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.
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.
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.
MetforminUse current BNF and SmPC eGFR thresholds, dose review and monitoring; do not infer safety from one creatinine value during acute illness.