drug nephropathy. Methods for the prevention of this pathological condition

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

The pathogenesis of drug nephritis is associated with immediate type I reactions (IT-I) and immune damage. renal tissue. Its development may be associated with the reception of any medicinal product, as well as with the introduction of vaccines and sera. The basis of toxic and drug nephropathies are morphofunctional disorders of the kidneys caused by the direct action of chemical compounds, as well as drugs or their metabolites on the 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 glomerular filtration barrier, interstitial cells of the medulla and epithelium of the nephron tubular system. A direct and pronounced nephrotoxic effect is exerted by antibiotics of the aminoglycoside group, especially neomycin, monomycin, kanamycin, streptomycin; moderate damage is caused by amphotericin B, polymyxin and gentamicin. The nephrotoxic effect of tetracycline is manifested if it accumulates in the body due to a decrease in the excretory function of the kidneys. Kidney damage occurs with prolonged 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 spasm of microvessels, thrombosis of the renal capillaries and the development of acute renal failure occur during angiographic studies with the introduction of radiopaque substances. With prolonged use of diuretics, laxatives, a violation of the concentration ability of the kidneys due to dystrophy of the epithelium of the tubules is possible.

The main signs of drug nephropathy include hematuria (erythrocyturia), proteinuria, nephrotic syndrome. Perhaps the development of oliguria against the background of acute renal failure. Some nephropathies (phenacetin) can be asymptomatic for a long time. With the manifestation of the disease, symptoms of chronic kidney failure(polyuria, isohypostenuria, decreased glomerular filtration rate, increased creatinine, anemia and arterial hypertension). Drug nephropathies are observed during treatment with benzylpenicillin, sulfonamides, anti-tuberculosis drugs (tubazid), gold and nitrofuran preparations, mercury salts, iron compounds with dextrans, novocaine.

The development of toxic nephropathy is possible with exogenous intoxication with heavy metals (Cd, Pb), which directly cause necrosis of the renal parenchyma. Allocate cadmium and lead nephropathy. An extended clinical picture in 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 (DN)- 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 vessels of the glomeruli, leading to the development of proteinuria, edema and arterial hypertension. diabetic nephropathy is the most common cause of death in most developed countries. Approximately 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 as a result of mutations in the genes of enzymes associated with excessive levels of 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, followed by the spread of atrophic processes to the nephron tubules. The appearance of glomerular hyperfiltration indicates the development of renal failure. A prognostically unfavorable sign of the course of nephropathy in patients with diabetes mellitus is nephrotic syndrome.

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 in Finns. The leading mechanism of the pathogenesis of familial nephrosis is the loss of a transmembrane protein, nephrin, as a result of gene mutations, and non-selective leakage of the protein through the glomerular membrane. Massive proteinuria develops by 35-38 weeks of gestation. Massive loss of protein leads to a delay in intrauterine development of the fetus. Newborns develop edema, up to ascites, and also sharply increase sensitivity to a respiratory bacterial infection. In severe congenital nephrosis with protein deficiency, an imbalance of hemostasis factors occurs and thrombophilia develops, and the synthesis of thyroid hormones (hypothyroidism) slows down. In the kidneys, sclerosis of the glomeruli occurs, interstitial fibrosis develops, atrophy of the tubules and the 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 gradually increases in the blood of children with the development of the final stages of CRF.

Nephropathy 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 and electrolyte metabolism, constantly increases. Changes in homeostasis at the organismic level lead to a regular morphological and functional restructuring of organs and tissues. In the kidneys, blood flow increases, the functional load on the nephrons increases, which leads to hypertrophy of the renal glomeruli, an increase in the 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 the urine per day during pregnancy increases by almost 2 times. With a complicated course of pregnancy, in the second half of it (preeclampsia), edema and degenerative changes in the endothelium of the glomerular capillaries occur in the kidneys, and the lumen of the vessels also sharply decreases. These pathological changes in the kidneys of pregnant women are known as "glomerular endotheliosis". With glomerular endotheliosis, the loss of protein from the body with urine can reach 10 g per day. Nephrotic syndrome (edema and other symptoms) develops, and arterial hypertension also appears. IN rare cases there is severe damage to the cortical layer of the kidneys or tubular necrosis with the development of acute renal failure in pregnant women.

Congenital anomalies of the kidneys. Modern technologies radiodiagnosis allow to detect abnormalities in the development of the kidneys in the fetus as early as the 20th week of its gestation. Congenital anomalies remain the main cause of end-stage kidney disease in children. A sign of abnormal formation of the urinary system is hydronephrosis. hydronephrosis – persistent expansion of the cavities of the renal pelvis and calyx with pathological changes interstitial tissue and atrophy of the renal parenchyma, caused by a violation of the outflow of urine. It is divided into two-sided and one-sided. Among the causes of bilateral hydronephrosis may be increased reflux of urine from the bladder into the ureters (reflux), atonic bladder and an oversized ureter, as well as abnormal narrowing of the ureters (atresia). Unilateral hydronephrosis occurs when the junction of the pelvis and ureter is narrowed, as well as when duplication of the kidney or horseshoe kidney. This anomaly is known in infants as the most common renal anomaly and is associated with hydronephrosis.

When taking medications, pathological conditions may occur, characterized by functional and organic lesions kidneys.

IN last years in connection with great welcome drug patients, the incidence of kidney damage (drug-induced nephropathy) increases (about 10-20% of all renal pathology). The kidneys can be affected both as a result of acute and chronic poisoning drugs - in case of overdose, with long-term use or with intolerance to drugs (with idiosyncrasy or geno- and fetal characteristics of the body). In most cases, drug-induced nephropathy is associated with a violation of the immune response to a number of drugs (antibiotics, anesthetics, sulfa drugs, salts heavy metals etc.) or vaccines and sera.
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 nephropathy, severe vasculitis often develops with involvement of the interstitial tissue in the process. The enzymopathic effect of certain drugs or their metabolites may be manifested in the predominant damage to the tubular-interstitial structures of the kidneys. Polymorphism of drug-induced nephropathies is characteristic, and one drug can cause renal damage different type, and the impact various medicines may cause similar nephropathy.

Clinic of drug-induced kidney injury

Clinical manifestations consist of common manifestations medicinal disease(fever, skin rash, intoxication) and signs of nephropathy - glomerulonephritis, interstitial nephritis, nephrotic syndrome, tubulopathy, urinary syndrome etc.
e. 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 injury

Diagnosis of drug nephropathy is difficult due to numerous extrarenal manifestations of drug disease, the absence of signs of kidney disease, polymorphism of drug nephropathy; great importance have anamnestic facts of taking medications when symptoms of nephropathy appear, the disappearance or decrease of the latter after discontinuation of drugs. Makes it much easier to diagnose laboratory methods increased sensitization of the body to the drug taken.

Differentiate drug-induced nephropathy from pyelonephritis, glomerulonephritis, interstitial nephritis and other kidney pathology.
Wherein crucial have a history of previous drug use, laboratory research 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 injury

Treatment consists primarily in the abolition of drugs, against which nephropathy develops. dietary and medicinal treatment depends on the nature of the nephropathy. With the immune genesis of nephropathy, hormones are indicated (prednisolone, triamcinolone, etc.).

Prevention is the careful collection allergic history, the lawful prescription of drugs, especially with increased sensitization to them, the prevention of the use of nephrotoxic drugs, the absence of kidney disease; in case of inevitability drug therapy urinalysis is monitored regularly.

Drug damage to the kidneys is very common in practice with long-term medication. After some therapeutic courses, pathologies occur in the body, characterized by damage to the kidneys 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 poisoning with drugs, and as a result of an overdose. In some cases, disruption is to blame immune system, which shows backlash for antibiotics and anesthetics. In this article, we will consider all the features of kidney damage after taking medication.

Features and characteristics of drug-induced kidney injury

The peculiarity of pathologies due to drug-induced kidney injury is that the disease is considered as a change morphological form liver. The deformation is due to long-term use medicines. The disease is quite frequent occurrence because today there is great amount medicines that can cause disorders in the functioning of the kidney organs.

Important! According to studies, we can say 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 preparations are dispensed by pharmacists without a prescription. The patient cannot receive broad 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 pills, it increases the likelihood 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 errors of doctors. According to statistics, death due to such situations takes the 5th position in the ranking. For this reason, take your medicines very carefully.

Causes of drug-induced kidney injury

Various drug-induced organ damage most often depend on a large number factors. Among such concomitant pathology conditions, the following can be distinguished:

The age of the patient;
Females and males have different tolerability of certain drugs;
Features of the trophic status;
In the position of pregnancy, a woman tolerates drugs differently;
The dosage and duration of the therapeutic course of drugs can play a fatal role;
How do drugs interact with each other if you have been prescribed several of them;
Various enzyme inductions or their polymorphism;
If a person has a liver pathology, then medication should be taken very carefully;
If the patient has systemic or chronic diseases;
In violation of the functioning of the kidneys.

Attention! Everyone knows the fact that the kidneys play a liver important role in the body, since it is they who biotransform drugs. That is, the first blow of the pills falls on these organs.

Symptoms of drug-induced kidney injury

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

The lion's share of all toxic nephropathies falls on drug damage. In this case, the reaction of the immune elements of the body 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 focus, which aggravates the situation. In general, the symptoms of pathologies resemble acute glomerulonephritis. Among the most obvious signs should highlight:

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 is tormented by convulsions and even heart contractions stop.

The toxic effects of sulfonamide substances, especially from streptocide and norsulfazol, are most often accompanied by bouts of fever, severe pain in the area of the joints, the skin and mucous membranes are affected, hemorrhagic rashes occur. If we consider the capillaries on the kidneys, we can see an endothelial lesion, in which the walls ulcerate and vascular permeability increases.

Features of the treatment process

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

cutting or It's a dull pain in the lumbar region;
An increase in the pressure indicator for a short period of time;
Often the patient is tormented by pain in the joints, in medicine called arthralgia;
Observed various changes in urinary secretions.

A urinalysis can reveal increased amount ESR, symptoms of anemia and moderate leukocytosis. It is worth noting that when acute renal failure is reached, the risk of death increases, so the disease is already dangerous. This is due to the fact that renal function may drop sharply or fall out. In this case, the entire standard set is displayed. clinical symptoms, that is, oligoanuria, a delay in the body of nitrogenous slags, a violation of water and acid balance etc.

As you can see, the disease delivers many unpleasant consequences. I am glad that any drug lesion is treatable, the main thing is to timely help. If the treatment is not timely, then it will really be possible to carry out only 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 drugs and methods to improve the human condition. Most often, diuretics, alkaline agents are prescribed. So we got acquainted with the features of drug damage to the kidneys.

Description:

When taking medications, pathological conditions may occur, characterized by functional and organic lesions of the kidneys.

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

Symptoms:

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

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

Causes of occurrence:

In most cases, drug-induced nephropathy is associated with a violation of the immune response to a number of drugs (antibiotics, anesthetics, sulfa drugs, salts of heavy metals, etc.) or to vaccines and sera. 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 nephropathy, severe vasculitis often develops with involvement of the interstitial tissue in the process. The enzymopathic effect of certain drugs or their metabolites may be manifested in the predominant damage to the tubular-interstitial structures of the kidneys. The polymorphism of drug-induced nephropathies is characteristic, and one drug can cause kidney damage of various types, and exposure to different drugs can cause similar nephropathy.

Treatment:

For treatment appoint:

Treatment consists primarily in the abolition of drugs, against which nephropathy develops. Dietary and drug treatment depends on the nature of the nephropathy. With the immune genesis of nephropathy, hormones are indicated (prednisolone, triamcinolone, etc.).

Prevention consists in a careful collection of an allergic history, the lawful prescription of drugs, especially with increased sensitization to them, the prevention of the use of nephrotoxic drugs, the absence of kidney disease; in case of inevitability of drug therapy, regular monitoring of urinalysis is carried out.

This is an acute or chronic lesion of the renal glomeruli, tubules, interstitium, caused by medication. It is manifested by polyuria, oligoanuria, nocturia, hematuria, back pain, asthenic, edematous and hypertensive syndromes. Diagnosed on the basis of 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, antiaggregants, antihypertensive drugs, ZPT. With persistent chronic dysfunction, kidney transplantation 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 has increased, manifested 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 precisely with taking medications.

To the group increased risk includes older patients age group who receive long-term maintenance combined treatment about chronic somatic diseases and are subject to diagnostic procedures with the use of nephrotoxic drugs. Their share in the number of nephrological patients reaches 66%.

Causes

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

Official medicines. Renal dysfunction occurs when taking antibacterial drugs(penicillins, cephalosporins, aminoglycosides, tetracyclines, fluoroquinolones, sulfonamides, anti-tuberculosis 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 sera. Up to 23% of cases of drug-induced nephrological pathology are caused by the introduction of anti-tetanus, anti-measles, anti-staphylococcal sera, ADS, ADS-M, DPT, gonovaccine. The risk of post-vaccination or serum nephropathies increases during immunization or the introduction of ready-made antibodies to patients with a burdened allergic history, hypersensitivity to the components of the immunodrug.
Paramedical drugs. According to observations, up to 80% of the population uses funds alternative medicine. At the same time, vasoconstrictor, cytopathic, crystalluric, dysmetabolic effects are often underestimated. medicinal plants. According to the FDA, up to 32% of Ayurvedic preparations contain mercury, arsenic, lead, aristolochic acid, recognized as one of probable causes Balkan endemic nephropathy, other nephrotoxic ingredients.

Pathogenesis

The basis for the development of drug nephropathy is a combination of several pathogenetic mechanisms. Some drugs have a direct damaging effect, leading to primary damage to the cells of the proximal tubules, reabsorbing nephrotoxic chemical compound. The tubular epithelium can also be destroyed during the precipitation of crystals against the background of the use of sulfanilamide 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 violation of the filtration capacity. An independent or aggravating factor for destruction is ischemic changes tissues caused by anaphylactic shock, thrombotic microangiopathy, inhibition of prostaglandins and the renin-angiotensin system, followed by 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 can develop as a result of precipitation of circulating in the blood immune complexes, as well as 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 impaired renal microcirculation, the 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 fibres.

Classification

Diagnostics

In the event of acute renal dysfunction associated in time with the use of potentially nephrotoxic drugs, diagnosis drug nephropathy usually presents no difficulty. More thorough diagnostic search required for gradual increase renal symptoms in the patient long time accepting a certain pharmaceutical drug. For the diagnosis of drug 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 in the material, a decrease or a significant increase in relative density, erythrocytes, leukocytes, cylinders, salt crystals can be determined. To assess the reabsorption function of the tubules, the study is often supplemented with a Zimnitsky test.
Blood chemistry. An increase in creatinine levels indicates a decrease in the filtration function, uric acid, urea, change in the content of potassium, calcium, sodium, phosphorus. An imbalance of ions is possible in violation of their reabsorption. With proteinuria, hypo- and dysproteinemia occurs.
Nephrological complex. Determination of the health of the body is based on data on the content of creatinine, urea, uric acid, macronutrients. Indicative is the appearance in the urine of protein, glucose, microalbumin. As additional method Reberg's hemorenal test, Sulkovich's test is 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 Scan supplement with ultrasound, which allows assessing renal blood flow, if necessary - with tomography (MRI, CT).
Intravenous urography. According to withdrawal data contrast medium characteristics of the blood supply to the kidneys and their functional activity. Excretory urography may be supplemented by nephroscintigraphy. Due to the possible aggravation of symptoms, the examination of patients with ARF is limited.
Needle biopsy of the kidneys. Histological examination biomaterial makes it possible to most accurately assess the state of glomeruli, tubules, interstitial tissue, capillaries, arterioles. Renal 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 are possible. Differential Diagnosis performed 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 counseling the patient.

Treatment of drug nephropathy

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

Corticosteroids. Glucocorticoid therapy with medium and high doses justified in the immune pathogenesis of nephropathy, is carried out for the rapid relief of autoimmune and allergic reactions. The immunosuppressive effect includes a decrease in interstitial edema, suppression of macrophage functions, limitation of leukocyte migration in inflamed tissues, inhibition of the synthesis of inflammatory mediators and antibodies. Glucocorticosteroids effectively stabilize cell and lysosomal membranes.
Symptomatic remedies. Renal dysfunction is accompanied by the occurrence of organ and systemic disorders that require emergency correction. To restore water and electrolyte balance, hemodynamics, microcirculation, tissue perfusion, infusion therapy with the introduction of colloidal, crystalloid solutions, antiplatelet agents, anticoagulants. In violation of renin-angiotensin regulation, antihypertensive drugs are usually required.
Renal Replacement Therapy. Extrarenal blood purification is prescribed to prevent severe uremic complications in severe functional insufficiency. Hemodialysis, peritoneal dialysis, hemofiltration, hemodiafiltration can be carried out in an intermittent mode until the restoration of renal function or continuously in severe chronic renal failure. At chronic course drug-induced nephropathy may require a kidney transplant.

Forecast 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 of adequate therapy significantly increases the risk lethal outcome. In patients with chronic nephrological diseases and burdened premorbid background, there is often a persistent decrease in the filtration capacity of the kidneys, which can be somewhat slowed down by prescribing drug therapy.

For the prevention of drug nephropathy, it is necessary to adjust the doses of drugs that are metabolized in the kidneys, in accordance with the values of creatinine clearance, to refuse the use of nephrotoxic drugs in the presence of risk factors ( elderly age, female gender, intercurrent diseases, decrease in BCC), exclusion of polypharmacy.