Synopsis
Interpret renal biochemistry through time, understand creatinine and eGFR limitations, distinguish acute from chronic dysfunction and avoid unsafe dosing or referral decisions based on one number.
- Serum creatinine is produced from muscle metabolism and influenced by muscle mass, diet, supplements, hydration, tubular secretion and some medicines; a 'normal' value can conceal major impairment in a frail person.
- Creatinine rises only after filtration has fallen and distribution has evolved. During acute kidney injury it lags the insult, so creatinine-based eGFR is mathematically precise but physiologically invalid at non-steady state.
- NICE detects AKI using a creatinine rise of at least 26 micromol/L within 48 hours, a rise of at least 50% within seven days, or defined oliguria, applied against a credible baseline.
- Chronic kidney disease requires abnormal structure or function present for more than three months. One eGFR below 60 cannot distinguish transient AKI, biological variation or established CKD.
- Classify chronic disease with both GFR category G1 to G5 and albuminuria category A1 to A3 because ACR materially changes renal and cardiovascular risk at the same eGFR.
- eGFR is indexed to 1.73 square metres. Drug dosing may require Cockcroft-Gault creatinine clearance or a de-indexed estimate, particularly for direct oral anticoagulants and extremes of body size.
- Do not use routine eGFR equations in pregnancy; follow serum creatinine and the renal-obstetric pathway. Interpret cautiously in amputees, severe muscle wasting, bodybuilders, oedema and rapidly changing function.
- Urea rises with reduced filtration but also dehydration, high protein intake, catabolism, corticosteroids and gastrointestinal bleeding; low urea occurs with low protein intake or severe liver dysfunction.
- A disproportionate urea rise can support reduced renal perfusion or upper gastrointestinal bleeding but no fixed urea-to-creatinine ratio diagnoses the cause reliably in an individual patient.
- Trends need context: a dilutional creatinine fall after large fluid balance does not necessarily mean renal recovery, and dialysis can lower values without restoring native function.
Key red flags
A qualifying creatinine rise over hours or days, falling urine output and a new precipitant supports AKI. Hyperkalaemia, acidosis, pulmonary oedema and uraemic features determine immediate severity.
Investigation priorities
Define a credible baseline, chronicity and speed of change.
Management branches
First recognised creatinine elevation or eGFR below the reference range.
- Retrieve baseline values, measure urine output, assess illness, volume, obstruction and medicines, and repeat urgently when AKI criteria or serious complications are possible.
- Perform urinalysis, ACR and appropriate imaging; classify an acute rise by NICE criteria rather than accepting the automated eGFR stage.
- If stable but chronicity is uncertain, repeat within the NICE timeframe to exclude rapid deterioration and then confirm persistence beyond three months before labelling CKD.
Key medicines
Direct oral anticoagulantsSelect agent and dose from the licensed indication using Cockcroft-Gault creatinine clearance, age, weight and interacting medicines, with pharmacy support when uncertain.Overestimated function increases bleeding risk. Recalculate during illness, weight change and renal decline; dialysis and very low clearance have drug- and indication-specific restrictions.
MetforminUse current BNF and SmPC eGFR thresholds, dose review and monitoring; do not infer safety from one creatinine value during acute illness.Manufacturer advice avoids use below the specified severe eGFR threshold. Temporarily review during AKI or major physiological stress and create an explicit restart plan after recovery.