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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
High-protein diets and resistance training are widely practiced among athletes and bodybuilders. While moderate protein intake supports muscle growth, chronic excessive intake can lead to glomerular hyperfiltration and increased renal workload. Furthermore, transient but extreme surges in blood pressure during maximal resistance exercise may cause repeated microvascular injury. The synergistic impact of these factors on renal function remains poorly recognized. We report a case of end-stage kidney disease (ESKD) in a bodybuilder likely resulting from the combined effects of exercise-induced hypertension and sustained high protein intake.
A 50-year-old man, a former professional bodybuilder with a 10-year history of untreated hypertension, presented with nausea and malaise after prolonged driving in hot weather. Clinical records, laboratory findings, imaging studies, and renal histopathology were comprehensively reviewed. Blood pressure, renal function markers (serum creatinine, cystatin C, inulin clearance), and echocardiographic data were analyzed to elucidate the interplay between hemodynamic stress, rhabdomyolysis, and renal injury.
On admission, the patient showed severe azotemia (serum creatinine 19.0 mg/dL, BUN 250 mg/dL) and biochemical evidence of rhabdomyolysis, with markedly elevated creatine kinase levels. Post-renal obstruction was excluded. Hemodialysis was initiated for uremic symptoms. Renal biopsy revealed advanced nephrosclerosis and secondary focal segmental glomerulosclerosis, with global sclerosis in 83% of glomeruli. Multiple tortuous arterioles were noted, indicating adaptive vascular remodeling due to repeated episodes of extreme hypertension (Hill, Kidney Int, 1974). Cystatin C (3.61 mg/L) was relatively low compared with creatinine, suggesting acute deterioration superimposed on chronic kidney injury. Inulin clearance confirmed ESKD (3.4 mL/min). Echocardiography demonstrated marked concentric left ventricular hypertrophy (LVMI 244.8 g/m², RWT 0.75), compatible with pressure-overload remodeling typical of resistance-trained athletes (Morganroth et al., Circulation, 1975). The patient denied anabolic steroid or nephrotoxic supplement use but reported chronic protein intake exceeding 3 g/kg/day for years.
The severity of renal injury was disproportionate to the patient’s resting hypertension (≈150/100 mmHg). During maximal resistance exercise, systolic pressure can transiently exceed 300 mmHg (MacDougall et al., J Appl Physiol, 1985), leading to recurrent glomerular and vascular stress. The combination of repeated exercise-induced hypertension, rhabdomyolysis episodes, and sustained protein overload likely accelerated irreversible nephrosclerosis. This case highlights the underappreciated risk of high-intensity resistance exercise and excessive protein intake on kidney health. Regular monitoring of blood pressure and renal function is recommended even in athletes without overt hypertension at rest.