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Bedford M, Stevens P, Coulton S, et al. Development of risk models for the prediction of new or worsening acute kidney injury on or during hospital admission: a cohort and nested study. Southampton (UK): NIHR Journals Library; 2016 Feb. (Health Services and Delivery Research, No. 4.6.)

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Development of risk models for the prediction of new or worsening acute kidney injury on or during hospital admission: a cohort and nested study.

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Appendix 2Variable relationships with acute kidney injury

Alanine transaminase

Alanine transaminase is a liver enzyme. It is often measured clinically to determine liver function. In the event of acute hepatocellular injury the ALT level rises. In cases of chronic liver damage and cirrhosis there may, however, be a reduced level of ALT as production of the enzyme is decreased. The relationship between ALT and AKI in this data set (Figure 25), suggest that only a low ALT level is associated with an increased risk of AKI.

FIGURE 25. Relationship between ALT level and AKI.

FIGURE 25

Relationship between ALT level and AKI.

Normal range (laboratory) = 0–70 U/l.

Range determined as normal for risk modelling = ≤ 50 U/l.

Amylase

Amylase is an enzyme produced in the pancreas that aids the digestion of carbohydrates. A raised level of AMY can signify the presence of pancreatitis, which we believe may carry a risk of AKI. However, as shown in Figure 26, the relationship between AMY level and AKI in this data set suggests that only a low AMY level is associated with an increased risk of AKI.

FIGURE 26. Relationship between AMY level and AKI.

FIGURE 26

Relationship between AMY level and AKI.

Normal range (laboratory) = 0–125 U/l.

Range determined as normal for risk modelling = ≤ 125 U/l.

Brain natriuretic peptide

Brain natriuretic peptide is an amino acid produced by the cardiac myocytes when they are under strain, and, in this way, BNP is associated with heart failure. Heart failure may result in reduced perfusion of the kidneys and thus carry a risk of AKI. The relationship between BNP level and AKI in this data set (Figure 27) suggests that, above a BNP of 25 ng/l, with a rising BNP value there is an increasing risk of AKI.

FIGURE 27. Relationship between BNP level and AKI.

FIGURE 27

Relationship between BNP level and AKI.

Normal range (laboratory) = 0–99 ng/l.

Range determined as normal for risk modelling = ≤ 25 ng/l.

Corrected calcium

Corrected calcium is the calcium, a mineral in the blood, corrected for the albumin level in the blood. Raised calcium levels can lead to dehydration, which can result in AKI. Low calcium levels can signify acute disease, which may have a risk of AKI. The relationship between calcium level and AKI in this data set (Figure 28) suggests that both low calcium and high calcium levels signify an increased risk of AKI, and that the risk increases the further away the value is from the normal range.

FIGURE 28. Relationship between calcium and AKI.

FIGURE 28

Relationship between calcium and AKI.

Normal range (laboratory) = 2.2–2.6 mmol/l.

Range determined as normal for risk modelling = 2.1–2.6 mmol/l inclusive.

C-reactive protein

C-reactive protein is a marker of infection or inflammation. Infection and, importantly, sepsis carry a significant risk of AKI. The higher the CRP level the greater the severity of the infection and, it would be expected, the higher the risk of AKI. The relationship between CRP level and AKI in this data set (Figure 29) suggests that the risk of AKI increases with rising CRP levels.

FIGURE 29. Relationship between CRP level and AKI.

FIGURE 29

Relationship between CRP level and AKI.

Normal range (laboratory) = ≤ 10 mg/l.

Range determined as normal for risk modelling = ≤ 10 mg/l.

Haemoglobin

Haemoglobin is the iron-containing oxygen transport metalloprotein in red blood cells. A low Hb level is a marker of acute or chronic disease, and we would therefore expect it to be associated with AKI. The relationship between Hb level and AKI in this data set (Figure 30) suggests that both low and high Hb levels signify an increased risk of AKI and that risk increases the further away the value is from the normal range.

FIGURE 30. Relationship between Hb and AKI.

FIGURE 30

Relationship between Hb and AKI.

Normal range (laboratory) = 11–15 g/l (women); 13–18 g/l (men).

Range determined as normal for risk modelling = 11–15 g/l inclusive if female, 13–18 g/l inclusive if male.

Glycated haemoglobin

Glycated haemoglobin gives an average of blood sugar readings over the last 120 days. A value of > 6.5% indicates a patient with diabetes. Patients with diabetes have an increased risk of AKI. A value of > 7.5% indicates that the diabetes is not well controlled; it would be expected that the higher the value, the worse the diabetic control and, therefore, the higher the risk of AKI. The relationship between HbA1c and AKI in this data set (Figure 31) suggests that having HbA1c tested (as probably defining diabetes) indicates an increased risk of AKI. This risk increases with rising HbA1c up to a value of approximately 12%, at which point the risk starts to decrease.

FIGURE 31. Relationship between HbA1c and AKI.

FIGURE 31

Relationship between HbA1c and AKI.

Normal range (laboratory) = 4–6.5% (Diabetes Control and Complications Trial).*

Range determined as normal for risk modelling = ≤ 7.5% (Diabetes Control and Complications Trial116).*

*The International Federation of Clinical Chemistry (www.ifcc.org) recommended standardisation of HbA1c following extraction of this data set.

Potassium

Potassium is an electrolyte that is essential for the normal functioning of cells, importantly cardiac cells. Maintaining the gradient across the cellular membrane is essential, and changes in this can lead to cardiac arrhythmias. K level itself in blood would not be expected to have a causal relationship with the development of AKI, but may be a reflection of acute illness and changes in electrolyte and fluid balance. The relationship between K level and AKI in this data set (Figure 32), suggests that both a low and a high K level indicates an increased risk of AKI and that risk increases the further away the value is from the normal range.

FIGURE 32. Relationship between K and AKI.

FIGURE 32

Relationship between K and AKI.

Normal range (laboratory) = 3.5–5.3 mmol/l.

Range determined as normal for risk modelling = 3.5–5.3 mmol/l, inclusive.

Magnesium

Magnesium is an electrolyte that is essential for the normal functioning of cells. The magnesium (Mg) level itself in blood would not be expected to have a causal relationship with the development of AKI, but may be a reflection of acute illness and changes in electrolyte and fluid balance. The relationship between Mg level and AKI in this data set (Figure 33), suggests that both a low and a high Mg level indicates an increased risk of AKI and that risk increases the further away the value is from the normal range.

FIGURE 33. Relationship between Mg and AKI.

FIGURE 33

Relationship between Mg and AKI.

Normal range (laboratory) = 0.70–1.05 mmol/l.

Range determined as normal for risk modelling = 0.7–1.0 mmol/l, inclusive.

Sodium

Sodium is an electrolyte that is essential for the normal functioning of cells. The Na level itself in blood would not be expected to have a causal relationship with the development of AKI, but may be a reflection of acute illness and changes in electrolyte and fluid balance. A low Na level may also signify diuretic medication use. The relationship between Na and AKI in this data set (Figure 34) suggests that both low and high Na levels indicate an increased risk of AKI, and that risk increases the further away the value is from the normal range.

FIGURE 34. Relationship between NA and AKI.

FIGURE 34

Relationship between NA and AKI.

Normal range (laboratory) = 136–145 mmol/l.

Range determined as normal for risk modelling = 136–145 mmol/l, inclusive.

Platelet count

Platelet count is a measure of the number of platelets in the blood. Platelets are essential for the clotting of the blood. The platelet level itself in blood would not be thought to have a causal relationship with the development of AKI. However, a low PLT may be related to haematological disease or acute illness, and a high PLT may also signify acute illness, specifically inflammation/infection. The relationship between PLT and AKI in this data set (Figure 35) suggests that both a low and a high PCT indicates an increased risk of AKI, and that risk increases the further away the value is from the normal range.

FIGURE 35. Relationship between PLT and AKI.

FIGURE 35

Relationship between PLT and AKI.

Normal range (laboratory) = 150–400 × 109/l.

Range determined as normal for risk modelling = 150– 400 × 109/l, inclusive.

White blood cell count

White blood cell count is a direct marker of infection. A low (< 4 × 109/l) or high (> 11 × 109/l) WBC can signify infection, and an infection brings a risk of AKI. The relationship between WBC and AKI in this data set (Figure 36) suggests that both a low and a high WBC indicates an increased risk of AKI, and that risk increases the further away the value is from the normal range.

FIGURE 36. Relationship between WBC and AKI.

FIGURE 36

Relationship between WBC and AKI.

Normal range (laboratory) = 4–11 × 109/l.

Range determined as normal for risk modelling = 1–11 × 109/l, inclusive.

Creatinine kinase

Creatinine kinase is a product of muscle breakdown. When excess muscle breakdown occurs, high levels of CK can cause damage to the kidneys and result in AKI. It would therefore be expected that the greater the CK the greater the risk of AKI. However, the relationship between creatinine kinase level and AKI in this data set (Figure 37) suggests that the fact that CK has been tested defines a patient with a higher risk of AKI; however, lower levels of CK seem to be related to higher risk of AKI.

FIGURE 37. Relationship between CK and AKI.

FIGURE 37

Relationship between CK and AKI.

Normal range (laboratory) = 0–142 U/l.

Range determined as normal for risk modelling = ≤ 1000 U/l.

Copyright © Queen’s Printer and Controller of HMSO 2016. This work was produced by Bedford et al. under the terms of a commissioning contract issued by the Secretary of State for Health. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising. Applications for commercial reproduction should be addressed to: NIHR Journals Library, National Institute for Health Research, Evaluation, Trials and Studies Coordinating Centre, Alpha House, University of Southampton Science Park, Southampton SO16 7NS, UK.

Included under terms of UK Non-commercial Government License.

Bookshelf ID: NBK344210

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