Kidney issues in liver failure

Renal dysfunction is a common and serious problem in patients with advanced liver disease. In particular, alterations in renal physiology in acute liver failure or cirrhosis with ascites can predispose patients to a specific functional form of renal failure known as hepatorenal syndrome (HRS).

Hepatorenal syndrome (HRS) is a type of progressive kidney failure seen in people with severe liver damage, most often caused by cirrhosis. As the kidneys stop functioning, toxins begin to build up in the body. Eventually, this leads to liver failure.

There are two forms of HRS. Type 1 HRS is associated with rapid kidney failure and an overproduction of creatinine. Type 2 HRS is associated with more gradual kidney damage. It generally progresses more slowly. Symptoms are generally subtler.

Renal failure is a late consequence of end‐stage liver disease (ESLD). Even with liver transplantation, pre transplant renal impairment remains a strong predictor of post transplant mortality. This review seeks to summarize and critically appraise common therapies used in this setting, including pharmacologic agents, procedures (transjugular intrahepatic portosystemic shunt, renal replacement therapy), and simultaneous liver‐kidney transplantation

Diagnosis of HRS

The presence of renal dysfunction is often missed in patients with cirrhosis. Because of a reduction in muscle mass in these patients, serum creatinine may be within the normal range, even with a very low GFR. The use of blood urea nitrogen (BUN) concentration as a measure of renal function is even less reliable, because BUN levels can be affected by the presence of gastrointestinal bleeding or by the amount of protein in the diet. It has been suggested that serum creatinine concentrations of 71 mcmol/L, 88 mcmol/L, 160 mcmol/L, 195 mcmol/L, and 354 mcmol/L, would reflect steady-state GFRs of 100 mL/min, 50 mL/min, 25 mL/min, 12 mL/min, and 6 mL/min, respectively

Therefore, a creatinine level > 88 mcmol/L in a patient with cirrhosis should alert the clinician to the presence of renal dysfunction.

HRS should only be diagnosed in patients with decreased renal function in the presence of advanced cirrhosis, chronic liver disease with severe liver failure and portal hypertension, or acute liver failure. Other forms of organic renal disease must be ruled out. Some patients with primary liver diseases are at higher risk for developing certain forms of kidney diseases,while some systemic processes can affect both the liver and the kidney.

Approach to Renal Failure in Cirrhosis

Patients with type 2 HRS are at particularly high risk for type 1. A thorough history and physical exam can detect intravascular volume depletion and arterial hypotension. A careful assessment of the patient’s history should identify preceding events such as gastrointestinal bleeding, overdiuresis, or aggressive paracentesis. Sepsis should be suspected in any cirrhotic patient with renal deterioration, even in the absence of symptoms. Fever and leukocytosis may not be present. Appropriate cultures should be obtained, including examination of the ascitic fluid to rule out SBP. Recent exposure to nephrotoxins such as NSAIDs, aminoglycosides, or radiocontrast dyes prior to the increase in serum creatinine level should be ruled out. If proteinuria and/or hematuria are present, additional investigations should be undertaken to rule out renal parenchymal diseases. Renal biopsy should be considered if there is a strong suspicion of glomerulonephritis. An abdominal ultrasound should be performed to determine whether the patient has postobstructive renal failure.