Chronic kidney disease: can progression be stopped? M.Yu. Shvetsov leading researcher, Ph.D.

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Viznachennya KHN

1.1.1: CNH is defined as a damaged structure or function that lasts for more than 3 months and has a negative impact on a healthy person.

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Significance of stages of chronic chronic nasal congestion

1.2.1: We recommend that CCN be classified based on cause, FCS category, and albuminuria category (ACA) (1B) 1.2.2: Classify the cause of CCN based on the evidence or presence of systemic disease not the presence of this sign in the results of natural or transmitted pathological characteristics. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30.

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Determinants of plasma levels of endogenous markers

Plasma levels of endogenous markers are determined by their production (G) by cells and intake from food, extrarenal elimination (E) through the intestines and liver, and renal elimination (UV). Renal excretion is the sum of filtration load (GFR X P), tubular secretion (TS), and reabsorption (TR). Stevens LA, Levey AS. J Am SocNephrol 20:2305-2313, 2009

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Some conditions affecting the correctness of GFR calculations

Acute kidney injury Racial characteristics Extreme muscle mass Extreme body size Diet (high protein, creatinine) Muscle wasting diseases Meat consumption Drug-induced underestimation (trimethoprim, cimetidine, fenofibrate) Dialysis Underestimation due to inhibition of intestinal creatinine kinase by antibiotics Overestimation due to large fluid loss

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Formula GFR-EPI, 2009

GFR = 141 X min (Scr/κ,1)α X max (Scr/κ,1)-1.209 X 0.993 age X 1.018 [for women] X 1.159 [for African Americans] Where is the serum creatinine level (mg/dL), κ corresponds to 0.7 for women and 0.9 for men, α corresponds to –0.329 for women and –0.411 for men, min corresponds to the minimum Sk/κ or 1, and max corresponds to the maximum Sk/κ or 1. Levey AS, Stevens LA, Schmid CH, Zhang YL , Castro AF 3rd, Feldman HI, Kusek JW, Eggers P, Van Lente F, Greene T, Coresh J; CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A New Equation to Estimate Glomerular Filtration Rate. Ann Intern Med 150(9):604–12. (2009)

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Albuminuria. Terminology

Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30.

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Formulation of the diagnosis

It is recommended to classify chronic kidney disease based on the CGA category: cause (i.e. in this case, patients with diabetes mellitus may have Diabetic kidney disease), GFR category and albuminuria category Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4; 158(11):825-30

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1.3: VALUE TO THE FORECAST

greens: low rhizic (as it does not contain any other markers of illness, no chemical substances); Zhovty: postmortem movement; orange: vysokyirizik; chervoniy-duzhevysokyirizik. Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30.

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Impact of GFR and albuminuria on overall and CV mortality

1,024,977 participants (128,505 with diabetes) from 30 population-based and cohort studies at high risk of cardiovascular events 13 cohort studies in chronic kidney disease the Chronic Kidney Disease Prognosis ConsortiumLancet. Nov 10, 2012; 380(9854): 1662–1673.

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Impact of GFR and albuminuria on DKD progression

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Management of patients with DKD

American Diabetes Association (ADA); Standards of Medical Care in DiabetesDiabetes Care Volume 39, Supplement 1, January 2016

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Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30.

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Diabetic nephropathy (diabetic kidney disease)

Diabetic nephropathy (DN) is a specific kidney damage in diabetes mellitus (DM), which is characterized by gradual sclerosis of renal tissue (mainly glomeruli and interstitium) and leads to progressive loss of all renal functions.

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Diabetic kidney disease

Develops in 40-45% of patients with diabetes On average, after 10-15 years of adequate therapy Among all patients with type 2 diabetes, 25-30% have diabetic kidney disease with GFR

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Screening for diabetic kidney disease

KDOQI Diabetes Guideline: 2012 Update

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Frequency of examination of patients with DKD

Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline. Ann Intern Med. 2013 Jun 4;158(11):825-30.

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Management of patients with CKD

Patients with GFR less than 30 ml/min per 1.73 m2 should be treated by a nephrologist. Early treatment may also slow the progression of decreased kidney function. It is necessary to carry out specific treatment for the disease that causes CKD. Therapy for CKD itself is syndromic in nature and nonspecific with respect to the cause of the disease.

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Clinical syndromes in CKD

hypertension, dyslipidemia, anemia, nutritional disorders, phosphorus-calcium metabolism disorders, neuropathy.

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“...previous recommendations emphasized escalation of therapy to achieve specific LDL cholesterol targets by increasing statin doses or using drug combinations. The unproven hypothesis associated with these recommendations is that more intensive therapy will reduce cardiovascular risk without increasing side effects... KDOQI Lipid Management in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2013 ClinicalPractice Guideline//Annals of Internal Medicine

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An additional weakness of this approach is that CKD patients with low LDL cholesterol and very high cardiovascular risk are undertreated. Given the lack of evidence in patients with and without CKD, the significant variability in LDL cholesterol levels and the risk of drug toxicity (including direct effects on muscle and liver and indirect effects due to drug interactions, KDOQI Lipid Management in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2013 ClinicalPractice Guideline//Annals of Internal Medicine

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“...this approach is no longer recommended for patients with CKD and the decision to prescribe statins is based on the 10-year risk of CV events...” KDOQI Lipid Management in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2013 ClinicalPractice Guideline//Annals of Internal Medicine

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Diagnosis of anemia

Anemia is diagnosed in adults and children >15 years of age with CKD at Hb concentration

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Use of iron supplements

When prescribing iron therapy, a balance must be struck between the benefits of avoiding the need for blood transfusions, the use of erythropoietins and symptoms associated with anemia and the risk of adverse individual reactions (i.e., anaphylactic and other reactions and unknown long-term effectiveness For adult patients with CKD with anemia, for those not receiving erythropoietin therapy, it is recommended to try starting IV iron therapy

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Use of erythropoietins

Rule out all correctable causes of anemia, including iron deficiency, before initiating erythropoietin therapy. When initiating erythropoietin therapy, a balance must be struck between the benefits of avoiding the need for blood transfusions, and the symptoms associated with anemia and the risk of individual adverse reactions (eg, stroke, loss of vascular access , hypertension) It is recommended to use erythropoietins with great caution, especially in cancer patients and patients who have had a stroke

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erythropoietin Beta intravenously or subcutaneously (20 IU/kg 3 times a week or 60 IU/kg once a week) erythropoietin receptor activator (120 - 360 mcg once a month, 60 - 180 mcg twice a month)

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Red blood cell transfusion

During therapy, it is recommended to avoid, if possible, transfusions of red blood cells, especially for patients who are planning a kidney transplant. Transfusion may be possible for patients with ineffective erythropoietin therapy, or when erythropoietin therapy is contraindicated. The decision should not be based on the hemoglobin level, but on the severity of the symptoms of anemia

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Phosphorus-calcium metabolism disorders.

Disorders of phosphorus-calcium metabolism begin when GFR decreases to less than 60 ml/min/1.73 m2, and the severity depends on the stage of CKD. The level of calcium, phosphorus and intact parathyroid hormone must be determined in patients with stage III CKD. every 12 months, in patients of stage IV. CKD every 3 months and in patients with stage V, the level of intact parathyroid hormone should be determined every 3 months, and the level of calcium and phosphorus every month.

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Correction of phosphorus-calcium metabolism

Calcium supplements Active metabolites of vitamins D2 and D3 (Alpha D3) Phosphorus binders (Renagel, lanthanum carbonate)

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Parathyroidectomy

Parathyroidectomy may be recommended for iPTH levels greater than 800 mg/mL and concurrent hypercalcemia and hyperphosphatemia uncontrolled by medications. The decision to undergo parathyroidectomy should be preceded by at least a 3-month course of vitamin D therapy, if it is ineffective.

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Replacement therapy

Performed for patients with stage V CKD Programmed hemodialysis Peritoneal dialysis Kidney transplantation

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Description of the presentation by individual slides:

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Lecture SP for chronic renal failure PM.02. MDK 02.01. SP for pathology of the urinary system State budgetary educational institution of secondary vocational education "Medical College No. 8 of the Moscow Department of Health" Therapy teacher Denyusheva E.K.

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Contents of the educational material for the theoretical lesson Chronic renal failure. Definition. Stages. Clinical manifestations of chronic renal failure. Forecast. Features of diet, drinking regimen and use of table salt. Drug therapy. Methods of dialysis and plasmapheresis. The essence of methods. Diet and drinking regimen of a patient on dialysis. Typical patient problems. Prevention. Clinical examination.

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After studying the topic, the student should know: definitions of the concepts “acute renal failure”, “chronic renal failure”; stage of chronic renal failure; clinical manifestations of chronic renal failure; features of diet for chronic renal failure; the essence of dialysis methods, plasmapheresis for chronic renal failure; the importance of diet in dialysis patients; typical patient problems; prevention, rehabilitation.

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Acute renal failure A syndrome of sudden, rapid decline or cessation of function of both kidneys (or a single kidney), leading to a sharp increase in nitrogen metabolic products in the body.

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Acute renal failure - clinical picture Develops within a few hours to 1-7 days. Lasts more than 24 hours. The prognosis is positive with timely treatment and correct treatment. ARF is always a complication of other pathological processes in the body.

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Acute renal failure - clinical stage I - initial (shock) - before the first kidney symptoms appear (from several hours to several days): Symptoms of intoxication Pallor Nausea Abdominal pain.

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Acute renal failure - clinical stage II - oligoanuric (from several days to 3-4 weeks): Oliguria or anuria - sharp levels of urea and other protein metabolic products in the blood (self-poisoning of the body) Symptoms of central nervous system damage: lethargy, adynamia, drowsiness, headache, convulsions; Symptoms of intoxication: diarrhea, abdominal pain, tachycardia, noisy deep breathing, signs of liver failure: enlarged liver, dry skin, dry tongue, covered with a brown coating.

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Acute renal failure - clinical stage III - recovery (up to 2 weeks) polyuria from 300 to 3000-5000 ml/day, the functions of all organs and systems are restored. Stage IV – recovery (from 20 days to several months) anatomical and functional restoration of renal activity to initial parameters. Erythropoiesis is restored within 1-2 years.

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Chronic renal failure - etiology Chronic glomerulonephritis (damage to the glomerular apparatus of the kidneys). Secondary kidney damage: - diabetes mellitus type 1 and 2; - arterial hypertension; - systemic connective tissue diseases; - viral hepatitis “B” and/or “C”; - systemic vasculitis; - gout; - malaria. Chronic pyelonephritis. Urolithiasis, urinary tract obstruction. Anomalies in the development of the urinary system. Polycystic kidney disease. Effect of toxic substances and drugs.

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Chronic renal failure - pathogenesis 1. Excretion of end products of nitrogen metabolism and foreign substances is impaired - accumulation of nitrogenous wastes in the body. 2. Violation of water and electrolyte balance: The first stage is polyuria, dehydration of the body  thirst, dry skin, drinking large amounts of liquid, The second stage is overhydration → edema, left ventricular heart failure. 3. Change in acid-base balance: acidosis, in the terminal stage vomiting, diarrhea → loss of sodium and chlorides → hypochloremic alkalosis occurs.

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Chronic renal failure - Latent clinic (decrease in glomerular filtration to 40-60 ml/min, diuresis 1.5 - 1.8 l/day) is not clinically manifested, mild fatigue and dry mouth are possible; BAC: slight disturbances in the electrolyte composition of the blood, sometimes protein in the urine. Compensated (glomerular filtration 15-40 ml/min, diuresis 1.8 - 2.5 l/day) clinical manifestations are more pronounced, persistent hypertension, nocturia, weakness, fatigue, loss of appetite, nausea, vomiting, weight loss, thirst , dryness and unpleasant taste in the mouth.

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Chronic renal failure - Intermittent clinic - electrolyte and acid-base balance is disturbed, diuresis is 1.0-1.5 l/day. general weakness, increased fatigue; decreased or lack of appetite, thirst, nausea, vomiting in the morning, on an empty stomach; stable DAG. Conservative therapy makes it possible to maintain performance. UAC: anemia. BAK: stable products of nitrogen metabolism (protein) - level of urea, creatinine. Objectively, loss of body weight, atrophy of subcutaneous tissue, dry, flabby skin with a yellowish tint, traces of scratching, bruising, muscle tone ↓, small muscle twitching, tremor of fingers and hands, smell of ammonia from the mouth, pain in bones and joints.

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Chronic renal failure - Terminal clinic (glomerular filtration below 15-20 ml/min) severe dysfunction of organs and systems, changes in them are irreversible; polyuria → oliguria; lethargy, apathy + inhibition and inappropriate behavior; a sharp decrease in appetite (up to anorexia), dryness and unpleasant taste in the mouth, frequent nausea; severe weakness, chilliness, sleep disturbance, itchy skin, tonic cramps of the calf muscles. The malignant nature of hypertension → a sharp decrease in vision, acute LV failure with pulmonary edema. Objectively: the face is puffy, gray-yellow in color, itchy skin, marks from scratching, dull and brittle hair. the tongue is coated, aphthous stomatitis, the abdomen is swollen, the voice is hoarse. The breath smells of ammonia, diarrhea, foul-smelling, dark-colored stools. Monoarthritis due to secondary gout, pain in the bones and spine (hyperparathyroidism), paresthesia and severe weakness in the lower extremities (polyneuropathy), nosebleeds. BAC: constant amount of urea, creatinine, uric acid, the electrolyte composition of the blood is disturbed.

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Chronic kidney disease - stages of CKD (chronic kidney disease) I: kidney damage with normal or increased GFR (90 ml/min/1.73 m2). No chronic renal failure. CKD II: moderate decrease in GFR (60-89 ml/min/1.73 m2). Initial stage of chronic renal failure. CKD III: moderate degree of reduction in GFR (30-59 ml/min/1.73 m2). Chronic renal failure is compensated. CKD IV: significant decrease in GFR (15-29 ml/min/1.73 m2). Decompensated chronic renal failure. CKD V: kidney damage with end-stage renal failure (< 15 мл/мин/1,73 м2).

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Chronic renal failure - diagnosis of UAC - anemia (↓ hemoglobin and red blood cells), signs of inflammation (acceleration of ESR, moderate > leukocyte count), tendency to bleeding (↓ platelet count). BAK - > products of nitrogen metabolism (urea, creatinine, residual nitrogen in the blood), disturbance of electrolyte metabolism (levels of potassium, phosphorus and ↓ calcium), total protein in the blood decreases, hypocoagulation (↓ blood clotting), cholesterol in the blood, total lipids. Urinalysis - proteinuria, hematuria, cylindruria (indicates the degree of kidney damage). Rehberg-Toreev test - to assess the excretory function of the kidneys - glomerular filtration rate (GFR). This indicator is the main one for determining the degree of renal failure and the stage of the disease.

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Chronic renal failure - diagnosis by ultrasound of the urinary system with pulsed Doppler (determining renal blood flow) - assess the severity of kidney damage. A puncture biopsy of the kidneys - to make an accurate diagnosis, determine the course of the disease, and assess the degree of kidney damage. X-ray (survey, contrast) examination of the kidneys is carried out only for patients with I – II degrees of renal failure.

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Chronic renal failure - treatment At stage I: treatment of the underlying disease. Stopping the exacerbation of the inflammatory process in the kidneys reduces the severity of renal failure. At stage II: + evaluate the rate of progression of renal failure and use drugs to slow down its rate. At stage III: identify and treat possible complications, use drugs to slow down the rate of progression of renal failure. Correction of impaired functions of all organs and systems. At stage IV: the patient is prepared for renal replacement therapy. At stage V: renal replacement therapy is carried out.

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Chronic renal failure - hemodialysis An extrahepatic method of blood purification, during which: - toxic substances are removed from the body, - disturbances in water and electrolyte balances are normalized. It is carried out by filtering blood plasma through the semi-permeable membrane of the artificial kidney apparatus. Treatment with maintenance hemodialysis is carried out at least 3 times a week, with a duration of one session of at least 4 hours.

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Chronic kidney disease. Chronic renal failure. 1 Definition 2 Formulation of diagnosis according to ICD-10 3 Clinical picture 4 Risk factors 5 Classification of CKD 6 Criteria for diagnosing CKD 7 Treatment 8 Prevention 9 Summary. Plan:.

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Renal filtration function The formula is simple, but it is also advisable to standardize the resulting value to the surface of the patient’s body. The Cockcroft-Gault formula has been successfully used widely for many years - not only in nephrology, but also in clinical pharmacology and other areas of medicine. In patients with a decrease in GFR less than 30 ml/min, this formula may give inaccurate results.

It is detected in clinics and hospitals by doctors of therapeutic specialties (therapists, cardiologists, endocrinologists). Patients with CKD are treated by a general practitioner. Specialized nephrological care is provided by a nephrologist, as well as specialists in replacement therapy. Consultation with a nephrologist is advisable in the following cases: GFR<30 мл/мин (ХБП 4–5 стадий). СКФ 30–60 мл/мин (ХБП 3 стадии) с быстрым снижением функции почек или с риском быстрого снижения функции почек: прогрессирующее снижение СКФ (более 15% за 3 месяца), протеинурия более 1 г/сут, выраженная и неконтролируемая артериальная гипертония, анемия (гемоглобин менее 110 г/л). При впервые выявленной сниженной скорости клубочковой фильтрации (СКФ) до 30–60 мл/мин следует оценить стабильность нарушения функции почек. Повторное обследование проводится через 2–4 недели и далее через 3–6 месяцев. Тактика ведения пациентов с ХБП

Blood pressure measurement, fundus examination, GFR and creatinine, lipid profile, glucose, complete blood count (hemoglobin), urinalysis, daily microalbuminuria (proteinuria). Frequency – annually. At stage 3: Plus additionally: potassium, sodium, calcium, phosphorus, uric acid. Frequency - once every six months, with a stable course (decrease in GFR less than 2 ml/min over 6 months) - annually For stages 4-5: Plus additionally: parathyroid hormone, bicarbonate. Frequency - once a quarter, with a stable course (decrease in GFR less than 2 ml/min over 6 months) - once every six months Diagnostic measures for CKD (K/DOQI, 2006)

Treatment: ACEI or ARB Diuretic or Non-DHP ant. Ca ACE inhibitor + ARB Diuretic or Non-DHP ant. Ca Addition of centrally acting drugs Replacement of Non-DGP ant. Sa on DGP ant. Ca + betta AB Addition alpha AB

Nephroprotective therapy consists of drugs that block the RAS - ACE inhibitors and angiotensin receptor blockers, which is associated with its key role in the progression of nephrosclerosis treatment

A heterogeneous group of drugs that differ in their effects on central and renal hemodynamics A pronounced antihypertensive effect that persists in drugs with prolonged action throughout the day Additional organo- and vasoprotective effects Do not cause metabolic disorders Non-hydropyridine drugs reduce intraglomerular pressure and proteinuria Nefidipines can increase intraglomerular pressure and proteinuria, cause activation of the sympathoadrenal system Nonhydropyridines cannot be combined with beta blockers, which limits the possibility of combined treatment of severe renal hypertension

For forms of CKD and diabetes mellitus, the drugs of choice are non-dihydropyridine calcium antagonists, which, unlike dihydropyridines, do not increase glomerular pressure and do not increase proteinuria.

A heterogeneous group of drugs that have different effects on electrolyte metabolism Have a pronounced antihypertensive effect and reduce the risk of cardiovascular complications Correction of hypertension usually requires small doses Effectiveness of diuretic combinations with different mechanisms of action: Saluretic + potassium-sparing Thiazide + loop Intermittent use of diuretics is ineffective In CKD 3B- 5 Thiazides are ineffective. The drugs of choice are loop diuretics. Sensitivity to them decreases as kidney function declines. The danger of aggravating hyperuricemia and urate crisis when using thiazides and loop diuretics. Aldosterone antagonists (aldactone, eplerenone) suppress the processes of myocardial remodeling and nephrosclerosis. The danger of hyperkalemia and breast cancer in men (aldactone)

Suppress the hyperreactivity of the sympathoadrenal system that develops in CKD Make an additional contribution to the suppression of the renin-angiotensin system Reduce the risk of cardiovascular complications “-” Frequent side effects: Bronchoobstruction Bradycardia Vasoconstriction Erectile dysfunction Depression, insomnia Metabolic disorders (rarely occur when using therapeutic doses) Not their combination with non-hydropyridine calcium antagonists is recommended. Beta-blockers do not have proven nephroprotective properties.

It consists of identifying and eliminating relevant risk factors. The fight against them remains important at the stage of secondary prevention, allowing, along with reducing the rate of deterioration of kidney function, to also reduce the risk of cardiovascular complications. prevention

Food. Limit the consumption of canned food, food concentrates, and instant foods as much as possible. Control your weight: avoid excess weight and do not lose it suddenly. Eat more vegetables and fruits, limit high-calorie foods and exclude canned food. Drink more liquid, 2-3 liters, especially in the hot season: fresh water, green tea, herbal teas, natural fruit drinks, compotes. Do not smoke, do not abuse alcohol. Exercise regularly (this is no less important for the kidneys than for the heart!) - if possible, 15-30 minutes a day or 1 hour 3 times a week. TEN GOLDEN RULES to keep your kidneys healthy

Painkillers (if it is impossible to completely refuse them, limit intake to 1-2 tablets per month), do not take diuretics on your own without a doctor’s prescription, do not self-medicate, do not get carried away with nutritional supplements, do not experiment on yourself by using “Thai herbs” with unknown composition, “fat burners” that allow you to “lose weight once and for all without any effort on your part.” Protect yourself from contact with organic solvents and heavy metals, insecticides and fungicides at work and at home (when repairing, servicing a machine, working in your garden, etc.), use protective equipment. Do not overexpose yourself to the sun, avoid hypothermia in the lumbar region, pelvic organs, and legs. Monitor blood pressure, blood glucose and cholesterol levels. Regularly undergo medical examinations to assess the condition of the kidneys (general urine test, blood creatinine, ultrasound - once a year).

Disability in patients with CKD cannot be assessed, since they depend on the etiology and characteristics of the course of nephropathy, response to pathogenetic and nephroprotective therapy. The overwhelming number of patients with CKD stages 4-5, regardless of the therapy, have varying degrees of permanent disability. EVN

A highly specialized, “nephrological”, but a general medical problem: the costs of renal replacement therapy constitute a significant part of national health care budgets; the main causes of end-stage renal failure are not primary kidney diseases (glomerulonephritis, hereditary kidney diseases), but secondary nephropathies (diabetic, hypertensive, ischemic); the main cause of death in patients with chronic kidney disease is not uremia, but cardiovascular complications, which occur in patients with impaired renal function tens of times more often than in the general population and have their own characteristics; summary

Chronic kidney disease at an early stage is not experienced by nephrologists, but by representatives of other specialties (endocrinologists, cardiologists), therapists and general practitioners, who are primarily approached and under the supervision of patients at risk of developing chronic kidney disease; the presence of chronic kidney disease limits many treatment and diagnostic methods widely used in the population (some antibiotics and antihypertensive drugs, non-steroidal anti-inflammatory drugs and analgesics, radiocontrast agents, other potentially nephrotoxic drugs, any drugs excreted by the kidneys) the task of monitoring patients with chronic kidney disease, ensuring effective nephroprotective therapy and achieving recommended target clinical and laboratory parameters can only be achieved through the joint efforts of the entire medical community

"renal failure" is used to refer to end-stage chronic kidney disease. The diagnosis of “Chronic kidney disease” (even in the absence of a decrease in GFR) implies inevitable further progression of the process and is intended to attract the attention of a doctor. It is the potential for loss of kidney function that is the most important point in understanding the term “chronic kidney disease”.