Chronic Renal Failure - Symptoms

Based on the degree of reduction of CF and treatment tactics, there are 3 stages of chronic renal failure.

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Initial stage of chronic renal failure (decrease in CF to 40-60 ml/min)

The first symptoms of chronic renal failure are non-specific “masks”: anemic, hypertensive, asthenic, gouty, osteopathic, as well as complications caused by a decrease in renal elimination of drugs, for example, an increase in the frequency of hypoglycemic conditions in stable diabetes with a selected dosage of insulin.

The initial stage of chronic renal failure is characterized by a latent course with polyuria, nocturia, and moderate anemia. Arterial hypertension is detected in 40-50% of cases. Decreased appetite is often observed.

• Water and electrolyte disturbances.
  • Polyuria with nocturia is an early symptom of chronic renal failure caused by impaired renal concentrating ability due to decreased tubular reabsorption of water. Since polyuria is "forced" in nature, when limiting the drinking regime in chronic renal failure, there is a risk of dehydration, hypovolemia and hypernatremia.
  • The addition of impaired tubular sodium reabsorption indicates the development of sodium wasting syndrome (salt-losing kidney). The latter is complicated by prerenal acute renal failure.
  • Hypokalemia also occurs in the polyuric stage of chronic renal failure in the case of overdose of saluretics, profuse diarrhea. It is represented by severe muscle weakness, ECG changes, and increased toxic effect of cardiac glycosides.
  • Sodium retention due to sodium intake with food in a volume exceeding its maximum excretion in chronic renal failure leads to hypervolemia with hyperhydration, volume overload of the myocardium, and also to volume-Na ⁺ -dependent hypertension.
• Arterial hypertension. The connection between hypertension and chronic renal failure should be assumed in its poorly controlled course with the absence of a nighttime decrease in blood pressure and in the early formation of left ventricular hypertrophy.
  • Volume-dependent Na ⁺ hypertension (90-95% of cases) is represented by chronic hypervolemia, hypernatremia and hyporeninemia, increases with increasing hyperhydration and Na overload and normalizes after fluid and salt restriction, taking saluretics or performing a hemodialysis session.
  • Hypertension in diabetic nephropathy, despite its volume-Na ⁺ -dependent nature, becomes uncontrollable early (with a decrease in CF to 30-40 ml/min), which sharply accelerates the progression of chronic renal failure, diabetic proliferative retinopathy and sometimes leads to pulmonary edema due to acute left ventricular failure, as well as retinal detachment.
  • Renin-dependent hypertension (5-10%) is characterized by a persistent increase in diastolic pressure. In this case, the level of renin and OPSS is increased, and cardiac output and blood sodium concentration are decreased. Blood pressure does not normalize after the administration of saluretics (and during hemodialysis), despite the correction of hyperhydration. Renin-dependent arterial hypertension is often malignant: it occurs with severe damage to the vessels of the fundus, central nervous system, myocardium (acute left ventricular failure).
  • As chronic renal failure progresses, one form of hypertension may transform into another, usually more severe. In pyelonephritis, hypertension, which usually responds well to hypotensive therapy, may become uncontrollable when one of the kidneys shrinks and atherosclerotic stenosis of the renal artery occurs.
• Anemia often develops in the early stages of chronic renal failure (with a decrease in CF to 50 ml/min) and increases with its progression, since as the kidneys shrink, the deficiency of endogenous epoetin increases. Epoetin-deficiency anemia is normocytic, normochromic, and progresses slowly. Its severity largely determines the severity of the asthenic syndrome, tolerance of physical activity in chronic renal failure, and the degree of loss of appetite. Anemia increases the risk of cardiovascular complications of chronic renal failure, susceptibility to infections, promotes secondary hemochromatosis, HBV and HCV infection due to frequent blood transfusions. Anemia is not typical for chronic renal failure in polycystic kidney disease, and is often absent in renovascular hypertension.
• Cardiomyopathy and progressive atherosclerosis. Progressive atherosclerosis affects the coronary, cerebral and renal arteries in chronic renal failure. In 15% of patients with terminal renal failure over 50 years of age, bilateral atherosclerosis of the renal arteries is diagnosed. The risk of acute myocardial infarction is high in patients with chronic renal failure with severe left ventricular hypertrophy and hyperlipidemia. Left ventricular hypertrophy and coronary heart disease, diagnosed in the initial stage of chronic renal failure in 30-40% of patients, progress on dialysis, leading to acute myocardial infarction, cardiomyopathy and chronic heart failure.

Conservative stage of chronic renal failure (CF 15-40 ml/min)

At this stage, conservative therapy is effective, supporting the residual renal function. Dialysis treatments are not used. The onset of this stage is indicated by the addition of asthenic syndrome to polyuria, decreased ability to work, decreased appetite up to the development of anorexia, weight loss, and the occurrence of azotemia.

• Azotemia. In chronic renal failure, a persistent increase in the level of nitrogenous waste products (creatinine, urea nitrogen, uric acid) in the blood is observed when the CF decreases below 40 ml/min. Of all the indicators of nitrogen metabolism, blood creatinine is the most specific for the diagnosis of chronic renal failure. It is more difficult to interpret an increase in the level of urea and uric acid in the blood (see "Gouty nephropathy"). With an increase in the blood urea content against the background of CF> 50 ml/min and a normal creatinine level, non-renal causes of azotemia are likely: dehydration, nutritional disorders (protein overload, starvation), hypercatabolism. If a direct relationship is found between the degree of increase in urea and uric acid in the blood and the severity of hypercreatininemia, this indicates in favor of the diagnosis of chronic renal failure.
• Compensated hyperchloremic acidosis is caused by a defect in tubular reabsorption of bicarbonates and a decrease in tubular secretion of H ⁺ and NH ₄⁺ -hohob. It is characteristic of the conservative stage of chronic renal failure. It increases hyperkalemia, hypercatabolism and accelerates the development of uremic hyperparathyroidism. Clinical symptoms are weakness, dyspnea.
• Hyperkalemia is one of the most common and life-threatening symptoms of chronic renal failure. Although the ability of the kidneys to maintain normal blood potassium concentrations is preserved for a long time and ceases only when the CF decreases below 15-20 ml/min (terminal chronic renal failure), early hyperkalemia often occurs under the influence of various factors. The risk of developing critical hyperkalemia is increased already in the initial stage of chronic renal failure in diabetes. Its pathogenesis, in addition to severe hyperglycemia with insulin deficiency and hypercatabolism, is associated with the syndrome of hyporeninemic hypoaldosteronism, with the formation of renal tubular acidosis type IV. In critical hyperkalemia (blood potassium level over 7 mEq/L), muscle and nerve cells lose their ability to excitate, which leads to paralysis, acute respiratory failure, diffuse damage to the central nervous system, bradycardia, atrioventricular block, and even complete cardiac arrest.
• Uremic hyperparathyroidism. In the conservative stage of chronic renal failure, hyperparathyroidism usually occurs subclinically in the form of episodes of ossalgia, myopathy. It progresses in patients with chronic renal failure on programmed hemodialysis.
• Metabolism and drug action disorders in chronic renal failure. Overdose and side effects of drugs occur in chronic renal failure significantly more often than in individuals with healthy kidneys. Side effects include nephrotoxic, affecting the residual renal function, and general toxic. Reduced excretion and metabolism of drugs by shrunken kidneys leads to their accumulation in the blood with an increase in the main effect, the degree of which is inversely proportional to the level of residual renal function. Drugs metabolized by the liver do not cause overdose and side effects in chronic renal failure.
• Nutritional status disorders. In patients with chronic renal failure with slowing of CF, decreased appetite, and increasing intoxication, spontaneous reduction in protein and energy consumption is observed; without appropriate correction, this leads, along with hypercatabolism, to nutritional status disorders. Hypoalbuminemia is closely associated with an increase in concomitant diseases, hospitalizations, and mortality in patients with chronic renal failure.

Causes of hyperkalemia in chronic renal failure

Severity of hyperkalemia	Reasons
Early hyperkalemia	Excessive dietary potassium intake Hypercatabolism Severe fluid restriction, oliguria Metabolic, respiratory acidosis Drugs that cause potassium to leave the cell
Terminal hyperkalemia	Hypoaldosteronism (hyporeninemic, selective) Competitive inhibition of the effect of aldosterone Disorders of tubular potassium secretion Salt-losing kidney At CF < 15-20 ml/min

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End-stage chronic renal failure (GFR less than 15 ml/min)

In the terminal stage, only renal replacement therapy is effective - dialysis methods (regular hemodialysis, CAPD) or kidney transplantation.

When the conservative stage of chronic renal failure passes into the terminal stage, the water-excreting function is impaired: "forced" polyuria is replaced by oliguria, hyperhydration develops. Hypertension often becomes uncontrollable, leads to a sharp decrease in vision, acute left ventricular failure with pulmonary edema. The symptoms of chronic renal failure at this stage are as follows: drowsiness, muscle weakness, nausea, vomiting with a sharp decrease in appetite, often up to anorexia, diarrhea (uremic enterocolitis). Skin itching is characteristic. Bleeding (nasal, gastrointestinal, uterine), pain in the bones and spine, convulsive muscle twitching are observed. In terminal uremia, the following are detected: ammonia odor from the mouth, pericarditis, damage to the peripheral nervous system and central nervous system, symptoms of decompensated metabolic acidosis: periodic breathing, secondary gout (with arthritis, tophi).

• Damage to the nervous system.
  • Early symptoms of uremic encephalopathy: memory loss, loss of ability to perform simple mathematical operations, sleep inversion.
  • In the late stage, uremic coma occurs. The comatose state in chronic renal failure is also caused by other reasons: cerebral edema due to critical hyperhydration or severe hypertensive crisis.
  • In diabetes, the addition of chronic renal failure increases the risk of hypoglycemic coma, since the rate of insulin metabolism decreases as the kidneys shrink. The absence of typical symptoms of hypoglycemia due to autonomous diabetic polyneuropathy is especially dangerous in diabetic nephropathy.
  • Peripheral sensory-motor polyneuropathy is characterized by restless legs syndrome, paresthesia, sometimes by severe muscle weakness, and disturbances in the circadian rhythm of arterial pressure. Paresis and sensory ataxia are typical for the late stage of sensory-motor neuropathy.
  • Autonomic neuropathy is characterized by hemodynamic instability (orthostatic, intradialytic hypotension), decreased sweating, “vagal denervation” of the heart with arrhythmias, risk of sudden cardiac arrest, gastric paresis, profuse nocturnal diarrhea, and impotence.
• Metabolic acidosis with high anion deficiency is caused by the retention of sulfates and phosphates. In addition, in conditions of renal anemia and tissue hypoxia in chronic renal failure, the risk of developing lactic acidosis is increased. With decompensated metabolic acidosis (with a decrease in blood pH), Kussmaul breathing occurs, other symptoms of CNS damage, up to acidotic coma.
• Pericarditis. Uremic pericarditis is a symptom of chronic renal failure in the terminal stage and is an indication for urgent hemodialysis. Typical are chest pains, often intense, associated with breathing and changes in body position, rhythm disturbances and pericardial friction rub. Pericarditis is the cause of death in 3-4% of patients with chronic renal failure.
• Respiratory system damage in chronic renal failure. Uremic interstitial pulmonary edema ("watery lung") is the most common respiratory system damage in chronic renal failure. It is important to distinguish it from acute left ventricular failure and RDS syndrome. When chronic renal failure is added to patients with diabetes, the risk of non-cardiogenic pulmonary edema increases. Since severe hyperglycemia is not accompanied by osmotic diuresis in patients with diabetic nephropathy with chronic renal failure, the developing hyperosmolar syndrome leads to critical hypervolemic hyperhydration with interstitial pulmonary edema. Obstructive sleep apnea syndrome often occurs in chronic renal failure.
• Acute bacterial pneumonia (staphylococcal, tuberculosis) also often complicates chronic renal failure. Tuberculosis in chronic renal failure is observed 7-10 times more often than in individuals with normal renal function.
• Gastrointestinal tract damage in severe uremia. The following symptoms of chronic renal failure are characteristic: anorexia, severe dyspeptic syndrome, glossitis, cheilitis, stomatitis, mumps, frequent diarrhea. Gastric bleeding with a mortality rate exceeding 50% occurs in every 10th dialysis patient due to peptic ulcers of the stomach, erosive esophagitis, angiodysplasia of the gastrointestinal mucosa. An additional risk factor for intestinal bleeding with perforation is diverticulosis of the colon, characteristic of polycystic disease. Uremic gastrointestinal tract damage leads to malabsorption syndrome, which is facilitated by anorexia, secretion disorders, atherosclerosis of the abdominal arteries and autonomic neuropathy of the gastrointestinal tract.