Kidneys and alcohol (alcoholic nephropathy)

Alcoholic nephropathy is associated with the effect of chronic alcohol on the immune system both due to the direct membrane-toxic effect with the influence on cytokine production and due to the disruption of immune regulation in the central nervous system and liver. An important role is played by sensitization to the alcohol hyaline antigen, bacterial antigens, and acceleration of HCV replication. Almost half of patients with visceral alcoholism have HCV-RNA, as well as an increase in the concentration of E. coli endotoxin, which activates the complement system via the alternative pathway.

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Causes alcoholic nephropathy

Among non-inflammatory nephritogenic factors, "alcoholic" hypertension and purine metabolism disorders are distinguished (see Gouty nephropathy ). The risk of developing hypertension increases with the amount of alcohol consumed and reaches 90% with consumption of more than 35 g/day. Morphologically, alcoholic glomerulonephritis is classified as a group of secondary IgA nephritis, it is characterized by a picture of mesangioproliferative nephritis (more often focal, less often diffuse).

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Symptoms alcoholic nephropathy

Symptoms of alcoholic nephropathy include the manifestation of symptoms of latent nephritis: persistent painless microhematuria, combined with minimal or moderate proteinuria (less than 2 g/day).

Acute nephritic syndrome, often accompanied by an increase in microhematuria, proteinuria, oliguria and a transient decrease in CF, is observed in more than 1/3 of patients on the first day after an alcoholic excess.

Hypertensive and nephrotic forms of alcoholic glomerulonephritis are diagnosed much less frequently. The nephrotic form is typical for rapidly progressing and diffuse fibroplastic variants of alcoholic glomerulonephritis. In the hypertensive form of alcoholic glomerulonephritis, purine metabolism disorders (hyperuricemia, hyperuricosuria) and obesity are often detected. Antihypertensive drugs satisfactorily control blood pressure. The following are typical for all forms of alcoholic glomerulonephritis:

• mesangial IgA deposits;
• severity of renal interstitial fibrosis;
• the presence of extrarenal symptoms of alcoholism.

In more than half of the cases, diseases such as alcoholic liver disease (chronic hepatitis, portal cirrhosis of the liver), chronic pancreatitis, alcoholic cardiomyopathy, and peripheral polyneuropathy are detected.

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Forms

The following clinical forms of glomerulonephritis are distinguished:

• latent;
• hypertensive;
• nephrotic.

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Diagnostics alcoholic nephropathy

Inspection and physical examination

The stigmas of alcoholism are revealed:

• macrocytic anemia;
• Dupuytren's contractures;
• giant mumps;
• erythema of the palms;
• gynecomastia.

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Laboratory diagnostics of alcoholic nephropathy

• General urine analysis: microhematuria, proteinuria.
• Decrease in the speed of the CF.
• Immunological blood test: persistent increase in IgA levels.
• Hyperuricemia, hyperuricosuria.

Instrumental diagnostics of alcoholic nephropathy

Ultrasound, X-ray and radionuclide diagnostic methods, liver biopsy are used.

Differential diagnosis

Diagnosis of alcoholic nephropathy is often difficult due to the non-specificity of hematuria and the variety of symptoms of alcoholic disease. First of all, to exclude urological diseases accompanied by hematuria (nephrolithiasis, tumors of the urinary system, tuberculosis of the kidney, necrotic papillitis in purulent pyelonephritis), a complex of radionuclide, ultrasound and X-ray diagnostic methods is used.

The next stage of differential diagnostics of alcoholic nephropathy is differentiation of alcoholic glomerulonephritis from acute nephritis, from primary and secondary IgA nephritis, from gouty and psoriatic nephropathy. In alcoholic glomerulonephritis, unlike acute nephritis and Berger's disease, macrohematuria is less often detected, the episode of hematuria is associated not with a previous acute infection of the upper respiratory tract (tonsillitis, pharyngitis), but with alcoholic excess. Symptoms of alcoholic liver disease, myocardium, pancreas are often present.

Liver biopsy plays an important role in establishing the alcoholic etiology of glomerulonephritis and choosing adequate therapy.

Rapidly progressive alcoholic nephritis should be differentiated from the following conditions:

• diffuse nephritis in subacute infective endocarditis;
• hepatorenal syndrome;
• endotoxic shock (see Acute renal failure);
• apostematous nephritis;
• secondary IgA nephritis in HIV carriers (IgA nephritis, which often develops in HIV-infected individuals of the white race, is characterized by diffuse extracapillary proliferation and a rapidly progressive course).

Treatment alcoholic nephropathy

First of all, it is necessary to completely eliminate alcoholic beverages, which leads to the rapid development of remission of nephritis in 50-60% of cases.

In alcoholic glomerulonephritis with purine metabolism disorders that are not corrected by abstinence and a low-purine diet, treatment with allopurinol is indicated.

In nephrotic and rapidly progressive forms of glomerulonephritis, glucocorticoids, cytostatics, and antiviral drugs (for HCV replication) are used, but the effectiveness of pathogenetic therapy for alcoholic CGN has not been proven.

When prescribing antihypertensive therapy, hepatotoxic drugs (methyldopa, thiazide diuretics, ganglionic blockers) should be avoided. Systematic administration of loop diuretics aggravates hyperuricemia, potassium and calcium deficiency, and in case of concomitant portal cirrhosis of the liver, provokes the development of hepatorenal syndrome. Of the antihypertensive drugs, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, and beta-blockers are the most preferable.

Treatment of chronic renal failure

The use of regular intermittent hemodialysis is difficult due to hemodynamic instability (liver cirrhosis with portal hypertension syndrome, hypovolemia, alcoholic cardiomyopathy with systolic dysfunction), severe hemorrhagic syndrome, metabolic disorders (respiratory alkalosis, hepatic encephalopathy). CAPD is more effective and safe.

In kidney transplantation for patients with alcoholic glomerulonephritis, there is an increased risk of infectious and oncological complications, as well as acute liver failure. In glomerulonephritis associated with alcoholic liver cirrhosis, combined transplantation is advisable - kidney and liver.

Forecast

The course and prognosis of alcoholic nephropathy are relatively favorable.

Almost half of the patients have a recurrent course of chronic glomerulonephritis with exacerbations after another alcohol excess and rapid (in 3-4 weeks) regression during abstinence. In parallel with a decrease in the severity of proteinuria, microhematuria, hypertension and normalization of CF, positive dynamics of cholestasis syndrome (reduction in liver size), purine metabolism disorders, cardiomyopathy (restoration of sinus rhythm) are noted.

The persistent course is characterized by constant activity of chronic glomerulonephritis, not clearly associated with alcohol excess.

Rapidly progressing course of alcoholic nephropathy with the outcome in irreversible renal failure in the 1-2nd year of nephritis is found in 3-6% of cases - with advanced alcoholic disease. The morphological basis of this variant is diffuse extracapillary or mesangiocapillary nephritis. A connection is noted between the rapidly progressing course of alcoholic chronic glomerulonephritis and persistent viral (HCV) infection, severe exacerbation of alcoholic pancreatitis.

In general, 15-20% of patients with chronic glomerulonephritis develop terminal chronic renal failure by the 10th year.

The criteria for an unfavorable prognosis for alcoholic chronic glomerulonephritis include:

• persistent proteinuria more than 1 g/day;
• formation of nephrotic syndrome;
• persistent hypertension;
• long-term (more than 10 years) alcohol consumption;
• HCV replication.

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