Cigarette Smoking and Chronic Kidney Disease Factors

Summary

Cigarette smoking is recognised as a modifiable risk factor that contributes substantially to the development and progression of chronic kidney disease (CKD) worldwide. Epidemiological studies have linked both active and past smoking to heightened incidence of albuminuria, reduced glomerular filtration rate and increased likelihood of progression to end-stage kidney disease. Mechanistic investigations point to acute haemodynamic alterations, oxidative stress, endothelial dysfunction and direct cellular toxicity in podocytes and tubular epithelium as key mediators of renal injury. In individuals with diabetes or hypertension, smoking amplifies underlying vulnerabilities, accelerating nephropathy and promoting fibrotic remodelling. Markers such as elevated blood urea nitrogen, plasma creatinine and urinary albumin excretion provide early indicators of smoking-associated damage. From a public health perspective, smoking cessation programmes, risk stratification based on cumulative exposure and the development of tailored biomarkers are critical for mitigating renal morbidity and mortality.

Research from Nature Portfolio

A large-scale retrospective cohort study in Korea involving over 23 million adults found that current and former smokers face a significantly increased hazard of end-stage kidney disease compared to non-smokers. The risk rose in direct proportion to smoking duration, daily cigarette consumption and pack-years, demonstrating a clear dose–response relationship. These findings underscore smoking as an independent predictor of adverse renal outcomes at the population level.

Cigarette Smoking and Chronic Kidney Disease Factors publication trend

The graph below shows the total number of articles in cigarette smoking and chronic kidney disease factors across all publications each year (not limited to Nature Index journals).

Technical terms

Estimated glomerular filtration rate (eGFR): A calculated index of kidney filtration capacity, typically derived from serum creatinine, age and sex.

Albuminuria: The presence of albumin in urine, indicating glomerular damage and serving as an early marker of kidney disease.

Nicotine metabolite ratio (NMR): The proportion of 3′-hydroxycotinine to cotinine in biological fluids, reflecting individual variation in nicotine metabolism.

Gremlin 1 (Grem1): A secreted antagonist of bone morphogenetic protein signalling implicated in fibrotic and inflammatory pathways within the kidney.

Podocyte: A specialised epithelial cell in the glomerulus that contributes to the filtration barrier and is vulnerable to nicotine-induced injury.

References

  1. Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression. Molecular Medicine (2023).
  2. The hidden impact: the rate of nicotine metabolism and kidney health. Frontiers in Endocrinology (2024).
  3. Nicotine Induces Podocyte Apoptosis through Increasing Oxidative Stress. PLOS ONE (2016).
  4. Nicotine-Induced Apoptosis in Human Renal Proximal Tubular Epithelial Cells. PLOS ONE (2016).
  5. Cigarette smoking: an important renal risk factor – far beyond carcinogenesis. Tobacco Induced Diseases (2002).
  6. Smoking and risk of incident end-stage kidney disease in general population: A Nationwide Population-based Cohort Study from Korea. Scientific Reports (2019).
  7. The Association Between Smoking and Renal Function in People Over 20 Years Old. Frontiers in Medicine (2022).

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