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Cirrhosis of the Liver Community
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Acites related to getting off peritoneal dialysis or due to cirrhosis of liver.

I've been on peritoneal dialysis for almost 5 years and recently had to discontinue due to peritonitis and inflammation of the peritoneal lining and convert to hemodialysis. After discontinuing peritoneal dialysis, I continued to accumulate fluid in the peritoneal cavity and I have had a total of 3 paracentesis with less being collected each time and I'm not collecting as much as I did from the start and I have talked to other people that have been on peritoneal dialyisis and some of them have had the same problem and we are all walking around like we're pregnant, men and women. Went to a gastroenterologist and before I even had the lab drawn he said I had cirrhosis of the liver because of the acities and he says that my liver and spleen are swollen and that I have portal hypertension. I have never had any problems with my liver, I don't drink. I do have hyperparathyroidism along with ESRD that I'm dealing with. This doctor is pushy and won't listen to a word I have to say and he knows everything and I don't know anything. So I'm thinking about getting a second opinion, he's wanting me to go ahead an have a liver and kidney transplant like yesterday and he's just too quick to not check out other causes for my problem and says that peritoneal dialysis had nothing to do with my problem, but I did not have this before I started peritoneal dialysis. I will include some of my lab results and would appreciate any information anyone can offer. Sorry for the long post but I wanted to include anything that I think would help.  Thanks

Hepatic Function Panel :

Total Protein 6.8 g/dL       6.3 - 8.2 g/dL
Albumin 4.5 g/dL               3.5 - 5.0 g/dL
Globulin 2.3 g/dL               2.0 - 4.0 g/dL
A/G ratio 2.0                         1.0 - 2.0
AST 41 U/L                       <=40 U/L
ALT 43 U/L                       <=41 U/L
Alkaline Phosphatase 312 U/L          38 - 126 U/L ( Dr. does not use this result as part of diagnosis ????)
Bilirubin, Total 0.4 mg/dL                  0.2 - 1.3 mg/dL
Bilirubin, Direct <0.2 mg/dl          0.0 - 0.3 mg/dl

CBC:

WBC 2.0 K/uL                  4.6 - 10.2 K/uL
RBC         3.28 M/uL          4.69 - 6.13 M/uL
Hemoglobin   9.9 g/dl          14.1 - 18.1 g/dl
Hematocrit 30.1 %          43.5 - 53.7 %
MCV 91.8 fL                  80.0 - 97.0 fL
MCH 30.2 pg                  27.0 - 31.2 pg
MCHC 32.9 g/dl                  31.8 - 35.4 g/dl
RDW 13.8 %                  11.6 - 14.8 %
Platelets 63 K/uL                  142 - 424 K/uL  (Platelets have been low since 2013)

COMPREHENSIVE METABOLIC PANEL:

Sodium       142 mEq/L                            135 - 145 mEq/L
Potassium 4.1 mEq/L                     3.4 - 5.1 mEq/L
Chloride       106 mEq/L                            101 - 112 mEq/L
CO2               28 mEq/L                             20 - 32 mEq/L
Albumin       3.9 g/dl                             3.7 - 5.3 g/dl
Alkaline Phosphatase 303 IU/L             34 - 154 IU/L  (This decreased a little from result above)
ALT =0.1 ng/mL indicates myocardial damage and increased risk.

Lipase 104 u/L              23 - 300 u/L

Peritoneal Fluid:

Gram Stain 2+ (1-9/LPF) WBC  
Gram Stain No organisms seen  
BODY FLUID CELL COUNT AND ANALYSIS

Fluid Specimen         Peritoneum  
Fluid Color                 Light Yellow  
Appearance Clear   Clear
Are clots, cell clumps, and/or debris present?   No  
RBC Fluid 208 cells/mm3               cells/mm3
WBC Fluid 413 cells/mm3               cells/mm3
Crystals, Fluid not applicable  

Culture        No Growth at 72 hrs  

FLUID ANALYSIS MANUAL DIFFERENTIAL

Segmented Neutrophils     1 %                    %
Mononuclear Cells             98 %                    %
Macrophages                     1 %                    %
Total Counted                    100  

3 Responses
683231 tn?1467326617
I am not a doctor. I’m a patient who has had cirrhosis for over 10 years which was caused by 37 years of infection with hep c.

Even though I have cirrhosis determined by liver biopsy back in 2008 and confirmed by Fibroscan testing in 2014 (score was 27) my lane results are in normal range except my platelet count which has risen a little after my hep c was cured to about 110 still well below minimum normal of 150.

Having low platelets is a common symptom of cirrhosis it is an indication I have portal hypertension. I also have a small amount of ascities but not as significant as yours.

Cirrhosis is a silent illness and be caused by more than excess alcohol consumption. You would never know you are having problems with your liver until you begin experiencing symptoms of liver failure like ascities to the point of looking pregnant.

Has your gastro performed a Fibroscan test it is similar to an ultrasound but produces a thump to estimate liver stiffness. Also you should have an abdominal ultrasound which can detect some of the signs of cirrhosis like a coursened echo texture on the liver surface which is consistent with cirrhosis. Another reason to have the ultrasound is to look for liver cancer tumors as those of us with cirrhosis are at in tased risk of HCC. Another test you should have is an upper endoscopy to look for esophageal varicies which if present can cause a dangerous bleeding episode. I had serious varicies back in 2012 that required banding.

You certainially are entitled to a second opinion but I suspect that as your doctor is much more expert than me as he is a hepatologist you will likely hear the same thing.



683231 tn?1467326617
Here is some information from NIDDK (National Institute of Diabeties and Digestive and Kidney Diseases)

“What causes cirrhosis?

Cirrhosis has various causes. Many people with cirrhosis have more than one cause of liver damage.

The list below shows common causes of cirrhosis in the United States.2 While chronic hepatitis C and alcohol-related liver disease are the most common causes of cirrhosis, the incidence of cirrhosis caused by nonalcoholic fatty liver disease is rising due to increasing rates of obesity.

Most Common Causes of Cirrhosis

Chronic hepatitis C. Hepatitis C is due to a viral infection that causes inflammation, or swelling, and damage to the liver. The hepatitis C virus spreads through contact with infected blood, such as from a needlestick accident, injection drug use, or receiving a blood transfusion before 1992. Less commonly, hepatitis C can be spread by sexual contact with an infected person or at the time of childbirth from an infected mother to her newborn.

Hepatitis C often becomes chronic, with long-term persistence of the viral infection. Chronic hepatitis C causes damage to the liver that, over years or decades, can lead to cirrhosis. Advanced therapies for chronic hepatitis C now exist, and health care providers should treat people with chronic hepatitis C before they develop severe fibrosis or cirrhosis. Unfortunately, many people first realize they have chronic hepatitis C when they develop symptoms of cirrhosis. More information is provided in the NIDDK health topic, Hepatitis C.

Alcohol-related liver disease. Alcoholism is the second most common cause of cirrhosis in the United States. Most people who consume alcohol do not suffer damage to the liver. However, heavy alcohol use over several years makes a person more likely to develop alcohol-related liver disease. The amount of alcohol it takes to damage the liver varies from person to person. Research suggests that drinking two or fewer drinks a day for women and three or fewer drinks a day for men may not injure the liver.3 Drinking more than these amounts leads to fat and inflammation in the liver, which over 10 to 12 years can lead to alcoholic cirrhosis.4

Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). In NAFLD, fat builds up in the liver; however, the fat buildup is not due to alcohol use. When the fat accompanies inflammation and liver cell damage, the condition is called nonalcoholic steatohepatitis, or NASH, with “steato” meaning fat, and “hepatitis” meaning inflammation of the liver. The inflammation and damage can cause fibrosis, which eventually can lead to cirrhosis.

Extra fat in the liver has many causes and is more common in people who

are overweight or obese.
have diabetes—a condition characterized by high blood glucose, also called high blood sugar.
have high blood cholesterol and triglycerides, called hyperlipidemia.
have high blood pressure.
have metabolic syndrome—a group of traits and medical conditions linked to being overweight and obese that makes people more likely to develop both cardiovascular disease and type 2 diabetes. Metabolic syndrome is defined as the presence of any three of the following: large waist size, high triglycerides in the blood, abnormal levels of cholesterol in the blood, high blood pressure, and higher than normal blood glucose levels. NASH may represent the liver component of the metabolic syndrome.
NASH now ranks as the third most common cause of cirrhosis in the United States. More information is provided in the NIDDK health topic, Nonalcoholic Steatohepatitis.

Chronic hepatitis B. Hepatitis B, like hepatitis C, is due to a viral infection that causes inflammation and damage to the liver. Chronic infection can lead to damage and inflammation, fibrosis, and cirrhosis. The hepatitis B virus spreads through contact with infected blood, such as by needlestick accident, injection drug use, or receiving a blood transfusion before the mid-1980s. Hepatitis B also spreads through sexual contact with an infected person and from an infected mother to child during childbirth.

In the United States, hepatitis B is somewhat uncommon, affecting less than 1 percent of the population, or fewer than one in 100 people.5 In many areas of the world, however, hepatitis B is common. In some parts of Africa and in most of Asia and the Pacific Islands, about 5 to 7 percent of the population has chronic hepatitis B. In some parts of Africa, more than 8 percent of the population has chronic hepatitis B.6 For these reasons, hepatitis B is likely the major cause of cirrhosis worldwide. However, in the United States, hepatitis B ranks well behind hepatitis C, alcohol-related liver disease, and NASH.

Therapies for chronic hepatitis B now exist and health care providers should treat people with chronic hepatitis B before they develop severe fibrosis or cirrhosis. Unfortunately, many people first realize they have chronic hepatitis B when they develop symptoms of cirrhosis.

Less Common Causes of Cirrhosis

Less common causes of cirrhosis include the following:

Autoimmune hepatitis. In this form of hepatitis, the body’s immune system attacks liver cells and causes inflammation, damage, and eventually cirrhosis. Normally, the immune system protects people from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. In autoimmune diseases, the body’s immune system attacks the body’s own cells and organs. Researchers believe genetics, or inherited genes, may make some people more likely to develop autoimmune diseases. At least 70 percent of those with autoimmune hepatitis are female.7 More information is provided in the NIDDK health topic, Autoimmune Hepatitis.

Diseases that damage, destroy, or block the bile ducts. Several diseases can damage, destroy, or block the ducts that carry bile from the liver to the small intestine, causing bile to back up in the liver and leading to cirrhosis. In adults, the most common of these diseases is primary biliary cirrhosis, a chronic disease that causes the small bile ducts in the liver to become inflamed and damaged and ultimately disappear. Primary sclerosing cholangitis is a disease that causes irritation, scarring, and narrowing of the larger bile ducts

Hemochromatosis
Wilson Disease
Rare viral infections of the liver. Hepatitis D, or hepatitis delta, and hepatitis E are two rare viral infections of the liver. Hepatitis D infection occurs only in people who have hepatitis B. People infected with chronic hepatitis B and chronic hepatitis D are more likely to develop cirrhosis than people infected with chronic hepatitis B alone.9

Hepatitis E is a virus found in domestic and wild animals, particularly pigs, and can cause hepatitis in humans. People with weakened immune systems, including people who are liver or kidney transplant recipients or who have acquired immune deficiency syndrome (AIDS), can develop chronic hepatitis E. Chronic hepatitis E can cause scarring of the liver and cirrhosis. Current treatments for chronic hepatitis D and E are experimental and only partially effective.

Other causes. Other causes of cirrhosis may include

reactions to medications taken over a period of time.
prolonged exposure to toxic chemicals.
parasitic infections.
chronic heart failure with liver congestion, a condition in which blood flow out of the liver is slowed. Liver congestion can also occur after surgery to correct a congenital heart problem—a heart problem that is present at birth.
Trauma to the liver or other acute, or short term, causes of damage do not cause cirrhosis.

Best of luck to you
1 Comments
https://www.niddk.nih.gov/health-information/liver-disease/cirrhosis
683231 tn?1467326617
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939491/

Liver cirrhosis leads to poorer survival in patients with end-stage renal disease
Ae Jin Kim, Hye Jin Lim, [...], and Jae Hyun Chang

Additional article information

Abstract
Background/Aims:
Liver cirrhosis (LC) is an important problem in patients withend-stage renal disease (ESRD). Few studies have investigated the inf luence ofLC on mortality in patients with ESRD. This study investigated the associationbetween LC and mortality among patients with ESRD and compare mortality betweentwo dialysis modalities.

Methods:
Adult patients (≥ 18 years of age) starting dialysis for ESRD were enrolledin the present study from 2000 to 2011. We analyzed 1,069 patients withESRD; of these, 742 patients were undergoing hemodialysis (HD) and 327 patientswere undergoing peritoneal dialysis (PD).

Results:
The prevalence of LC was 44 of 1,069 patients (4.1%). The cumulative 1-,3-, and 5-year survival rates of noncirrhotic patients were 93%, 83%, and 73%, respectively,whereas the equivalent survival rates of cirrhotic patients were 90%,68%, and 48%, respectively (p = 0.011). After adjustment, LC was an independentrisk factor for death in patients with ESRD. No difference in mortality associatedwith LC was found between the HD and PD subgroups.

Conclusions:
Of the patients with ESRD, cirrhotic patients had poorer survivalthan noncirrhotic patients. Among patients with ESRD and LC, survival of patientsundergoing PD may be comparable with that of patients undergoing HD.
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317787 tn?1473362051
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