About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page Users Online: 657

 Table of Contents  
EDITORIAL
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
Iran
Login to access the Email id


DOI: 10.4103/1319-6308.123366

Rights and Permissions

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 2021 Jun 25];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

1.Barratt J, Topham P. Urine proteomics: The present and future of measuring urinary protein components in disease. CMAJ 2007;177:361-8.  Back to cited text no. 1
[PUBMED]    
2.Israni AK, Kasiske BL. Laboratory assessment of kidney disease: Clearance, urinalysis, and renal biopsy. In: Brenner BM, editor. Brenner and Rector's the Kidney. 8 th ed. Philadelphia: Saunders; 2007. p. 738-42.  Back to cited text no. 2
    
3.Abuelo JG. Proteinuria: Diagnostic principles and procedures. Ann Intern Med 1983;98:186-91.  Back to cited text no. 3
    
4.Chitalia VC, Kothari J, Wells EJ, Livesey JH, Robson RA, Searle M, et al. Cost-benefit analysis and prediction of 24-hour proteinuria from the spot urine protein-creatinine ratio. Clin Nephrol 2001;55:436-47.  Back to cited text no. 4
    
5.Schardijn GH, Statius van Eps LW. Beta 2-microglobulin: Its significance in the evaluation of renal function. Kidney Int 1987;32:635-41.  Back to cited text no. 5
    
6.Marchewka Z, KuŸniar J, D³ugosz A. Enzymuria and beta2-mikroglobulinuria in the assessment of the influence of proteinuria on the progression of glomerulopathies. Int Urol Nephrol 2001;33:673-6.  Back to cited text no. 6
    
7.Poortman JR. Post-exercise proteinuria in humans. J Am Med Assoc 1985;253:236-40.  Back to cited text no. 7
    
8.Zambraski EJ, Bober MC, Goldstein JE, Lakas CS, Shepard MD. Changes in renal cortical sialic acids and colloidal iron staining associated with exercise. Med Sci Sports Exerc 1981;13:229-32.  Back to cited text no. 8
    
9.Poortmans JR, Vanderstraeten J. Kidney function during exercise in healthy and diseased humans. An update. Sports Med 1994;18:419-37.  Back to cited text no. 9
    
10.Von Leube W. Über ausscheidung von Eiweiss in harn des gesunden menschen. Virkows Arch Pathol Anat Physiol 1878;72:145-7.  Back to cited text no. 10
    
11.Bellinghieri G, Savica V, Santoro D. Renal alterations during exercise. J Ren Nutr 2008;18:158-64.  Back to cited text no. 11
    
12.Sentürk UK, Kuru O, Koçer G, Gündüz F. Biphasic pattern of exercise-induced proteinuria in sedentary and trained men. Nephron Physiol 2007;105:22-32.  Back to cited text no. 12
    
13.Gündüz F, Kuru O, Sentürk UK. Effect of nitric oxide on exercise-induced proteinuria in rats. J Appl Physiol 2003;95:1867-72.  Back to cited text no. 13
    
14.Hansen JM, Olsen NV, Feldt-Rasmussen B, Kanstrup IL, Déchaux M, Dubray C, et al. Albuminuria and overall capillary permeability of albumin in acute altitude hypoxia. J Appl Physiol 1994;76:1922-7.  Back to cited text no. 14
    
15.Koçer G, Sentürk UK, Kuru O, Gündüz F. Potential sources of oxidative stress that induce postexercise proteinuria in rats. J Appl Physiol 2008;104:1063-8.  Back to cited text no. 15
    
16.Suzuki K, Sato H, Kikuchi T, Abe T, Nakaji S, Sugawara K, et al. Capacity of circulating neutrophils to produce reactive oxygen species after exhaustive exercise. J Appl Physiol 1996;81:1213-22.  Back to cited text no. 16
    
17.Rose BD. Pathophysiology of Renal Disease. 2 nd ed. New York: McGraw-Hill; 1987. p. 11-6.  Back to cited text no. 17
    
18.Poortmans JR, Haggenmacher C, Vanderstraeten J. Postexercise proteinuria in humans and its adrenergic component. J Sports Med Phys Fitness 2001;41:95-100.  Back to cited text no. 18
    
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
    
20.Poortmans JR, Labilloy D. The influence of work intensity on postexercise proteinuria. Eur J Appl Physiol Occup Physiol 1988;57:260-3.  Back to cited text no. 20
    
21.Winterborn MH, Bradwell AR, Chesner IM, Jones GT. The origin of proteinuria at high altitude. Postgrad Med J 1987;63:179-81.  Back to cited text no. 21
    
22.Kinra Wg Cdr Prateek, Richa Dr, Singh Wg Cdr Vishal, Gomez Gp Capt G. Proteinuria in Indian aviators. Int J Agile Syst Manage 2008;52:44-53.  Back to cited text no. 22
    
23.Soylu A, Kavukçu S, Yilmaz O, Astarcioðlu H, Ozkal S, Türkmen M, et al . Renal failure in high altitude: Renal functions, renal pathology and bone mineralization in rats with ablation nephropathy at 1200 m altitude. Pathol Res Pract 2007;203:795-800.  Back to cited text no. 23
    
24.Cogo A, Ciaccia A, Legorini C, Grimaldi A, Milani G. Proteinuria in COPD patients with and without respiratory failure. Chest 2003;123:652-3.  Back to cited text no. 24
    
25.Dittrich S, Haas NA, Bührer C, Müller C, Dähnert I, Lange PE. Renal impairment in patients with long-standing cyanotic congenital heart disease. Acta Paediatr 1998;87:949-54.  Back to cited text no. 25
    
26.Afshar R, Sanavi S, Fakharian MA, Ahmadzadeh M. The pattern of proteinuria following karate (kumite) competitions. NDT Plus 2008;5:376.  Back to cited text no. 26
    
27.Sanavi S, Sarhadi M, Afshar R. Urinary abnormalities following karate (kumite) competitions. NDT Plus 2010;3:596-601.  Back to cited text no. 27
    
28.Mousavi M, Sanavi S, Afshar R. Effects of continuous and intermittent trainings on exercise-induced hematuria and proteinuria in untrained adult females. NDT Plus 2011;4:217-22.  Back to cited text no. 28
    
29.Peeri M, Kohanpour MA, Sanavi S, Matinhomaee H, Mirsepasi M. Effects of different intensities of aerobic exercise on proteinuria in hypoxia and normoxia conditions in young football players. Dial Traspl 2012;33:84-8.  Back to cited text no. 29
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
References

 Article Access Statistics
    Viewed2724    
    Printed54    
    Emailed0    
    PDF Downloaded121    
    Comments [Add]    

Recommend this journal