Renal Emergencies

Definition

Renal emergencies are acute, life-threatening conditions arising from sudden impairment of kidney function or acute complications of chronic kidney disease (CKD) that demand immediate intervention within minutes to hours to prevent irreversible organ damage or death.

10-15%

ICU admissions with AKI

50-80%

Mortality in severe AKI with MOF

13%

Global CKD prevalence

6-7×

Higher mortality with AKI in hospitalized

Major Renal Emergencies

CRITICALAcute Kidney Injury (AKI) with anuria

CRITICALLife-threatening Hyperkalemia (K⁺ > 6.5)

CRITICALSevere Pulmonary Edema (flash)

CRITICALSevere Metabolic Acidosis (pH < 7.1)

HIGHUremic Encephalopathy / Pericarditis

HIGHHUS / TTP (Thrombotic Microangiopathy)

HIGHRapidly Progressive Glomerulonephritis

MODERATERhabdomyolysis-induced AKI

MODERATEAcute Urinary Obstruction

MODERATEHypertensive Renal Crisis

KDIGO Definition of AKI

•Increase in serum creatinine ≥ 0.3 mg/dL within 48 hours
•Increase in serum creatinine ≥ 1.5× baseline within 7 days
•Urine output < 0.5 mL/kg/hr for 6 hours

Stage	Serum Creatinine	Urine Output
Stage 1	1.5–1.9× baseline OR ≥0.3 mg/dL increase	<0.5 mL/kg/hr for 6–12 hr
Stage 2	2.0–2.9× baseline	<0.5 mL/kg/hr for ≥12 hr
Stage 3	≥3× baseline OR ≥4 mg/dL OR initiation of RRT	<0.3 mL/kg/hr for ≥24 hr OR anuria ≥12 hr

Pre-Renal (55-60%)

• Hypovolemia (hemorrhage, dehydration, burns)
• Decreased cardiac output (CHF, cardiogenic shock)
• Systemic vasodilation (sepsis, anaphylaxis)
• Renal vasoconstriction (NSAIDs, ACEi/ARBs, hepatorenal)
FENa < 1%, BUN/Cr > 20:1, UOsm > 500

Intrinsic Renal (35-40%)

• ATN – ischemic (most common) or nephrotoxic
• Acute Interstitial Nephritis (AIN) – drugs, infections
• Glomerulonephritis – RPGN, lupus nephritis
• Vascular – TMA, renal artery thrombosis, cholesterol emboli
FENa > 2%, Muddy brown casts, UOsm < 350

Post-Renal (5-10%)

• BPH (most common in elderly males)
• Bilateral ureteric stones/tumors
• Retroperitoneal fibrosis
• Neurogenic bladder
Hydronephrosis on USG, bladder distension

Emergency Management Algorithm

1

ABCs – Secure airway, assess breathing, establish IV access

2

Volume status – JVP, lung auscultation, fluid challenge if hypovolemic

3

Urgent labs – BMP, CBC, ABG, urinalysis, FENa, urine microscopy

4

Imaging – Renal USG (rule out obstruction), bladder scan

5

Stop nephrotoxins – NSAIDs, aminoglycosides, contrast, ACEi/ARBs

6

Treat cause – Fluids for prerenal, relieve obstruction, treat sepsis

7

Assess for emergent dialysis – AEIOU indications (see Dialysis section)

K⁺ > 6.5 mEq/L or ANY ECG changes = MEDICAL EMERGENCY. Cardiac arrest from VFib/asystole can occur within minutes. Treat the ECG, not just the number.

ECG Changes – Progressive Sequence

5.5-6.0

Tall, peaked T waves (precordial leads)

6.0-6.5

Prolonged PR interval, flattened P waves

6.5-7.0

Loss of P waves, widened QRS complex

7.0-8.0

Sine wave pattern, merging QRS-T

> 8.0

VFib → Asystole → CARDIAC ARREST

Emergency Treatment Protocol (C-BIG-K-D)

Step	Drug / Intervention	Dose	Onset	Mechanism
C	Calcium Gluconate 10%	10-20 mL IV over 2-3 min	1-3 min	Stabilizes cardiac membrane
B	NaHCO₃ (if acidotic)	50-100 mEq IV over 5 min	15-30 min	Shifts K⁺ intracellularly
I	Insulin + Glucose	10U regular insulin + 50mL D50W	15-30 min	Shifts K⁺ intracellularly (↓ 0.5-1.0)
G	Nebulized Salbutamol	10-20 mg nebulized over 15 min	15-30 min	β2-mediated K⁺ shift (↓ 0.5-1.0)
K	Kayexalate / Patiromer	SPS 15-30g PO/PR; Patiromer 8.4g	1-6 hr	K⁺ elimination (GI exchange)
D	Dialysis (Hemodialysis)	Emergent HD session	Immediate	Definitive K⁺ removal

Pearl: Monitor blood glucose q1h for 6 hours after insulin-dextrose to catch late hypoglycemia. Repeat calcium gluconate if ECG changes persist after 5 minutes. Always recheck K⁺ at 1, 2, and 4 hours.

Pathophysiology

Oliguric/anuric AKI or ESRD → inability to excrete sodium and water → rapid fluid accumulation → increased hydrostatic pressure → alveolar flooding. Often exacerbated by concurrent hypertension and reduced oncotic pressure (hypoalbuminemia).

Clinical Presentation

• Acute-onset severe dyspnea, orthopnea
• Pink frothy sputum
• Bilateral crackles/rales (base → apex)
• SpO₂ < 90%, tachypnea, diaphoresis
• ↑ JVP, S3 gallop, peripheral edema
• CXR: bilateral alveolar infiltrates, Kerley B lines, pleural effusion

Emergency Management – "LMNOP"

L – Lasix (Furosemide) 80-200mg IV (if residual function)
M – Morphine 2-4mg IV (caution in renal failure)
N – Nitrates: GTN infusion 10-200 mcg/min
O – Oxygen: High-flow, CPAP/BiPAP, intubation PRN
P – Position (upright, legs dependent)
→ EMERGENT DIALYSIS / ULTRAFILTRATION if diuretic-resistant (most AKI patients)

When Does It Become an Emergency?

Renal failure impairs H⁺ excretion and HCO₃⁻ regeneration. pH < 7.1 or HCO₃⁻ < 8 mEq/L is life-threatening → impaired cardiac contractility, vasodilation, arrhythmias, coma.

High Anion Gap (HAGMA) – "GOLDMARK"

G – Glycols (ethylene, propylene)
O – Oxoproline (acetaminophen metabolite)
L – L-Lactate (type A: shock, type B: metformin)
D – D-Lactate (short bowel syndrome)
M – Methanol
A – Aspirin (salicylates)
R – Renal failure (uremia) ★
K – Ketoacidosis (DKA, alcoholic, starvation)

Emergency Treatment

• NaHCO₃ infusion – only if pH < 7.1 or HCO₃⁻ < 8
• Target pH 7.2 (not normal) to avoid overshoot alkalosis
• Dose: HCO₃⁻ deficit = 0.5 × wt × (24 – actual HCO₃⁻); give 50% over 4-8hr
• Monitor for: hypocalcemia (ionized Ca²⁺), hypokalemia, volume overload
• Emergent dialysis if pH < 7.1 refractory to bicarb, or toxic ingestion
• Treat underlying cause simultaneously

Anion Gap Calculation

AG = Na⁺ − (Cl⁻ + HCO₃⁻)

Normal: 8-12 mEq/L | Corrected for albumin: AG + 2.5 × (4 − albumin)

The Classic Pentad of TTP

🩸

MAHA

🔴

Thrombocytopenia

🧠

Neuro Symptoms

🫘

Renal Failure

🌡️

Fever

Feature	TTP	Typical HUS	Atypical HUS
Cause	ADAMTS13 deficiency	STEC (E. coli O157:H7)	Complement dysregulation
Predominant	Neuro (70%)	Renal (90%)	Renal (100%)
Key Lab	ADAMTS13 < 10%	Stool Shiga toxin +	Low C3, Factor H/I
Treatment	PLASMA EXCHANGE (PLEX)	Supportive (NO antibiotics)	Eculizumab (anti-C5)

⚠️ TTP is fatal in >90% without plasma exchange. Do NOT wait for ADAMTS13 results. Start PLEX immediately if clinical suspicion + schistocytes on smear + thrombocytopenia. Mortality drops to ~10-20% with timely PLEX.

AEIOU – Indications for Emergent Dialysis

A

Acidosis

Severe metabolic acidosis (pH < 7.1) refractory to NaHCO₃

E

Electrolytes

Refractory hyperkalemia (K⁺ > 6.5 despite medical therapy), severe hypercalcemia

I

Intoxication

Dialyzable toxins: methanol, ethylene glycol, lithium, salicylates, metformin

O

Overload

Diuretic-resistant pulmonary edema / volume overload

U

Uremia

Uremic encephalopathy, pericarditis, seizures, bleeding (BUN > 100 mg/dL typically)

IHD

Intermittent Hemodialysis

• 3-5 hr sessions
• Rapid solute/fluid removal
• Best for: hyperkalemia, intoxication
• Risk: hemodynamic instability

CRRT

Continuous RRT (CVVHD/CVVHDF)

• 24hr continuous therapy
• Gentle, slow fluid removal
• Best for: hemodynamically unstable ICU patients
• Dose: 20-25 mL/kg/hr effluent

PD

Peritoneal Dialysis (Acute)

• Via Tenckhoff catheter
• Resource-limited settings
• Hemodynamically stable
• Less efficient than HD/CRRT

Drug	Normal Dose	GFR <30	HD Supplement
Vancomycin	15-20 mg/kg q8-12h	15-20 mg/kg LOAD, then trough-guided	Redose post-HD
Gentamicin	5-7 mg/kg/day	AVOID or extend interval (q48-72h)	Redose post-HD
Enoxaparin	1 mg/kg q12h	1 mg/kg q24h (CrCl <30)	Use UFH instead
Metformin	500-2000 mg/day	CONTRAINDICATED	Dialyzable
Morphine	2-10 mg q4h PRN	↓ 50-75%, active metabolite accumulates	Some removal
Meropenem	1g q8h	1g q12h (GFR 10-25); 500mg q12h (GFR <10)	Supplement post-HD

🚫 Nephrotoxins to STOP in AKI

NSAIDs Aminoglycosides ACEi / ARBs IV Contrast Amphotericin B Metformin Cisplatin Lithium Calcineurin inhibitors

Stage	GFR (mL/min/1.73m²)	Description
G1	≥ 90	Normal or high
G2	60–89	Mildly decreased
G3a	45–59	Mild-moderate decrease
G3b	30–44	Moderate-severe decrease
G4	15–29	Severely decreased
G5	< 15	Kidney failure (ESRD)

Overview of Renal Emergencies