Chronic renal failure: symptoms

Based on the degree of decrease in CF and medical tactics, there are 3 stages of chronic renal failure.

[1], [2], [3], [4], [5]

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

The first symptoms of chronic renal failure are nonspecific "masks": anemic, hypertonic, asthenic, gouty, osteopathic, as well as complications caused by a decrease in renal elimination of drugs, for example, the increase in hypoglycemic states with stable diabetes on a selected dosage of insulin.

The initial stage of chronic renal failure is characterized by a latent flow with polyuria, nicturia, moderately severe anemia. In 40-50% of cases, arterial hypertension is detected. Often there is a decrease in appetite.

• Water-electrolyte disturbances.
  • Polyuria with nicture is an early symptom of chronic kidney failure caused by a violation of the concentration ability of the kidneys due to a decrease in tubular water reabsorption. Since polyuria is "forced", limiting the drinking regimen with chronic renal failure causes the risk of dehydration, hypovolemia and hypernatremia.
  • Attachment of a violation of the tubular reabsorption of sodium indicates the development of the syndrome of sodium loss (salting 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 a sharp muscle weakness, ECG changes, increased toxic effect of cardiac glycosides.
  • The delay of sodium due to the intake of sodium in the volume exceeding its maximum excretion in chronic renal failure leads to hypervolemia with hyperhydration, volume overload of the myocardium, and also to the volume of Na ^- dependent hypertension.
• Arterial hypertension. The relationship between hypertension and chronic renal insufficiency should be assumed in the case of its uncontrolled course with no nighttime decrease in arterial pressure and with the early formation of hypertrophy of the ventricular ventricle.
  • Volume-Na ⁺ -dependent hypertension (90-95% of cases) is represented by chronic hypervolemia, hypernatremia and giporeninemia, increases with increasing hyperhydration and Na overload and normalizes after restriction of fluid and salt, saluretics or hemodialysis sessions.
  • Hypertension with diabetic nephropathy, despite the volume-Na ⁺ -dependent character, early becomes uncontrolled (with a decrease in CF to 30-40 ml / min), which dramatically 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. At the same time, the level of renin and OPSS is increased, and the cardiac output and the concentration of sodium of blood are reduced. The arterial pressure is not normalized after prescribing 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).
  • With the progression of chronic renal failure, one form of hypertension can be transformed into another, usually more severe. In pyelonephritis, hypertension, usually responding well to antihypertensive therapy, can become uncontrolled by shrinking one of the kidneys, joining atherosclerotic stenosis of the renal artery.
• Anemia often develops in the early stage of chronic renal failure (with a decrease in CF to 50 ml / min) and with its progression increases, as the deficiency of endogenous epoetin grows as the buds shrivel. Epo-ethyne-deficient anemia is normocytic, normochromic, progressing slowly. Its severity largely determines the severity of the asthenic syndrome, tolerability of physical activity in chronic renal failure, the degree of decrease in appetite. Anemia increases the risk of cardiovascular complications of chronic renal failure, sensitivity to infections, promotes secondary hemochromatosis, infection with HBV and HCV due to frequent blood transfusions. Anemia is not characteristic of chronic renal failure in polycystic kidney disease, often absent in renovascular hypertension.
• Cardiomyopathy and progressive atherosclerosis. Progressing atherosclerosis affects coronary, cerebral and renal arteries in chronic renal failure. 15% of patients with terminal renal failure older than 50 years are diagnosed with bilateral atherosclerosis of the renal arteries. High risk of acute myocardial infarction in patients with chronic renal failure with severe left ventricular hypertrophy and hyperlipidemia. Hypertrophy of the left ventricle and IHD, diagnosed in the initial stage of chronic renal failure in 30-40% of patients, progress on dialysis, leading to AMI, cardiomyopathy and chronic heart failure.

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

At this stage, effective conservative therapy, which maintains the residual function of the kidneys. Dialysis methods of treatment do not apply. About the onset of this stage is evidence of adherence to polyuria asthenic syndrome, decreased ability to work, a decrease in appetite until the development of anorexia, weight loss, the emergence of azotemia.

• Azotemia. In chronic renal failure, a persistent increase in the level of nitrogenous slag (creatinine, urea nitrogen, uric acid) of blood is observed with a decrease in CF below 40 ml / min. Of all the parameters of nitrogen metabolism, blood creatinine is most specific for the diagnosis of chronic renal failure. It is more difficult to treat the increase in the level of urea and uric acid in the blood (see "Gouty nephropathy"). With an increase in the blood urea concentration on the background of CF> 50 ml / min and the normal level of creatinine, there are likely non-primary causes of azotemia: dehydration, eating disorders (protein overload, starvation), hypercatabolism. If a direct relationship is found between the degree of urea and uric acid increase in the blood and the severity of hypercreatininaemia, this indicates a 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. Enhances hyperkalemia, hypercatabolism and accelerates the development of uremic hyperparathyroidism. Clinical symptoms are weakness, dyspnea.
• Hyperkalemia is one of the most frequent and life-threatening symptoms of chronic kidney failure. Although the ability of the kidneys to maintain normal blood potassium concentration persists for a long time and stops 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 giporeninemic hypoalldosteronism, with the formation of renal tubular acidosis of type IV. With critical hyperkalemia (blood potassium level more than 7 meq / liter), the muscle and nerve cells lose their ability to become irritable, which leads to paralysis, acute respiratory failure, diffuse CNS damage, bradycardia, atrioventricular blockage up to complete cardiac arrest.
• Uremical hyperparathyroidism. In the conservative stage of chronic renal failure, hyperparathyroidism usually proceeds subclinically in the form of episodes of ossalgia, myopathy. Progresses in patients with chronic renal failure on programmed hemodialysis.
• Metabolic disorders and drug effects in chronic renal failure. Overdosage and side effects of drugs occur in chronic renal failure significantly more often than in individuals with healthy kidneys. Among the side effects are nephrotoxic, affecting the residual function of the kidneys, and general toxic. Reduction of excretion and metabolism of drugs with wrinkled 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, with chronic renal failure do not cause an overdose and side effects.
• Nutritional status disorders. In patients with chronic renal failure with a slowing of CF, a decrease in appetite, an increase in intoxication, there is a spontaneous decrease in protein and energy intake; without appropriate correction this leads along with hypercatabolism to violations of the status of nutrition. Hypoalbuminemia is closely associated with an increase in concomitant diseases, hospitalizations and mortality of patients with chronic renal insufficiency.

Causes of hyperkalemia in chronic renal failure

Severity of gynecology	Causes
Early hyperkalemia	Excessive intake of potassium from food Hypercatabolism Severe fluid restriction, oliguria Metabolic, respiratory acidosis Medicines that cause the release of potassium from the cell
Terminal hyperkalemia	Hypoaldosteronism (giporeninemichesky, selective) Competitive inhibition of the effect of aldosterone Violations of tubular secretion of potassium Salting kidney With CF <15-20 ml / min

[6], [7], [8], [9], [10], [11], [12], [13],

The terminal stage of chronic renal failure (CF less than 15 ml / min)

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

When the conservative stage of chronic renal failure passes into the terminal one, the water-elimination function is violated: "forced" polyuria is replaced by oliguria, hyperhydration develops. Hypertension often acquires a little-controlled course, leading to a sharp decrease in vision, acute left ventricular failure with pulmonary edema. Symptoms of chronic kidney failure at this stage are: drowsiness, muscle weakness, nausea, vomiting with a sharp decrease in appetite, often right up to anorexia, diarrhea (uremic enterocolitis). Itchy skin itch. Observe bleeding (nasal, gastrointestinal, uterine), pain in the bones and spine, convulsive twitching of the muscles. With terminal uremia, odor of ammonia from the mouth, pericarditis, damage to the peripheral nervous system and the central nervous system, symptoms of decompensated metabolic acidosis: periodic respiration, secondary gout (with arthritis, tofusi).

• The defeat of the nervous system.
  • Early symptoms of uremic encephalopathy: memory loss, ability to simple mathematical actions, sleep inversion.
  • In the late stage comes uremic coma. The coma in chronic kidney failure is due to other causes: brain edema due to critical hyperhydration or severe hypertensive crisis.
  • In diabetes, adherence to chronic renal failure increases the risk of hypoglycemic coma because the rate of insulin metabolism decreases as the kidney shrinks. Especially dangerous in diabetic nephropathy is the absence of typical symptoms of hypoglycemia due to autonomic diabetic polyneuropathy.
  • Peripheral sensory-motor polyneuropathy is represented by the syndrome of "restless legs", paresthesia, sometimes - a sharp muscle weakness, violations of the daily rhythm of blood pressure. For the late stage of sensory-motor neuropathy pareses and sensory ataxia are typical.
  • 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 night diarrhea, impotence.
• Metabolic acidosis with a high anionic deficiency is caused by the delay of sulfates, phosphates. In addition, in the 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 the pH of the blood), Kussmaul breathes, other symptoms of CNS damage, up to the acidotic coma.
• Pericarditis. Uremic pericarditis is a symptom of chronic renal failure in the terminal stage and serves as an indication for urgent hemodialysis. Typical chest pains, often intense, associated with breathing and changes in body position, rhythm disturbances and pericardial friction noise. Pericarditis is the cause of death of 3-4% of patients with chronic renal failure.
• The defeat of the respiratory system in chronic renal failure. Uremical interstitial edema of the lungs ("water lung") - the most common lesion of the respiratory system in chronic renal failure is important to distinguish from acute left ventricular failure and RDS syndrome. With the addition of chronic renal failure in diabetics, the risk of non-cardiogenic pulmonary edema increases. Since chronic renal failure in patients with diabetic nephropathy expressed hyperglycemia is not accompanied by osmotic diuresis, the developing hyperosmolar syndrome leads to critical hypervolemic hyperhydration with interstitial edema of the lungs. In chronic renal failure, there is often a syndrome of nocturnal apnea of the obstructive type.
• Acute bacterial pneumonia (staphylococcal, tubercular) also often complicates chronic renal failure. Tuberculosis in chronic renal failure is observed 7-10 times more often than in persons with normal renal function.
• Lesion of the digestive tract with pronounced uremia. Characteristic of the following symptoms of chronic renal failure: anorexia, pronounced dyspeptic syndrome, glossitis, cheilitis, stomatitis, mumps, frequent diarrhea. Gastric bleeding with mortality 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 the diverticulosis of the large intestine, characteristic of polycystic disease. Uremical damage to the gastrointestinal tract leads to a syndrome of impaired absorption, which is promoted by anorexia, impaired secretion, atherosclerosis of the abdominal arteries and autonomic neuropathy of the gastrointestinal tract.