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Abstract
Hepatorenal syndrome (HRS) is defined as the development of renal failure in patients with severe liver disease (acute or chronic), in the absence of any other cause of renal pathology. It is diagnosed after exclusion of other causes of renal failure in hepatic patients such as hypovolaemia, drug nephrotoxicity, sepsis or glomerulonephritis.
Two types of HRS are observed in clinical practice:
1. Type I HRS: is an acute form of HRS in which rapid decline of renal function takes place over days or weeks in cirrhotic patients.
2. Type II HRS: more common, mostly observed in cirrhotic patients with diuretic resistant ascites with gradual slow decline of renal functions over months.
Patients with functional renal failure of cirrhosis are particularly sensitive to decreases in plasma volume. Thus indicators of moderately impaired renal function are of great clinical importance and monitoring renal function is pivotal. While patients with severely impaired renal function exhibit increased serum creatinine concentrations, detection of slightly or moderately decreased glomerular filtration rate by serum parameters is rather difficult.
In clinical practice, serum creatinine is the most widely used method as non-invasive estimator of GFR to diagnose patients with hepatorenal syndrome. Serum creatinine concentration has some disadvantages such as its concentration depends on sex and muscle mass and shows marked increases only at severely reduced creatinine clearance values. Thus while sufficient for the diagnosis of hepatorenal syndrome, serum creatinine determination can miss less severely impaired renal function.
Recently, the protease inhibitor cystatin C has been suggested as a sensitive marker of glomerular filtration rate and as an early indicator of impaired renal function, possibly superior to serum creatinine. Cystatin C is a non-glycosylated low molecular weight protein produced by nucleated cells at a constant rate, freely filtered by the glomeruli, and catabolised in the tubuli. Its renal clearance was found to be very similar to that of exogenous substances such as 51Cr-EDTA.
Cystatin C serum concentration appears to be independent of sex or muscle mass and its determination is not affected by hyperbilirubinaemia or haemolysis. The rate of synthesis of this protein is also not affected by inflammatory conditions or age.
The aim of the present work was to verify the value of serum cystatin C concentrations in cirrhotic patients with or without HRS as well as its correlation with Child-Pugh score and renal resistive index.
This study was conducted on seventy subjects classified into three groups; group I consisted of thirty patients with Chronic Hepatitis C (CHC) and liver cirrhosis without HRS, group II including thirty patients with liver cirrhosis and HRS and group III composed of ten healthy subjects with matching age and sex as control group.
All patients and controls were subjected to the following:
1. Proper and detailed history taking and thorough clinical examination.
2. Routine laboratory investigations including:
A-Complete blood picture.
B-Liver function tests: serum alanine aminotrsanferase (ALT), serum aspartate aminotransferase (AST), serum bilirubin (total and direct), serum albumin, prothrombin time and activity, serum alkaline phoaphatase .
C-Renal function tests: blood urea and serum creatinine, uric acid, Na, K and creatinine clearance.
D-fasting and 2hr-postprandial blood sugar and lipid profile (triglycerides, cholesterol, VLDL, LDL, HDL).
E-complete urine analysis.
3. Viral markers for hepatitis B (HBs Ag) and hepatitis C (anti-HCV) by ELISA.
4. Ultrasound examination of the abdomen.
5. Renal Doppler ultrasound.
6. Estimation of serum cystatin C.
Statistical analysis of data obtained from the present study revealed the following results:
• Serum level of cystatin C significantly higher in patients with HRS than in those with liver cirrhosis without HRS and controls.
• A significant positive correlation was found between serum cystatin C on one hand and, Child-Pugh score, serum bilirubin and prothrombin time on the other hand, while significant negative correlation was observed between serum cystatin c on one hand and, serum albumin on the other hand.
• In groups I and II, significant positive correlation was found between serum cystatin c and serum creatinine and RRI while significant negative correlation was recorded between serum cystatin c and creatinine clearence.
• Serum cystatin C shows 90% specificity, 86.7 % sensitivity, a positive predictive value of 85% and accuracy of 87.5%. Regarding RRI, it records 90% specificity, 93% sensitivity and a positive predictive value of 90% and accuracy of 92.5%. Regarding Serum creatinine, it records 90% specificity, 75% sensitivity and a positive predictive value of 80% and accuracy of 85% in the prediction of decreased creatinine clearance <80 ml/min in group I.
• ROC curve analysis showed that the diagnostic potential of cystatin C and RRI to detect patients with a creatinine clearance of less than 80 ml/min was superior to that of creatinine.
• It is noted that the cutoff limits for cystatin C; those calculated from control group or those from the ROC curve were very similar. For creatinine, the cutoff limit was markedly lower in cirrhotic patients than the upper reference limit for the general population. This is the consequence of lower plasma concentrations of creatinine in cirrhotic patients compared with controls with similar creatinine clearance values.
• Serum cystatin C, it shows 90% specificity, 100 % sensitivity, a positive predictive value of 100% and accuracy of 95%. Regarding RRI, it records 90% specificity, 100% sensitivity and a positive predictive value of 100% and accuracy of 95%. Regarding Serum creatinine, it records 90% specificity, 100% sensitivity and a positive predictive value of 100% and accuracy of 92% in the prediction of decreased creatinine clearance <80 ml/min in group II.