OVERVIEW
Post-hepatitis cirrhosis, ethanol cirrhosis, biliary cirrhosis and schistosomiasis cirrhosis can cause renal damage. Patients not only have clinical evidence of liver primary disease as well as hepatic decompensation and portal hypertension secondary to cirrhosis, but also the kidneys can be involved, which is collectively called cirrhotic renal damage.
Etiology
There are many causes of cirrhosis, mainly viral hepatitis, chronic alcoholism, nutritional deficiencies, intestinal infections, poisoning by drugs or industrial poisons and chronic cardiac insufficiency.
Symptoms
Cirrhotic renal damage can be clinically manifested as glomerulopathy, renal tubular acidosis, and hepatorenal syndrome in severe cases.
1. Glomerular injury
Clinical manifestations of renal involvement are mostly mild, and different degrees of hematuria and proteinuria are often found in laboratory tests. A few with nephrotic syndrome may have renal damage, and a variety of immunoglobulins in the blood are elevated, especially IgA, and the level of complement C3 may be decreased. It may also be accompanied by abnormal immune markers, including antinuclear antibodies, rheumatoid factor, positive circulating immune complexes, and cryoglobulinemia. The most common type of glomerular lesion in cirrhosis is IgA nephropathy. The manifestations are diffuse IgA-based deposition in the tethered zone, which may be accompanied by IgG, IgM, and C3 deposition; the tethered matrix may be widened and inserted into the glomerular basement membrane and endothelial cells in a double-tracking sign and produce basement membrane thickening-like changes; and electron-dense material is deposited in the tethered zone and/or in the walls of the capillaries. In addition, patients with post-hepatitis cirrhosis can often present the manifestations of hepatitis B or C-related nephritis, such as membranoproliferative nephritis, membranous nephropathy, intracapillary proliferative nephritis, glomerulosclerosis, and so on.
2.Renal tubular acidosis
The incidence of chronic liver disease combined with renal tubular acidosis is about 30%, in which renal tubular acidosis has the highest incidence in primary biliary cirrhosis, followed by chronic active hepatitis, post-hepatitis cirrhosis and cirrhosis of unknown cause, and the incidence in alcoholic cirrhosis is lower. The vast majority of patients have incomplete distal renal tubular acidosis, while the incidence of complete distal renal tubular acidosis is less than 10%. Clinical manifestations of renal tubular acidosis are polydrinking, polyuria, nocturia, and even uremia, muscle weakness, nausea and vomiting.
Examination
The common tests for cirrhotic kidney injury include routine blood test, routine urine test, complement binding test, ultrasound, liver function test, renal function test, renal histopathology test and so on.
Different degrees of hematuria and proteinuria can be found, as well as elevated levels of various immunoglobulins in the blood, especially IgA, and the level of complement C3 can be decreased. It may also be accompanied by abnormal immune markers, including antinuclear antibodies, rheumatoid factor, positive circulating immune complexes, and cryoglobulinemia.
Laboratory tests include acidosis, alkaluria, hypokalemia, and decreased urinary concentrating function.
Diagnosis
Diagnosis is made by combining the history of cirrhosis, hematuria, renal function tests, and renal histopathology. The main points of diagnosis are as follows.
1. History of liver cirrhosis.
2. The presence of urinary system abnormalities such as hematuria, proteinuria and abnormal renal function tests.
3. Various immunoglobulins in the blood are elevated, especially IgA, and the level of complement C3 may be decreased.
Treatment
1. Treatment of cirrhosis
(1) Pay attention to rest, and in the late stage, bed rest should be emphasized, and nutritious diet should be given.
(2) Use liver-protecting drugs and treatment for ascites, splenorenal vein anastomosis for portal hypertension, splenectomy for splenomegaly and hypersplenism.
2.Treatment of cirrhosis with glomerular damage
Most of the kidneys with mild clinical manifestations or lack of symptoms do not need to be treated. For a few patients with rapid deterioration of renal function or nephrotic syndrome, appropriate treatment should be given after renal pathologic changes have been clarified. The treatment of nephritis can refer to the treatment of primary glomerulonephritis, but avoid the use of hormones and cytotoxic drugs if liver function is impaired.
3. Treatment of hepatic tubular acidosis
If it is incomplete renal tubular acidosis, no special treatment can be given without clinical manifestations. If there is acidosis, sodium citrate should be given to symptomatic treatment, and timely correction of potassium, calcium and other electrolyte disorders. Hypokalemia is easily induced during the use of diuretics or intravenous glucose infusion in these patients, and attention should be paid to the treatment.