What could cause the acute decline in renal function in an 86‑year‑old woman with stage 0 chronic lymphocytic leukaemia, hypogammaglobulinaemia, hypertension, hyperlipidaemia, recurrent bacterial sinus infections, mild dementia and arthritis presenting with nausea and abdominal pain?

Acute Kidney Injury in an 86-Year-Old with Multiple Comorbidities

This patient's precipitous GFR drop from 59 to 18 mL/min/1.73 m² represents KDIGO Stage 3 acute kidney injury superimposed on pre-existing chronic kidney disease, and the most likely causes are prerenal azotemia from volume depletion (nausea, poor oral intake), medication-induced injury (NSAIDs, ACE inhibitors, ARBs, diuretics), or infection-related AKI given her recurrent bacterial infections and immunocompromised state from CLL with hypogammaglobulinemia. 1, 2

Immediate Diagnostic Approach

Confirm AKI and Establish Baseline

• Retrieve all serum creatinine values from the past 3–12 months to confirm this represents acute deterioration rather than unrecognized chronic decline; a GFR of 59 suggests baseline CKD Stage 3A, making the current GFR of 18 (Stage 4-5) highly suspicious for superimposed AKI. 2
• Apply KDIGO criteria: an absolute creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% increase from baseline within 7 days confirms AKI; in elderly patients with reduced muscle mass, baseline creatinine may underestimate true GFR, so absolute criteria are critical. 1, 2, 1

Identify the Etiology

Prerenal causes (most common in this presentation):

• Volume depletion from nausea, vomiting, poor oral intake, or excessive diuretic use is the leading reversible cause. 1, 2
• Medications altering glomerular hemodynamics—ACE inhibitors, ARBs, NSAIDs—constitute a major prerenal trigger, especially when combined ("triple whammy" with diuretics). 2, 1

Intrinsic renal causes:

• Acute tubular necrosis from prolonged hypoperfusion or nephrotoxic drug exposure (aminoglycosides, contrast agents if recent imaging). 1, 2
• Acute interstitial nephritis from antibiotics used for recurrent sinus infections (beta-lactams, fluoroquinolones). 1

Infection-related AKI:

• Recurrent bacterial sinus infections in an immunocompromised host (CLL with hypogammaglobulinemia) may progress to sepsis-associated AKI; hypogammaglobulinemia increases susceptibility to encapsulated bacteria (Streptococcus pneumoniae, Haemophilus influenzae). 3, 4, 5
• Obtain blood cultures, urine cultures, and chest radiograph immediately; in any patient with unexplained AKI and infection risk, empiric broad-spectrum antibiotics should be started without awaiting culture results. 2

Postrenal obstruction:

• Although less common (accounting for <3% of AKI), urinary retention or bilateral ureteral obstruction must be excluded, particularly in elderly women with arthritis who may have reduced mobility and delayed voiding. 1

Essential Laboratory and Imaging Workup

• Urinalysis with microscopy: muddy-brown casts suggest ATN; white-cell casts indicate pyelonephritis or interstitial nephritis; absence of casts with low urine sodium (<20 mEq/L) favors prerenal azotemia. 1, 2
• Comprehensive metabolic panel (sodium, potassium, calcium, bicarbonate, BUN, creatinine) to detect life-threatening hyperkalemia or metabolic acidosis requiring urgent intervention. 2
• Renal ultrasound to assess kidney size (small kidneys suggest chronic disease) and exclude hydronephrosis from obstruction. 1, 2
• Complete blood count: neutropenia from CLL bone marrow infiltration or prior chemotherapy increases infection risk; anemia is common in both CKD and CLL. 2

Immediate Management Priorities

Medication Review and Nephrotoxin Elimination

• Discontinue all nephrotoxic agents immediately: NSAIDs, ACE inhibitors, ARBs, diuretics, and any recent antibiotics (aminoglycosides, vancomycin). 2, 1
• Review all medications for dose adjustment in severe renal impairment (GFR <30 mL/min); many drugs require reduction or avoidance at this level. 6

Volume Resuscitation

• If clinically hypovolemic (dry mucous membranes, orthostatic hypotension, elevated BUN-to-creatinine ratio), administer isotonic crystalloids (normal saline or lactated Ringer's) to restore renal perfusion; avoid colloids and hydroxyethyl starch, which worsen kidney injury. 2
• Monitor closely for fluid overload given age and potential heart failure risk. 1

Infection Management

• If infection is suspected (fever, leukocytosis, elevated inflammatory markers), start empiric broad-spectrum antibiotics immediately after obtaining cultures; hypogammaglobulinemia in CLL predisposes to severe bacterial infections that can rapidly progress to septic AKI. 2, 4, 5
• Consider intravenous immunoglobulin (IVIG) in CLL patients with recurrent severe infections and documented hypogammaglobulinemia, although cost-effectiveness is debated. 3, 5

Electrolyte and Acid-Base Correction

• Monitor serum creatinine and electrolytes every 4–6 hours initially in Stage 3 AKI to detect progression and complications. 2
• Treat severe metabolic acidosis with intravenous sodium bicarbonate; if refractory, consider urgent dialysis. 2
• Manage hyperkalemia aggressively (calcium gluconate for cardiac protection, insulin-glucose, sodium polystyrene sulfonate, or dialysis if severe). 2

Indications for Nephrology Consultation

• Stage 3 AKI (GFR 18 mL/min) warrants immediate nephrology referral for consideration of renal replacement therapy and specialized management. 2, 6
• AKI persisting >48 hours despite initial management requires specialist input to guide further diagnostics (possible renal biopsy if glomerulonephritis or vasculitis suspected). 2
• Pre-existing CKD Stage 3A with acute deterioration to Stage 4-5 necessitates nephrology involvement for long-term planning, including preparation for dialysis or transplant evaluation. 6

Special Considerations in This Patient

Age-Related Renal Decline

• Renal function declines by approximately 1% per year after age 40; by age 86, physiologic GFR may have declined 40–50% from young-adult levels, making elderly patients particularly vulnerable to AKI from any insult. 1, 7
• Serum creatinine alone underestimates renal impairment in elderly patients due to reduced muscle mass; a "normal" creatinine may mask significant CKD. 1, 8

CLL-Associated Immunodeficiency

• Hypogammaglobulinemia in CLL increases risk of recurrent bacterial infections (especially encapsulated organisms), which are a leading cause of morbidity and mortality in this population. 3, 4, 5
• Infection is the commonest cause of death in CLL patients, and any acute illness should prompt aggressive infection workup and early antimicrobial therapy. 3, 9

Medication Toxicity Risk

• Elderly patients with CKD and cancer have up to 60% prevalence of renal insufficiency, yet many receive drugs contraindicated in renal impairment; avoid co-prescribing additional nephrotoxins (NSAIDs, COX-2 inhibitors). 8

Common Pitfalls to Avoid

• Do not dismiss a modest absolute creatinine rise as "insignificant" merely because the percentage change seems small; even a 0.3 mg/dL increase is associated with four-fold higher mortality. 2
• Do not rely on estimated GFR equations (MDRD, CKD-EPI) during acute changes; they require steady-state creatinine and were validated only in stable CKD patients. 2
• Do not delay nephrology consultation or renal replacement therapy when clear indications exist (Stage 3 AKI, refractory acidosis, hyperkalemia); delayed dialysis increases mortality. 2
• Do not overlook infection as a precipitant in immunocompromised patients; failure to promptly recognize and treat infection markedly increases AKI progression risk. 2
• Do not continue nephrotoxic medications during AKI recovery; inappropriate continuation is a major preventable cause of delayed recovery. 2

Follow-Up Planning

• Reassess kidney function at 3 months after the AKI episode to determine progression to CKD or acute kidney disease (AKD). 2
• Schedule early follow-up within 1–2 weeks given Stage 3 AKI severity and high risk of CKD progression. 2
• Document the AKI episode clearly in the medical record and educate the patient to avoid NSAIDs and seek prompt medical attention for intercurrent illnesses. 2
• Even if creatinine appears to recover, AKI is associated with sustained increased risk of CKD, cardiovascular disease, and mortality, necessitating long-term monitoring. 2