Clinical interpretation of elevated serum creatinine levels (lecture)

Measurement of serum creatinine is an important test for assessing kidney function. Among several methods of laboratory measurement of creatinine, isotope dilution mass spectrometry is considered the most accurate. The colorimetric Jaffe method is commonly used in clinical practice, but is subject to interference by a range of substances. The amount of creatinine the body produces each day depends on the person's muscle mass. Plasma creatinine levels vary substantially (with coefficient of variability from 8% to 27%), mostly due to the effects of diet and of intra- and inter-patient variability in the production, tubular secretion, and renal and extra-renal excretion and degradation of creatinine. There are pre-renal, renal and post-renal causes of elevated creatinine. Urea/serum creatinine ratio can help distinguish pre-renal from renal causes. A ratio >100 suggests pre-renal causes, whereas a ratio <40 suggests renal causes. The typical rise in serum creatinine in acute kidney injury is 88 to 177 µmol/L/day. Suspicion of rapidly progressive glomerulonephritis or rhabdomyolysis should arise in cases of more prominent rise in serum creatinine. Rises in creatinine are delayed for approximately [12–24] hours following kidney injury. When evaluating the causes of increased serum creatinine, significant importance is attached to the analysis of the drugs that the patient was taking. Antibacterial and antiviral agents, nonsteroidal anti-inflammatory agents, and proton pump inhibitors have the greatest nephrotoxic potential. A decrease in glomerular filtration rate under the influence of inhibitors of the renin-angiotensin-aldosterone system is more often a sign of the effective action of the drugs than of acute kidney injury. Diuretics do not cause acute kidney injury if not used excessively. Rise in serum creatinine is associated with an increased risk of end-stage renal disease and death, although some causes of the increased serum creatinine are reversible. Keywords: laboratory measurement, kidney injury, nephrotoxicity of drugs.

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Journal
Experimental and Clinical Medicine
Published
2025-06-30
DOI
https://doi.org/10.35339/ekm.2025.94.2.bzb
Primary Topic
Venous Thromboembolism Diagnosis and Management
Type
article
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article

Clinical interpretation of elevated serum creatinine levels (lecture)

M. Bereznyakova, Л. В. Карабут, І. G. Bereznyakov, V.G. Nesterenko et al.
Experimental and Clinical Medicine
Venous Thromboembolism Diagnosis and Management
article

Clinical interpretation of elevated serum creatinine levels (lecture)

M. Bereznyakova, Л. В. Карабут, І. G. Bereznyakov, V.G. Nesterenko, T. I. Tyupka, Yuliia Avidzba, O. Zalubovska, M. Lytvynenko
article en

Abstract

Measurement of serum creatinine is an important test for assessing kidney function. Among several methods of laboratory measurement of creatinine, isotope dilution mass spectrometry is considered the most accurate. The colorimetric Jaffe method is commonly used in clinical practice, but is subject to interference by a range of substances. The amount of creatinine the body produces each day depends on the person's muscle mass. Plasma creatinine levels vary substantially (with coefficient of variability from 8% to 27%), mostly due to the effects of diet and of intra- and inter-patient variability in the production, tubular secretion, and renal and extra-renal excretion and degradation of creatinine. There are pre-renal, renal and post-renal causes of elevated creatinine. Urea/serum creatinine ratio can help distinguish pre-renal from renal causes. A ratio >100 suggests pre-renal causes, whereas a ratio <40 suggests renal causes. The typical rise in serum creatinine in acute kidney injury is 88 to 177 µmol/L/day. Suspicion of rapidly progressive glomerulonephritis or rhabdomyolysis should arise in cases of more prominent rise in serum creatinine. Rises in creatinine are delayed for approximately [12–24] hours following kidney injury. When evaluating the causes of increased serum creatinine, significant importance is attached to the analysis of the drugs that the patient was taking. Antibacterial and antiviral agents, nonsteroidal anti-inflammatory agents, and proton pump inhibitors have the greatest nephrotoxic potential. A decrease in glomerular filtration rate under the influence of inhibitors of the renin-angiotensin-aldosterone system is more often a sign of the effective action of the drugs than of acute kidney injury. Diuretics do not cause acute kidney injury if not used excessively. Rise in serum creatinine is associated with an increased risk of end-stage renal disease and death, although some causes of the increased serum creatinine are reversible. Keywords: laboratory measurement, kidney injury, nephrotoxicity of drugs.

Experimental and Clinical MedicineVol. 94(2)
Ukrainian Engineering Pedagogics Academy (UA), Kharkiv National Medical University (UA)
Openalex Percentile: Top 58%
Venous Thromboembolism Diagnosis and Management
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