Synopsis
Interpret concurrent heart and kidney dysfunction by congestion, perfusion and time course, preserve beneficial heart-failure therapy where safe and recognise dialysis-level emergencies.
- Cardiorenal syndrome describes bidirectional heart–kidney dysfunction; identify acute versus chronic change and whether congestion, low perfusion, drugs, sepsis or intrinsic renal disease dominates.
- Raised venous pressure is a major renal insult in decompensated HF; a congested patient with rising creatinine may still need effective decongestion.
- NICE does not recommend loop diuretics to treat AKI itself, but does recommend considering them for fluid overload or oedema while renal function is recovering or awaiting renal replacement.
Key red flags
Hypotension, cool peripheries, oliguria and rising lactate/creatinine; diuretic escalation alone may worsen perfusion.
Investigation priorities
Define AKI trajectory and treatment toxicity.
Management branches
HF with worsening renal function
- Confirm baseline and AKI trajectory; record urine output, weight, BP, JVP/oedema, perfusion and recent medicines/illness.
- Check electrolytes, bicarbonate, urinalysis, ECG and cause-directed imaging; consider sepsis, obstruction, bleeding and nephrotoxins.
Key medicines
FurosemideAcute overload: if loop-naive, commonly 20–40 mg IV initially; if already taking loop diuretic, use an initial IV dose higher than the pre-admission oral dose and titrate to response. Chronic doses are individualised to the lowest effective level.
RamiprilHF commonly starts at 1.25 mg orally once daily and titrates toward 10 mg/day as tolerated; lower starting doses/smaller increments are considered when eGFR ≤45.