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Year : 2013  |  Volume : 13  |  Issue : 2  |  Page : 57-59

Sport related proteinuria

1 Clinical Fellow of Nephrology, Internist, Clinical Department, Iranian Comprehensive Hemophilia Care Center, Tehran, Iran
2 Department of Exercise Physiology, Islamic Azad University, Central Tehran Branch, Tehran, Iran

Date of Web Publication20-Dec-2013

Correspondence Address:
Suzan Sanavi
Clinical Fellow of Nephrology, Internist, Clinical Department, Iranian Comprehensive Hemophilia Care Center, Tehran
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-6308.123366

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How to cite this article:
Sanavi S, Kohanpour MA. Sport related proteinuria. Saudi J Sports Med 2013;13:57-9

How to cite this URL:
Sanavi S, Kohanpour MA. Sport related proteinuria. Saudi J Sports Med [serial online] 2013 [cited 2022 Aug 10];13:57-9. Available from: https://www.sjosm.org/text.asp?2013/13/2/57/123366

There are large amount of proteins in the plasma; however, the urine is virtually protein-free due to selectivity of glomerular barrier. Normal individuals excrete less than 150 mg/dl of total protein and only about 30 mg/dl of albumin. Small and medium-size proteins are filtered in considerable quantities and although the large plasma proteins are severely restricted from crossing the glomerular barrier, a small percentage does make it through. However; the proximal tubule is capable of taking up filtered proteins. [1] The initial step for the uptake of larger proteins is endocytosis at the luminal membrane. This energy-requiring process is increased in proportion to the concentration of protein in the glomerular filtrate until a maximal rate of vesicle formation. These vesicles merge with lysosomes which degrade the protein to low-molecular-weight (LMW) fragments. These end-products then exit the cells into the interstitial fluid and finally to the peritubular capillaries. This mechanism is easily saturated so that increasing glomerular permeability and filtered proteins can cause more excretion of proteins. [2]

Moreover, the magnitude and pattern of proteinuria depend upon the mechanism of renal injury leading to protein losses. Both charge and size selectivity normally prevents virtually all of plasma albumin and other high-molecular-weight (HMW) proteins from crossing the glomerular wall. Disruption of this barrier can induce leakage of plasma proteins into the urine (glomerular proteinuria). The glomerular endothelial cell forms a penetrated barrier that holds back particles > 100 nm, but offers little impediment to passage of most proteins. The glomerular basement membrane traps most large proteins (>100 kDa), while the podocytes through the slit diaphragms allow passage of small solutes and water. Smaller proteins (<20 kDa) are freely filtered, but are readily reabsorbed by the proximal tubule. Another mechanism of proteinuria occurs when there is excessive production of a protein that exceeds the capacity of tubular uptake. [3]

When proteinuria was detected by screening, it must be confirmed and quantified in a timed urine collection, which may help to distinguish type of proteinuria, provide useful prognostic information and assist in monitoring the response to therapy. [4] Higher amounts of albumin and HMW proteins suggest glomerular proteinuria, whereas isolated increases in LMW proteins (e.g., Beta 2-microglobulin [B2M]) are more suggestive of tubular proteinuria. B2M is freely filtered at the glomerulus and is avidly taken up and catabolized by the proximal tubule. Not surprisingly; therefore, detectable urinary levels of B2M have been associated with many pathologic conditions involving the proximal tubule. [5],[6]

Regardless of renal diseases, various physiologic setting including exercise can induce a transient increase in urinary protein excretion, which is benign and reversible. Sport-related proteinuria (SRP), which is probably attributed to a temporary hemodynamic impairment partially of glomerular, but principally of tubular function usually disappears within 24-36 h. [7],[8],[9] SRP following marching was first observed in soldiers in 1878 and its prevalence ranges from 18% to 100% depending on the exercise type and intensity. A higher incidence of proteinuria has been observed in some heavy exercises relating to muscular work, which may ameliorate following prolonged training. [10],[11]

Post-exercise proteinuria (PEP) may be related to the loss of glomerular wall negative charge, [7],[8] relative preservation of glomerular filtration despite decreased renal blood flow with resultant increased capillary permeability, [7],[9] proteinuria out of proportion of maximal tubular reabsorption capacity following heavy exercise, [7],[8],[9],[12],[13] hypoxia [14] and oxidative stress produced by free radicals owing to enhanced oxygen consumption in muscles. [15],[16] PEP can present either with glomerular or glomerulotubular (mixed) patterns. [7],[17] It is suggested that the sympathetic stimulation, decreased renal blood flow, increased filtration fraction and glomerular permeability alterations during strenuous exercise can lead to glomerular proteinuria, while tubular proteinuria results from partial tubular-reabsorption inhibition. [7],[18],[19]

The pattern of PEP depends on the exercise intensity rather than its duration, so that light and moderate exercises are preponderantly accompanied by glomerular proteinuria and heavy exercise is associated with mixed proteinuria. [7],[12],[19],[20]

Moreover, proteinuria may be influenced by different environmental factors including the high altitude-induced hypoxia. The effects of hypoxia on proteinuria have been studied in few researches and some investigators have suggested significant increase in proteinuria under hypoxia conditions [21],[22] while others have not. [23] Alterations in the albumin excretion rate closely related to the degree of hypoxia have been also reported, which is mediated by increased capillary permeability leading to greater filtered proteins exceeding the tubular reabsorptive capacity. [21] It is known that patients subject to hypoxia suffer from glomerulomegaly, glomerulosclerosis and proteinuria, which interfere with intact kidney performance. [24],[25]

To determine various factors affecting the SRP, we conducted multiple studies on professional and untrained healthy athletes. Whereas most investigations regarding SRP had been performed on long-standing aerobic exercises, we decided to evaluate the proteinuria in short-term anaerobic karate (kumite) competitions in professional athletes. Karate is often regarded as a "hard" martial art, which demonstrates strength and power. A significantly increased proteinuria of mixed type with glomerular predominance was found in both genders. [26],[27] Then, we assessed the effects of training (continuous and intermittent) on SRP in untrained young females that revealed no significant effect on the magnitude of proteinuria. [28] Thereafter, the influences of different intensities of aerobic exercise, consisting of 6 sessions of 30 min running with intensities of 55, 70 and 85% of maximal heart rate (MHR), on proteinuria in hypoxia and normoxia conditions in young football players were analyzed. [29] Urinary protein significantly increased at the intensity of ≥70% MHR while mixed proteinuria, with glomerular predominance, appeared at 85% MHR. These findings may be related to decreasing blood pH due to overproduction of organic acids, which results in increased glomerular permeability and tubular reabsorption inhibition in heavy exertion. Furthermore, elevated amino acid levels beyond the tubular reabsorption capacity, in peritubular capillaries, resulting from increased tubular catabolism may contribute to reabsorption inhibition. However; no significant difference in proteinuria was detected between hypoxia (equivalent to the height of 2,500 m above sea level) and normoxia conditions. It seems that further researches regarding SRP must be performed particularly in higher altitudes.

  References Top

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17.Rose BD. Pathophysiology of Renal Disease. 2 nd ed. New York: McGraw-Hill; 1987. p. 11-6.  Back to cited text no. 17
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19.Poortmans JR, Brauman H, Staroukine M, Verniory A, Decaestecker C, Leclercq R. Indirect evidence of glomerular/tubular mixed-type postexercise proteinuria in healthy humans. Am J Physiol 1988;254:F277-83.  Back to cited text no. 19
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