Acute Kidney Injury — Advanced

FEUrea is the preferred fractional excretion index when patients are taking diuretics. Loop diuretics increase urinary sodium excretion and thus can make FENa falsely high, reducing its reliability to detect pre-renal (functional) AKI. FEUrea is less affected by diuretics and better differentiates pre-renal azotaemia (low FEUrea, indicating avid urea reabsorption) from intrinsic tubular injury (higher FEUrea). Urine eosinophils are neither sensitive nor specific for intrinsic renal disease and are not recommended for routine use. Renal ultrasound is appropriate when obstruction is suspected but does not differentiate pre-renal from intrinsic tubular injury. Urine osmolality may be influenced by diuretics and is less reliable in this setting.

The presentation is highly suggestive of a pulmonary–renal syndrome such as anti-GBM disease or ANCA-associated vasculitis. Urgent serology for anti-GBM antibodies and ANCA will rapidly help distinguish causes and guide specific early treatments (e.g. plasma exchange for anti-GBM). While high clinical suspicion may require early treatment, starting high-dose steroids or plasma exchange empirically without serology may be appropriate in some centres when delays are expected, but the best immediate diagnostic step to direct therapy is urgent serology. Renal biopsy is important for diagnosis and prognostication but may be deferred until initial serology and stabilisation; biopsy is invasive and may not be the initial immediate test in a patient with pulmonary haemorrhage. Treating as ATN would miss immune-mediated rapidly progressive glomerulonephritis and delay specific therapy.

Uraemic complications such as pericarditis or encephalopathy indicate severe toxin accumulation and are widely regarded as urgent indications for dialysis irrespective of serum creatinine level. Absolute indications for RRT commonly include life-threatening electrolyte disturbances refractory to medical therapy, severe metabolic acidosis not responding to treatment, refractory pulmonary oedema, and uraemic complications (pericarditis/encephalopathy). A specific numeric creatinine threshold is not used because clinical context varies. Oliguria by itself (e.g. 6 hours) is not an absolute indication; duration, trends and associated derangements matter. Mild acidosis responsive to bicarbonate does not necessitate immediate RRT. CKD stage 3 with a stable clinical state does not by itself mandate urgent dialysis.

In patients with sepsis and risk of AKI, balanced crystalloids are generally preferred over 0.9% saline because large volumes of chloride-rich saline may be associated with hyperchloraemic metabolic acidosis and worse renal outcomes in some studies. Hydroxyethyl starch solutions are associated with increased risk of AKI and should be avoided. Hypertonic saline is not appropriate for routine sepsis resuscitation. Albumin may have a role in some patients (e.g. hypoalbuminaemia) but is not first-line for initial resuscitation to protect the kidney. Withholding fluids in a fluid-responsive, hypotensive septic patient is inappropriate; vasopressors are used once adequate intravascular volume is restored.

The most evidence-based preventive measure for contrast-associated AKI in patients with reduced eGFR is adequate intravascular volume expansion with isotonic crystalloid (e.g. 0.9% saline or balanced crystalloids) before and after contrast exposure, unless contraindicated by fluid overload. Routine use of N-acetylcysteine has not been consistently shown to prevent contrast nephropathy and is not universally recommended. Withholding antihypertensives may be appropriate in selected patients (e.g. renin–angiotensin system blockers in volume-depleted patients) but is not a primary prevention strategy for contrast AKI. Diuretics during contrast administration are not recommended and can worsen renal perfusion. Routine sodium bicarbonate infusion has not demonstrated consistent benefit over saline and is not standard for all patients.

Loop diuretics are useful to manage fluid overload and to attempt to convert oliguric to non-oliguric AKI, which may aid fluid management, but randomized data do not show that diuretics reduce progression to RRT or improve survival. They should be used judiciously; high-dose diuretics are not proven to reduce mortality. Thiazides are not preferred in oliguric AKI because they are weaker and less effective when urine output is low. Diuretics, when indicated, do not intrinsically worsen renal perfusion if used appropriately; withholding them entirely may leave volume overload untreated. Continuous loop infusion or combination therapy may be used for diuretic resistance, but they do not prevent AKI progression to CKD.

The clinical features indicate acute lower urinary tract obstruction (acute urinary retention) causing post-renal AKI. Immediate bladder decompression with urethral catheterisation is the appropriate first step and is often rapidly diagnostic and therapeutic. CT urogram or imaging may be helpful if upper tract obstruction or ureteric injury is suspected after initial stabilisation, but they should not delay catheterisation. Antegrade nephrostomy is indicated for upper tract obstruction not relieved by lower tract catheterisation or when urethral access is not possible; it is not first-line for simple urinary retention. Starting antibiotics without addressing obstruction fails to relieve the cause and risks worsening renal injury. Elective review next week would be inappropriate given acute retention and rising creatinine.

When hyperkalaemia is accompanied by ECG changes (peaked T waves, widened QRS), the immediate priority is to stabilise the cardiac membrane with intravenous calcium (calcium gluconate or calcium chloride) to reduce the risk of malignant arrhythmia. This should be done before attempts to shift potassium intracellularly (insulin/dextrose, nebulised beta-agonist) or remove potassium. Insulin+dextrose and nebulised salbutamol are important next steps to lower serum potassium but do not immediately stabilise the myocardium. Oral potassium binders act slowly and are not appropriate as the sole immediate therapy in the presence of ECG changes. Urgent dialysis may be required to remove potassium definitively, but calcium should be given immediately to protect the heart while preparing for dialysis or other therapies.

Patients who experienced severe AKI (e.g. stage 3) or required renal replacement therapy during admission should have timely nephrology follow-up after discharge because of high risk of incomplete recovery and progression to chronic kidney disease. Those with transient low-stage AKI that resolved and patients with minor fluctuations or reversible causes often do not require routine nephrology follow-up beyond primary care unless other risks exist. The 58-year-old who required temporary dialysis is high risk and needs specialist follow-up for monitoring, medication reconciliation and planning if CKD or dialysis dependence emerges.

In haemodynamically unstable ICU patients, continuous renal replacement therapy (CRRT) is commonly preferred because it provides gentle, continuous solute and fluid removal with less haemodynamic perturbation compared with conventional intermittent haemodialysis. Intermittent haemodialysis (IHD) may cause rapid fluid and osmotic shifts that worsen hypotension. Peritoneal dialysis is generally not practical for rapid clearance needs in unstable, ventilated ICU patients, and has limitations in sepsis and with intra-abdominal concerns. Intermittent haemofiltration with very high flow rates or SLEDD may be used in some centres, but CRRT is the standard for immediate haemodynamic stability in many ICUs.