In patients with cirrhosis, adrenal insufficiency (AI) is reported during sepsis and septic shock and is associated with increased mortality. Consequently, the term “hepato‐adrenal syndrome” was proposed. Some studies have shown that AI is frequent in stable cirrhosis as well as in cirrhosis associated with decompensation other than sepsis, such as bleeding and ascites. Moreover, other studies showed a high prevalence in liver transplant recipients immediately after, or some time after, liver transplantation. The effect of corticosteroid therapy in critically ill patients with liver disease has been evaluated in some studies, but the results remain controversial. The 250‐μg adreno‐cortico‐tropic‐hormone stimulation test to diagnose AI in critically ill adult patients is recommended by an international task force. However, in liver disease, there is no consensus on the appropriate tests and normal values to assess adrenal function; thus, standardization of normal ranges and methodology is needed. Serum total cortisol assays overestimate AI in patients with cirrhosis, so that direct free cortisol measurement or its surrogates may be useful measurements to define AI, but further studies are needed to clarify this. In addition, the mechanisms by which liver disease leads to adrenal dysfunction are not sufficiently documented. This review evaluates published data regarding adrenal function in patients with liver disease, with a particular focus on the potential limitations of these studies as well as suggestions for future studies. (HEPATOLOGY 2012)
Summary
Background Renal function in patients with cirrhosis is important prognostically, both before and following liver transplantation. Its prognostic impact is reflected by the inclusion of serum creatinine in the model for end‐stage liver disease score, which is now used for recipient prioritization on liver transplantation waiting lists in the USA.
Aim To review the accuracy of the surrogate markers for the assessment of renal function, i.e. glomerular filtration rate, particularly in patients with cirrhosis.
Method We reviewed the available literature in PubMed regarding the markers for GFR evaluation and the factors which affect their accuracy in cirrhosis.
Results Although creatinine is widely available, it is an unreliable marker of glomerular filtration rate, particularly in patients with cirrhosis. Clearance of exogenous markers is considered the ‘gold standard’, but this methodology has many drawbacks, particularly poor applicability. Several mathematical formulae for estimated glomerular filtration rate are used to overcome some of these limitations: Cockcroft‐Gault and Modification of Diet in Renal Disease formulae are the most frequently applied, but they are based on serum creatinine.
Conclusions Due to the inaccuracy of serum creatinine and its derived formulae in estimating glomerular filtration rate, alternative serum markers, such as cystatin C, and new formulae are desirable. These need formal evaluation in patients with cirrhosis so as to have a reliable surrogate of glomerular filtration rate, and to obviate many problems that are associated with using creatinine and estimated glomerular filtration rate.
Bilirubin (Bil) interferes with creatinine (Cr) measurement. Different laboratory methods are used to overcome this problem. Model for end-stage liver disease (MELD) scoring incorporates Cr and is used to prioritize patients for liver transplantation. Thus, MELD scores may vary with different Cr measurements influencing patients' priority. Our aim was to evaluate 4 different Cr assays (O'Leary modified Jaffe [mJCr], compensated [rate blanked] kinetic Jaffe [cJCr], enzymatic [ECr], and standard kinetic Jaffe [JCr]) in patients with abnormal liver function tests and assess changes in MELD score. A total of 403 consecutive samples from 158 patients' Cr assays were evaluated.. Bland-Altman plots and MELD scores were also evaluated for each assay. Agreement was found to be poor among all Cr assays. Increased variability in Cr occurred with increasing Bil concentrations: Bil Ͻ100 mol/L Յ3-point MELD variation -3-point difference in 2%; Bil Ն400mol/L Յ7-point MELD variation -Ն3-point difference in 78%. When MELD was Ն25 (mJCr as reference; mean, 30.5 points), MELD variation was greatest: mean, 28 (MELD cJCr), 27.5 (MELD ECr), and 28.4 (MELD JCr) (P Ͻ 0.001). In conclusion, there is poor agreement among different assays for Cr. As Bil concentration rises, there is greater variability in each creatinine measurements and thus greater variability in MELD scores that, this affect prioritization for liver transplantation. Liver Transpl 13: 523-529, 2007.
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