Drug-induced nephropathy. Methods for preventing this pathological condition

Toxic nephropathies. Drug-induced kidney damage. Long-term use medicines leads to isolated or combined with other organ damage to the kidneys. According to the mechanism of action on renal tissue, drug nephritis, toxic kidney (nephrotoxic nephritis) and drug nephropathy are distinguished.

The pathogenesis of drug-induced nephritis is associated with immediate type I reactions (IRT-I) and immune damage renal tissue. Its development may be associated with the intake of any medicine, as well as with the introduction of vaccines and serums. Toxic and drug-induced nephropathies are based on morphofunctional disorders of the kidneys caused by the direct effect of chemical compounds, as well as drugs or their metabolites on renal tissue. The high intensity of renal blood flow, the multiple circulation of all blood, and with it drugs, through the kidneys create the most “favorable” conditions for damage to the filtration barrier of the glomeruli, interstitial cells of the medulla and the epithelium of the nephron tubular system. Antibiotics of the aminoglycoside group, especially neomycin, monomycin, kanamycin, streptomycin, have a direct and pronounced nephrotoxic effect; moderate damage is caused by amphotericin B, polymyxin and gentamicin. The nephrotoxic effect of tetracycline occurs if it accumulates in the body due to a decrease in the excretory function of the kidneys. Damage to the kidneys occurs with long-term use of non-steroidal anti-inflammatory drugs (acetylsalicylic acid, butadione), which contribute to the disruption of oxidative phosphorylation in the epithelium of the nephron tubular apparatus. Severe consequences in the form of microvascular spasm, thrombosis of the renal capillaries and the development of acute renal failure occur during angiographic studies with the introduction of radiocontrast agents. With long-term use of diuretics and laxatives, the concentrating ability of the kidneys may be impaired due to dystrophy of the tubular epithelium.

The main signs of drug-induced nephropathies include hematuria (erythrocyturia), proteinuria, nephrotic syndrome. Oliguria may develop against the background of acute renal failure. Some nephropathy (phenacetin) can be asymptomatic for a long time. When the disease manifests itself, symptoms of chronic renal failure(polyuria, isohyposthenuria, decreased glomerular filtration rate, increased creatinine levels, anemia and arterial hypertension). Drug-induced nephropathies are observed during treatment with benzylpenicillin, sulfonamides, anti-tuberculosis drugs (tubazid), gold and nitrofuran drugs, mercury salts, iron compounds with dextrans, novocaine.

The development of toxic nephropathies is possible with exogenous intoxication with heavy metals (Cd, Pb), which directly cause necrosis of the renal parenchyma. There are cadmium and lead nephropathies. The detailed clinical picture of toxic nephropathies caused by heavy metals is associated with a decrease in glomerular filtration rate, the development of oliguria or anuria, proteinuria, arterial hypertension, aminoaciduria and glycosuria.

DiAbetic nephropathy (AN)- This general concept, which combines various types of kidney damage in diabetes mellitus, including glomerulosclerosis, infection urinary tract and papillary necrosis. Diabetic glomerulosclerosis (diabetic nephropathy) is a disease characterized by the appearance of specific degenerative changes in the glomerular vessels, leading to the development of proteinuria, edema and arterial hypertension. Diabetic nephropathy is the most common cause of death in most developed countries. About 25% of patients with type 1 diabetes suffer from DN 7-10 years after the diagnosis of the underlying disease. The main risk factors for diabetic nephropathy are uncontrolled levels of hyperglycemia and arterial hypertension, and hereditary predisposition. It has been established that DN develops due to mutations in the genes of enzymes associated with excess homocysteine in the blood. With DN, there is a thickening of the filtration barrier, hyalinosis of the afferent and efferent arterioles, sclerosis of the renal glomeruli with the subsequent spread of atrophic processes to the nephron tubules. The appearance of glomerular hyperfiltration indicates the development of renal failure. Nephrotic syndrome is a prognostically unfavorable sign of the course of nephropathy in patients with diabetes mellitus.

Congenital nephrotic syndrome(congenital nephrosis, familial nephrosis) is an autosomal recessive disease that manifests itself in the first three months of life and is fatal. Congenital nephrosis occurs in various ethnic groups, most often among Finns. The leading mechanism of the pathogenesis of familial nephrosis is the loss of the transmembrane protein nephrin as a result of gene mutations and non-selective leakage of the protein through the glomerular membrane. Massive proteinuria develops already by 35-38 weeks of gestation. Massive loss of protein leads to intrauterine growth retardation. Newborns develop edema, even ascites, and also sharply increase sensitivity to respiratory bacterial infection. In severe congenital nephrosis with protein deficiency, an imbalance of hemostatic factors occurs and thrombophilia develops, and the synthesis of thyroid hormones slows down (hypothyroidism). In the kidneys, sclerosis of the glomeruli occurs, interstitial fibrosis develops, tubular atrophy and loss of morphological differences between the cortical and medulla layers of the renal tissue. At the age of 3 to 8 years, the level of creatinine and urea in the blood of children gradually increases with the development of the final stages of chronic renal failure.

Nephropathies during pregnancy. As the fetus develops in the body of a pregnant woman, the functional load on the cardiovascular and endocrine systems, as well as on water-electrolyte metabolism, constantly increases. Changes in homeostasis at the organismal level lead to a natural morphofunctional restructuring of organs and tissues. Blood flow in the kidneys increases, the functional load on the nephrons increases, which leads to hypertrophy of the renal glomeruli, increased intensity of glomerular filtration and other changes. Physiological proteinuria is a reflection of the special functional state of the kidneys during pregnancy. Excretion of protein in urine per day during pregnancy increases almost 2 times. With a complicated course of pregnancy, in the second half (preeclampsia), swelling and dystrophic changes in the endothelium of the glomerular capillaries occur in the kidneys, and the lumen of the blood vessels sharply decreases. These pathological changes in the kidneys of pregnant women are known as "glomerular endotheliosis". With glomerular endotheliosis, protein loss from the body in the urine can reach 10 g per day. Nephrotic syndrome develops (swelling and other symptoms), and arterial hypertension appears. IN in rare cases severe damage to the renal cortex or tubular necrosis is observed with the development of acute renal failure in pregnant women.

Congenital kidney anomalies. Modern technologies radiology diagnostics make it possible to detect abnormalities in the development of the kidneys in the fetus as early as the 20th week of gestation. Congenital anomalies remain the leading cause of end-stage kidney disease in children. A sign of improper formation of the urinary system is hydronephrosis. Hydronephrosis – persistent expansion of the cavities of the renal pelvis and calyces with pathological changes interstitial tissue and atrophy of the renal parenchyma caused by impaired urine outflow. It is divided into bilateral and unilateral. Among the causes of bilateral hydronephrosis may be increased reflux of urine from the bladder into the ureters (reflux), atonic bladder and a huge ureter, as well as abnormal narrowing of the ureters (atresia). Unilateral hydronephrosis occurs when there is narrowing of the junction of the pelvis and ureter, as well as when duplex kidney or horseshoe kidney. This anomaly is known to be the most common renal anomaly in infants and is associated with hydronephrosis.

When taking medications, pathological conditions characterized by functional and organic lesions kidney

IN last years in connection with great welcome patients taking medications, the incidence of kidney damage (drug-induced nephropathy) increases (about 10-20% of all renal pathology). The kidneys can be damaged as a result of both acute and chronic poisoning medicines - in case of overdose, in case of long-term use or in case of drug intolerance (due to idiosyncrasy or geno- and fetatic characteristics of the body). In most cases, drug-induced nephropathies are associated with impaired immune response to a number of drugs (antibiotics, anesthetics, sulfa drugs, salts heavy metals etc.) or for vaccines and serums.
These kidney lesions are characterized mainly by damage to the renal glomeruli with the deposition of antigen-antibody complexes in their structures and the appearance of glomerular functional disorders. With allergic nephropathies, severe vasculitis often develops, involving interstitial tissue. The enzymopathic effect of some drugs or their metabolites may manifest itself in preferential damage to the tubular-interstitial structures of the kidneys. Polymorphism of drug-induced nephropathies is characteristic, and one drug can cause renal damage different types, and the impact various medications may cause similar nephropathy.

Clinic of drug-induced kidney damage

Clinical manifestations consist of common manifestations medicinal disease(fever, appearance of skin rash, intoxication) and signs of nephropathy - glomerulonephritis, interstitial nephritis, nephrotic syndrome, tubulopathy, urinary syndrome etc.
d. Acute and chronic renal failure can occur very often.

A feature of the development of drug-induced glomerulonephritis is the absence of significant hematuria and arterial hypertension.

Diagnosis of drug-induced kidney damage

Diagnosis of drug-induced nephropathy is difficult due to numerous extrarenal manifestations of drug-induced disease, lack of signs of kidney disease, and polymorphism of drug-induced nephropathy; great importance have a history of taking medications when symptoms of nephropathy appear, disappearance or reduction of the latter after discontinuation of the drugs. Significantly facilitates diagnosis laboratory methods increased sensitization of the body to the drug taken.

They differentiate drug-induced nephropathy from pyelonephritis, glomerulonephritis, interstitial nephritis and other kidney pathologies.
Wherein crucial have a history of previous use of medications, laboratory test the body's sensitivity to the drug. In unclear cases, puncture biopsy of the kidneys can play a significant role in differentiation.

Treatment of drug-induced kidney damage

Treatment consists primarily of discontinuing medications that cause nephropathy. Dietary and drug treatment depends on the nature of nephropathy. For immune genesis of nephropathies, hormones (prednisolone, triamcinolone, etc.) are indicated.

Prevention consists of careful collection allergic history, lawful prescription of medications, especially with increased sensitization to them, avoidance of the use of nephrotoxic drugs, absence of kidney disease; in case of unavoidability drug therapy Urinalysis is regularly monitored.

Drug-induced kidney damage is very common in practice with long-term use of medications. After some therapeutic courses, pathologies arise in the body, characterized by kidney damage at the functional and organic level. According to statistics, it can be seen that over the past few years, drug-induced nephropathy has increased by 20%. It is worth noting that negative impact drugs is displayed both in acute chronic drug poisoning and due to overdose. In some cases, malfunction is to blame immune system which shows negative reaction to antibiotics and anesthetics. In this article, we will look at all the features of kidney damage after taking medications.

Features and characteristics of drug-induced kidney damage

The peculiarity of pathologies due to drug-induced kidney damage is that the disease is considered as a change morphological form liver. Deformation occurs due to long-term use medicines. The disease is quite common occurrence, because today there is great amount medications that can cause disorders in the functioning of the renal organs.

Important! According to studies, it can be said that among the main side effects after medications are jaundice - in 2.5%, hepatitis - in 40% and kidney failure acute form– in 25% of hospital patients.

If we take into account the subclinical nature of drug-induced damage to the renal organ, it should be noted that it is possible to determine the frequency in rare cases. Complications after taking medications have become much more common in practice. This fact is influenced by the fact that most drugs and medications are dispensed by pharmacists without a prescription. The patient cannot obtain extensive information about the features of the drug, so the risk of side effects increases. Thus, if you drink 5 at the same time different types tablets, then the likelihood increases negative consequences by 4%, if 10 - then by 10%, and if you take about 30-60 drugs, then the risk increases by 60%.

Attention! It should be noted that half of all negative consequences after taking antibiotics are due to the incompetence or gross mistakes of doctors. According to statistics, death due to such situations occupies 5th position in the ranking. For this reason, take medications very carefully.

Causes of drug-induced kidney damage

Various drug-induced organ damage most often depends on large quantities factors. Among such accompanying circumstances of pathology, the following can be distinguished:

Age of the patient;
Females and males have different tolerances to certain drugs;
Features of tropholic status;
During pregnancy, a woman tolerates medications differently;
The dosage and duration of the therapeutic course of drugs can play a fatal role;
How do medications interact with each other if you have been prescribed several of them?
Various enzyme inductions or their polymorphisms;
If a person has liver pathology, then medications should be taken very carefully;
If the patient has systemic or chronic diseases;
In case of impaired renal function.

Attention! Everyone knows the fact that the kidneys and liver play important role in the body, since they are the ones who biotransform drugs. That is, the first impact of the tablets falls on these organs.

Symptoms of drug-induced kidney damage

In general, the symptoms resemble ordinary human poisoning. The first signs can be replaced in the urinary secretions, where changes occur. Most cases of drug damage do not make themselves known to the person. Only if the dose of the drug is greatly exaggerated or complications arise. In such cases side effects may cause significant discomfort.

The lion's share of all toxic nephropathies is caused by drugs. In this case, a reaction of the body’s immune elements and chemical reagents is observed. The kidneys contain components of allergic zones, such as mast cells, interleukins and immunoglobulin. Thus, with drug-induced kidney damage, all these components enter directly into the lesion, which aggravates the situation. In general, the symptoms of pathologies resemble acute glomerulonephritis. Among the most obvious signs, it should be highlighted:

A person is tormented by general malaise and weakness;
The patient becomes irritable and may show aggression;
During this period there is increased swelling of the whole body;
The frequency and volume of urinary emission decreases, which in medicine is called oligoanuria;
In parallel with drug damage, arterial hypertension is very often observed, which can increase so much that a person suffers from convulsions and even stops heartbeats.

The toxic effects of sulfonamide substances, especially from streptocide and norsulfazole, are most often accompanied by attacks of fever, severe pain in the joint area, the skin and mucous membranes are affected, and hemorrhagic rashes occur. If you look at the capillaries on the kidneys, you can notice endothelial damage, in which the walls become ulcerated and vascular permeability increases.

Features of the treatment process

In most cases, the presence toxic nephropathy leads to the formation of interstitial type nephritis, hemolytic-uremic syndrome and acute renal failure. In acute or chronic nephritis, a person experiences the following symptoms:

Cutting or It's a dull pain in the lumbar region;
Increase in blood pressure for a short period of time;
Often the patient suffers from pain in the joints, medically called arthralgia;
Observed various changes in urinary secretions.

When performing a general urine test, you can find increased amount ESR, symptoms of anemia and moderate leukocytosis. It is worth noting that when acute renal failure is achieved, the risk of death increases, which is why the disease is already dangerous. This is due to the fact that renal function may sharply decrease or disappear. In this case, the entire standard set appears clinical symptoms, that is, oligoanuria, retention of nitrogenous wastes in the body, impaired water and acid balance etc.

As you can see, the disease causes many unpleasant consequences. The good news is that any drug-induced injury can be treated, the main thing is to provide timely assistance. If treatment is not done in a timely manner, then it will only be possible to carry out detoxification or symptomatic therapy. Initially, the doctor determines the composition of the elements that led to the lesion, and taking this into account, prescribes necessary medications and methods for improving the human condition. Diuretics and alkaline agents are most often prescribed. So we got acquainted with the features of drug-induced kidney damage.

Description:

When taking medications, pathological conditions characterized by functional and organic kidney damage may occur.

In recent years, due to the increased use of medications by patients, the frequency of kidney damage (drug-induced) has been increasing (about 10-20% of all renal pathology). The kidneys can be affected as a result of both acute and chronic drug poisoning - with an overdose, with prolonged use or with intolerance to drugs (due to idiosyncrasy or geno- and fetatic characteristics of the body).

Symptoms:

Clinical manifestations consist of general manifestations of a drug-induced disease (fever, appearance of a skin rash) and signs of nephropathy - glomerulonephritis, interstitial, tubulopathy, etc. Acute and.

A feature of medicinal development is the absence of significant and.

Causes:

In most cases, drug-induced nephropathies are associated with impaired immune response to a number of drugs (antibiotics, anesthetics, sulfonamides, heavy metal salts, etc.) or to vaccines and serums. These kidney lesions are characterized mainly by damage to the renal glomeruli with the deposition of antigen-antibody complexes in their structures and the appearance of glomerular functional disorders. With allergic nephropathies, severe vasculitis often develops, involving interstitial tissue. The enzymopathic effect of some drugs or their metabolites may manifest itself in preferential damage to the tubular-interstitial structures of the kidneys. Polymorphism of drug-induced nephropathies is characteristic, and one drug can cause renal lesions of different types, and exposure to different medications can cause similar nephropathy.

Treatment:

For treatment the following is prescribed:

Treatment consists primarily of discontinuing medications that cause nephropathy. Dietary and drug treatment depends on the nature of nephropathy. For the immune genesis of nephropathies, hormones (prednisolone, triamcinolone, etc.) are indicated.

Prevention consists of carefully collecting an allergic history, lawfully prescribing medications, especially with increased sensitization to them, avoiding the use of nephrotoxic drugs, and the absence of kidney disease; If drug therapy is unavoidable, regular monitoring of urine analysis is carried out.

This is an acute or chronic lesion of the renal glomeruli, tubules, interstitium, caused by taking medications. Manifested by polyuria, oligoanuria, nocturia, hematuria, lower back pain, asthenic, edematous and hypertensive syndromes. Diagnosed based on general and biochemical analyzes blood, urine, ultrasound, ultrasound, CT, MRI of the kidneys, excretory urography, nephroscintigraphy, renal tissue biopsy. Treatment includes detoxification therapy, corticosteroids, drug infusions, anticoagulants, antiplatelet agents, antihypertensive drugs, PTA. If persistent chronic dysfunction occurs, a kidney transplant is required.

ICD-10

N14.0 N14.1 N14.2

General information

According to the observations of domestic and foreign urologists, in recent years the frequency of drug-induced kidney damage, manifested by various options acute and chronic nephropathies. This is primarily due to the expansion of the arsenal medications used in therapy various diseases, and the potential nephrotoxicity of most drugs. In 10-11% of patients with kidney disease requiring replacement therapy, nephrological pathology is associated specifically with taking medications.

To the group increased risk includes older patients age group who receive long-term supportive care combination treatment regarding chronic somatic diseases and are exposed diagnostic procedures with the use of nephrotoxic drugs. Their share of nephrology patients reaches 66%.

Causes

Drug-induced nephropathy with the use of pharmaceutical and paramedical drugs that have nephrotoxic effects. Typically, the prerequisites for the development of kidney damage are uncontrolled use of medications without taking into account contraindications (self-medication), side effects due to unreasonable prescription or incorrect combination of medications, hereditary predisposition, Availability concomitant pathology(diabetes mellitus, hypertension, nephrological diseases, etc.). Damage to kidney tissue can be caused by:

Official medicines. Renal dysfunction occurs when taking antibacterial drugs(penicillins, cephalosporins, aminoglycosides, tetracyclines, fluoroquinolones, sulfonamides, antituberculosis drugs), analgesics, NSAIDs, diuretics, barbiturates, cytostatics, H2-histamine receptor blockers, ACE inhibitors, phenothiazines, etc. When using X-ray contrast, the development of contrast-induced nephropathy is possible.
Vaccines and serums. Up to 23% of cases of drug-induced nephrological pathology are caused by the administration of antitetanus, antimeasles, antistaphylococcal serums, ADS, ADS-M, DPT, and gonovaccines. The risk of post-vaccination or serum nephropathies increases when immunization or administration of ready-made antibodies to patients with a burdened allergic history or hypersensitivity to the components of the immunodrug.
Paramedics. According to observational data, up to 80% of the population uses funds alternative medicine. At the same time, vasoconstrictor, cytopathic, crystalluric, and dysmetabolic effects are often underestimated medicinal plants. According to the FDA, up to 32% of Ayurvedic drugs contain mercury, arsenic, lead, aristolochic acid, recognized as one of the probable causes Balkan endemic nephropathy, other nephrotoxic ingredients.

Pathogenesis

The basis for the development of drug-induced nephropathy is a combination of several pathogenetic mechanisms. Some medications have a direct damaging effect, leading to primary damage to the cells of the proximal tubules that reabsorb nephrotoxic chemical compound. Tubular epithelium can also be destroyed by precipitation of crystals due to the use of sulfonamide drugs, myoglobin obstruction during rhabdomyolysis due to the use of statins, monoamine oxidase inhibitors, phenothiazine derivatives, and some anesthetics.

The resulting tubular dysfunction provokes a secondary impairment of filtration capacity. An independent or aggravating factor in destruction becomes ischemic changes tissues caused by anaphylactic shock, thrombotic microangiopathy, inhibition of prostaglandins and the renin-angiotensin system with subsequent vascular spasm.

A separate link in the pathogenesis is damage to the glomerular and tubular basement membranes immune complexes, which include the drug or its metabolites as an antigen. Glomerulopathy and tubulopathy may develop as a result of sedimentation of circulating blood immune complexes, and in the reaction of antibodies to chemical substances, associated with structural renal elements.

At immune mechanism The leading cause of nephropathy is a hyperergic reaction with disruption of renal microcirculation, release of histamine and other inflammatory mediators. Prolonged tissue ischemia in combination with alteration cellular elements potentiates collagenogenesis and tissue sclerosis with replacement functional elements connective tissue fibers.

Classification

Diagnostics

If acute renal dysfunction occurs, time-related with the use of potentially nephrotoxic drugs, making a diagnosis drug-induced nephropathy usually not difficult. More thorough diagnostic search required with gradual increase renal symptoms in the patient, long time receiving a certain pharmaceutical drug. For the diagnosis of drug-induced nephropathies, laboratory and instrumental methods are recommended to assess the morphological structure and functional ability of the kidneys:

General urine analysis. At different options pathological condition a decrease or significant increase in relative density, red blood cells, white blood cells, cylinders, and salt crystals can be detected in the material. To assess the reabsorption function of the tubules, the study is often supplemented with the Zimnitsky test.
Blood chemistry. A decrease in filtration function is indicated by an increase in creatinine levels, uric acid, urea, changes in the content of potassium, calcium, sodium, phosphorus. An imbalance of ions is possible when their reabsorption is impaired. With proteinuria, hypo- and dysproteinemia occurs.
Nephrological complex. Determination of organ performance is based on data on the content of creatinine, urea, uric acid, and macroelements. The appearance of protein, glucose, and microalbumin in the urine is indicative. As additional method Rehberg's hemorenal test and Sulkowicz's test are recommended.
Sonography. Ultrasound of the kidneys reveals an increase or decrease in the size of the organ, diffuse and focal changes in the parenchyma and medulla. Ultrasound scanning complemented by ultrasound scanning, which allows assessing renal blood flow, and, if necessary, tomography (MRI, CT).
Intravenous urography. According to hatching data contrast agent the characteristics of the blood supply to the kidneys and their functional activity. Excretory urography can be supplemented with nephroscintigraphy. Due to the potential for worsening symptoms, testing of patients with acute renal failure is limited.
Needle biopsy of the kidneys. Histological examination biomaterial makes it possible to most accurately assess the condition of glomeruli, tubules, interstitial tissue, capillaries, arterioles. Kidney biopsy results are particularly valuable for selection medical tactics in patients with chronic drug-induced nephropathies.

IN general analysis blood, a moderate acceleration of ESR, an increase in the level of eosinophils, a decrease in the content of erythrocytes and hemoglobin is possible. Differential diagnosis carried out with acute and malignant glomerulonephritis, nephropathy with gout, lupus, autoimmune vasculitis, urolithiasis, renal tuberculosis, idiopathic interstitial nephritis. In addition to a urologist or nephrologist, an anesthesiologist-resuscitator, toxicologist, rheumatologist, immunologist, phthisiatrician, infectious disease specialist, and oncologist may be involved in consulting the patient.

Treatment of drug-induced nephropathy

Medical tactics for managing patients with drug-induced nephrological pathology take into account the clinical and morphological form and features of the pathogenesis of the disease. In any case, treatment begins with discontinuation of the drug that caused the nephropathy. In acute processes, methods aimed at eliminating the damaging compound are justified - taking antidotes (if available), gastric lavage, hemosorption, accelerating excretion (prescribing sorbents, laxatives). Therapy is carried out taking into account the filtering and reabsorption functions. Depending on the clinical situation may be used:

Corticosteroids. Glucocorticoid therapy with moderate and high doses justified in the immune pathogenesis of nephropathy, carried out for the rapid relief of autoimmune and allergic reactions. The immunosuppressive effect includes reducing interstitial edema, suppressing the functions of macrophages, limiting leukocyte migration in inflamed tissues, and inhibiting the synthesis of inflammatory mediators and antibodies. Glucocorticosteroids effectively stabilize cellular and lysosomal membranes.
Symptomatic remedies. Renal dysfunction is accompanied by the occurrence of organ and systemic disorders that require emergency correction. It is used to restore water and electrolyte balance, hemodynamics, microcirculation, and tissue perfusion. infusion therapy with the introduction of colloid, crystalloid solutions, antiplatelet agents, anticoagulants. If renin-angiotensin regulation is impaired, antihypertensive drugs are usually required.
Renal replacement therapy. Extrarenal blood purification is prescribed to prevent severe uremic complications in severe functional failure. Hemodialysis, peritoneal dialysis, hemofiltration, hemodiafiltration can be carried out intermittently until renal function is restored or continuously in case of severe chronic renal failure. At chronic course drug-induced nephropathy may require kidney transplantation.

Prognosis and prevention

The outcome of the disease depends on the timeliness of treatment and the degree of damage to the renal parenchyma. If acute nephropathy does not occur irreversible changes in the anatomical structure of the organ, the prognosis is favorable. The occurrence of massive destruction and acute renal failure in the absence adequate therapy significantly increases the risk fatal outcome. Patients with chronic nephrological diseases and aggravated premorbid background often experience a persistent decrease in the filtration capacity of the kidneys, which can be somewhat slowed down by prescribing drug therapy.

To prevent drug-induced nephropathy, it is necessary to adjust the doses of drugs that are metabolized in the kidneys, in accordance with the values of creatinine clearance, and avoid the use of nephrotoxic drugs in the presence of risk factors ( elderly age, female gender, intercurrent diseases, decreased blood volume), exclusion of polypharmacy.