Hepatorenal syndrome is a progressive, functional renal insufficiency with progressive oliguria or anuria, elevated blood urea nitrogen and creatinine that occurs late in the course of severe liver disease, but no obvious organic lesions on renal pathology.
Characteristics of hepatorenal syndrome
1. occurring in patients with liver failure, often with refractory ascites, without shock, and non-pharmacological renal damage.
2, oliguria, 24h urine output <500ml, dilatation not diuretic.
3, normal or slightly abnormal urinary routine, no proteinuria.
4. blood creatinine >150umol/L; 5. urinary sodium concentration <10mmol/L.
Etiology
Advanced cirrhosis and hepatocellular carcinoma are often complicated by severe hepatic failure with idiopathic, progressive, pre-renal renal failure, which may have no obvious or only mild non-specific renal histological changes. The main mechanisms for the sudden onset of unexplained oliguria and azotemia in patients are as follows.
1. Increased renal sympathetic tone
In severe cirrhosis or advanced hepatocellular carcinoma with extensive damage to hepatocytes, resulting in severe impairment of liver function, pneumoperitoneum, dehydration, upper gastrointestinal bleeding and discharge of peritoneal fluid can lead to a decrease in effective circulating blood volume, reflexively causing increased excitability of the sympathetic-adrenomedullary system, resulting in constriction of the small inlet arteries, increased synthesis and secretion of renin, and increased concentration of catecholamines in the blood, resulting in a decrease in glomerular filtration rate and inducing Functional renal failure.
2.Increased pseudo-neurotransmitters
In hepatic failure, metabolites in blood cannot be removed, and pseudoneurotransmitters replace normal peripheral sympathetic neurotransmitters, resulting in decreased peripheral vascular tone, causing small artery dilation, decreased blood pressure, decreased renal blood perfusion, and decreased glomerular filtration rate, leading to hepatorenal syndrome.
Clinical manifestations
1. Pre-azotemia
Liver loss of compensation, normal or slightly high blood urea nitrogen (BUN) and urine creatinine (Cr), decreased Na, progressive oliguria, and insensitivity to diuretics.
2.The azotemia stage
Blood BUN is significantly elevated, Cr is moderately elevated, and Na further decreases.
3.End stage
No urine, blood pressure drops, even in deep coma.
Examination
1.Urinary routine
Negative or trace protein, normal urine sediment or may have a small amount of red blood cells, white blood cells, clear, granular tubular or bile-stained renal tubular cells tubular.
2.Urinal fluid examination
Urine specific gravity is often >1.020, urine osmolality >450mmol/L, urine/blood osmolality <1.5, urine sodium is usually <10mmol/L.
3.Blood biochemical examination
(1) Hyponatremia.
(2) Low blood chloride.
(3) Elevated BUN and Scr.
(4) Liver function ① ALT is elevated. (2) Albumin is decreased. (3) Elevated bilirubin. ④Lower cholesterol. (⑤) Elevated blood ammonia.
Diagnosis
1.Evidence of liver disease and signs of liver failure.
2.24-hour urine output <500ml for more than 2 days with elevated BUN.
3, No original history of renal disease (or normal renal function).
Differential diagnosis
1.Simple pre-renal azotemia
There are prerenal factors, such as severe hypotension, massive diuresis, ascites discharge or blood loss, and renal function can be rapidly restored after experimental rehydration.
2.Acute renal tubular necrosis
(1) Urinary sodium > 40 mmol/L.
(2) Urine/blood creatinine <10.
(3) Ratio of urine/blood osmolality <1.
(4) Urine specific gravity is low, <1.015.
(5) Urine routine has more protein, cellular tubular and granular tubular.
3. Pseudohepatorenal syndrome
Toxic poisoning, severe sepsis or diffuse intravascular coagulation can damage both liver and kidney, causing the so-called “pseudohepatorenal syndrome”, but it is not caused by severe liver disease, so it is not difficult to distinguish.
Treatment
1.Treatment of primary disease
Because the kidney failure of this disease is functional, so actively improve the patient’s liver function, to improve kidney function has a better effect, if the situation allows should actively take surgery, radiotherapy, chemotherapy, interventional therapy and other treatment for intrahepatic tumors and liver cirrhosis.
2.Supportive therapy
Discontinue any drugs that induce azotemia and damage the liver, give low protein and high sugar diet to reduce the development of azotemia and hepatic encephalopathy, and use liver-protective and enzyme-lowering drugs at the same time.
3.Remove the triggering factors
Upper gastrointestinal bleeding, hepatocellular carcinoma rupture bleeding, large amount of discharge fluid, high dose of diuretics, combined with serious infection, surgery, etc. are common causes of hepatorenal syndrome, which should be prevented and treated in time.
4.Correct water-electrolyte and acid-base balance
On the basis of replenishing effective blood volume, increase urine volume and urinary sodium excretion, and actively correct K, Na, Cl, Mg and acid-base imbalance.
5.Volume expansion therapy
Use plasma, whole blood, albumin or dextrose and other plasma preparations to expand the volume, and also give furosemide (tachyphylaxis) to reduce vascular resistance and improve renal blood flow. If the pulmonary capillary wedge pressure, then dilation is not appropriate.
6.Application of vasoactive drugs
Application of dopamine and phentolamine can dilate renal blood vessels, improve renal blood flow and reduce renal vascular resistance.
7.Prostaglandin PI and 654-2
Both have a protective effect on the kidney.
8.Chinese medicine treatment
Chinese medicinal preparation Danshen injection in static drip can treat functional renal failure and reduce BUN level.
Prognosis
The prognosis of this disease is poor, and most of them die from various complications of liver or renal failure within 3-10 days after the occurrence of hepatorenal syndrome.