12.3 Acute Kidney Injury (AKI), Chronic Kidney Disease & Management

Acute Kidney Injury (AKI), Chronic Kidney Disease & Management

Statutory and Clinical Framework: Renal dysfunction affects up to 20% of acute hospital admissions in Ireland and is associated with substantial morbidity and mortality. Under NMBI clinical competence standards, Registered General Nurses must be skilled in early recognition of kidney dysfunction, monitoring subtle urinary output trends, understanding nephrotoxic pharmacology, managing vascular and peritoneal dialysis access, and identifying urgent indications for renal replacement therapy.

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Acute Kidney Injury (AKI): Definition & KDIGO Staging

Acute Kidney Injury (AKI) is characterized by an abrupt, rapid decline in renal excretory and filtration function occurring over hours to days (within 48 hours to 7 days). This leads to the accumulation of nitrogenous metabolic waste products (blood urea nitrogen and serum creatinine) and the loss of fluid, electrolyte, and acid-base regulation.

In Irish acute hospitals, clinical diagnostic criteria and staging adhere strictly to the international Kidney Disease: Improving Global Outcomes (KDIGO) criteria:

KDIGO Staging Criteria for Acute Kidney Injury

[!NOTE] The Primacy of Hourly Urine Output Monitoring: Serum creatinine is a delayed, lagging biomarker; it typically takes 24 to 48 hours after an acute renal insult for serum creatinine to rise significantly. In contrast, oliguria (<0.5 mL/kg/hr) occurs immediately upon hypoperfusion. Measuring urine output hourly via a closed urometer drainage system provides the earliest possible alert for evolving AKI.

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Etiological Classification of AKI: Pre-renal, Intrinsic & Post-renal

AKI is partitioned pathophysiologically into three distinct categories:

+-----------------------------------------------------------------------------+
|                     THE THREE ANATOMICAL CATEGORIES OF AKI                  |
+-----------------------------------------------------------------------------+
| 1. PRE-RENAL HYPOPERFUSION (~60% of cases):                                 |
|    - Intact nephrons; decreased renal blood flow and perfusion pressure     |
|    - Reversible if perfusion restored promptly                             |
|                                                                             |
| 2. INTRINSIC / INTRA-RENAL (~35% of cases):                                 |
|    - Direct structural and cellular damage to renal parenchyma              |
|    - Most commonly Acute Tubular Necrosis (ATN) from ischaemia or toxins    |
|                                                                             |
| 3. POST-RENAL OBSTRUCTION (~5% of cases):                                   |
|    - Mechanical obstruction of urinary collecting system below kidneys      |
|    - Hydronephrosis, retrograde pressure transmission                       |
+-----------------------------------------------------------------------------+

1. Pre-renal AKI (~60% of Ward Presentations)

Pre-renal AKI is caused by renal hypoperfusion without structural damage to renal parenchyma. Glomerular Filtration Rate (GFR) drops because renal perfusion pressure falls below the autoregulatory range (mean arterial pressure < 65 mmHg).

Etiology

• Absolute Hypovolaemia: Haemorrhage, severe gastrointestinal fluid losses (vomiting, diarrhoea, fistulae), excessive diuresis, extensive burns, severe dehydration.
• Relative Hypovolaemia / Effective Circulatory Depletion: Sepsis (systemic vasodilation and capillary leak), anaphylaxis, decompensated congestive heart failure (cardiorenal syndrome), liver cirrhosis with ascites (hepatorenal syndrome).
• Renovascular Compromise: Renal artery stenosis, renal vein thrombosis.
• Haemodynamic Drug Interactions — The 'Triple Whammy':
  • NSAIDs: Inhibit cyclooxygenase (COX), blocking the production of vasodilatory prostaglandins (prostacyclin, PGE2) that maintain blood flow through the afferent arteriole. This causes afferent arteriolar constriction and drops intraglomerular pressure.
  • ACE Inhibitors / ARBs: Inhibit Angiotensin II, preventing vasoconstriction of the efferent arteriole. This dilates the efferent arteriole, dissipating glomerular filtration pressure.
  • Diuretics: Deplete intravascular circulating volume, reducing renal plasma inflow.
  • The Combination: Prescribing a Diuretic + ACEi/ARB + NSAID simultaneously ('The Triple Whammy') removes both autoregulatory defence mechanisms in a hypovolaemic patient, precipitating immediate catastrophic pre-renal failure.

2. Intrinsic / Intra-renal AKI (~35% of Cases)

Intrinsic AKI involves structural parenchymal damage to glomeruli, renal tubules, interstitium, or microvasculature.

Etiology

• Acute Tubular Necrosis (ATN) (~85% of intrinsic cases):
  • Ischaemic ATN: Uncorrected, prolonged pre-renal hypoperfusion leading to renal tubular cell ischaemia, sloughing, and necrosis.
  • Nephrotoxic ATN: Direct cellular damage from exogenous or endogenous toxins:
    • Aminoglycosides (Gentamicin, Amikacin): Accumulate inside proximal tubular cells, causing cellular necrosis. Therapeutic drug monitoring (trough levels) is mandatory in Irish hospitals.
    • Glycopeptides (Vancomycin): Nephrotoxic, especially when combined with aminoglycosides or piperacillin-tazobactam.
    • Iodinated Radiocontrast Media: Contrast-Induced Nephropathy (CIN) occurs 24–48 hours post-CT or angiography. High-risk patients require pre- and post-procedure hydration with 0.9% NaCl.
    • Endogenous Toxins: Myoglobin from rhabdomyolysis (crush injuries, prolonged immobilization, statins) precipitates in tubules and causes direct cytotoxicity; Haemoglobin from intravascular haemolysis; Bence-Jones light chains in multiple myeloma.
• Acute Interstitial Nephritis (AIN): Drug-induced allergic hypersensitivity reaction (penicillins, cephalosporins, NSAIDs, PPIs, allopurinol). Features: sterile pyuria, eosinophiluria, systemic rash, and fever.
• Glomerulonephritis: Rapidly Progressive Glomerulonephritis (RPGN), ANCA vasculitis, post-streptococcal GN, lupus nephritis. Characterized by haematuria, red blood cell casts, proteinuria, and hypertension.

3. Post-renal AKI (~5% of Cases)

Post-renal AKI results from mechanical obstruction to urine flow anywhere from the renal pelvis down to the external urethral meatus. Retrograde backpressure increases Bowman's capsule pressure, arresting glomerular filtration.

• Etiology: Benign Prostatic Hyperplasia (BPH, leading cause in elderly men), prostate carcinoma, bilateral ureteric calculi, retroperitoneal fibrosis, pelvic malignancies (cervical, ovarian, colorectal), neurogenic bladder, or a blocked indwelling urethral catheter (encrustation, sediment, kinked tubing).
• Diagnosis: Immediate bedside bladder ultrasound scanning (showing large urinary volume > 300–500 mL in urinary retention) and urgent formal renal ultrasonography (showing bilateral hydronephrosis and dilated ureters).

Biochemical Differentiation: Pre-renal versus Intrinsic ATN

Multidisciplinary Nursing Management of AKI

Managing AKI requires a systematic, aggressive nursing and medical response centered on perfusion restoration, complication prevention, and pharmacological auditing.

1. The Nephrotoxic Medication Audit ('DAMN' Drugs)

Upon recognizing AKI, the nurse must immediately review the patient's medication administration record (kardex) with the prescriber to withhold the 'DAMN' drugs:

+-----------------------------------------------------------------------------+
|                  THE 'DAMN' NEPHROTOXIC DRUG AUDIT                          |
+-----------------------------------------------------------------------------+
| D - DIURETICS (Furosemide, Bumetanide, Spironolactone)                     |
|     -> Exacerbate intravascular volume depletion and worsen pre-renal AKI.  |
|                                                                             |
| A - ACE INHIBITORS / ARBs (Ramipril, Lisinopril, Losartan, Candesartan)     |
|     -> Dilate efferent arterioles, abolishing glomerular filtration         |
|        pressure.                                                            |
|                                                                             |
| M - METFORMIN                                                               |
|     -> Does not cause direct renal injury, but accumulates in renal         |
|        impairment, precipitating fatal METFORMIN-ASSOCIATED LACTIC ACIDOSIS |
|        (MALA). Must be suspended immediately when eGFR drops < 30 mL/min.   |
|                                                                             |
| N - NSAIDs (Ibuprofen, Naproxen, Diclofenac, Celecoxib)                     |
|     -> Constrict afferent arterioles, directly choking glomerular blood     |
|        supply.                                                              |
+-----------------------------------------------------------------------------+

2. Haemodynamic Fluid Resuscitation versus Fluid Restriction

• In Pre-renal AKI: Administer prescribed isotonic balanced crystalloid fluid challenges (e.g., Hartmann's 250–500 mL boluses) and re-evaluate vital signs and urine output. Ensure mean arterial pressure (MAP) is maintained ≥ 65 mmHg.
• In Established Oliguric Intrinsic ATN: Once intravascular volume is restored, continuing aggressive IV fluids does not revive dead tubular cells; it simply floods the lungs. Institute strict fluid restriction: daily allowance equals measured previous 24-hour fluid output + 500 mL (insensible loss allowance).

3. Monitoring Life-Threatening AKI Complications

• Hyperkalaemia: Monitor serum electrolytes at least twice daily; maintain continuous ECG telemetry; execute the hyperkalaemia protocol if K+ > 6.0 mmol/L.
• Pulmonary Edema: Monitor respiratory rate, SpO2, and auscultate lung bases hourly for bilateral crepitations. AKI patients cannot excrete water; excessive fluids cause acute pulmonary extravasation.
• Metabolic Acidosis: Kidneys fail to regenerate bicarbonate (HCO3-) or excrete hydrogen ions (H+). Assess for Kussmaul breathing (deep, rapid, sighing respirations as lungs blow off CO2 to compensate for systemic acidaemia; Arterial Blood Gas: pH < 7.20, HCO3- < 12 mmol/L).
• Uraemic Complications: Urea and toxic nitrogenous wastes accumulate across body tissues:
  • Uraemic Encephalopathy: Confusion, cognitive slowing, asterixis (flapping tremor demonstrated when patient dorsiflexes wrists with arms extended), myoclonus, and seizures.
  • Uraemic Pericarditis: Severe central pleuritic chest pain relieved by leaning forward; auscultation reveals a high-pitched superficial pericardial friction rub.
  • Uraemic Bleeding: Uremic toxins inhibit platelet aggregation (platelet factor 3 release), causing epistaxis, GI bleeding, and prolonged bleeding time despite normal platelet counts.

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Chronic Kidney Disease (CKD): Staging & Systemic Complications

Chronic Kidney Disease (CKD) is defined as abnormalities of kidney structure or function present for greater than 3 months, evidenced by either markers of kidney damage (persistent proteinuria, albuminuria, pathological sediment, imaging abnormalities) or an estimated Glomerular Filtration Rate (eGFR) < 60 mL/min/1.73 m².

KDIGO Staging of Chronic Kidney Disease

Major Systemic Complications of CKD

1. Anemia of Chronic Kidney Disease

• Pathophysiology: Loss of functional peritubular capillary fibroblasts in the renal cortex leads to deficient Erythropoietin (EPO) synthesis. Uraemic toxins also suppress bone marrow erythropoiesis and shorten red blood cell survival. Compounded by chronic gastrointestinal micro-bleeding and iron deficiency.
• Clinical Signs: Fatigue, lethargy, pallor, exertional dyspnoea, palpitations, exacerbation of angina.
• Management:
  • Correct Iron Deficiency First: Erythropoietin therapy is completely ineffective if iron stores are depleted. Administer oral iron or intravenous iron (e.g., ferric carboxymaltose) to maintain serum ferritin > 100 to 200 µg/L and transferrin saturation (TSAT) > 20%.
  • Erythropoiesis-Stimulating Agents (ESAs): Subcutaneous or IV administration of recombinant human erythropoietin (Epoetin alfa/beta) or longer-acting Darbepoetin alfa.
  • Safety Target: Maintain haemoglobin between 100 and 120 g/L. Exceeding 120–130 g/L increases the incidence of severe hypertension, vascular access thrombosis, stroke, and cardiovascular mortality.

2. CKD-Mineral and Bone Disorder (CKD-MBD / Renal Osteodystrophy)

• Pathophysiology:
  1. The failing kidney cannot excrete phosphate, causing Hyperphosphataemia.
  2. Loss of functional renal mass diminishes the enzyme 1-alpha-hydroxylase, preventing the activation of 25-hydroxyvitamin D into active 1,25-dihydroxyvitamin D (Calcitriol).
  3. Lack of calcitriol reduces intestinal calcium absorption, producing Hypocalcaemia.
  4. Hyperphosphataemia and hypocalcaemia chronically stimulate parathyroid glands to secrete massive amounts of Parathyroid Hormone (PTH), establishing Secondary Hyperparathyroidism.
  5. High PTH leaches calcium and phosphate from skeletal bones, producing osteitis fibrosa cystica, osteomalacia, bone pain, and pathological fractures, while causing metastatic calcification in coronary arteries and peripheral vessels (calciphylaxis).
• Management:
  • Dietary Phosphate Restriction: Limit high-phosphate foods (dairy, cheese, nuts, colas, processed meats).
  • Phosphate Binders: Must be taken immediately before or with meals to bind dietary phosphate in the gut lumen, forming insoluble complexes excreted in faeces. Calcium-based binders (Calcium Acetate, Calcium Carbonate) or non-calcium binders (Sevelamer carbonate, Lanthanum carbonate).
  • Active Vitamin D Analogues: Calcitriol or Alfacalcidol to suppress PTH.
  • Calcimimetics: Cinacalcet (increases sensitivity of calcium-sensing receptors on parathyroid glands, suppressing PTH secretion without raising calcium).

3. Cardiovascular Disease in CKD

Cardiovascular disease (accelerated atherosclerosis, left ventricular hypertrophy, heart failure, lethal arrhythmias) is the leading cause of death in patients with CKD. Uraemia, chronic fluid overload, vascular calcification, and hypertension accelerate coronary disease. Strict blood pressure control (target <130/80 mmHg), statin therapy, and smoking cessation are paramount.

Renal Replacement Therapy (RRT): Indications & Nursing Care

When conservative medical therapy fails to maintain life in severe AKI or Stage 5 CKD, Renal Replacement Therapy (RRT) is required.

Emergency Indications for Dialysis: The 'AEIOU' Mnemonic

Every candidate must memorize the five statutory clinical triggers for emergency renal replacement therapy:

+-----------------------------------------------------------------------------+
|                   THE 'AEIOU' EMERGENCY DIALYSIS CRITERIA                   |
+-----------------------------------------------------------------------------+
| A - ACIDOSIS                                                                |
|     -> Severe metabolic acidosis refractory to medical management           |
|        (Arterial pH < 7.15 to 7.20; Serum Bicarbonate < 10-12 mmol/L).       |
|                                                                             |
| E - ELECTROLYTES                                                            |
|     -> Severe, refractory hyperkalaemia (Serum K+ > 6.5 mmol/L) with        |
|        persistent ECG abnormalities unresponsive to medical shift therapy.  |
|                                                                             |
| I - INGESTIONS / INTOXICATIONS                                              |
|     -> Overdose of dialysable toxic substances:                             |
|        * Lithium                                                            |
|        * Salicylates (Aspirin)                                              |
|        * Ethylene Glycol (Antifreeze)                                       |
|        * Methanol (Toxic Alcohol)                                           |
|        * Theophylline                                                       |
|                                                                             |
| O - OVERLOAD                                                                |
|     -> Acute fluid overload / pulmonary edema refractory to high-dose IV    |
|        loop diuretics.                                                      |
|                                                                             |
| U - URAEMIA                                                                 |
|     -> Severe symptomatic end-organ uraemic complications:                  |
|        * Uraemic Encephalopathy (confusion, asterixis, seizures)            |
|        * Uraemic Pericarditis (friction rub, pleuritic pain, tamponade risk)|
|        * Uraemic Platelet Bleeding / Uraemic Gastropathy                    |
+-----------------------------------------------------------------------------+

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Modalities of Renal Replacement Therapy

+-----------------------------------------------------------------------------+
|                       HAEMODIALYSIS vs PERITONEAL DIALYSIS                  |
+---------------------------------------+-------------------------------------+
|            HAEMODIALYSIS              |         PERITONEAL DIALYSIS         |
| - Blood pumped through external       | - Patient's peritoneal membrane     |
|   artificial dialyser                 |   serves as the semi-permeable filter|
| - Access: AV Fistula, AV Graft, or    | - Access: Permanently implanted     |
|   Tunnelled Central Line (Permacath)  |   Tenkhoff catheter in abdomen      |
| - Schedule: 4 hours, 3 times per week | - Schedule: CAPD (4 manual exchanges|
| - Rapid solute & fluid removal        |   daily) or APD (overnight cycler)  |
| - Key Risk: Hypotension, bleeding,    | - Key Risk: PERITONITIS             |
|   vascular access thrombosis          |   (cloudy dialysate effluent)       |
+---------------------------------------+-------------------------------------+

1. Haemodialysis (HD) & Arteriovenous (AV) Fistula Nursing Care

In haemodialysis, blood is pumped via an extracorporeal circuit through a hollow-fibre dialyser. Solutes diffuse across semi-permeable membranes down concentration gradients into dialysate solution, while excess fluid is removed via hydrostatic ultrafiltration.

Vascular Access Modalities

• Arteriovenous Fistula (AVF): The surgical joining (anastomosis) of a native artery directly to a native vein (most commonly radiocephalic [Brescia-Cimino] at the wrist or brachiocephalic at the elbow). The high arterial pressure causes the vein to dilate and thicken ('arterialise') over 6 to 12 weeks. Represents the gold standard vascular access due to lowest infection and thrombosis rates.
• Arteriovenous Graft (AVG): A synthetic polytetrafluoroethylene (PTFE) tube bridging an artery and vein. Used when native veins are inadequate; matures in 2–4 weeks; carries higher thrombosis and infection rates than AVF.
• Central Venous Haemodialysis Catheters: Dual-lumen non-tunnelled catheters (Vascath, femoral or internal jugular; temporary emergency access) or cuffed tunnelled catheters (Permacath, internal jugular vein; intermediate access). Highest risk of catheter-related bloodstream infections (CRBSI) and central venous stenosis.

[!CAUTION] STRICT RULES FOR AV FISTULA STEWARDSHIP (CRITICAL OSCE PITFALL):

1. Daily Patency Assessment: Every shift, the nurse must assess the fistula:
   • Auscultation: Place a stethoscope over the fistula to listen for a continuous, low-pitched, musical rushing sound (the bruit).
   • Palpation: Gently palpate the fistula site to feel a continuous, soft, buzzing mechanical vibration (the thrill).
   • Emergency: If the thrill or bruit is absent, the fistula has thrombosed. Alert the vascular surgeon and nephrologist immediately; urgent intervention within 24 hours can rescue the access.
2. ABSOLUTE LIMB RESTRICTION: The limb with an AV fistula or graft must be protected at all costs:
   • NEVER take blood pressure measurements on the fistula arm (cuff inflation causes stasis and acute thrombosis).
   • NEVER perform venepuncture or insert peripheral IV cannulas in the fistula arm.
   • NEVER administer IV infusions or subcutaneous injections in that arm.
   • Place a distinct warning wristband on the arm and hang a prominent sign above the hospital bed ('NO BP / NO BLOOD DRAWS ON THIS ARM').
   • Instruct the patient to avoid tight clothing, restrictive watches, carrying heavy shopping bags, or sleeping on the fistula arm.

2. Peritoneal Dialysis (PD) & Peritonitis Care

Peritoneal dialysis instills 1.5 to 2.5 litres of sterile dialysate solution into the peritoneal cavity through a surgically implanted silicone Tenkhoff catheter. The vascular peritoneal membrane acts as a semi-permeable filter. Dextrose concentrations (1.36%, 2.27%, or 3.86%) create an osmotic gradient pulling fluid into the peritoneal space.

• Continuous Ambulatory Peritoneal Dialysis (CAPD): Patient performs 4 to 5 manual bag exchanges throughout the day under gravity.
• Automated Peritoneal Dialysis (APD): An automated cycling machine performs multiple exchanges overnight while the patient sleeps.

Peritoneal Dialysis-Associated Peritonitis

Peritonitis is the most frequent, debilitating, and potentially fatal complication of peritoneal dialysis. Contamination occurs during connection/disconnection procedures or via touch contamination of the transfer set.

• Cardinal Clinical Signs:
  1. Cloudy / Turbid Dialysate Effluent: The clear dialysate drainage becomes hazy, cloudy, or milky. Bedside diagnostic test: Attempt to read printed newspaper text through the drained effluent bag. If the print is obscured, suspect peritonitis immediately!
  2. Abdominal Pain: Diffuse, generalized abdominal cramps or sharp pain.
  3. Peritoneal Irritation: Abdominal rebound tenderness and guarding.
  4. Systemic Symptoms: Fever, nausea, vomiting, chills, malaise.

+-----------------------------------------------------------------------------+
|                 EMERGENCY MANAGEMENT OF PD PERITONITIS                      |
+-----------------------------------------------------------------------------+
| 1. IMMEDIATE EFFLUENT INSPECTION:                                           |
|    - Examine drained effluent bag against printed text; note cloudiness.    |
|                                                                             |
| 2. URGENT LABORATORY INVESTIGATION:                                         |
|    - Send effluent specimen immediately for:                                |
|      * Peritoneal fluid white blood cell (WBC) count and differential       |
|        (Diagnosis confirmed if WBC > 100/mcL with > 50% neutrophils)        |
|      * Gram stain                                                           |
|      * Aerobic and anaerobic cultures                                       |
|                                                                             |
| 3. EMPIRICAL ANTIMICROBIAL THERAPY:                                         |
|    - DO NOT discontinue peritoneal dialysis!                                |
|    - Instigate broad-spectrum Intraperitoneal (IP) Antibiotics added        |
|      directly into the dialysate bags (typically combining vancomycin or    |
|      cefazolin for Gram-positives with gentamicin or ceftazidime for        |
|      Gram-negatives).                                                       |
|    - Intraperitoneal heparin (500 units/L) is added to dialysate to prevent  |
|      fibrin clots from blocking the Tenkhoff catheter.                      |
+-----------------------------------------------------------------------------+