Renal failure: what you need to know

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Renal failure: what you need to know

I. Anatomy and physiology of the kidneys: the basis of understanding renal failure

For a complete understanding of pathogenesis, clinical manifestations and methods of treating renal failure (Mon), a clear idea of ​​the structure and functions of the kidneys is necessary. The kidneys are paired organs located in the retroperitoneal space on both sides of the spine.

  • Macroscopic structure: Each kidney has a bean -shaped shape and is surrounded by a fibrous capsule. Inside the kidneys, a cortical layer (external) and brain layer (internal) is distinguished. The brain layer consists of renal pyramids, the peaks of which (papillae) open into small renal cups. Small cups merge into large renal cups, which, in turn, form the renal pelvis. The pelvis goes into the ureter, according to which the urine enters the bladder.

  • Microscopic structure (nephron): The main structural and functional unit of the kidney is nephron. Each nephron consists of:

    • Renal body (glomerulus): Capillary glomerulus (Glomerula), surrounded by the capsule of Bowman-Smumlyansky. Glumber is a network of interwoven capillaries in which blood plasma filters.
    • Proximal convoluted tubules: The longest and most convincing section of the nephron, in which reabsorption of most of the filtered water, electrolytes, glucose, amino acids and other substances occurs.
    • Henle loops: U-shaped structure consisting of descending and rising knees. He plays a key role in the concentration and breeding of urine.
    • Distant convoluted tubules: Participates in the regulation of electrolyte balance and pH of blood.
    • Collective tube: Collects urine from several nephrons and transports it to the renal cups.

  • Kidney functions: The kidneys perform many vital functions:

    • Excretory (excretory): Removing the final metabolic products (urea, creatinine, uric acid), toxins, excess water, electrolytes and drugs from the body. The filtering of blood plasma in glomerulus and the subsequent reabsorption of nutrients and the secretion of harmful substances in the tubules provide urine.
    • Regulatory:
      • Water-electrolyte balance: Maintaining the optimal volume of fluid in the body and the concentration of electrolytes (sodium, potassium, chlorine, calcium, phosphorus).
      • Acid-base balance (pH of blood): Regulation of the concentration of bicarbonates and other buffer systems.
      • Arterial pressure: The synthesis of renin, hormone participating in the regulation of blood pressure.
      • Erithophoes: The synthesis of erythropoetin, hormone, stimulating the formation of red blood cells in the bone marrow.
      • Vitamin D metabolism: Activation of vitamin D necessary for the absorption of calcium in the intestine and maintaining bone health.
    • Endocrine: The synthesis of hormones, such as renin, erythropoetin and the active form of vitamin D.

Violation of any of these functions leads to serious consequences for the body and is the basis of the pathophysiology of renal failure.

II. Definition and classification of renal failure

Renal failure (Mon) is a clinical syndrome characterized by a progressive decrease in the function of the kidneys leading to a violation of the water-electrolyte, acid-base balance, the accumulation of nitrogenous slags and other toxic substances (uremia) in the body.

There are various PN classifications based on the speed of development, the severity of lesion and etiology.

  • By speed of development:

    • Acute renal failure (OPN): Quick (within a few hours or days) reduction of kidney function. Usually reversible with timely and adequate treatment.
    • Chronic renal failure (KHPN): A gradual (for several months or years) irreversible decrease in kidney function.

  • In the severity of the lesion (based on the speed of glomerular filtration – SKF): Classification of KHPN according to the stages proposed by the National Kidney Foundation (NKF) is the most common and allows you to evaluate the severity of kidney damage and choose the optimal treatment tactics:

    • Stage 1: SKF ≥ 90 ml/min/1.73 m2 (kidney damage with normal or increased SCF). There may be signs of kidney damage, such as proteinuria or changes in urinary sediment.
    • Stage 2: SKF 60-89 ml/min/1.73 m2 (kidney damage with a slight decrease in SKF).
    • Stage 3: SKF 30-59 ml/min/1.73 m2 (moderate decrease in SKF).
    • Stage 4: SKF 15-29 ml/min/1.73 m2 (pronounced decrease in SKF).
    • Stage 5: SKF <15 ml / min / 1.73 m2 (terminal stage of the start of lack of lack). We will need replace the initial therapy (dializ or transplant).

  • By etiology (reason):

    • Tubeelon Mon: It is caused by a decrease in renal blood flow (for example, due to dehydration, blood loss, heart failure).
    • Renal Mon: It is caused by damage to the kidney tissue (for example, glomerulonephritis, pyelonephritis, acute tubular necrosis).
    • PN Pon: It is caused by obstruction of the urinary tract (for example, stones, tumors, strictures).

Understanding the classification of PN is necessary to determine the prognosis, the choice of tactics of treatment and monitor the patient’s condition.

III. Acute renal failure (OPN): causes, pathogenesis, clinical picture, diagnosis and treatment

Acute renal failure (OPN) is a sudden decrease in the function of the kidneys, leading to delayed nitrogen slag and impaired water-electrolyte balance.

  • Causes of the OPN:

    • Interchanting causes (reduction of renal blood flow):
      • Hypovolemia (dehydration, blood loss, burns).
      • Heart failure (decrease in cardiac output).
      • Sepsis (vascular expansion and reduction of blood pressure).
      • Medicines (NSAIDs, ACE inhibitors, diuretics).
    • Renal causes (damage to the renal fabric):
      • Acute tubular necrosis (Two) is the most common cause of the Renal OPN, caused by ischemia of the kidneys (for example, with prolonged hypotension) or nephrotoxic substances (for example, aminoglycosides, radiocontraduate substances).
      • Acute glomerulonephritis (inflammation of the glomeruli).
      • Acute interstitial nephritis (tissue inflammation between tubules).
      • Thrombotic microangiopathy (TMA) – damage to the small vessels of the kidneys.
    • Wrestling reasons (obstruction of the urinary tract):
      • Stones in the urinary tract.
      • Urinary tumors.
      • Urinary strictures.
      • An increase in the prostate gland.

  • Pathogenesis of OPN:

    • Business OPN: A decrease in renal blood flow leads to a decrease in glomerular filtration (SKF) and delayed nitrogen slag. The kidneys are trying to compensate for a decrease in blood flow due to the activation of the renin-angiotensin-aldosterone system (RAS), which leads to sodium and water delay.
    • Renal OPN: Damage to the kidney tissue leads to impaired filtration, reabsorption and secretion in the tubules. TIN is characterized by damage to the epithelial cells of the tubules, which leads to their necrosis and obstruction of the tubules. Glomerulonephritis is characterized by inflammation of the glomeruli, which leads to a decrease in the permeability of the filtration membrane and proteinuria.
    • Wrestling OPN: Options of urinary tract leads to an increase in pressure in renal pelvis and tubules, which reduces SKF. Long -term obstruction can lead to irreversible damage to the renal tissue.

  • Clinical picture of the OPN:

    • Oliguria or anuria: Decrease in diuresis (amount of urine) less than 400 ml per day (oliguria) or complete absence of urine (anuria). However, in some cases, CPS can occur with normal or even increased diuresis (Neoliguric OPN).
    • Swelling: The delay in fluid in the body leads to the appearance of edema on the legs, face and lungs (pulmonary edema).
    • Improving blood pressure: The delay in sodium and water leads to an increase in the volume of circulating blood and an increase in blood pressure.
    • Electrolyte balance violations: Hyperkalemia (increasing the level of potassium in the blood) is the most dangerous complication that can lead to heart rhythm disturbances. Hyponatremia (decreasing the level of sodium in the blood) – can lead to neurological symptoms.
    • Acidosis: Violation of the excretion of acids from the body leads to metabolic acidosis.
    • Uremia: The accumulation of nitrogen slag (urea, creatinine) in the blood leads to uremic intoxication, which is manifested by nausea, vomiting, weakness, drowsiness, itching of the skin, pericarditis, encephalopathy.

  • Diagnosis of the OPN:

    • Anamnesis and physical examination: It is important to establish the possible causes of the OPS (for example, taking nephrotoxic drugs, the presence of a history of kidney diseases). Physical examination allows you to assess the state of hydration, blood pressure, the presence of edema.
    • Blood tests:
      • Creatinin and urea: an increase in the level of creatinine and urea in the blood is the main sign of the OPN.
      • Electrolytes (potassium, sodium, chlorine): to identify electrolyte balance disorders.
      • Blood gases: to detect metabolic acidosis.
      • General blood test: to identify anemia and other changes.
    • Urine analysis:
      • Proteinuria: The presence of protein in the urine may indicate damage to glomeruli.
      • Urine sediment: the presence of cylinders (hyalin, granular, epithelial) may indicate damage to the tubules.
      • Microgematuria: the presence of red blood cells in the urine may indicate damage to glomeruli or urinary tract.
      • Opmolar urine: to assess the concentration ability of the kidneys.
    • Ultrasound study of the kidneys (ultrasound): To exclude obstruction of the urinary tract.
    • Kidney biopsy: In some cases, a kidney biopsy may be required to establish the cause of the Renal CPN.
    • Determination of glomerular filtration rate (SKF): SKF is calculated based on the level of creatinine in the blood and allows you to evaluate the function of the kidneys.

  • Treatment of OPN:

    • Elimination of the cause of the CPS: Treatment should be aimed at eliminating the cause that caused the OPN. For example, with a crossroads, it is necessary to restore the volume of circulating blood, with a triumphant OPN – to eliminate the obstruction of the urinary tract.
    • Correction of water-electrolyte balance: Introduction of solutions for dehydration correction and electrolyte disorders. With hyperkalemia, drugs that reduce the level of potassium in the blood are prescribed (for example, calcium gluconate, glucose insulin, potassium -binding resins).
    • Acidosis correction: Introduction of a solution of sodium bicarbonate to correct metabolic acidosis.
    • Diuretic therapy: The purpose of diuretics (for example, furosemide) to stimulate diuresis. Caution should be used diuretics for an interruption of the CPS, as they can aggravate dehydration.
    • Dialysis: In severe UPS, especially with the development of uremia, hyperkalemia, pulmonary edema or severe acidosis, dialysis (hemodialysis or peritoneal dialysis) may be required to remove nitrogenous slag and excess of fluid from the body.
    • Nutrition: Restriction of protein and potassium consumption with food.

The prognosis of the OPN depends on the cause, severity and timeliness of treatment. With timely and adequate treatment, the function of the kidneys is usually restored. However, in some cases, CPS can lead to chronic renal failure or death.

IV. Chronic renal failure (HPN): causes, pathogenesis, clinical picture, diagnosis and treatment

Chronic renal failure (HPN) is a slow and irreversible decrease in the function of the kidneys, leading to the accumulation of nitrogenous toxins and a violation of the water-electrolyte, acid-base balance.

  • Causes of KHPN:

    • Diabetes mellitus (diabetic nephropathy): The most common reason for KHPN. A high level of glucose in the blood leads to damage to the glomerulus of the kidneys.
    • Arterial hypertension (hypertensive nephropathy): Increased blood pressure leads to damage to the blood vessels.
    • Glomerulonephritis: Inflammation of the glomerulus of the kidneys.
    • Pyelonephritis: Chronic kidney inflammation.
    • Polycystic kidney: A hereditary disease characterized by the formation of many cysts in the kidneys.
    • Uroline disease (obstructive nephropathy): Long -term obstruction of the urinary tract can lead to damage to the renal tissue.
    • Reflux-Nefropathy: The reverse casting of urine from the bladder to the kidneys.
    • Medicines: Long -term intake of certain drugs (for example, NSAIDs, analgesics) can lead to CPN.
    • Hereditary kidney diseases: For example, alport syndrome.

  • Pathogenesis of CKD:

    • Loss of nephrons: Damage to the renal tissue leads to the death of nephrons.
    • Hyperfiltration: The remaining nephrons are trying to compensate for the loss of function, increasing their filtration load (hyperfiltration). Hyperfiltration over time leads to damage to glomeruli and the progression of CPN.
    • Proteinuria: Damage to the glomeruli leads to an increase in the permeability of the filtration membrane and loss of protein in urine (proteinuria). Proteinuria is one of the factors of the progression of CPN.
    • Sclerosis: Damage to the renal tissue leads to the development of sclerosis (replacing the normal tissue with connective tissue). Sclerosis leads to a further decrease in kidney function.
    • Activation Raus: A decrease in the function of the kidneys leads to the activation of the renin-angiotensin-aldosterone system (RAAS), which contributes to sodium and water delay, increased blood pressure and the progression of CPN.
    • Fibroz: Damage and inflammation in the kidneys stimulate the production of growth factors, which lead to fibrosis, that is, the replacement of the normal tissue of the kidneys with scar tissue. This is an irreversible process that worsens the function of the kidneys.

  • Clinical picture of KHPN: The clinical picture of KHPN develops gradually, as the disease progresses. In the early stages of KHPN can be asymptomatic.

    • General symptoms:
      • Weakness and fatigue.
      • Decrease in appetite.
      • Nausea and vomiting.
      • Itching of the skin.
      • Sleep violation.
    • Symptoms associated with impaired water-electrolyte balance:
      • Swelling.
      • Increasing blood pressure.
      • Convulsions.
      • Heart rhythm disturbances.
    • Symptoms associated with uremic intoxication:
      • Uremic smell from the mouth.
      • Uremic pleurisy and pericarditis.
      • Encephalopathy (violation of consciousness, cramps, coma).
      • Anemia.
      • Osteodistrophy (violation of bone metabolism).
    • Symptoms associated with impaired endocrine kidney function:
      • Anemia (reduction in erythropoietin production).
      • Osteodistrophy (violation of activation of vitamin D).
      • Violation of reproductive function.

  • CHPN diagnostics:

    • Anamnesis and physical examination: It is important to establish possible causes of CPN (for example, diabetes mellitus, arterial hypertension, a history of kidney disease). Physical examination allows you to evaluate blood pressure, edema, skin condition.
    • Blood tests:
      • Creatinin and urea: an increase in the level of creatinine and urea in the blood is the main sign of KHPN.
      • Electrolytes (potassium, sodium, chlorine, calcium, phosphorus): to identify electrolyte balance disorders.
      • Blood gases: to detect metabolic acidosis.
      • General blood test: to detect anemia.
      • Paratgormon (PTG), vitamin D: to assess the state of bone metabolism.
    • Urine analysis:
      • Proteinuria: The presence of protein in the urine is an important sign of HPN and a factor in the progression of the disease.
      • Urine sediment: to detect signs of inflammation or damage to the renal tissue.
    • Ultrasound study of the kidneys (ultrasound): To assess the size and structure of the kidneys, the exclusion of uterine obstruction.
    • Kidney biopsy: In some cases, a kidney biopsy may be required to establish the cause of CPN and assess the degree of damage to the renal tissue.
    • Determination of glomerular filtration rate (SKF): SKF is calculated on the basis of the level of creatinine in the blood and allows you to evaluate the function of the kidneys and the stage of KHPN. For a more accurate assessment of SKF, additional markers can be used, such as cystatin S.

  • CHPN treatment: CHPN treatment is aimed at slowing the progression of the disease, monitoring symptoms and preventing complications.

    • Treatment of the underlying disease: It is important to treat the underlying disease that led to CPN (for example, diabetes mellitus, arterial hypertension, glomerulonephritis).
    • Control of blood pressure: Maintaining blood pressure at a level below 130/80 mm Hg. Art. Slets the progression of HPN. To control blood pressure, ACE inhibitors, angiotensin II (sconces), diuretics and other antihypertensive drugs are used. ACE and sconces also have nephroprotective effects, reducing proteinuria.
    • Decrease in proteinuria: A decrease in proteinuria slows down the progression of CPN. To reduce proteinuria, ACE, sconces and other drugs are used.
    • Protein consumption restriction: The restriction of protein consumption with food reduces the formation of nitrogenous toxins and reduces the load on the kidneys.
    • Control of phosphorus and calcium: To prevent osteodistrophy, it is necessary to maintain a normal level of calcium, phosphorus and parathormone in the blood. To reduce the level of phosphorus, phosphate -binding drugs (for example, Severmer, Lantan) are used. To increase the level of calcium and activation of vitamin D, vitamin D preparations are used (for example, calcitriol, alfacalcedel).
    • Anemia correction: Erythropoietin preparations (for example, epietin, darbepoetin) are used to correct anemia.
    • Acidosis correction: To correct metabolic acidosis, a sodium bicarbonate solution is used.
    • Diet: A special diet with a restriction of protein, phosphorus, potassium and sodium.
    • Plast Presidential Personal Therapy (ZPT): At the terminal stage of KHPN (SKF <15 ml/min/1.73 m2), renal replacement therapy is required:
      • Hemodializ: The procedure for cleaning blood from nitrogenous toxins and excess fluid using a special apparatus (“artificial kidney”).
      • Peritoneal dialysis: The blood purification procedure using the peritoneal membrane, which is used as a filter.
      • Kidney transplantation: Transplanting donor kidney. It is the most effective method of treating the terminal stage of KHPN, as it allows you to restore the function of the kidneys and improve the quality of the patient’s life.

The forecast of CPN depends on the cause, severity and timeliness of treatment. With adequate treatment, you can slow down the progression of the disease and improve the quality of the patient. However, KHPN is a progressive disease, which can ultimately lead to death.

V. Complications of renal failure: pathogenesis, prevention and treatment

The renal failure, both acute and chronic, leads to numerous complications that affect almost all organs and systems of the body. These complications significantly worsen the quality of life of patients and are the main cause of mortality.

  • Cardiovascular complications: Are the most common cause of death in patients with CPN.

    • Arterial hypertension: Sodium and water delay, RAS activation, increased activity of the sympathetic nervous system. Treatment: restriction of salt, diuretics, ACE inhibitors/sconces, beta-blockers, calcium channel blockers.
    • Heart failure: Overload with volume, arterial hypertension, coronary heart disease, uremic cardiomyopathy. Treatment: limiting fluid and salt, diuretics, ACE/sconces, beta-blockers, digoxin.
    • Corny heart (coronary heart disease): Accelerated atherosclerosis, hypergomocysteinemia, anemia, disturbances in phosphorus-calcium metabolism. Treatment: modification of risk factors (smoking, dyslipidemia, arterial hypertension, diabetes mellitus), antiplatelets, statins, beta-blockers, nitrates, revascularization (angioplasty, shunting).
    • Heart rhythm disturbances: Hyperkalemia, hypokalemia, acidosis, uremia. Treatment: correction of electrolyte disorders and acidosis, antiarrhythmic drugs, implantation of the cardioverter-defibrillator.
    • Pericarditis: Uremic intoxication, inflammation. Treatment: intensive dialysis, anti -inflammatory drugs.
    • Stroke: Arterial hypertension, atherosclerosis, blood coagulation disorders. Treatment: prevention of arterial hypertension and atherosclerosis, antiplatelets, anticoagulants (with caution).

  • Complications from bone tissue and mineral metabolism (mineral and bone violations for KHPN – MKN -HPN):

    • Secondary hyperparathyroidism: A decrease in the level of calcitriol (active form of vitamin D) leads to a decrease in the absorption of calcium in the intestines and hypocalcemia. Hypokalcemia stimulates the production of parathormone (PTG), which leads to parachitaic gland hyperplasia and an increase in the level of PTH.
    • Hyperphosphatemia: A decrease in the excretion of phosphorus by the kidneys leads to hyperphosphatemia. Hyperphosphatemia suppresses the production of calcitriol and contributes to the development of secondary hyperparathyroidism.
    • Renal osteodistrophy: Violation of bone metabolism, including osteomalization, omnes fibrosis, adynamic bone disease and mixed uremic osteodistrophy.
    • Calcification of soft tissues: The deposition of calcium in soft tissues, such as blood vessels, heart, lungs and skin. Treatment: restriction of phosphorus in a diet, phosphate -binding preparations, vitamin D, calcium drugs (reduce PTH levels), parathyroidctomy (removal of parathyroid glands).

  • Hematological complications:

    • Anemia: Reducing erythropoetin production, iron deficiency, bone marrow inhibition with uremic toxins, blood loss. Treatment: erythropoetin preparations, iron preparations, blood transfusion (in extreme cases).
    • Blood coagulation disorders: Platelet dysfunction, violation of the synthesis of coagulation factors. Treatment: desmopressin, erythropoetin, transfusion of platelets (in extreme cases), dialysis.

  • Neurological complications:

    • Uremic encephalopathy: The accumulation of uremic toxins in the brain. Symptoms: violation of consciousness, cramps, coma. Treatment: dialysis.
    • Peripheral neuropathy: Damage to the peripheral nerves with uremic toxins. Symptoms: numbness, tingling, pain in the limbs. Treatment: dialysis, symptomatic treatment (analgesics, antidepressants).
    • Restless legs syndrome: Unpleasant sensations in the legs, causing an irresistible desire to move them. Treatment: dialysis, iron preparations, dopaminergic drugs.

  • Gastrointestinal complications:

    • Anorexia, nausea, vomiting: Uremic intoxication, violation of motor skills of the gastrointestinal tract. Treatment: anti -rate drugs, improvement of appetite, dialysis.
    • Uremic gastritis and colitis: Inflammation of the mucous membrane of the stomach and colon with uremic toxins. Treatment: antacids, proton pump inhibitors, dialysis.
    • Constipation: Reducing intestinal motility, taking phosphate -binding drugs. Treatment: high fiber diet, laxatives.

  • Dermatological complications:

    • Itching of the skin: Uremic intoxication, calcium deposition in the skin, dry skin. Treatment: antihistamines, softening creams, dialysis.
    • Change of skin color: Pallor (anemia), grayish tint (deposition of uremic toxins).
    • Dry skin: Violation of the function of the sweat glands.

  • Immunological complications:

    • Increased susceptibility to infections: Violation of the function of leukocytes, a decrease in the immune response. Prevention: vaccination, observance of hygiene rules. Treatment: antibiotics.

VI. Diet with renal failure: principles and recommendations

The diet plays a key role in managing renal failure, both acute and chronic. The correctly compiled diet helps to reduce the load on the kidneys, control the electrolyte balance, reduce the level of blood toxins and prevent the development of complications. The basic principles of the diet in renal failure include the restriction of protein, phosphorus, potassium and sodium.

  • Protein restriction:

    • Purpose: to reduce the formation of nitrogenous slag (urea, creatinine), which accumulate in the blood with renal failure.
    • Recommendations:
      • Restriction of protein consumption up to 0.6-0.8 g/kg of body weight per day with CPN without dialysis.
      • Higher protein consumption (1.0-1.2 g/kg of body weight per day) with CPN on dialysis, since dialysis leads to protein loss.
      • Preference is given to proteins of high biological value (meat, fish, eggs, dairy products).
      • Plant proteins (legumes, nuts) contain more phosphorus and potassium, so their consumption should be limited.
    • Important: protein restriction should not be excessive, as this can lead to insufficient nutrition and loss of muscle mass.

  • The Fosphorus Restriction:

    • Purpose: to prevent hyperphosphatemia, which contributes to the development of secondary hyperparathyroidism and calcification of soft tissues.
    • Recommendations:
      • Restriction of phosphorus consumption up to 800-1000 mg per day.
      • Avoid products with a high phosphorus content: dairy products, cheese, nuts, legumes, chocolate, carbonated drinks.
      • Carefully study the composition of the products on labels, as phosphorus is often added to food as a preservative.
      • Use phosphate -binding drugs prescribed by a doctor to reduce the level of phosphorus in the blood.

  • Potassium restriction:

    • Purpose: to prevent hyperkalemia, which can lead to heart rhythm disturbances.
    • Recommendations:
      • Limiting potassium consumption until 2000-3000 mg per day.
      • Avoid products with a high potassium content: bananas, oranges, tomatoes, potatoes, spinach, avocados, dried fruits.
      • Soak potatoes and other vegetables in water

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