Systemic disease and the kidneyLiver disease and renal dysfunction
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
References (19)
- et al.
Renal failure in patients with cirrhosis
Med Clin North Am
(2009 Jul) Cirrhotic glomerulonephritis: incidence, morphology, clinical features, and pathogenesis
Am J Kidney Dis
(1987 Mar)- et al.
Renal dysfunction is the most important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis
Clin Gastroenterol Hepatol
(2011 Mar) - et al.
Proceedings of Consensus Conference on Simultaneous Liver Kidney Transplantation (SLK)
Am J Transplant
(2008 Nov) The kidney in liver disease
(1996)- et al.
Kinetic serum creatinine assays. II. A critical evaluation and review
Clin Chem
(1980 Apr) - et al.
Plasma cystatin C as a marker of renal function in patients with liver cirrhosis
Scand J Clin Lab Invest
(2002) - et al.
Bile acids, oxidative stress, and renal function in biliary obstruction
Semin Nephrol
(1997 Nov) - et al.
Nitric oxide and renal function in cirrhotic patients with ascites: from physiopathology to practice
Eur J Gastroenterol Hepatol
(2004 Jun)