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Acute Renal Failure (Acute Kidney Injury) (ARF)

Definition Complications of ARF

Clinical syndrome Oliguria
Rapid ↓ in Renal Excretory Function (occurring over hours → days) Hyperkalaemia
Oliguria ( <400ml/day) Pulmonary Edema
Anuria Metabolic Acidosis
↑ Serum Creatinine (SCr) Uremic symptoms
↑ Blood Urea Nitrogen (BUN)
Management
Importance Fluid Management
Occurs in 5% of all Hospital Admissions Pre-Renal Renal Post-Renal
Hospital Morbidity & Mortality (common cause) (30-70%) (with Volume deficit) (without Volume deficit)
Severity of underlying illness Fluid Replacement, Fluid Restriction Remove Obstruction
Complications of ARF Correction of Na+, K+ restriction
Intravascular Volume Fluid Intake =
Iatrogenic cases (50%) Contraction Output + 50ml
Sepsis • Blood Transfusion IV Frusemide
Fluid, Electrolyte imbalance • Normal Saline,
Drug Hartmann solution
Nephrotoxicity Control BP
Reversible if diagnosed & treated promptly (many cases) Hyperkalaemia
If patient survives, renal function returns to Normal or Near Normal Mild ( <6.5 mmol/L) Moderate → Severe ( >6.5 mmol/L)
(ECG – Bradycardia peaked T waves to
Diagnostic Evaluation idioventricular rhythm)
Establish Diagnosis Fluid Therapy IV Calcium Gluconate (10%)
Serum Biochemistry IV Insulin + Glucose
Symptoms & Signs Salbutamol
Elucidation of Cause Haemodialysis, Haemofiltration (if Anuric)
Clinical assessment – Presenting symptoms, Drug History, Hospital course, PE Pulmonary Edema
Urine Examination Sit up, Give ↑ flow O2 mask
Blood Tests Venous Vasodilator – Morphine IV/ IV Nitrate
Renal Imaging Loop Diuretic – Frusemide IV
Renal Biopsy Haemodialysis, Haemofiltration (if no response)
Continuous +ve airway pressure ventilation therapy
Metabolic Acidosi s
pH < 7.1 or with HCO3 >10mmol/L
Mild – Fluid Therapy
Supportive Treatment
Uraemic signs & symptoms
• Pericarditis
Urine Evaluation • Uraemic Encephalopathy
Dipstick Urinalysis Urine Microscopy Urine Biochemical Indices • Bleeding
Proteinuria Examination of Distinguish from • GI Complications
Haemoglobin sediment of Pre-renal ARF Hyperkalaemia
Leucocytes centrifuged speciment Intrinsic/ Renal ARF Fluid overload
Cells Urine Osmolality Acidosis
Casts ( > 350mosm/kg in Pre-Renal) SCr > 600 umol/L
Crystals Fractional Excretion of Na+ Urea > 30 mmol/L
Pyuria ( <1% in Pre-Renal) Dialysis
Peritoneal Dialysis
Haemodialysis
Ultrasound
Continuous Renal Re placement Therapy (CRRT )

Outcome & Long Term Prognosis

Mortality rate – 50%
Causes of Death
Sepsis
Cardiovascular causes
Pulmonary dysfunction
Mortality & Cause
Pre-Renal - 7%
Normal Acute Obstruction Toxin related - 30%
Following Trauma, Major Surgery - 50-70%
Renal Biopsy Mortality rates ↑
After excluding Pre-Renal, Post-Re nal causes of ARF Older patients
Cause of Intrinsic/ Renal ARF is unclear Multiple Organ Failure (MOF)
Useful when Clinical assessment, Urinalysis, Laboratory investigations Sepsis
suggest a diagnosis other than Ischaemic or Nephrotoxic Inj ury Patients who survive ARF episode, mostly recover sufficient renal function
Anti-glomerular basement membrane disease Never recover renal function (5-10%)
Glomerulonephritis (RPGN ) Long term dialysis
Vasculitis Transplantation
Allergic Interstitial Nephritis
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Acute Renal Failure

Pre-Renal (Volume Responsive) (55%) Renal (Intrinsic) (40%) Post-Renal (5-10%)
Hypovolaemia Acute Tubular Necrosi s Obstruction
Vomiting, Diarrhoea (Necrosis of Tubular Epithelial Cells) Between External Urethral meatus & Bladder neck
Haemorrhage Ischaemia Toxins Bilateral Ureteric Obstruction
Burns As for Prerenal ARF Exogenous (Drugs) Unilateral Ureteric Obstruction
Aminoglycosides (one fun ctioning Kidney)
↓ Effective Circulating Volume Amphotericin B
Cardiac Failure Radiographic contrast Bladder Neck Obstruction (most common)
Septic Shock Endogenous
Cirrhosis Rhabdomyolysis Early Stage of Obstruction (hours → days)
Anaphylaxis Haemolysis Continued glomerular filtration
Gradual distension
Drugs Interstitial Nephritis • Proximal Ureter
ACE Inhibitors Allergic Infection Infiltration • Renal Pelvis
Diuretics Antibiotics Bacterial Lymphoma • Renal Calyces
Penicillins Leptosprosis Leukaemia ↑ Tubular Hydrostatic Pressure
Sulfonamides Viral Sarcoidosis
NSAIDs Hantavirus Later Stage of Obstruction
Alveolar Vasoconstriction occurs
Diseases of Glomeruli/ Renal Microvasculature ↓ GFR
Glomerulonephritis, Vasculitis, HUS, DIVC,
Toxaemia of Pregnancy, Accelerated Hypertension

Intratubular Deposition & Obstruction

Myeloma proteins, Uric Acid
Pathogenesis Pathogenesis (Acute Tubular Ne crosis) Pathogenesis

Hypovolaemia Renal Hypoperfusion Obstruction

(↓ Effec tive Circulating Volume) ↓ ↓
↓ Tubular Ischaemia Back-Pressure
Systemic Arterial Pressure ↓ (Proximal Tubule) ↓
↓ (Thick Ascending Limb LOH) Inhibit Filtration
Renal Hypoperfusion ↓ ↓
↓ Cellular Apoptosis Inflammation Swelling, Pressure ↑
GFR ↓ (Necrosis) ↓ ↓
↓ ↓ Capillary Compress Blood Vessel
Prerenal Azotemia Back Leak Disruption of Normal sludging ↓
(Renal Parenchyma Not Damaged) Of Epithelial Integrity Ischaemia
Glomerular ↓ ↓
Filtrate Cell Sloughing Acute Kidney Injury
↓
Luminal Obstruction
↓
Acute Kidney Injury
(Acute Tubular Necrosis)

Pathogenesis

Myoglobin, Aminoglycoside
Haemoglobin antibiotic
↙ ↘ ↓
Inhibit NO Promote Accumulate in
↓ Intrarenal Renal Tubular
Multiple Intrarenal Oxidative Epithelial cells
Myeloma Vasoconstriction Stress ↓
↓ ↓ Cause
Immunoglobulin Ischaemia Oxidative
light chain Stress
↓
Directly Injury to
toxic to Tubular
Tubular Epithelial
Epithelial Cells
Cell ↓
↑ Tubular
Anticancer obstruction,
Drugs compromise
tubular
transport of
solute

Type of ARF
Pre-Renal Intrarenal Post-Renal
BUN:Creatini ne > 20:1 10:1 – 20:1 10:1 – 20:1
FENa (Fractional Excretion of Sodium) < 1% > 1% > 1%
Urine Specific Gravity > 1.020 1.010 – 1.020 1.010 – 1.020
Ultrasound Normal Normal Hydronephrosis
Urine Osmolality 350-600 < 300 Normal