Causes and treatment of acute kidney injury in an elderly male

AKI is an abrupt, potentially reversible fall in glomerular filtration over hours to days, with retention of nitrogenous waste. Standard criteria: rise in serum creatinine by ≥0.3 mg/dL in 48 hours, or ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/hour for 6 hours.

Tubular frailty is the key ageing change — tubular cells in the elderly injure easily, progress readily to acute tubular necrosis (ATN), and recover slowly. If the kidney has not recovered by about 3 months, it is left as chronic kidney disease.

AKI is commoner in older adults because of frequent systemic illness (diabetes, myeloma), polypharmacy, and the renal ageing process itself. The cause is usually multifactorial, not single.

Ageing reduces urine concentrating power (falls about 30 mOsmol/kg per decade), raises the thirst threshold, and lowers total body water to about 54% of body weight (65% in the young) — so dehydration develops very easily.

Renal dysautonomia and loss of the autonomic vascular reflex mean the aged kidney is damaged during both hypotensive and hypertensive episodes.

Prerenal: dehydration is the main cause; also haemorrhage and shock (cardiogenic and septic).

Renal (intrinsic): ATN from persisting prerenal causes or from nephrotoxins (aminoglycosides, contrast); rapidly progressive damage from primary or secondary glomerular disease; acute interstitial nephritis.

Postrenal (obstructive): stones, tumour, stricture and — the key one in a male — prostatic hypertrophy.

Renal vasculitis becomes commoner with age and is probably the commonest primary cause of renal failure in older adults; granulomatosis with polyangiitis and microscopic polyangiitis both rise with age. Crescentic glomerulonephritis peaks at 60–79 years and typically presents as rapidly evolving AKI.

Vascular causes: renovascular atherosclerosis and ischaemic nephropathy; reversible renal failure after an ACE inhibitor in bilateral renal artery stenosis; intrarenal atheroembolism, from which the kidney rarely recovers.

Urinary tract infection / pyelonephritis is the commonest infection in the elderly, and its pathogenesis is strongly linked to obstructive uropathy; risk is raised further by urethral and vaginal atrophy, bed-rest puddling and catheterisation.

Add in a man specifically: myeloma kidney, tumour lysis syndrome, rhabdomyolysis after a long lie, and heat-related illness.

Prostatic hypertrophy occurs to some degree in nearly all ageing men; in a proportion it causes slow outflow obstruction with gradual loss of kidney function.

It is often recognised too late, because the patient becomes polyuric rather than oliguric. By the time obstruction is diagnosed, damage may be irreversible, and relief of obstruction restores function only partially.

Urinary indices behave differently in the elderly: a high urinary sodium, fractional excretion of sodium or fractional excretion of urea does not exclude prerenal AKI, because the aged kidney normally loses sodium and urea.

Serum creatinine underestimates the damage. Renal function falls by about 50% before creatinine rises, and reduced muscle mass plus net tubular creatinine reabsorption in the elderly delay the rise further.

Practical work-up: volume status and postural blood pressure, complete drug chart, bladder scan and ultrasound KUB for obstruction, urinalysis with microscopy, serum potassium and bicarbonate, creatine kinase, serum and urine protein electrophoresis, and ANCA / anti-GBM if a rapidly progressive picture is suspected.

Prerenal and postrenal causes matter most — their early identification and treatment may prevent the development of, or reverse, established AKI. Catheterise or place a nephrostomy promptly; restore extracellular volume; treat sepsis; stop nephrotoxic drugs.

Correct complications: hyperkalaemia (the elderly are already predisposed because of low aldosterone and reduced tubular response, and worsen further on NSAIDs, ACE inhibitors, beta blockers and potassium-sparing diuretics), metabolic acidosis and fluid overload. Adjust every drug dose to the measured GFR.

Specific therapy: withdraw the culprit drug in interstitial nephritis, with steroids if needed; steroids with cyclophosphamide for vasculitis and crescentic glomerulonephritis, used as in younger adults but with closer attention to side effects.

Dialysis: temporary or permanent support may be needed. AKI is treated much the same in old and young, but older patients are more vulnerable to dialysis-related complications — haemodynamic instability, bleeding and disequilibrium syndrome.

Prognosis: age by itself is not an important determinant of survival in AKI. Failure to recover by about 3 months leaves chronic kidney disease.

Prevention is paramount: maintain an adequate extracellular volume and tailor drug dosing to GFR. Perioperatively, estimate GFR (CKD-EPI is regarded as most accurate, Cockcroft–Gault as most sensitive), stop nephrotoxic drugs before surgery, review diuretics against the planned procedure, titrate aminoglycoside dosing intervals to plasma levels, and optimise renal perfusion with haemodynamic monitoring.

Writing "oliguria" for obstructive uropathy in a man — it is classically polyuric.

Using FENa >1% to call it ATN in an 80-year-old — the aged kidney loses sodium anyway.

Saying "old age makes AKI fatal" — age itself is not an important survival determinant.

Forgetting that the cause is usually multifactorial; listing only one.

Quoting a normal creatinine as reassurance in a sarcopenic patient.

Omitting renal vasculitis, which is the commonest primary cause of renal failure in this age group.