cirrhotic kidney damage
Introduction
Introduction to cirrhotic renal damage Post-hepatitis cirrhosis, alcoholic cirrhosis, biliary cirrhosis and schistosomiasis cirrhosis can cause kidney damage, cirrhosis causing kidney damage for a variety of reasons, and portal cirrhosis is a common liver Hardening type, accounting for about half of all cirrhosis, causes many causes of portal cirrhosis, mainly viral hepatitis, chronic alcoholism, nutritional deficiencies, intestinal infections, drug or industrial poisoning, and chronic cardiac insufficiency. A glomerular diffuse sclerosis caused by cirrhosis causes abnormalities in kidney anatomy and function. basic knowledge The proportion of sickness: 0.003%-0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: upper gastrointestinal bleeding, hepatic encephalopathy, liver and kidney syndrome, kidney stones, fracture, peritonitis, pneumonia, cirrhosis, ascites
Cause
Causes of cirrhotic renal damage
(1) Causes of the disease
There are many causes of cirrhosis, mainly viral hepatitis, chronic alcoholism, nutritional deficiencies, intestinal infections, drug or industrial poisoning and chronic heart failure, etc., cirrhosis caused by glomerular diffuse sclerosis lesions, kidney anatomy And the function has an exception.
(two) pathogenesis
The pathogenesis of hepatic glomerulosclerosis is still unclear and is currently considered to be related to the following factors:
1. Significant IgA deposition in glomerular deposits associated with immune complexes. As the antigen may come from the digestive tract of bacteria, viruses or food components, due to liver cirrhosis, hepatocyte Kupffer cell dysfunction, the diseased liver cannot be cleared from Exogenous antigens in the intestine, and then due to the formation of collateral circulation, so that these antigenic substances directly enter the blood circulation without the liver treatment to stimulate the production of antibodies, it is reported that patients with cirrhosis often have higher Escherichia coli antibodies in the serum and Immunoglobulins, whose levels are consistent with liver histological changes, that is, the more severe the destruction and fibrosis of the hepatic lobular structure, the higher their level, the animal experiments have also proved similar changes, because many patients with cirrhosis are caused by viral Hepatitis has evolved, and many patients with cirrhosis have long-term HBsAg in their serum. Therefore, the immune complex formed by hepatitis B antigen can cause glomerular damage, and the autoimmune mechanism plays a certain role in the occurrence and development of this disease. effect.
2. Changes in renal hemodynamics In decompensated cirrhosis, glomerular filtration rate and renal plasma flow vary widely, from supernormal values to severe renal failure, the mechanism by which this abnormal value occurs. It is unclear that the supernormal value is hardly noticed [inulin clearance value >200ml/(min·1.73m2)], and in many cases the glomerular filtration rate is normal, but the glomerular filtration rate (GFR) of severely ill patients and Renal plasma flow is mostly reduced, and the mechanism of renal hemodynamic decline is unknown. It may be secondary to changes in the circulation of the body. The total plasma volume increases during cirrhosis, but its distribution is concentrated in the vascular bed of the portal and viscera, making the effective plasma. Decreased volume, renal cortical ischemia in patients with decompensated cirrhosis, decreased renal plasma flow, and evidence of redistribution of renal plasma flow in patients with cirrhosis using 133I sodium urate, and vasoconstriction in the superficial region of renal cortex, A temporary increase in inulin and creatinine clearance was observed in patients with GFR decline and normal with m-hydroxylamine, demonstrating that vasoactive drugs can change glomerular filtration rate faster, and prostaglandin A in patients with decompensated cirrhosis Small kidney Ball filtration rate, renal plasma flow and urinary sodium excretion are increased, angiotensin in patients with cirrhosis and ascites, causing natriuretic and diuretic, ascites caused by increased intra-abdominal pressure, can affect glomerular filtration Rate and renal plasma flow, with peritoneal puncture and drainage, continuous measurement of glomerular filtration rate and effective renal plasma flow, found that within 1h after puncture, there was a significant rise, taking prone position lying, glomerulus There is a temporary improvement in the filtration rate. A small amount of ascites is removed, and the cardiac output can be temporarily increased. When a large amount of ascites is removed, the cardiac output is decreased, and the plasma volume is reduced due to re-generation of ascites.
3. Sodium excretion damage Many studies have shown that patients with decompensated portal cirrhosis often have significant sodium retention, the discharged urine is almost free of sodium, ascites and edema are formed during sodium load, and there is an increase in sodium excretion at night. In reverse, urinary sodium chloride excretion depends on glomerular filtration and tubular reabsorption, and it has been demonstrated in patients with cirrhosis and in animal experiments that all nephron segments increase sodium reabsorption.
The mechanism of renal tubular reabsorption of sodium chloride during cirrhosis is unclear. There may be several factors: renal hemodynamics, physical factors around the renal tubules, aldosterone and natriuretic hormone, which cannot be explained by a single factor. Clinical and experimental conditions, there is evidence to strongly support the mechanism of sodium retention in cirrhosis as a reduction in effective circulating plasma volume. Patients with sclerotherapy who have sodium retention in the water tank can be immersed in the head and neck to cause natriuretic and diuretic due to blood. Volume redistribution, central blood volume increased, and total blood volume and plasma composition did not change, further studies found that associated with mineralocorticoids, plasma aldosterone increased in patients with cirrhosis, due to increased adrenal secretion, renin-angiotensin-stimulated As a result, hormone degradation is reduced, but there is evidence that aldosterone plays only a limited role in sodium chloride retention in cirrhosis, because inhibition of aldosterone does not occur in sodium, while sodium retention, edema and ascites can occur in excessive aldosterone secretion. In the cirrhosis of the liver, the above description shows that there are other mechanisms involved in salt retention, and it is believed that there may be a kind of inhibition of the proximal end. Renal unit reabsorbs sodium, when its activity decreases, glomerular filtration rate decreases and intrarenal blood flow changes in each nephron, cortical surface nephron (relative sodium loss) to cortical proximal medullary unit ( The filtrate of the relative sodium retention is redistributed. In the sodium retention of animal experiments, it is important that the physical factors such as the filtration fraction increase the colloid osmotic pressure.
Renal tubular acidosis can be a renal manifestation of a systemic immune disease. From these patients (slow live liver, primary biliary cirrhosis, cryptogenic cirrhosis), renal biopsy can show distal convoluted tubules and The plasmonic tissue is damaged by sensitized monocytes or autoantibodies. It is similar to renal tubular acidosis caused by immunological damage after cadaveric kidney transplantation, and hepatocyte surface antigen and Tamm- in patients with autoimmune liver disease. The Horsfall glycoprotein has a cross-reactivity, and this protein is present in the ascending and distal tubular cells of the medulla, and the anti-tamm-Horsfall glycoprotein antibody is produced in patients with autoimmune liver disease associated with renal tubular acidosis. In addition, animal experiments have shown that the patient's lymphocytes have a cytotoxic effect on renal tubular cells, and renal damage mainly in the distal tubule may be related to the above mechanism.
Another pathogenesis of renal tubular acidosis in primary biliary cirrhosis may be related to copper metabolism disorders. Copper is mainly excreted through the bile. When the disease progresses to cause biliary obstruction, copper cannot be excreted from the liver, mainly relying on plasma copper blue. Protein production, but the rate of ceruloplasmin synthesis in liver disease is reduced, so systemic copper retention occurs, copper toxicity damages renal tubules, in hepatolenticular degeneration, whole body tissues (liver, kidney, brain and cornea) have copper deposition, serum Copper decreased and urinary copper excretion increased, impairing renal tubular uric acidification, manifested as proximal and distal type, due to direct damage of copper toxicity, and considered reversible, with the long-term treatment with penicillamine, It can improve the copper after it is discharged from the body.
Prevention
Cirrhosis-induced renal damage prevention
1. Find a clearer cause of cirrhosis with glomerular damage and remove the cause to prevent glomerular damage.
2, pay attention to protect the liver, avoid harmful stimuli, prevent further damage to liver function to prevent progressive damage to the kidneys.
There is no special treatment for cirrhosis with glomerular damage, but most of them can find more obvious predisposing factors. Therefore, removing the cause has important practical significance for preventing the occurrence of glomerular damage, because the disease is transformed by cirrhosis. Come, it should be mainly for the treatment of liver disease itself, should pay attention to protect the liver, avoid harmful stimuli, prevent further damage of liver function to prevent progressive damage to the kidney.
Complication
Complications of cirrhotic renal damage Complications upper gastrointestinal bleeding hepatic encephalopathy hepatorenal syndrome kidney stone fracture peritonitis pneumonia cirrhosis ascites
Common complications of cirrhosis are: upper gastrointestinal bleeding, hepatic encephalopathy, bacterial infection and hepatorenal syndrome.
Upper gastrointestinal bleeding upper gastrointestinal bleeding is the main complication of cirrhosis, 50% manifested as massive hemorrhage, bleeding rate up to 40% 72h after hemorrhage, liver cirrhosis, liver tissue fibrosis and connective tissue hyperplasia, so that the liver The blood vessels are damaged, distorted and occluded, and the vascular network in the liver is greatly reduced, causing the portal vein blood flow to be blocked. The blood of the portal vein passes through the collateral circulation and flows to the esophageal venous plexus, causing venous congestion, dilatation, and venous vascular tube at these sites. The wall becomes thinner, and the thinned blood vessel wall can cause bleeding due to factors such as rough food, chemical stimulation and increased intra-abdominal pressure. The clinical symptoms are hematemesis (dark red or bright red) and black stool.
2. Hepatic encephalopathy The product of protein metabolism in the body is a substance containing nitrogen. When these nitrogenous substances are retained in the blood beyond a certain level, they may cause central nervous system dysfunction with neuropsychiatric abnormalities and coma as the main symptoms. Induced by harmful substances from the intestine entering the brain.
3. Bacterial infection in patients with cirrhosis due to reduced immunity, the body's immune function is significantly reduced, susceptible to intestinal bacteria and toxins, and various infections, such as bronchitis, pneumonia, urinary tract infection, tuberculous peritonitis, primary Peritonitis and the like.
4. Hepatorenal syndrome decompensated cirrhosis of the liver when there is a large amount of ascites, due to insufficient circulating blood and other factors, functional renal failure, that is, hepatorenal syndrome, manifested as oliguria (less than 400ml urine) /d), azotemia, hyponatremia, urinary sodium excretion decreased, and urine routine examinations are often no abnormalities, renal histology is normal or mild lesions, it is the late stage of cirrhosis renal dysfunction, very Danger.
5. The serious complications of renal tubular renal acidosis are renal calcinosis and kidney stones. Because of the decrease of H secretion, persistent alkaline urine, high calcium urine and low uric acid environment, calcium salt is easy to sink. In the kidneys and urinary tract, due to negative calcium balance, secondary hyperparathyroidism, decreased blood calcium and phosphorus levels can cause osteomalacia and spontaneous fractures, reduced H-Na exchange, increased K-Na exchange, urine Loss of potassium can cause hypokalemia. In addition, due to the reduced ability of the kidney to excrete ammonia, it can induce or aggravate hepatic encephalopathy.
Symptom
Symptoms of cirrhotic renal damage Common symptoms Liver failure Hepatic insufficiency Liver palm nephrotic syndrome Proteinuria Hypotension Spider Huangqi oliguria nausea
The clinical manifestations of cirrhosis can be divided into two phases, namely, liver function compensation period and liver function decompensation period, and some may stay in the compensation period for a long time, and may not enter the decompensation period.
1. Liver function compensation period is the early stage of cirrhosis, mild symptoms, common loss of appetite, fatigue, nausea and vomiting, abdominal distension, upper abdominal discomfort or dull pain, normal bowel movements or loose stools, complexion, sallow, face, neck, On the upper chest, back, shoulders and upper limbs, spider mites or telangiectasia can be seen, liver palm, liver slightly swollen, smooth surface, hard texture, mild tenderness, mild to moderate spleen, liver The function is checked in the normal range or mildly abnormal.
2. Decompensated liver function, clinical manifestations of liver dysfunction, such as weight loss, fatigue, irregular hypothermia, dark complexion, pigmentation and anemia, various gastrointestinal symptoms such as nausea, vomiting, loose stools, abdominal distension, etc. Symptoms and bleeding of the nose, gums, gastrointestinal tract and purpura, mild to moderate jaundice, male patients with loss of libido, testicular atrophy, hair loss, breast development, female patients with amenorrhea, infertility, and portal hypertension Performance, splenomegaly, accompanied by white blood cells, red blood cell and platelet count reduction, lower esophageal and gastric varices, often due to rupture of hematemesis, melena and shock, abdominal wall and umbilical varicose veins, nucleus rupture caused by blood in the stool, ascites is The most prominent manifestation of cirrhosis.
The size of the liver is different. It is usually large and small, the texture is hard, nodular, and sometimes tender. About half of the patients have mildly elevated serum bilirubin, and total cholesterol, especially cholesterol, is usually lower than normal. Decreased, globulin increased, albumin/globulin ratio decreased or inverted, -globulin increased significantly in protein electrophoresis, zinc turbidity test was positive, BSP retention often exceeded 10%, SGPT increased significantly, thrombin The prolonged original time, blood IgG, IgA, IgM increased, IgG was the most significant, HBsAg can be positive, and some patients were positive for serum autoantibodies.
3. Cirrhosis secondary to renal damage in patients with cirrhosis glomerulonephritis and renal tubular acidosis, early patients often have no obvious clinical symptoms, only a small amount of proteinuria, cirrhosis secondary to IgA nephropathy patients with renal function deterioration In order to be slow and benign, some patients have mesangial cells, endothelial cells and/or epithelial cells proliferating, with mesangial area and subendothelial immune complex deposition. These patients often have proteinuria and hematuria, and edema may also occur. , high blood pressure and renal dysfunction.
The clinical manifestations of cirrhosis secondary to renal tubular acidosis are similar to those of non-hepatic diseases. Most of them are incomplete distal renal tubular acidosis. A few patients have polyuria, polydipsia, nocturia, poor urine concentration and hypokalemia. , muscle weakness and other manifestations, patients with severe liver disease symptoms and signs, but also persistent alkaline urine, high calcium urine, low acid uric acid, combined with urinary calculi and secondary hyperparathyroidism, liver disease In the case of renal tubular acidosis, in addition to the reduced ability of the kidney to excrete H, it is often accompanied by significant hypokalemia. In addition, due to the reduced ability of the kidney to excrete ammonia, hepatic encephalopathy can be induced or aggravated.
Examine
Examination of cirrhotic renal damage
1. Urine examination has proteinuria, hematuria and tubular urine, often gross hematuria, generally considered that renal failure is not caused by glomerular lesions, liver tubular renal acidosis can be expressed as persistent alkaline urine, high calcium Urine, hyponattomic acid, combined with urinary calculi.
2. Serum examination serum examination can be seen, a variety of immunoglobulin hyperplasia, especially IgA most prominent, IgA concentration increased, cryoglobulinemia and serum C3 concentration decreased, liver excretion of renal tubular acidosis in addition to kidney excretion H In addition to reduction, it is often accompanied by significant hypokalemia.
3. Pathology
(1) Pathological changes of liver cirrhosis: the liver is significantly reduced, the hardness is increased, the weight is reduced, the liver surface is diffuse fine nodules, histological changes, the normal hepatic lobular structure disappears, replaced by false leaflets, hepatocytes in the pseudolobule Different degrees of degeneration, necrosis and regeneration can be present, and the portal area is significantly widened by connective tissue hyperplasia, in which inflammatory cell infiltration of varying degrees can be seen, and most of them are small bile duct-like structures (false bile duct), which are confirmed by electron microscopy. These pseudobiliary ducts are actually composed of newborn hepatocytes, which may be a manifestation of hepatocyte regeneration and kidney stones caused by renal calcinosis.
(2) Liver cirrhosis and kidney damage: The characteristic pathological changes of this disease are:
The mesangial matrix is broadened and can be inserted into the double-track sign between GBM and endothelial cells, resulting in a similar change in GBM.
The 2 mesangial zone has diffuse IgA-based deposition with IgG and/or IgM and/or C3 deposition.
3 Electron dense deposits in the mesangial area and/or capillary wall.
4 The basement membrane-like material and some sediments are visible in a circular loose zone.
5 glomerular sclerosis.
In addition, many authors have observed that patients with cirrhosis can be characterized by membranous nephropathy, intravascular proliferative nephritis, membrane proliferative nephritis, crescentic nephritis and focal glomerular sclerosis. Patients with biliary cirrhosis are reported to present with IgM-associated membranous nephropathy and cutaneous vasculitis.
4. Renal biopsy: under the electron microscope, the glomerular mesangial matrix has granular deposits such as glomerular sclerosis; round sparse areas in the basement membrane and some sediments, immunoglobulins, especially IgA and C3 deposits, although Each term is not specific, but if it is four items, it is a special change of hepatic glomerular sclerosis. "Hepatic glomerulosclerosis" can be changed at different times, and only glomerular sclerosis is in the early stage. There is no sediment, and the above typical lesions appear in the late stage.
5. Other examinations: routine liver, gallbladder, spleen, kidney B-ultrasound, X-ray examination, can be found typical of hepatosplenomegaly or atrophic sclerosis, as well as kidney shape changes and urinary calculi.
Diagnosis
Diagnosis and differential diagnosis of cirrhotic renal damage
Diagnostic criteria
First of all, the diagnosis of cirrhosis should be clarified. Clinically, according to the medical history, obvious liver, spleen, liver atrophy, hardening, positive liver function test, esophageal X-ray swallowing examination showed esophageal or gastric varices, liver biopsy It is found that typical symptoms such as pseudolobular formation can be clearly diagnosed, but it is often necessary to distinguish it from other types of liver cirrhosis. The liver should be differentiated from chronic active hepatitis and primary liver cancer. Ascites needs to be differentiated from tuberculous peritonitis. Identification of sexual pericarditis.
When hematuria patients with hematuria, proteinuria and tubular urine should consider cirrhosis with glomerular damage, patients with renal biopsy can help to confirm the diagnosis, the disease is mainly glomerular immunoglobulin deposition IgA-based and small amounts of IgG, IgM and/or C3, some patients have mesangial deposits without cell proliferation, glomerular proliferation including mesangial, endothelial or epithelial cells, with mesenteric and subendothelial The immunomorphological characteristics of sediments are:
1. The glomerular mesangial matrix has granular deposits under electron microscope.
2. Glomerular sclerosis.
3. A round sparse zone appears in the basement membrane and in certain deposits.
4. Immunoglobulins, especially IgA and C3 deposits.
Although each term is not specific, it is a special change of hepatic glomerulosclerosis, and "hepatic glomerular sclerosis" can be changed at different times. In the early stage, only glomerular sclerosis There is no sediment, and the above-mentioned typical lesions appear in the late stage. The laboratory tests may have glomerulonephritis, laboratory changes of renal tubular acidosis, such as proteinuria, hematuria, alkaline urine, hypercalciuria and bird road stones. Etc., and there are hyponatremia and a variety of immunoglobulins, blood IgA rise is particularly prominent, when serum C3 levels decline, the diagnosis can be established.
Differential diagnosis
The clinical manifestations of cirrhosis secondary to renal tubular acidosis are similar to those of non-hepatic patients and should be differentiated. In addition, the liver should be differentiated from chronic active hepatitis and primary liver cancer. Ascites should be differentiated from tuberculous peritonitis and constrictive pericarditis.
1, cirrhosis secondary to renal tubular acidosis
(1) The vast majority of patients with incomplete distal renal tubular acidosis, a small number of patients with polyuria, poor drinking night urine and poor concentration of hypokalemia and muscle weakness, patients with severe liver disease symptoms and signs, but also Persistent alkaline urine, hypercalciuria, hypocapnia and so on, can be combined with urinary calculi and secondary hyperparathyroidism.
(2) In patients with hepatic tubular renal acidosis, in addition to the reduced ability of the kidney to excrete H+, it is often accompanied by significant hypokalemia. In addition, due to the reduced ability of the kidney to excrete ammonia, hepatic encephalopathy can be induced or aggravated.
2. Chronic active hepatitis
The disease has a long course of disease, more than one year, and it can last for several years to several decades. Patients with fatigue, liver pain, loss of appetite and other symptoms persist, there will be liver splenomegaly, impotence, women's irregular menstruation and so on.
3, primary liver cancer
It is one of the common malignant tumors in China, with high mortality. It is divided into two major categories: primary liver cancer and secondary liver cancer.
4, tuberculous peritonitis
The vast majority of tuberculosis lesions secondary to other organs, the path of infection of this disease can be directly spread by intra-abdominal tuberculosis or disseminated by blood. Most of the onset is slow, patients often have fatigue, fever, abdominal distension, abdominal pain, chills, high fever and other symptoms.
5, constrictive pericarditis
Common causes are tuberculosis and suppurative infection followed by mold or viral infection. Common symptoms are difficulty breathing, fatigue, loss of appetite, upper abdominal distension or pain. Difficulty in breathing is labor-related, mainly related to decreased stroke volume.
