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Effects of active smoking on renal function.


Smoking is a medical term designating acute or chronic intoxication caused by tobacco consumption; it is sometimes specified active smoking as opposed to passive smoking which qualifies the involuntary inhalation of tobacco smoke contained in the surrounding air, or inhalation deposits secondarily in air suspension. Furthermore dependence, smoking is responsible for many diseases such as cancer and cardiovascular disease, either active or passive. Smoking is the leading cause of preventable death in the world, making it a major health issue [2].

Smoking has been identified as an important factor in the progression of various renal diseases.

Recently it has been shown that smoking harms renal hemodynamics and protein excretion in the absence of kidney disease [11]. Smoking increases the risk of progression of renal insufficiency in patients with primary renal disease. The deleterious effects of smoking were also discussed in dialysis and renal transplant. It seems that cessation smoking slows the progression of kidney disease in smokers. It therefore seemed interesting to note that in addition to well-known vascular and pulmonary disease, kidney also pays a price, sometimes high, smoking [4]. An interaction between smoking and kidney damage had already been established. It was only in 1997 that the nephrologists rediscovering tobacco as a risk factor for renal impairment [7].

This work aims to highlight the impact of active smoking on some parameters indicating the good renal functions. In the first place, we will discuss the distribution of smokers and nonsmokers dialysis; in the second place, we will study the changes in biochemical and hematological parameters between smokers and nonsmokers.


Experimental Principle:

The experiment took place at the Laboratoiy of Biochemistiy and hemodialysis service.

* At the hemodialysis service we studied the distribution of smokers and nonsmokers amongst dialysis patients from the data described in the register of service.

* In the laboratory of biochemistry, the study included a cohort of 44 men aged between 20-45 years divided into 02 groups:

A control group: 22 non-smoking men.

A treatment group: 22 male smokers who consume a pack of 20 cigarettes a day for a period of 7 to 10 years.

* These people came to the laboratory to make an assessment, some were voluntary.

* We have chosen non-hypertensive and non-diabetic people.

* A survey sheet was prepared which reads: age, the first consumer age for smoking and number of cigarettes consumed per day.

* The blood collection is done in anticoagulant tubes.

* The work is based on the study of changes in biochemical parameters of different indicators kidney alterations (urea, creatinine, albumin, uric acid), as well as changes in hematological factors (the number of red blood cells, hemoglobin, speed sedimentation and platelet number) between smokers and nonsmokers.

Statistical Study:

The results are given as mean [+ or -] standard deviation (X [+ or -] SD) and schematically represented as histograms. As for the data statistical processing test, we chose the analysis of variance with a single criteria followed by Newman-Keuls test using Sigma Stat software.


Distribution of smokers and nonsmokers dialysis:

The rate of smokers in the dialysis service is higher (p <0.05) than that of non-smokers (Figure 1).

Study of biochemical parameters:

--Blood urea: urea is the major form of nitrogen metabolism. There is a significant increase (p<0.05) of urea in smokers compared to non smokers (Figure 2).

--Blood creatinine level: creatinine is a metabolic product of creatine, primarily eliminated by the kidneys and excreted in the urine. Its level reflects the functional state of the kidneys. The creatinine level is higher (p <0.01) in the group of smokers compared to non-smokers (Figure 3).

--Blood uric acid: uric acid is the metabolism product of nucleic acids of the dead cells when uric acid in the blood increases, especially in overweight people, it can cause kidney disease.

Uric acid in the smoking group marks a very highly significant (p <0.001) and this compared to those nonsmokers (Figure 4).

--Blood albumin: albumin is a small protein found in the blood, which is not eliminated in the urine when the kidneys are functioning normally. If albumin pass into the urine (albuminuria) is that kidney function is impaired. Smokers have lower albumin levels (p <0.05) than that of nonsmokers (Figure 5).

Study of haematological parameters:

--Red blood cells (RBC): we noticed a non-significant (p> 0.05) in the number of red blood cells in smokers compared with non-smokers (Figure 6).

--Hemoglobin (Hb): in the same way, hemoglobin decreased insignificantly (p> 0.05) in the group of smokers compared to non-smokers (Figure 7).

--Sedimentation Rate: a highly significant (p <0.01) of the sedimentation rate in smokers (Figure 8).

--Platelets: smokers have a higher number of platelets than non-smokers, this difference was significant p <0.05 (Figure 9).


The number of smokers in the hemodialysis service is higher than that of non-smokers, this result us to say that tobacco is a risk factor renal failure.

Cigarette smoking alters kidney function in holy people (non-diabetic, non-hypertensive or renal failure), smoking increases microalbuminuria in proportion to the number of cigarettes smoked, suggesting an impairment of the endothelium which can lead to accelerated decline renal function.

Other studies have shown that patients with hypertension, diabetics and patients with kidney disease are at increased risk of worsening renal function than non-smokers (Klungsoysr et al. 2006). A prospective study of 23 500 people for over 20 years shows a relative risk of renal failure 2.5% in smokers and tobacco-attributable risk of 31% [10].

Our results show that smokers have elevated levels of urea, creatinine, uric acid with decreased albumin levels. These factors are accompanied by the decrease in the number of red blood cells, the hemoglobin with an increased erythrocyte sedimentation rate and the number of thrombocytes. In general, these disturbances may be due to lesions of the renal parenchyma which can be induced by the effect of nicotine which is responsible for cell proliferation processes and synthesis of extracellular matrix promoting interstitial fibrosis, for the heavy metals as cadmium and lead in the smoke that accumulates in the kidney and favor tubular damage, or free radical CO [7].

Increasing the level of urea, creatinine and uric acid gives an idea about the disruption of the glomerular filtration process and the decrease in albumin leads to nephrotic syndrome and glomerulonephritis. Cigarette smokers have a risk of hyperuricaemia univariate two times higher than in non-smokers. A significant association between smoking cigarettes and high levels of uric acid has been well demonstrated in the work of Alderman. Other studies confirm this significant relationship between smoking and hyperuricemia [8].

Whether active or passive, smoking operates as a major risk factor for arterial and independent members and cardio-vascular diseases [12]. Another study noted 67.4% of patients with hyperuricemia are smokers.

The decrease in the number of red blood cells and hemoglobin is due to the decrease in erythropoietin, most smokers have a risk of anemia due to moderate to severe renal impairment.

Excessive tobacco can be result in polycythemia because this situation created a real oxy-carbon poisoning, so there was an extra oxygen demand and production of red blood cells increases to cope. We can observe in some heavy smokers a real polycythemia.

The decrease in hemoglobin causes a more rapid sedimentation of red blood cells, tobacco causes chronic renal failure is a common cause of elevated sedimentation rate.


Tobacco is a kidney triggering factor and also the progression to a more advanced stage. Toxic harmful effects of cigarettes come mainly from tobacco components; nicotine is against indications for kidney. Accumulated by people with kidney failure, this substance should be excreted in the urine. The deleterious effects of nicotine could therefore explain the increased cardiovascular risks in these smokers.

This study clearly showed that renal function is threatened by the danger of smoking. The disturbances in smokers are due to the harmful effects of tobacco on the glomerular and tubular functioning.


Article history:

Received 28 September 2015

Accepted 15 November 2015

Available online 24 November 2015


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[2] Daff, B.M., S.C. Sarr, 2003. Enquete Mondiale sur la Sante.

[3] Klungsoysr, O., J.F. Nygard, T. Sorensen and I. Sandanger, 2006. Cigarette smoking and incidence of first depressive episode: An 11-year population-based follow-up study. Am J Epidemiol, 163: 421-32.

[4] 2002. Smoking and the kidney. J Am Soc Nephrol., 13: 1663-1672.

[5] Orth, S.R., E. Ritz, 2002. Adverse effect of smoking on renal function in the general population: are men at higher risk?. Am J Kidney Dis., 40: 864-866.

[6] Orth, S.R., E. Ritz and R.W. Schrier, 1997. The renal risks of smoking. Kidney Int., 51: 1669-1677.

[7] Orth, S.R., T. Schroeder, E. Ritz and P. Ferrari, 2005. Effects of smoking on renal function in patients with type 1 and type 2 diabetes mellitus. Nephrol Dial Transplant, 20: 2414-2419.

[8] Polidori, M.C., P. Mecocci, W. Stahl and H. Sies, 2003. Cigarette smoking cessation encreases plasma levels of several antioxidant micronutrients and improves resistance towards. Br j Nutr., 90(1): 147-150.

[9] Tomita, M., S. Mizumo and H. Yamanaka, 2000. Does hyperuricemia affect mortality? A prospective cohort study of japanese male workers. j Epidemiol, 10(6): 403-409.

[10] Warmoth, L., M.M. Regalado, j. Simoni, R.B. Harrist and D.E. Wesson, 2005. Cigarette smoking enhances increased urine albumin excretion as a risk factor for glomerular filtration rate decline in primary hypertension. Am j Med Sci., 330: 111-119.

[11] Youssef, H., P. Olivier, V. Bruno and B. Michel, 2009. Tabagisme et rein. Rev Med Suisse, 5: 457-462.

[12] Zanetti, H., 1998. Smoking and attitudes to a non-smoking policy among hospital staff, j Hum Hypertens, 112: 57-62.

Corresponding Author: Djabali Nacira, Department of biology, Faculty of sciences, El-Tarf University, El Tarf, 36000, Algeria Tel: 00213 794741479 ; E-mail:

Djabali Nacira

Department of biology, Faculty of sciences, El-Tarf University, El Tarf, 36000, Algeria
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Author:Nacira, Djabali
Publication:Advances in Environmental Biology
Article Type:Report
Date:Nov 1, 2015
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