Renin is increased (as well as sodium retention in kidneys) secondary to a fall in systemic vascular resistance.FibroTest is a biomarker for fibrosis that may be used instead of a biopsy.Other laboratory studies performed in newly diagnosed cirrhosis may include:

Serology for hepatitis viruses, autoantibodies (ANA, antismooth muscle, antimitochondria, anti-LKM)
Ferritin and transferrin saturation: markers of iron overload as in hemochromatosis, copper and ceruloplasmin: markers of copper overload as in Wilsons disease
Immunoglobulin levels (IgG, IgM, IgA) – these immunoglobins are nonspecific, but may help in distinguishing various causes. Cholesterol and glucose
Alpha 1-antitrypsinMarkers of inflammation and immune cell activation are typically elevated in cirrhotic patients, especially in the decompensated disease stage:

C-reactive protein (CRP)
Procalcitonin (PCT)
Presepsin
soluble CD14
soluble CD163
soluble CD206 (mannose receptor)
soluble TREM-1A recent study identified15 microbial biomarkers from the gut microbiota. These could potentially be used to discriminate patients with liver cirrhosis from healthy individuals. Pathology
The gold standard for diagnosis of cirrhosis is a liver biopsy. This is usually carried out as a fine-needle approach, through the skin (percutaneous), or internal jugular vein (transjugular). Endoscopic ultrasound-guided liver biopsy (EUS), using the percutaneous or transjugular route, has become a good alternative to use. EUS can target liver areas that are widely separated, and can deliver bi-lobar biopsies. A biopsy is not necessary if the clinical, laboratory, and radiologic data suggest cirrhosis. Furthermore, a small but significant risk of complications is associated with liver biopsy, and cirrhosis itself predisposes for complications caused by liver biopsy.Once the biopsy is obtained, a pathologist will study the sample.
Hepatic encephalopathy
Hepatic encephalopathy is a potential complication of cirrhosis. It may lead to functional neurological impairment ranging from mild confusion to coma. Goal of treatment is reducing ammonia. This can can achieved by administering lactulose or lactitol to increase potassium. Hydration and nutritional support is also provided. Protein uptake is encouraged. The underlying cause may also need to be identified and treated. Causes include alcohol use, excess protein, gastrointestinal bleeding, infection, constipation, and vomiting/diarrhea. Drugs like benzodiazepines, diuretics, or narcotics can also precipitate hepatic encephalopathy. A low protein diet is recommended with gastrointestinal bleeding. Rifaximin is administered if mental state does not improve in 48 hours. Antibiotic treatment may need to be continued for at least 3 months. The grading or severity of hepatic encephalopathy is determined by mental status. Hepatorenal syndrome
Hepatorenal syndrome is a serious complication of end-stage cirrhosis when kidney damage is also involved. Spontaneous bacterial peritonitis
People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis. Portal hypertensive gastropathy
Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in people with portal hypertension, and is associated with cirrhosis severity. Infection
Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize (for example, worsening encephalopathy but no fever). Moreover, infections in cirrhosis are major triggers for other complications (ascites, variceal bleading, hepatic enecphalopathy, organ failures, death). Hepatocellular carcinoma
Hepatocellular carcinoma is the most common primary liver cancer, and the most common cause of death in people with cirrhosis.