Renal dysfunction in patients with cirrhosis: Where do we stand?

Abstract

Patients with cirrhosis and renal failure are high-risk patients who can hardly be grouped to form precise instructions for diagnosis and treatment. When it comes to evaluate renal function in patients with cirrhosis, determination of acute kidney injury (AKI), chronic kidney disease (CKD) or AKI on CKD should be made. First it should be excluded the prerenal causes of AKI. All cirrhotic patients should undergo renal ultrasound for measurement of renal resistive index in every stage of liver dysfunction and urine microscopy for differentiation of all causes of AKI. If there is history of dehydration on the ground of normal renal ultrasound and urine microscopy the diuretics should be withdrawn and plasma volume expansion should be tried with albumin. If the patient does not respond, the correct diagnosis is HRS. In case there is recent use of nephrotoxic agents or contrast media and examination shows shock, granular cast in urinary sediment and proteinuria above 0.5 g daily, acute tubular necrosis is the prominent diagnosis. Renal biopsy should be performed when glomerular filtration rate is between 30-60 mL/min and there are signs of parenchymal renal disease. The acute renal function is preferable to be assessed with modified AKIN. Patients with AKIN stage 1 and serum creatinine ≥ 1.5 mg/dL should be at close surveillance. Management options include hemodynamic monitoring and management of fluid balance and infections, potentially driving to HRS. Terlipressin is the treatment of choice in case of established HRS, administered until there are signs of improvement, but not more than two weeks. Midodrine is the alternative for therapy continuation or when terlipressin is unavailable. Norepinephrine has shown similar effect with terlipressin in patients being in Intensive Care Unit, but with much lower cost than that of terlipressin. If the patient meets the requirements for transplantation, dialysis and transjugular intrahepatic portosystemic shunt are the bridging therapies to keep the transplant candidate in the best clinical status. The present review clarifies the latest therapeutic modalities and the proposed recommendations and algorithms in order to be applied in clinical practice.

Liver disease and renal dysfunction

“…Intercurrent illness such as peritonitis or gastrointestinal haemorrhage should also be excluded as this may be contributing to or precipitating renal dysfunction. 6,21 Management Treatment should target the underlying aetiology and will depend on the severity. It may include supportive and antimicrobial therapies, specific treatments for HRS and the Urine outflow obstruction due to, for example, prostatic hypertrophy, a pelvic mass or bleeding in the urinary tract Chronic kidney disease and liver disease Hepatorenal syndrome type 2 Polycystic kidney and liver disease Glomerulonephritis (e.g.…”

Cirrhosis and Renal Dysfunction

“…Prerenal azotemide tedavi; izotonik intravenöz sıvı resüsitas-yonu, diüretiklerin kesilmesi ile renal kan akımı ve övoleminin sağlanması, gastrointestinal kanaması olanlarda eritrosit süspan-siyonu ve plazma genişletici verilerek hemodinamik stabilitenin korunması (replasmanda hedef hemoglobin 7 gr/dL), ciddi asiti olan hastalarda geniş volümlü parasentezin 8 gr/L albümin infüzyonu eşliğinde yapılması ve bakteriyel enfeksiyon varsa agresif tedavi edilmesi (3. kuşak sefalosporinler) ilkelerini kapsamalıdır. Yine sirozda ve asiti olan hastalarda nefrotoksik ajanlardan, kontrast maddelerden ve hipotansiyona yol açabilecek ajanlardan kaçınılmalıdır (21,22). Tablo III'te dikkatle kullanıl-ması ve kaçınılması gereken ilaçlara kısaca değinilmiştir (18).…”

Clinical Spectrum of Renal Dysfunction in Cirrhosis of Liver

“…However nevertheless, serum creatinine which is used to analyze MELD score, should be interpreted with caution, since there is no universal standardized creatinine assay; there are interlaboratory variations, interactions with bilirubin and great influence by numerous nonrenal factors such as body weight, race, age, and gender. 14 Our study showed that esophageal varices (66.7%), use of diuretics (47.6%) and presence of diarrhoea and vomiting (23.8% each) were major cause of acute kidney injury alone or in combination. Whereas along with this the risk factors for development of hepatorenal syndrome was studied which showed that presence of subacute bacterial peritonitis (88 % vs 18.3%, p<0.0001), GI bleed (50% vs 23.2%, p=0.022) were major factors that were significantly associated with development of HRS.…”

“…Martín-Llahí et al (14) discussed this drawback by the absence of specific markers that may help in the identification of the cause of renal failure in cirrhosis. We also recommend the need to exert an effort to build-up a new battery of laboratory markers of renal failure that may be useful for the differential diagnosis.…”