of AMH. Expert Opinion

2. The assessment of the asymptomatic microhematuria patient should include a careful history, physical examination, and laboratory examination to rule out benign causes of AMH such as infection, menstruation, vigorous exercise, medical renal disease, viral illness, trauma, or recent urological procedures. Clinical Principle

3. Once benign causes have been ruled out, the presence of asymptomatic microhematuria should prompt a urologic evaluation. Recommendation (Evidence Strength Grade C)

4. At the initial evaluation, an estimate of renal function should be obtained (may include calculated eGRF, creatinine, and BUN) because intrinsic renal disease may have implications for renal related risk during the evaluation and management of patients with AMH. Clinical Principle

5. The presence of dysmorphic red blood cells, proteinuria, cellular casts, and/or renal insufficiency, or any other clinical indicator suspicious for renal parenchymal disease warrants concurrent nephrologic workup but does not preclude the need for urologic evaluation. Recommendation (Evidence Strength Grade C)

6. Microhematuria that occurs in patients who are taking anti-coagulants requires urologic evaluation and nephrologic evaluation regardless of the type or level of anti-coagulation therapy. Recommendation (Evidence Strength Grade C)

7. For the urologic evaluation of asymptomatic microhematuria, a cystoscopy should be performed on all patients aged 35 years and older. Recommendation (Evidence Strength Grade C)

8. In patients younger than age 35 years, cystoscopy may be performed at the physician's discretion. Option (Evidence Strength Grade C)

9. A cystoscopy should be performed on all patients who present with risk factors for urinary tract malignancies (e.g., irritative voiding symptoms, current or past tobacco use, chemical exposures) regardless of age. Clinical Principle

10. The initial evaluation for AMH should include a radiologic evaluation. Multi-phasic computed tomography (CT) urography (without and with intravenous (IV) contrast), including sufficient phases to evaluate the renal parenchyma to rule out a renal mass and an excretory phase to evaluate the urothelium of the upper tracts, is the imaging procedure of choice because it has the highest sensitivity and specificity for imaging the upper tracts.

 

[Michael Scally MD]

Tabatabaee SM, Elahi R, Savaj S. Bile Cast Nephropathy Due to Cholestatic Jaundice After Using Stanozolol in 2 Amateur Bodybuilders. Iran J Kidney Dis. 2015;9(4):331-4. http://www.ijkd.org/index.php/ijkd/article/view/2059

Elevated level of bile can cause bile cast nephropathy, which can be seen in patients with severe cholestatic liver disease. Stanozolol is a C17alpha-alkylation steroid derived from dihydrotestosterone and its major adverse effect is cholestatic jaundice. We report 2 bodybuilders who received stanozolol for 6 weeks and developed icterus. Serum total bilirubin was around 50 mg/dL. Liver biopsy showed intrahepatic cholestasis. In spite of fluid and albumin therapy, serum creatinine increased and the patients experienced oliguria. Urine sediment showed granular cast and normal erythrocyte count. Protein excretion in 24-hour urine was less than 1000 mg in both patients. Hemodialysis was started on and renal biopsy revealed acute tubular epithelial cell damage along with bile pigment (cast) deposition, compatible with bile cast-related nephropathy. Serum bilirubin decreased gradually and urine output increased. Serum creatinine was around 1.5 mg/dL in both of the patients 2 months after discharge.

 

[Michael Scally MD]

[Open Access] Acute Kidney Injury Associated With Androgenic Steroids and Nutritional Supplements

Almukhtar SE, Abbas AA, Muhealdeen DN, Hughson MD. Acute kidney injury associated with androgenic steroids and nutritional supplements in bodybuilders. Clin Kidney J. 215;8(4):415-9. http://ckj.oxfordjournals.org/content/8/4/415.full

Four bodybuilders who injected anabolic steroids and ingested commercial protein (78-104 g/day) and creatine (15 g/day) products presented with serum creatinine levels between 229.84 and 335.92 micromol/L (2.6-3.8 mg/dL).

Renal biopsies revealed acute tubular necrosis.

Four weeks after discontinuing injections and supplements, serum creatinine was in the normal range and estimated glomerular filtration rate > 1.00 mL/s (60 mL/min), including two patients with biopsies showing >30% interstitial fibrosis and tubular atrophy.

The findings highlight a risk for acute and potentially chronic kidney injury among young men abusing anabolic steroids and using excessive amounts of nutritional supplements.

 

[Sworder]

Robles-Diaz M, Medina-Caliz I, Lucena MI, Andrade RJ. Editorial: showing due DILIgence - the lessons from anabolic steroids; authors' reply. Aliment Pharmacol Ther. 2015;41(3):324. http://onlinelibrary.wiley.com/doi/10.1111/apt.13059/full


Neuberger J. Editorial: showing due DILI-gence - the lessons from anabolic steroids. Aliment Pharmacol Ther. 2015;41(3):321-3. http://onlinelibrary.wiley.com/doi/10.1111/apt.13048/full

"Although AAS can be taken topically or orally, most use them intramuscularly so putting the users at increased risk of blood borne viruses, including Hepatitis B and C and HIV."

Lol these researchers..

 

[Big_paul]

Shit I'm sitting in a hospital right now with fucked up kidneys, and with the same symptoms.

I never worried much about liver because I never had an issue with my liver before, even after using dbol for years.

It nothing but low dose trt from here on.

 

[Oregongearhead]

Shit I'm sitting in a hospital right now with fucked up kidneys, and with the same symptoms.

I never worried much about liver because I never had an issue with my liver before, even after using dbol for years.

It nothing but low dose trt from here on.

High creatinine/BUN Paul ? Speedy recovery !

 

[Big_paul]

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.

 

[Oregongearhead]

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 ...

 

[Big_paul]

I take 100mg metroprolol and 20mg lysinapril. BP was still hard to keep steady. Could be kidney disease was responsible . When I first starting taking it, I'd pass out if I stood to fast. Strong stuff. Better than pushing daisys though.

 

[Burrr]

BP, and anyone else... what can we do to minimize kidney damage as gear users? Stay hydrated and watch BP come to mind, anything else?

 

[roastdawg]

BP, and anyone else... what can we do to minimize kidney damage as gear users? Stay hydrated and watch BP come to mind, anything else?

You said it bro, stay hydrated and watch bp. And avoid diuretics. Those are the keys imo.

 

[Big_paul]

For myself, I'm a little shocked Im having problems with my kidneys. Maybe I shouldn't because the kidneys have to excrete much of the gear we use.

Will do much better staying hydrated.

For us as body builder, its a trade. I like the way I look, and I'm willing to take some abuse to continue to enjoy the body building lifestyle, as long as it doesn't shave 20 years off my life.

 

[Big dog]

For myself, I'm a little shocked Im having problems with my kidneys. Maybe I shouldn't because the kidneys have to excrete much of the gear we use.

Will do much better staying hydrated.

For us as body builder, its a trade. I like the way I look, and I'm willing to take some abuse to continue to enjoy the body building lifestyle, as long as it doesn't shave 20 years off my life.

I just read your post and I'm sorry to hear about your kidneys. I just found out my kidneys are only putting out at 38%. Can you say where your at with this?

 

[Big_paul]

I just read your post and I'm sorry to hear about your kidneys. I just found out my kidneys are only putting out at 38%. Can you say where your at with this?

It was a combination of dehydration and steroids. I was traveling and wasn't keeping myself hydrated.

Took a couple days in the hospital, with a constant iv to get my kidney function back to normal.

Lesson learned, when you use steroids, stay hydrated. Bp and heart rate were all screwed up.

 

[roastdawg]

It was a combination of dehydration and steroids. I was traveling and wasn't keeping myself hydrated.

Took a couple days in the hospital, with a constant iv to get my kidney function back to normal.

Lesson learned, when you use steroids, stay hydrated. Bp and heart rate were all screwed up.

What were your bp and heart rate at?

 

[Big_paul]

Resting heart rate was 120. Bp wasn't crazy high, but any time I go to the ER I get admitted because of s heart attack I had smoking crack 30 years ago. Guess i had that coming since i was the first guy in the neighbor hood that knew make crack. I think about that all the time. How many lives i fuckec up.

They see an inverted t-wave and they keep me.

First time anyone ever told me my kidneys were struggling though.