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REVIEW ARTICLE
Year : 2019  |  Volume : 19  |  Issue : 4  |  Page : 124-128

Gym nephropathy ‘bodybuilding versus kidney damaging’


Gawad Nephrology Clinic, Alexandria, Egypt

Date of Submission25-Aug-2019
Date of Decision13-Sep-2019
Date of Acceptance06-Oct-2019
Date of Web Publication25-Nov-2019

Correspondence Address:
Dr. Mohammed Abdel Gawad
14 May Bridge, Smouha Class Buildings, Building A, Smouha, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jesnt.jesnt_32_19

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  Abstract 


Nonnutritional and nutritional supplements are widely used by bodybuilders. Abuse of these supplements can cause kidney injury by different mechanisms. We refer to any kidney injury caused by any of these supplements as ‘gym nephropathy.’ Anabolic-androgenic steroids are taken by athletes to gain muscle, but they may induce kidney injury through multiple pathways. Creatine supplementation is safe to be used, and it is capable of increasing muscle strength and mass; however, the indiscriminate use of it may induce acute kidney injury. Many bodybuilders abuse oral and injectable vitamins, which may cause acute kidney injury. High protein improves the training adaptations to exercise with no harm as long as the renal functions are normal; however, the theoretical risks should be reviewed carefully with some individuals. Energy drink-induced renal failure has been also reported. In this article, we review different forms of kidney injury secondary to supplements abused by bodybuilders.

Keywords: acute kidney injury, anabolic-androgen steroids, bodybuilder, creatine monohydrate, endstage renal disease, energy drinks, focal segmental glomerulosclerosis, high-protein diet, nephrolithiasis, vitamin


How to cite this article:
Gawad MA, Kalawy HA. Gym nephropathy ‘bodybuilding versus kidney damaging’. J Egypt Soc Nephrol Transplant 2019;19:124-8

How to cite this URL:
Gawad MA, Kalawy HA. Gym nephropathy ‘bodybuilding versus kidney damaging’. J Egypt Soc Nephrol Transplant [serial online] 2019 [cited 2019 Dec 13];19:124-8. Available from: http://www.jesnt.eg.net/text.asp?2019/19/4/124/271563




  Introduction Top


Nonnutritional and nutritional supplements are widely used by bodybuilders all over the world. Abuse of these supplements can cause kidney injury by different mechanisms (summarized in [Table 1]). We refer to any kidney injury caused by these supplements as ‘gym nephropathy.’ Nonnutritional supplements used are anabolic-androgenic steroids (AAS), growth hormone, insulin-like growth factor, L-thyroxin, beta-2 agonists, anti-estrogens, beta-human chorionic gonadotropin, and erythropoietin. Nutritional supplements used are creatine, vitamins, protein, amino acids, glutamine, L-arginine, pre-workout energy drinks, L-carnitine, liver albumin, and omega 3. In the following, we summarize the different available evidence of kidney injuries secondary to these supplements.
Table 1 Summary of different supplements used by bodybuilders and their harmful effect on kidney

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Anabolic-androgenic steroids

AAS are taken by athletes to improve performance, gain muscle, and lose body fat [1]. A meta-analysis and meta-regression analysis [2] of 187 studies was performed to investigate moderators of the prevalence rate of AAS. It showed that the highest prevalence rate was in the Middle East; the lowest prevalence was in Asia.

AAS can induce kidney injury through multiple pathways such as stimulating renin–angiotensin–aldosterone system, enhancing the production of endothelin, producing reactive oxygen species, overexpression of profibrotic and proapoptotic mediators, as well as inflammatory cytokines [3]. In the following, we discuss the different forms of kidney injury secondary to AAS abuse.

Focal segmental glomerulosclerosis and global sclerosis

Prolonged use of AAS induces focal segmental glomerulosclerosis and global sclerosis. A cohort study [4] of 10 bodybuilders was done after long-term abuse of AAS for a duration varied from 10 to 20 years. The clinical presentation included proteinuria (mean, 10.1 g/d) and renal insufficiency (mean serum creatinine, 3.0 mg/dl). Renal biopsy was done, and it revealed focal segmental glomerulosclerosis in nine patients and glomerulomegaly in one patient. Seven biopsies revealed more than or equal to 40% tubular atrophy and interstitial fibrosis. Among eight patients with mean follow-up of 2.2 years, one progressed to end-stage kidney disease, and the other seven received renin–angiotensin system blockade, and one also received corticosteroids. All seven patients discontinued anabolic steroids, leading to stabilization or improvement in serum creatinine, and a reduction in proteinuria. Of these seven patients, one patient resumed anabolic steroid abuse and experienced relapse of proteinuria and renal insufficiency.

A case report was presented by Hartung et al [5] of a 27-year-old male bodybuilder on high-protein diet with more than 2 g/kg body weight per day, AAS (testosterone), and beta-2 agonist tablets (clenbuterol) for 18 months. He was referred to the hospital because of azotemia, with high serum creatinine, proteinuria, and hematuria. Renal biopsy was performed and revealed nephrosclerosis with pronounced global glomerulosclerosis and diffuse chronic tubulo‐interstitial damage. The patient commenced hemodialysis treatment three times a week and was prepared for renal transplantation. Another case report [6] of a 26-year-old male bodybuilder, giving positive history of AAS intake in addition to other supplements, accidentally discovered to have end-stage kidney disease. His renal ultrasound showed grade III hyper-echogenicity, and his renal biopsy revealed glomerulosclerosis of 100% of the available glomeruli.

de Francesco Daher et al. [7] showed that there is a subclinical kidney injury among AAS users, which was evident by monocyte chemoattractant protein-1 is higher in AAS users than nonusers. Although serum creatinine and cystatin C levels were within normal ranges, they showed a tendency to be higher in AAS users.

Bile acid nephropathy

Renal dysfunction in the setting of cholestatic liver disease is multifactorial. Acute kidney injury (AKI) may develop secondary to hypoperfusion, from tubular bile cast obstruction and directly through tubular toxicity of bile acids. Drug-induced hepatotoxicity is a common cause of acute hepatic injury and may be associated with a cholestatic injury pattern [8].

A case report was presented by Luciano et al [9] of AKI due to bile acid nephropathy in a 41-year-old bodybuilder man who developed severe cholestatic liver disease in the setting of AAS use. Six weeks before evaluation, he received AAS (nandrolone injection, testosterone injection, oral methandrostenolone), supplements (details of which were not known) and protein shakes. Urine microscopy demonstrated bile-stained granular casts, and bile-stained renal tubular epithelial cell casts. Light and electron microscopy evaluation of the kidney biopsy specimen showed evidence of tubular injury, and multiple greenish-brown casts were present within the distal tubular lumens. Another case report [8] was presented of a 56-year-old man with a diagnosis of bile cast nephropathy, as a complication of drug-induced severe hyperbilirubinemia due to the abuse of intramuscular anabolic steroids bought on the internet to increase muscular mass for body-building training. Kidney biopsy showed tubular damage with intratubular bile casts obstructing the renal tubules. The patient developed AKI and needed dialysis treatment for 4 weeks until renal function recovered.

Two cases of severe cholestasis and bile acid nephropathy from AAS were successfully treated with plasmapheresis. The first was a case of 35-year-old male [10] who presented with elevated serum creatinine of 2.2 mg/dl and total bilirubin 37.9 mg/dl at the first day of hospitalization. The diagnosis of bile cast nephropathy was supported owing to the prolonged exposure to high levels of bilirubin and increase in creatinine. However, bile cast nephropathy could not be confirmed by renal biopsy owing to patient refusal. The patient’s status was getting worse although of supportive care, so the decision was to initiate urgent plasma exchange on day 3 of admission and to replace it with donors’ fresh frozen plasma. He tolerated all six sessions well, and he was completely asymptomatic after 3 months with a creatinine level of 1.08 mg/dl and a total bilirubin level of 1.2 mg/dl. The second case was a 31-year-old man [11] who was hospitalized for severe jaundice with total bilirubin of 53 mg/dl and elevated serum creatinine of creatinine 2 mg/dl. Bile acid nephropathy was supported by renal biopsy. Plasmapheresis was initiated to alleviate his pruritus and reduce the burden of circulating bile acids. He underwent five sessions of plasmapheresis. Six weeks after discharge, he was asymptomatic with total bilirubin of 1.2 mg/dl and serum creatinine of 0.9 mg/dl.

Renal artery thrombosis

AAS are responsible for a number of hemostatic defects, including higher platelet number, enhanced platelet aggregation, increased synthesis of procoagulant factors, and impaired fibrinolysis.

A case report [12] was presented of a 34-year-old bodybuilder diagnosed as having right renal artery thrombosis owing to hypercoagulable state secondary to the use of unknown AAS. He was admitted to surgical emergency department with right midabdominal pain that was radiating to the right flank area, azotemia with serum creatinine level of 1.82 mg/dl, elevated D-dimer level, hematuria, and proteinuria. Coagulation profile parameters were within normal limits, and further screening tests for hypercoagulability were ordered; factor V Leiden, fibrinogen level, protein C and S, antithrombin III, antiphospholipid antibody, homocysteine, and anti-double-stranded DNA were all within normal limits. Right kidney infarction was diagnosed by computed tomography angiography. The patient underwent selective intra-arterial thrombolysis, but owing to bleeding complications after selective intra-arterial thrombolysis treatment, he required urgent nephrectomy. After operation, patient required CRRT. Patient was released from the hospital in a general good condition; he did not require renal replacement therapy. Serum creatinine level at discharge was 3 mg/dl.

Creatine monohydrate

Creatine supplementation has been recognized as one of the most efficient dietary supplements capable of increasing muscle strength and lean mass [13], as well as high-intensity exercise performance [14]. However, the indiscriminate use of this supplement has raised concerns regarding its safety, especially in relation to kidney function [15].

Available evidence which suggests the safety of creatine monohydrate

A randomized, double-blind, placebo-controlled trial [16] was performed where the participants were randomly allocated to receive either creatine or placebo. Twelve participants received creatine (20 g/d for 5 days followed by 5 g/d throughout the trial) and 14 participants were on placebo. All of the participants were engaged in resistance training and consumed a high-protein diet (≥1.2 g/kg/d). After a follow-up of 3 months, there was no statistically significant difference observed for 51Cr-EDTA clearance, serum and urinary urea, electrolytes, proteinuria, and albuminuria between the two groups.

Acute kidney injury

Although there is available evidence of the safety of creatine use, there are reports of creatine monohydrate-induced kidney injury. A case report [17] was presented of a 32-year-old man who presented with a 2-week history of nausea and weakness. At presentation, his laboratory studies showed serum urea of 111 mg/dl and serum creatinine of 4.3 mg/dl. He had a history of creatine monohydrate consumption (20 g/day for 3 days and maintenance dose of 1 g/day for 3 weeks) for body-building purposes for 3 weeks during the past month. Renal biopsy revealed normal glomeruli but there was mononuclear interstitial infiltrations and focal tubular disappearance, and he was diagnosed as having creatine monohydrate supplement-induced interstitial nephritis. The patient stopped creatine and received two consecutive days of methylprednisolone pulse therapy (500 mg/day) followed by 60 mg daily prednisolone. After starting corticosteroid therapy, the patient’s serum creatinine level decreased to 1.8 mg/dl, and his general condition improved profoundly.

Another case report [18] was presented of an 18-year-old man who presented with a 2-day history of nausea, vomiting, and stomach ache while consuming induction (20 g/day for 5 days) and maintenance (1 g/day for the next 6 weeks) dosages of creatine monohydrate for bodybuilding purposes. The initial laboratory studies showed serum urea of 111 mg/dl and serum creatinine of 2.27 mg/dl. Urinalysis revealed only proteinuria. The renal biopsy revealed focal tubular injury with dilatation of tubular lumina and flattening of the tubular epithelial cells. The glomeruli appeared to be normal. A diagnosis of acute tubular necrosis was done. Twenty-five days after stopping the creatine supplements, and on supportive treatment, the patient’s renal function returned to normal value and proteinuria normalized.

Vitamins

Many bodybuilders abuse oral and injectable vitamins. A 22-year-old man [19] presented to the Emergency Department with features of acute pancreatitis. Serum creatinine was 8.6 mg/dl, and serum calcium was 13.8 mg/dl (normal range, 8.6–10.3 mg/dl). Drug history showed that the patient was taking monthly intramuscular 50 ml of cholecalciferol (each ml contains 50 000 IU vitamin D) to improve muscle gain in the past 2 years. Computed tomography showed nephrocalcinosis and left renal stone. Renal biopsy showed moderate interstitial fibrosis and tubular atrophy surrounding numerous interstitial calcium deposits. The patient was considered as having only AKI secondary to hypercalcemia and pancreatitis-related complications. Therapy was initiated in the form of prednisone, intense hydration, furosemide, and hemodialysis. Two weeks after acute pancreatitis recovery, serum creatinine remained 1.8 mg/dl and serum calcium was within the normal range.

Another case of a previously healthy 24-year-old man [20] was admitted with a 2-month history of progressively worsening epigastric pain, nausea, vomiting, fatigue, and malaise. He reported abuse of an injectable veterinary vitamin compound, which contains 20 000 000 IU of vitamin A, 5 000 000 IU of vitamin D3, and 6800 IU of vitamin E per 100 ml vial. Laboratory studies (serum) evidenced creatinine 3.1 mg/dl, 25-OH-vitamin D more than 150 ng/ml (toxicity >100), and total calcium 13.6 mg/dl. Ultrasound abdomen and pelvis demonstrated signs of parenchymal nephropathy. The diagnosis was hypercalcemia and AKI secondary to vitamin D (and possibly vitamin A) intoxication. He was treated with vigorous intravenous hydration associated with diuretic and corticosteroids. On the fifth day of hospitalization a single dose of the osteoclast inhibitor pamidronate disodium 90 mg was added. The patient evolved with serum calcium and renal function normalization.

A case series from Brazil [21] consisted of 16 cases that used an excessive and prolonged intramuscular injection of veterinary supplements containing vitamins A, D, and E. Main signs and symptoms upon admission were nausea, vomiting, weight loss, epigastric pain, and headache. At hospital admission, the mean laboratory values were creatinine 3.9±5.2 mg/dl, serum calcium was 12±2.2 mg/dl, and serum vitamin D concentration was 135±75 ng/ml. AKI was diagnosed in 13 patients secondary to hypercalcemia. So, in conclusion, excessive use of veterinary vitamin supplements that contain high doses of vitamin A, D, and E is associated with AKI.

High-protein diet

The International Society of Sports Nutrition’s position stand on protein states that ‘protein intakes of 1.4–2.0 g/kg/day for physically active individuals is not only safe but may improve the training adaptations to exercise training’ [22].

Available evidence that suggests the safety of high-protein diet in individuals with normal kidney function

Some trials are available to identify if significantly increasing protein intake would affect clinical markers of health (i.e. lipids and kidney function) as well as performance and body composition in young males with extensive resistance training experience. All trials have been shown that high-protein intake in individuals with normal kidney function positively affect body composition with no deleterious effects on health.

A crossover study [23] was done on 14 healthy resistance-trained males; half of them received normal protein and the other half received high-protein diet for 2 months, then alter their protein intake for another 4 months then repeat for another 6 months. At the end, each group had 6 months of normal protein (>2.5 g/kg/day) and 6 months of high-protein diet (>3.5 g/kg/day). The end result showed no harm from high-protein diet as long as the renal functions are normal.

In another randomized crossover trial [22], 12 healthy resistance-trained men underwent a 16-week intervention. Each participant was maintained for 8 weeks on their normal or habitual diet (2.6 ± 0.8 g/kg/day) and 8 weeks on a high-protein diet (3.3 ± 0.8 g/kg/day). There were no significant changes in creatinine, blood urea nitrogen, and estimated glomerular filtration rate between the two groups at the end of the study.

Theoretical risks of high-protein diet

Nevertheless, although there are no clear renal-related contraindications to high-protein diets in individuals with healthy kidney function, the theoretical risks should be reviewed carefully with some individuals. High-protein consumption has been found, under various conditions, to lead to glomerular hyperfiltration and hyperemia; acceleration of CKD; increased proteinuria; diuresis, natriuresis, and kaliuresis with associated blood pressure changes; increased risk for nephrolithiasis; and various metabolic alterations [24].

Pre-workout (energy drinks)

Energy drink-induced renal failure has been reported infrequently. According to the Food and Drug Administration’s Center for Food Safety and Applied Nutrition Adverse Event Reporting System, between 2004 and 2012, the Food and Drug Administration has received 166 reports of adverse events associated with energy drink consumption. Only three of the 166 (0.18%) described renal failure, and none were reported with Red Bull specifically [25]. Red Bull contains caffeine, taurine, B vitamins, and simple sugars in a buffer solution.

A 40-year-old man [26] presented with elevated serum creatinine 5.5 mg/dl, from a baseline of 0.9 mg/dl. There is a history of daily ingestion of 100–120 oz of Red Bull energy drink for 2–3 weeks. Resolution of renal dysfunction occurred within 2 days of discontinuation of Red Bull and persisted through 10 months of follow-up. Rechallenge was not attempted.

Combined effect

Some case reports had renal injury owing to a combined use of some of the aforementioned supplements. Four bodybuilders who injected anabolic steroids and ingested commercial protein (78–104 g/day) and creatine (15 g/day) presented with AKI. 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 was more than 60 ml/min, including two patients with biopsies showing more than 30% interstitial fibrosis and tubular atrophy [27].

Acknowledgements

The authors searched PubMed for different types of supplements in relation to kidney harm, injury, and pathology.

The authors currently manage a lot of cases presented to them in their clinic with nephropathies secondary to supplements abuse.

The authors have an ongoing study in the form of survey to measure the awareness of bodybuilder regarding the safety and harmfulness of supplements.

The authors also agree to provide post-publication update on the article.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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