Elsevier

Medicine

Volume 39, Issue 8, August 2011, Pages 492-496
Medicine

Systemic disease and the kidney
Liver disease and renal dysfunction

https://doi.org/10.1016/j.mpmed.2011.05.002Get rights and content

Abstract

Renal dysfunction frequently complicates liver disease and, when present, adversely affects prognosis. While a number of conditions can affect both the liver and the kidney acutely (e.g. paracetamol), many hepatotoxic insults (e.g. alcohol or viral hepatitis) cause more problems associated with cirrhosis. This review focuses mainly on the renal dysfunction associated with this chronic liver damage. Chronic liver disease is implicated in changes in vascular reactivity and tone, resulting in a systemic vasodilatation and renal vasoconstriction. In its extreme form it leads to the most feared of all renal complications of liver disease, the hepatorenal syndrome (HRS), which is frequently fatal. The recognition and early management of both the renal dysfunction and liver disease are important to survival. The key therapeutic issues revolve around optimizing the circulating volume, reversing the maladaptive haemodynamic changes, removal of other potential nephrotoxins and early treatment of infection.

Section snippets

Difficulties in measuring renal function

Using serum creatinine as a marker of renal function has many shortcomings in normal individuals and is even more problematic in patients with cirrhosis as the concentration is frequently lower than expected if true glomerular filtration rate (GFR) is measured, falsely reassuring the unwary. Malnutrition, a reduced muscle mass, and impaired creatine synthesis by a failing liver result in low creatinine production rates, and tubular secretion of creatinine is increased in cirrhosis.2 Finally,

Immune events in cirrhosis

Liver disease is accompanied by increased bacterial translocation from the gut to the portal and systemic circulation. Bacterial products activate the cellular immune system, increasing nitric oxide (NO) production and causing an increase, and probably phenotypic change, in circulating immunoglobulin (Ig) (especially IgA). It is not known whether this reflects an increase in production or a reduction in clearance, or both, but it may explain the link between cirrhosis and a number of

Haemodynamic events in cirrhosis

The destruction of the architecture in the cirrhotic liver, and functional changes in hepatocytes and other hepatic cell lines (e.g. Ito cells) lead to an increase in the resistance to portal blood flow. There is an accompanying systemic vasodilatation, due to the action of NO and other mediators.7 This leads to a reduction in systemic vascular resistance (SVR) in most vascular beds, leading to a fall in mean arterial pressure (MAP) and a compensatory increase in cardiac output (CO) (Ohm’s law:

Acute kidney injury (AKI) in liver disease

The classification of AKI into pre-renal, intrinsic renal and post-renal causes is useful when evaluating renal failure in patients with liver disease. The causes of AKI are far more commonly intravascular volume depletion, sepsis and drugs than the hepatorenal syndrome (HRS), and early recognition and treatment can prevent significant morbidity and mortality.

HRS is an extreme but potentially reversible form of functional renal failure that occurs in up to 40% of patients with advanced liver

Rationalization of drug treatment

Removing all potential nephrotoxins is essential in minimizing further renal parenchymal damage. This includes non-steroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and aminoglycoside antibiotics. Ascites and/or oedema are frequently treated with spironolactone (100–400 mg/day), which may provoke hyperkalaemia. Furosemide (40–160 mg/day) is often added if ascites proves resistant, but both drugs risk reducing intravascular

Management of HRS

Several trials have evaluated the ability of medical therapies to reverse the circulatory changes that generate HRS with varying degrees of reproducibility and success. Renal vasodilators such as dopamine and prostaglandin E1 analogues do not lead to any improvement, and some treatments (endothelin antagonists) are detrimental to renal function. The greatest success has been with vasoconstrictor therapy, which attempts to improve renal perfusion by reversing the loss of vascular tone in the

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