Management of acute kidney injury

Recognise and stage first. AKI is defined by a rise in serum creatinine of ≥0.3 mg/dL within 48 hours, or ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/h for 6 hours. In older adults the incidence is higher because of systemic illness, polypharmacy and the renal ageing process itself, and it is frequently multifactorial.

Classify the cause, because two of the three categories are reversible. Prerenal — dehydration is the main cause in the elderly, plus haemorrhage and cardiogenic or septic shock. Renal — acute tubular necrosis from persistence of prerenal causes and/or nephrotoxins such as aminoglycosides, rapidly progressive glomerular damage, and acute interstitial nephritis. Postrenal — stones, tumour, stricture and prostatic hypertrophy. Prerenal and postrenal causes are of particular importance because their early identification and treatment may prevent or reverse the injury.

Immediate bedside assessment. Assess volume status; catheterise or bladder-scan to exclude retention; send urinalysis and microscopy for casts and cells; arrange renal ultrasound within 24 hours if obstruction is possible; and review every single drug, prescribed and over-the-counter.

The five therapeutic priorities. (i) Restore renal perfusion with judicious fluid, guided by clinical reassessment — but give it cautiously, because senile hypofiltration and diastolic cardiac failure predispose older people to cardiac failure and lung congestion after a saline load. (ii) Relieve obstruction promptly. (iii) Stop nephrotoxins — NSAIDs, ACE inhibitors and ARBs, diuretics, aminoglycosides, contrast, PPIs. (iv) Treat sepsis with appropriately dosed antibiotics. (v) Correct the consequences — hyperkalaemia, acidosis, fluid overload — and re-dose every drug to the current GFR.

Interpret the urinary indices with geriatric caution. The urinary indices used for diagnosing AKI — urinary sodium, fractional excretion of sodium and fractional excretion of urea — may be slightly different in older adults from those accepted for younger people, because the aged kidney wastes sodium and urea at baseline. A higher-than-expected value therefore does not exclude prerenal AKI. Importantly, age per se is not an important determinant of survival in AKI.

Dialysis, recovery and prevention. Temporary or permanent dialysis may sometimes be needed. Although AKI is treated similarly in older and younger patients, older patients are more vulnerable to dialysis-related complications — haemodynamic instability, bleeding and disequilibrium syndrome. If the kidney does not recover after approximately three months, the condition remains as chronic kidney disease. Because treatment options are limited, prevention is paramount: maintain adequate extracellular volume, avoid nephrotoxins, and tailor drug dosage to the GFR.

There is still no drug that treats AKI — but three practice points have changed. (a) Fluid choice: balanced crystalloids are preferred to 0.9% saline, which causes hyperchloraemic acidosis; and there is no role for low-dose dopamine, mannitol, or loop diuretics to "convert" oliguric to non-oliguric AKI — diuretics are for volume overload only. (b) Timing of dialysis: the STARRT-AKI trial showed that accelerated initiation of renal replacement therapy gave no mortality benefit and left more patients dialysis-dependent at 90 days, supporting a watchful, indication-driven rather than number-driven strategy. (c) Systems of care: electronic AKI alerts, nephrotoxin stewardship, and structured post-AKI follow-up — because survivors of AKI carry a markedly elevated risk of subsequent CKD, recurrent AKI and cardiovascular death, and older survivors are the group least likely to be followed up.

no recovery by 3 months = CKD.