---

Acute Kidney Injury (AKI): Full Clinical Approach for the Medical Officer

---

1. DEFINITION (KDIGO 2026)

KDIGO 2026 update: The new staging system now incorporates structural biomarkers (NGAL, TIMP-2•IGFBP7, etc.) in addition to SCr and urine output - a "B+" designation means biomarker-positive AKI, which carries a higher risk of progression even at lower functional stages.

---

2. KDIGO 2026 STAGING

---

3. CATEGORIZATION: THE FIRST CLINICAL STEP

A. Prerenal AKI (~40-55% of all AKI)

• Hypovolemia: vomiting, diarrhea, bleeding, burns, NGT suction
• Reduced effective arterial blood volume: heart failure, cirrhosis, nephrotic syndrome
• Drugs: NSAIDs (block prostaglandin-mediated afferent dilation), ACEi/ARBs (block angiotensin-mediated efferent constriction), diuretics
• Sepsis (distributive shock)

B. Intrinsic (Parenchymal) AKI

• ATN is the most common intrinsic cause, especially in critically ill patients
• Sepsis-associated AKI can occur even without overt hypotension (complex microvascular and inflammatory mechanisms)

C. Postrenal (Obstructive) AKI

• Urethral: BPH (most common in older males), urethral stricture, bladder neck obstruction
• Ureteric: stones, blood clots, retroperitoneal fibrosis, pelvic malignancy
• Always check bladder catheter patency - most easily missed cause

---

4. APPROACH TO THE PATIENT IN OPD/ED

Step 1: Stabilize the Patient First

Step 2: History - Targeted Questions

• When did the patient last pass urine? How much?
• Any vomiting, diarrhea, fever, poor oral intake? (volume loss)
• Any burning micturition, poor stream, inability to void? (obstructive)
• Drug history: NSAIDs, ACEi/ARBs, diuretics, aminoglycosides, contrast agents, herbal medicines, PPI
• Baseline renal status: known CKD? Diabetes, hypertension?
• Recent procedures: surgery, contrast study, cardiovascular intervention
• Symptoms of systemic disease: rash, joint pains, hematuria, frothy urine
• Any myalgia, dark urine? (rhabdomyolysis)
• Alcohol, toxins, snakebite (common in government hospital settings)

Step 3: Physical Examination

Step 4: Investigations (Prioritized)

• Serum creatinine + BUN (establish AKI and stage)
• Electrolytes: Na, K, HCO3 (hyperkalemia and acidosis are emergencies)
• ABG or venous blood gas (acid-base status)
• Blood glucose
• CBC: hemoglobin, platelet count (TTP/HUS if thrombocytopenic with AKI)
• Urine dipstick + microscopy: the single most important diagnostic test for intrinsic AKI
• Renal ultrasound: mandatory - rules out obstruction, assesses kidney size, echogenicity

Caveat: FeNa is unreliable if the patient is on diuretics. Use FEUrea (<35% = prerenal) instead. FeNa is also low in early contrast nephropathy, myoglobinuria, and acute GN even with intrinsic AKI.

• CPK, urine myoglobin (rhabdomyolysis)
• LFTs, coagulation (hepatorenal syndrome, DIC)
• ANCA, ANA, anti-GBM, C3/C4, ASOT, blood cultures (suspected GN/vasculitis)
• Serum protein electrophoresis, Bence Jones proteins (myeloma)
• HIV, hepatitis B/C serology (associated nephropathies)
• LDH, peripheral smear (TTP/HUS)
• Bladder scan or post-void residual (obstructive)

---

5. MANAGEMENT

A. General Supportive Measures (All AKI)

1. Establish IV access, start monitoring (vitals, urine output, fluid balance)
2. Foley catheter: essential for urine output monitoring + rules out/treats outlet obstruction
3. Review and stop ALL potentially nephrotoxic drugs: NSAIDs, aminoglycosides, IV contrast agents, ACEi/ARBs in acute setting, metformin (lactic acidosis risk), SGLT2 inhibitors
4. Avoid nephrotoxic contrast: if imaging is needed, use lowest possible dose of low/iso-osmolar contrast; ensure adequate hydration pre/post procedure
5. Dose-adjust all medications for the degree of renal impairment
6. Nutritional support: do not restrict protein intake below normal in AKI (KDIGO 2026 recommends 0.8-1.2 g/kg/day; avoid excess)

---

B. Fluid Management (KDIGO 2026 + Evidence)

• Hypovolemic patient: give IV fluids
• Euvolemic or hypervolemic patient: do NOT give fluids (can cause fluid overload, worse outcomes)

• Crystalloids are preferred over colloids (hydroxyethyl starches - HES - are contraindicated; associated with severe AKI and death)
• Balanced crystalloids (Ringer's Lactate, PlasmaLyte) are preferred over 0.9% normal saline - NS can cause hyperchloremic metabolic acidosis with renal vasoconstriction
• Albumin can be considered in specific scenarios: septic shock with large crystalloid volumes already given, or hepatorenal syndrome

• Give boluses of 250-500 mL over 15-30 minutes, then reassess
• Avoid static targets (CVP, JVP) - use dynamic assessments: passive leg raise (PLR) test, point-of-care ultrasound (POCUS) for IVC collapsibility, capillary refill time
• PLR: raise legs to 45° from supine for 1-2 minutes. If SBP rises >10% or pulse pressure increases - fluid responsive
• Re-assess after each bolus. Stop fluids once hemodynamics stabilize or patient becomes fluid-unresponsive

---

C. Hemodynamic Management

• Target MAP ≥65 mmHg (higher targets of 65-80 mmHg may be appropriate in patients with chronic hypertension or with septic AKI)
• If fluid-resuscitated but still hypotensive, start norepinephrine as first-line vasopressor
• Vasopressin as second agent if norepinephrine dose is escalating
• Dopamine at "renal dose" (1-3 µg/kg/min) is NOT recommended - does not protect kidneys, increases arrhythmia risk (KDIGO 2012 and 2026 - Grade 1A against use)
• In septic shock with vasopressor dependency: consider IV hydrocortisone 200 mg/day (50 mg Q6h)

---

D. Management of Specific AKI Types

Prerenal AKI

• Identify and correct the underlying cause
• Volume replacement for hypovolemia: see above
• For cardiorenal syndrome: treat heart failure (cautious diuretics, optimization of cardiac output)
• For hepatorenal syndrome: albumin 1 g/kg/day (max 100g) + vasoconstrictors (terlipressin 0.5-2 mg IV Q4-6h where available, or midodrine + octreotide); refer to hepatologist for liver transplantation evaluation

ATN (Ischemic/Toxic/Septic)

• No specific pharmacological treatment reverses established ATN - management is supportive
• Ensure adequate perfusion, avoid ongoing nephrotoxin exposure
• Diuretics (furosemide) may convert oliguric to non-oliguric ATN (easier to manage fluid balance) but do NOT improve survival, hasten recovery, or delay need for RRT. Use only for fluid overload, not to "protect" the kidneys
• N-acetylcysteine (NAC) 600 mg BD oral: reasonable for contrast nephropathy prevention in high-risk patients (evidence modest, but low cost and safe)
• For contrast AKI prevention: IV normal saline or sodium bicarbonate pre/post procedure (1 mL/kg/h for 3-12 hours before and after contrast), hold nephrotoxins

Obstructive (Postrenal) AKI

• Immediate drainage is the definitive treatment:
  • Urethral catheter for bladder neck/urethral obstruction (BPH, stricture)
  • Suprapubic catheter if urethral catheterization fails
  • Percutaneous nephrostomy or ureteral stenting for ureteric obstruction
• After relief: anticipate post-obstructive diuresis (can be massive - >200 mL/hr). Replace 50-75% of urine output with IV fluids. Monitor electrolytes closely (Na, K, Mg)

AIN (Drug-Induced)

• Stop the offending drug immediately
• If drug cannot be identified or improvement is slow, consider renal biopsy to confirm diagnosis
• Short course of steroids (prednisolone 0.5-1 mg/kg/day for 4-8 weeks) is used in confirmed AIN, especially if eosinophilia/systemic allergy features present - evidence is moderate but practice is widespread

Rhabdomyolysis-associated AKI

• Aggressive IV fluid resuscitation: 1-1.5 L/hr of crystalloid to target urine output 200-300 mL/hr until myoglobin clears
• Urinary alkalinization with sodium bicarbonate (target urine pH >6.5) - controversial but widely practiced
• Monitor for hypocalcemia (early phase), hypercalcemia (recovery phase), and hyperkalemia

---

E. Management of Complications (Life-Threatening - Address Immediately)

1. Hyperkalemia

In government hospital setting: calcium gluconate + insulin-dextrose + sodium bicarbonate (if acidotic) + furosemide is the practical first-line combination available everywhere.

• Peaked T waves (earliest) → widened QRS → sine wave pattern → VF

2. Metabolic Acidosis

• Treat the underlying cause
• If pH <7.2 or HCO3 <15 mEq/L: sodium bicarbonate infusion (1-2 mEq/kg IV over 2-4 hours)
• Severe acidosis (pH <7.1) with volume overload: indication for dialysis
• Avoid hyperchloremic solutions (0.9% saline) that worsen acidosis

3. Fluid Overload/Pulmonary Edema

• Upright posture, oxygen
• Furosemide IV: 40-80 mg IV bolus (if some residual renal function)
• High-dose furosemide may be needed in AKI (tubular secretion is impaired): up to 200-400 mg IV
• If refractory: urgent dialysis/ultrafiltration

4. Uremia

• Uremic pericarditis or encephalopathy = emergency indication for dialysis - do not delay
• BUN >100 mg/dL with symptoms warrants urgent nephrology consultation

---

F. Indications for Renal Replacement Therapy (RRT/Dialysis)

• Anuria (no urine for >6 hours despite adequate volume)
• Severe oliguria (<200 mL/12 hours)
• BUN rapidly rising or >100-150 mg/dL with symptoms

• Intermittent hemodialysis (IHD): standard if hemodynamically stable
• Continuous RRT (CRRT): preferred in hemodynamically unstable patients, patients with cerebral edema, when slow fluid removal is desired (septic shock on vasopressors)
• Peritoneal dialysis (PD): available in some government hospitals - can be used where HD is not available; less efficient but can be lifesaving

Do not delay dialysis waiting for specific BUN or creatinine cutoffs if clinical indications are present.

---

6. NEPHROLOGY REFERRAL CRITERIA

• AKI stage 2-3
• Suspected GN (active urinary sediment + proteinuria + hematuria + systemic features)
• AKI of unclear cause
• AKI in CKD patients
• Any indication for RRT
• AKI not responding to initial treatment

---

7. MONITORING DURING ADMISSION

---

8. POST-AKI FOLLOW-UP (KDIGO 2026)

• All patients with AKI should have creatinine, urine ACR, and BP checked at 3 months
• Patients without CKD at 3 months still have increased risk for new-onset CKD and should be monitored
• Patients with CKD at 3 months: managed per KDIGO 2024 CKD guidelines
• Restart ACEi/ARBs carefully once stable (usually 4-6 weeks after episode), based on electrolytes and eGFR
• Advise patient to avoid NSAIDs, herbal nephrotoxins, and dehydration

---

9. QUICK DECISION FLOWCHART FOR THE GOVERNMENT HOSPITAL MO

Patient with Suspected AKI
         │
         ▼
1. URGENT: Check K+, ABG, ECG
   → Hyperkalemia/acidosis? → Treat immediately (calcium gluconate, insulin-dextrose)
         │
         ▼
2. Catheterize → Measure urine output
   → Bladder full on catheter? → Postrenal AKI → Decompress → Reassess
         │
         ▼
3. Assess volume status (clinically + POCUS if available)
   → Hypovolemic? → IV fluids (Ringer's Lactate preferred)
   → Euvolemic/hypervolemic + oliguric? → Do NOT fluid challenge blindly
         │
         ▼
4. Urine dipstick + microscopy + urine Na + renal USG
   → Casts/cells → Intrinsic AKI → Specific workup (ANCA, C3/C4, etc.)
   → Bland sediment → Prerenal (if FeNa <1%) or postrenal
         │
         ▼
5. Stop all nephrotoxins, adjust drug doses
         │
         ▼
6. Monitor creatinine, K+, urine output Q12-24h
   → Stage 2-3 AKI / not responding / unclear cause → Nephrology referral
         │
         ▼
7. AEIOU indications → Arrange RRT

---

Key References

• Brenner and Rector's The Kidney, 10e - Ch. 29: Prevention and Management of Acute Kidney Injury (Weisbord & Palevsky)
• Harrison's Principles of Internal Medicine, 22e (2025) - AKI and Sepsis chapters
• Frameworks for Internal Medicine - AKI clinical framework
• KDIGO 2026 AKI/AKD Guideline Draft (first major update since 2012 - incorporates biomarkers, revised staging with structural criteria, updated fluid/hemodynamic and RRT guidance)
• KDIGO 2012 AKI Guideline (still valid for core principles, being superseded by 2026)

---

• Renal ultrasound is your most important non-lab investigation - it quickly separates postrenal from other causes and identifies CKD (small kidneys)
• When in doubt about volume status and no POCUS available, do a careful passive leg raise test or give a cautious 250 mL fluid challenge and re-examine in 30 minutes
• Balanced crystalloids (RL) are cheaper and safer than NS for resuscitation - avoid large volumes of 0.9% NS
• Track urine output religiously - a patient who makes urine is usually improving; persistent oliguria despite adequate fluids needs urgent escalation
• The most missed diagnosis is postrenal AKI from BPH - always catheterize an oliguric elderly male patient first