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AKI IN CIRRHOSIS

John Thomas

INR. Serum Creatinine) takes into account renal function in determining 3-month mortality & need for transplantation • AKI is potentially reversible if detected and treated early . WHY IS AKI IN CIRRHOSIS SIGNIFICANT? • Incidence of AKI in Cirrhosis: ~20% of hospitalised cirrhotic patients • AKI is a powerful predictor of death in decompensated liver disease • AKI is one of the most important predictors of pre-transplant and post- transplant mortality • Pre-transplant creatinine is the most important predictor of survival post- transplant • MELD Score (Bilirubin.

DEFINITION • Acute Kidney Injury: • Rapid decline in renal function over a period of hours – days (exact definition depends on criteria used) • Spectrum from mild impairment to severe renal failure • Typically quantified by the decline in baseline eGFR/urine output or rise in baseline serum creatinine • Three major criteria: RIFLE. Failure. AKIN. Loss of Kidney Function & End-stage Kidney disease (2004) • Acute Kidney Injury Network (2007) • Kidney Disease Improving Global Outcomes (2012) . Injury. KDIGO • Risk.

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CAUSES OF AKI • PRE-RENAL • Hypovolemia • Altered vascular hemodynamics • INTRA-RENAL • Acute Tubular Necrosis • Acute Interstitial Nephritis • Acute Glomerulonephritis • POST-RENAL • Urinary tract obstruction .

CAUSES OF AKI IN CIRRHOSIS AKI Pre-renal Intra-renal Post-renal (75%) (25%) (<1%) Volume Volume Non- ATN Responsive (67%) responsive (33%) Drugs e.g. GI blood loss Diarrhoea Diuresis Sepsis Ischaemia Nephrotoxics NSAIDs .

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PATHOPHYSIOLOGY • Cirrhotic patients are at a high risk of developing AKI: • Hyperdynamic circulatory state – renal blood flow is very susceptible to further decreases in effective arterial blood volume • Intravascular volume depletion – GI bleeding/diarrhoea/diuretic use • Sepsis – further decrease in effective arterial blood volume • Exposure to nephrotoxic agents e.g. NSAIDs/Contrast agents/ABs • Cirrhosis: Hyperdynamic circulatory state .

PATHOPHYSIOLOGY • Decreased clearance of bacterial DNA from gut (f) reduced function of mononuclear phagocyte system + porto-systemic shunting of blood (f) portal hypertension (thus bypassing Kupffer cells in the Liver)  Increased NO production • Spectrum: • Relative hypovolaemia  sodium & water retention (ascites formation) + increased intravascular volume + increased cardiac output • Progressive cirrhosis  worsening vasodilatation  high-output cardiac failure (heart becomes insufficient to maintain perfusion pressure) + decreased renal blood flow .

PATHOPHYSIOLOGY • Precipitating events: • Rapid fluid losses • Sepsis • Can cause both pre-renal AKI and intrinsic renal AKI/ATN .

so it is a delayed marker of renal impairment • SCr can remain within normal range despite significant renal damage due to renal reserve • SCr is underestimated in cirrhotics – note: SCr is the end-product of muscle creatine. • Severe hyperbilirubinemia can result in false measurements of SCr • Other markers to do: • Gold-standard: • a . inexpensive • Cons: • SCr alone is not helpful in distinguishing causes of AKI • SCr lags behind actual renal injury . DIAGNOSIS OF AKI IN CIRRHOSIS • Serum Creatinine • Pros: Simple. and used as a marker of renal perfusion as it is freely filtered but no reabsorbed/secreted in the renal tubules. In Cirrhotics. there is greatly reduced muscle mass  significantly reduced creatinine from muscles  patients will appear to have a normal SCr despite a very low glomerular filtration rate (less creatinine accumulates in serum).

e. concentrated urine • Renal • High urinary sodium (>40mEq/L) • High fractional excretion of sodium (2%) • Low urine osmolality (<350mOsm/kg) • Granular/Epithelial casts in urine • However. in Cirrhosis – the physiological changes result in a sodium avid state + often many patients are on diuretics  this can make Urinary sodium and FENa an unreliable marker to differentiate between Pre-renal and Renal. DIFFERENTIATING CAUSES OF AKI – NOT EASY • Key principle: Tubular function (to reabsorb Na) maintained in pre-renal/HRS but not in ATN • Pre-renal/HRS • Low urinary sodium (<20mEq/L) • Low fractional excretion of sodium (<1%) • Raised urine osmolality (>500mOsm/kg) i. .

the diagnosis of HRS is unlikely • HRS Type 1: • Abrupt deterioration in renal function that occurs mostly in an inpatient setting and often develops after a precipitating event. and urine output is usually approximately 600 mL/day . • Of note. particularly spontaneous bacterial peritonitis • Doubling of SCr to a level greater than 2.2) • Low Mean Arterial Pressure (median 74 mmHg) • Low serum sodium (median 127 mEq/L) • If these features are absent.5 mg/dL (or a greater than twofold to threefold increase in SCr) from baseline in < 2 weeks • HRS Type 2: • Steady or slowly progressive course that occurs mostly in an outpatient setting in patients with refractory ascites.6 mg/dL and rarely exceed 6 mg/dL. SCr levels in HRS are approximately 3. DIAGNOSIS OF HRS • A diagnosis of exclusion • Prerequisites: • Ascites – the same mechanisms leading to ascites lead to formaiton of HRS • Advanced liver disease (median Child Pugh score is 11.

Renal replacement therapy (volume overload/metabolic acidosis/hyperkalaemia) • a . maintain renal perfusion. TREATMENT • Treatment of AKI depends on the cause • Basic principle: • Pre-renal AKI: Volume repletion • ATN: Remove nephrotoxics.

TREATMENT OF HRS .