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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2018  |  Volume : 29  |  Issue : 2  |  Page : 326-331
Complementary bodybuilding: A potential risk for permanent kidney disease

1 Department of Medicine, Faculty of Medicine, Kuwait University, Safat, Kuwait
2 Department of Medicine, Al-Amiri Hospital, Kuwait City, Kuwait
3 Department of Histopathology, Al-Amiri Hospital, Kuwait City, Kuwait

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Date of Web Publication10-Apr-2018


We report our experience of renal disease associated with bodybuilders who had been on high-protein diet, anabolic androgenic steroids (AASs), and growth hormone (GH) for years. A total of 22 adult males who volunteered information about use of high protein diet and AAS or GH were seen over a six-year period with renal disease. Kidney biopsy revealed focal segmental glomerulosclerosis (FSGS) in eight, nephroangiosclerosis in four, chronic interstitial nephritis in three, acute interstitial nephritis in two, nephrocalcinosis with chronic interstitial nephritis in two, and single patients with membranous glomerulopathy, crescentic glomerulopathy, and sclerosing glomerulonephritis. Patients with FSGS had a longer duration of exposure, late presentation, and worse prognosis. Those with interstitial disease had shorter exposure time and earlier presentation and had improved or stabilized after discontinuation of their practice. There is a need for health education for athletes and bodybuilders to inform them about the risks of renal disease involved with the use of high-protein diet, AAS, and GH.

How to cite this article:
El-Reshaid W, El-Reshaid K, Al-Bader S, Ramadan A, Madda JP. Complementary bodybuilding: A potential risk for permanent kidney disease. Saudi J Kidney Dis Transpl 2018;29:326-31

How to cite this URL:
El-Reshaid W, El-Reshaid K, Al-Bader S, Ramadan A, Madda JP. Complementary bodybuilding: A potential risk for permanent kidney disease. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2020 Jun 6];29:326-31. Available from: http://www.sjkdt.org/text.asp?2018/29/2/326/229269

   Introduction Top

Anabolic androgenic steroids (AASs) and growth hormone (GH) have been used by professional athletes and elite bodybuilders since the 1930s due to their enhancing effects on muscle growth.[1] This pattern of practice spread in the last three decades to a much larger number of noncompetitive athletes in the general population who sought more masculine physique. The use of these substances is neither supervised nor recommended by physicians. Therefore, they are internationally banned and their intake is considered abuse. Their side effects are serious and include hypertension, accelerated atherosclerosis, reduced fertility, liver toxicity, and suppression of immune system.[2] Mood changes with the use of AAS are common and vary from aggression and violence to different pattern of impulsive behavior.[3] The abuse of these substances is common worldwide and still ongoing due to cultural and social understanding of muscular male built.

Glomerular changes of focal segmental glomerulosclerosis (FSGS) and electrolyte imbalance have been reported in professional body-builders.[4],[5],[6] In this prospective study, we present the renal outcome in 22 patients who presented with renal disease associated with use of AAS and GH over a six-year period.

   Patients and Population Top

Study design

This is a prospective study that included all bodybuilders who were referred to nephrology unit at Al-Amiri Hospital in the period from January 2011 to December 2016 with impaired renal function or proteinuria and/or hematuria. All patients had been on high-protein diet (20–30 g/kg/day) and multiple AASs, especially testosterone injections up to 250 mg/day intramuscularly in addition to GH on average of 100 mg/day. All had normal serum complements, and the screening revealed negative antinuclear antibody, antineutrophil cytoplasmic antibody, antiglomerular basement membrane antibodies, IgA level, and hepatitis B and C serology before inclusion into the study. They were all subjected to kidney biopsy, after informed consent, to define their underlying renal disease and prognosis. Patients were subjected to a kidney biopsy to define their kidney disease and its prognosis. For analytical purposes, they were then divided into three main groups according to the biopsy result: FSGS, nephroangiosclerosis, and interstitial nephritis.

Subsequently, they were instructed to adhere to low-protein (0.4 g/kg/day/) diet, avoid AAS, GH and nonsteroidal anti-inflammatory drugs (NSAIDs), and were treated with angiotensinconverting enzyme or angiotensin-receptor antagonists.

   Statistical Analysis Top

Analysis of data was performed using the Statistical Package for the Social Sciences (SPSS) version 20.0 for Windows (SPSS Inc., Chicago, IL, USA). P value of <0.05 was used as the cutoff level for significance. Variables are expressed as mean ± standard deviation (SD) unless otherwise specified. However, since the duration of exposure and treatment were not normally distributed, they were expressed as a median and interquartile range. ANOVA with repeated measures was used to compare the age among the groups while Kruskal–Wallis test was used for the duration of exposure and treatment.

   Results Top

A total of 25 patients were diagnosed with kidney disease that had developed after entering a bodybuilding program. Three patients were excluded: two had refused kidney biopsy and one patient with a biopsy-proven early focal segmental glomerulosclerosis (FSGS) had lost follow up. The remaining 22 patients were available on follow-up and were included in the study.

Demographical data

All patients were Middle Eastern males. They were adults with a mean age ± SD of 29 ±7 years.

Aided bodybuilding methods

All patients had used high-protein diet (20-30 g/kg/day) and multiple AAS, especially testosterone injections up to 250 mg/day intramuscularly in addition to that average dose of 100 mg/day. Patients with nephrocalcinosis had consumed an average of 10 L of milk every day, instead of water, in an attempt to promote their protein intake.

Clinicopathological correlations

Kidney biopsy in the 22 patients revealed FSGS in eight [Figure 1], nephroangiosclerosis in four [Figure 2], chronic interstitial nephritis in three, acute interstitial nephritis in two, nephrocalcinosis with chronic interstitial nephritis in two [Figure 3], and single patients with membranous glomerulopathy, crescentic glomerulopathy and sclerosing glomerulonephritis [Table 1]. The difference among patients in the three major groups, i.e., those with FSGS, interstitial disease, and nephroangiosclerosis is shown in [Table 2].
Figure 1: Photomicrograph of kidney biopsy showing a glomerulus with segmental sclerosis and mesangial cell proliferation.

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Figure 2: Photomicrograph of the kidney biopsy showing an ischemic glomerulus next to medium-sized arteries with intimal thickening, medial hypertrophy with hyalinosis.

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Figure 3: Photomicrograph of the kidney biopsy showing a glomerulus with mesangial sclerosis next to tubules containing calcium deposits (black arrowheads) which had extended into the interstitium.

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Table 1: Clinical presentation of the bodybuilders with renal disease.

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Table 2: Exposure and treatment time among the patients in the three main groups of bodybuilders.

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Patients with FSGS had a longer duration of exposure (42 ± 8 months, P = 0.001), late presentation, and worse prognosis (5 ± 15 months, P = 0.002). However, those with the interstitial disease had shorter exposure time (20 ± 17 months, P = 0.001) and earlier presentation and had improved or stabilized after discontinuation of their practice (41 ± 14 months, P = 0.002). Those with nephroangiosclerosis had a presentation and prognosis that is between the former groups.

   Discussion Top

FSGS is produced by many mechanisms.[7] The lack of florid nephrotic state and IgM deposition were against a primary immunological disease. In addition, they had normal-sized kidneys and no history of diabetes or morbid obesity, infections, intravenous substance abuse, or HIV infection. The only relevant insult in their medical history was the use of high-protein diet, pharmacological doses of AAS, and GH. There was no family history of a similar glomerulopathy

Two insults were prominent in the interstitium. The first was the milk-induced hyper-calcemia and nephrocalcinosis in patients who had used milk instead of water as a mean of more protein intake. The second was the use of NSAIDs for musculoskeletal pains while using less water in addition to the use of diuretics and laxatives as a mean for muscle shaping. Hypertensive changes were present in all patients, but four had it as a primary histopathological change. The etiology of the latter is intriguing. Repetitive effect of episodic severe elevations of blood pressure associated with weight lifting may have been a factor yet direct toxic effect from high-protein diet, and the pharmacological doses of drugs may have been the major insult.[8] The mechanism of injury leading to either FSGS or nephroangiosclerosis is hard to define since all patients had consumed the same drugs. However, those with FSGS had longer exposure time and less florid presentation indicating a low-dose and chronic disease in contrast to those with nephroangiosclerosis.

The development of other lesions such as membranous glomerulopathy and crescentic glomerulopathy may have been an incidental finding yet a drug-induced injury to glomerular basement membrane, or podocyte cannot be excluded.

The use of AAS to promote wound healing in World War II and in those in concentration camps is well documented. However, abuse of such drugs in sports started in 1940 and especially during the cold war between the west and east.[9] Their emerging systemic side effects on the heart, liver, and mood led to their ban in Olympic Games in 1976. Interestingly, the direct toxic effect of such banned drugs on the glomeruli has been clearly documented and has been shown to be mediated through specific testosterone receptors in the glomeruli.[10],[11] Moreover, the usual dose testosterone replacement therapy hardly exceeds 250 mg IM every three weeks. Our patients had consumed pharmacological doses of such drug reaching up to100 times the usual therapeutic one and in cases for many years.

Interestingly, GH had limited success in the treatment of short stature children yet is still being promoted as a bodybuilding agent. Experimental reports in mice have shown its renal toxicity and induction of glomerulosclerosis through an increase of renal blood flow and glomerular filtration rate.[12] Moreover, it has demonstrated that its target site was specifically on the glomerular podocyte.[13] In fact, FSGS was reported in a patient with acromegaly who had failed all therapeutic drug regimens yet improved after treatment transsphenoidal microsurgery of the adenoma.[14]

The last insult came with the addition of high-protein diet to their regimen. The optimal protein requirement for sedentary and healthy adults hardly exceeds 0.8 g/kg/day as recommended by the US Food and Nutrition.[15] Further analysis of data on high-protein intake indicated three observations. The first one was that the increase in protein synthesis for strength and power athletes was limited to <2.4 g/kg/day and hence beyond that was considered “protein overload.”[16] The second one was that protein intake under 2.8 g/kg did not impair renal function in well-trained athletes.[17] Finally, a harmful effect of high protein-diet mediated by progressive glomerulosclerosis due to glomerular hyperfiltration was shown in a “rat made diabetic with streptozocin” and children as well as young adults with juvenile diabetes.[18] Our patients had consumed 30–50 g/kg/day. Moreover, their kidneys may have been insulted by the AASs and GH as well as other factors such as NSAIDs and calcium deposition which may have additive element in accelerating in the development of FSGS.

   Conclusion Top

There is increased recognition of association of renal disease in athletes and bodybuilders who use anabolic steroids and high-protein diet. The athletes and their trainers should be educated about the health risks of these interventions and need to consult a medical practitioner for screening for any development of kidney disease.

Conflict of interest: None declared.

   References Top

Kanayama G, Pope HG Jr. History and epidemiology of anabolic androgens in athletes and non-athletes. Mol Cell Endocrinol 2018; 464:4-13.  Back to cited text no. 1
Eisenberg ER, Galloway G. Anabolic-androgenic steroids. In: Lowinston Joyce H., editor. Substance Abuse. 4th ed., Vol. 25. USA Lippincott Williams & Wilkins; 2005. p. 43460.  Back to cited text no. 2
Westlye LT, Kaufmann T, Alnæs D, Hullstein IR, Bjørnebekk A. Brain connectivity aberrations in anabolic-androgenic steroid users. Neuroimage Clin 2017;13:62-9.  Back to cited text no. 3
Herlitz LC, Markowitz GS, Farris AB, et al. Development of focal segmental glomerulosclerosis after anabolic steroid abuse. J Am Soc Nephrol 2010;21:163-72.  Back to cited text no. 4
Hartung R, Gerth J, Fünfstück R, Gröne HJ, Stein G. End-stage renal disease in a bodybuilder: A multifactorial process or simply doping? Nephrol Dial Transplant 2001;16:163- 5.  Back to cited text no. 5
Mayr FB, Domanovits H, Laggner AN. Hypokalemic paralysis in a professional bodybuilder. Am J Emerg Med 2012;30:1324.e5-8.  Back to cited text no. 6
D’Agati V. Pathologic classification of focal segmental glomerulosclerosis. Semin Nephrol 2003;23:117-34.  Back to cited text no. 7
Paczuła A, Więcek A, Piecha G. The role of endogenous cardiotonic steroids in pathogenesis of cardiovascular and renal complications of arterial hypertension. Postepy Hig Med Dosw (Online) 2016;70:243-50.  Back to cited text no. 8
Catlin DH, Fitch KD, Ljungqvist A. Medicine and science in the fight against doping in sport. J Intern Med 2008;264:99-114.  Back to cited text no. 9
Zeier M, Schönherr R, Amann K, Ritz E. Effects of testosterone on glomerular growth after uninephrectomy. Nephrol Dial Transplant 1998;13:2234-40.  Back to cited text no. 10
Zeier M, Gafter U, Ritz E. Renal function and renal disease in males or females – Vive la petite difference. Nephrol Dial Transplant 1998;13:2195-8.  Back to cited text no. 11
Hisano S, Latta K, Kreig RJ, Chan JC. Growth hormone and renal function. Nephrology 1997;3:309-14.  Back to cited text no. 12
Reddy GR, Pushpanathan MJ, Ransom RF, et al. Identification of the glomerular podocyte as a target for growth hormone action. Endocrinology 2007;148:2045-55.  Back to cited text no. 13
Yoshida H, Akikusa B, Saeki N, et al. Effect of pituitary microsurgery on acromegaly complicated nephrotic syndrome with focal segmental glomerulosclerosis: Report of a rare clinical case. Am J Kidney Dis 1999;33:1158-63.  Back to cited text no. 14
National Research Council (U.S.) Subcommittee on Tenth Edition of RDAs. Recommended Dietary Allowances. 10th ed. Washington, DC: National Academy Press; 1989.  Back to cited text no. 15
Fern EB, Bielinski RN, Schutz Y. Effects of exaggerated amino acid and protein supply in man. Experientia 1991;47:168-72.  Back to cited text no. 16
Poortmans JR, Dellalieux O. Do regular high protein diets have potential health risks on kidney function in athletes? Int J Sport Nutr Exerc Metab 2000;10:28-38.  Back to cited text no. 17
Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: The role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease. N Engl J Med 1982;307:652-9.  Back to cited text no. 18

Correspondence Address:
Dr. Wael El-Reshaid
Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat
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DOI: 10.4103/1319-2442.229269

PMID: 29657200

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  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


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