Major kidney diseases in children

When examining kidney diseases in children, it is very important to carefully question the mother or the child (if he is older) about any urinary disorders and the time of their appearance. It is necessary to find out how much urine the patient excretes. Is there frequent urination (pollakiuria), pain when urinating?

It is important to find out how much the child drinks, whether there is thirst. When it appeared; what preceded the current illness; whether the child had acute respiratory diseases, tonsillitis, scarlet fever before; whether the child has had any vaccinations; how many days after the illness or vaccination did urinary problems appear.

From the anamnesis, it is possible to identify a number of complaints characteristic of kidney diseases: headaches, lower back pain, as well as the appearance of edema and changes in skin color (paleness - with nephritis, especially with a nephrotic component, pale gray tint - with pyelonephritis, etc.).

When examining kidney disease in children, a change in skin color is characteristic - pallor, puffiness of the face - facies nephritica.

The characteristic "renal" or "marbled" pallor is caused either by vascular spasm (with increased blood pressure) or by compression of the vessels due to edema. Less often, pallor is determined by anemia.

Edema syndrome also has several clinical variants. With a slight expression of edema syndrome, an increase in body weight, a decrease in diuresis, an acceleration of the resorption of a blister with a skin water test are noted, and occasionally pastosity of the eyelids can be noted. Obvious edema (peripheral, hydrothorax, ascites, up to anasarca) develops with diffuse kidney diseases. Their formation can be very rapid.

Edema in kidney diseases is initially located on the face, less on the trunk and limbs. To detect hidden edema, the patient is systematically weighed and the hydrophilicity of the tissues is determined using the McClure-Aldrich "blister test". A syringe with a thin needle is injected intradermally into the forearm with 0.2 ml of isotonic sodium chloride solution, after which a blister forms on the skin, which in a healthy child of the first year of life is absorbed in 15-20 minutes, from 1 year to 5 years - in 20-25 minutes, in older children and adults - after 40 minutes.

It is necessary to pay attention to the shape and size of the abdomen, which change with the development of ascites.

The pathogenesis involves an increase in the volume of circulating blood and extravascular fluid, the development of hypoalbuminemia and hyponicia of the blood. Later, hypovolemia increases with an increase in the production of renin and aldosterone. The secretion of atrial natriuretic peptide decreases and the excretion of sodium in the urine decreases.

Pain syndrome is often combined with dysuria and is determined by organic (anomalies in the development of the urinary system) or functional obstruction of the urinary tract and stretching of the kidney capsule. Pain is localized in the lower abdomen and in the lumbar region, radiating along the ureter and to the inguinal region. Pain syndrome is especially characteristic of microbial inflammatory processes in the kidneys and urinary tract (cystitis, urethritis).

Hypertensive syndrome usually develops with an increase in the content of vasoconstrictors such as biogenic amines and activation of the renin-aldosterone-angiotensin systems, leading to an increase in arterial pressure equally in both systolic and diastolic pressure. This is accompanied by pallor and headache. Hypertensive syndrome is especially characteristic of acute and chronic nephritis, anomalies and diseases of the renal arteries, acute and chronic renal failure. The opposite picture - a decrease in arterial pressure - can be observed in dysmetabolic nephropathy and tubulopathy before the formation of chronic renal failure.

In diffuse kidney lesions, hypertension is observed, which can be transient or long-lasting. In connection with hypertension in nephritis, a change in the borders of the heart is often observed (expansion to the left), increased tones are heard, especially I at the apex, and in the second intercostal space on the right (aorta) - an accentuation of the II tone.

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Acute glomerulonephritis (poststreptococcal)

Acute glomerulonephritis (poststreptococcal) occurs most often in school-age children, naturally after a certain period of time after a streptococcal infection of the nasopharynx or respiratory tract. Much less often, nephritis occurs after an infection of another localization. The interval after infection with beta-hemolytic streptococcus group A can be 7-14 days. Symptoms are manifested by general malaise, headache and weakness with the gradual addition of pallor and slight swelling of the skin with predominant localization of edema on the eyelids, back of the hands and feet. The color of urine can change, up to the color of "meat slops", its amount is slightly reduced. Urine tests reveal a large number of erythrocytes, an increase in the amount of protein, leukocyte and erythrocyte casts. Relatively rarely and as a sign of a severe form of the disease, blood pressure may increase and attacks of encephalopathy with a convulsive syndrome may occur. A sudden and sharp increase in blood pressure creates a risk of cardiac decompensation.

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Nephrotic syndrome

This syndrome, or symptom complex, is observed mainly in preschool children and may be related to a wide range of diseases of both the kidneys themselves and systemic ones. The criteria for nephrotic syndrome are considered to be a triad: proteinuria, moreover, significantly expressed, hypoalbuminemia and edema. The latter may be not only periorbital or of the entire face, but also be quite widespread and accompanied by the accumulation of edematous transudate in cavities, most often in the abdominal cavity in the form of ascites, then in the pleural cavities (pleural effusion). Nephrotic syndrome is often accompanied by persistent abdominal pain, vomiting and diarrhea. Hypovolemia that occurs with widespread edema, vomiting and diarrhea leads to arterial hypotension and circulatory collapse. Edema and hypovolemia are the basis for hospitalization and infusion therapy. Infection - the risk of peritonitis - poses a great danger to patients with ascites.

The basis for the development of primary nephrotic syndrome are immunopathological processes and the direct effect of proinflammatory cytokines, which create high permeability of glomerular structures for protein.

Congenital nephrotic syndrome is inherited in an autosomal recessive manner. In essence, it is fundamentally different from the acquired forms of the disease, since the leading cause here is microdysplasia of the kidneys by the type of their microcystosis. Sometimes, edema of the placenta is already noted at birth. In a child, pronounced edema syndrome is detected in the first year of life in parallel with proteinuria and hypoalbuminemia.

Nephritis in hemorrhagic capillary toxicosis (Schonlein-Henoch disease) accompanies some cases of this disease and is manifested almost exclusively by hematuria during periods of increased cutaneous hemorrhagic syndrome. Only in individual patients is relatively rapid chronicization of kidney damage observed, sometimes with the dominance of nephrotic syndrome.

Interstitial nephritis

Interstitial nephritis is an acute or chronic non-specific inflammatory disease with inflammation localized mainly in the interstitial tissue of the kidneys. The disease reflects the kidneys' reaction to toxic effects, viruses, hypoxia, drug-induced damage, circulation of vasotropic interleukins and immune complexes. Acute interstitial nephritis is characterized by papillary necrosis and signs of cortical hypoxia. Acute renal failure may develop.

Clinical manifestations are often poorly expressed. The basis for recognition is an isolated urinary syndrome with a mononuclear profile of leukocyturia and functional changes with a predominant picture of dysfunction or insufficiency of the tubules. It is possible to detect a decrease in the secretory and excretory function of the tubules, a decrease in the concentration capacity, a decrease in the excretion of ammonia with a tendency to increase the loss of sodium and potassium.

Urinary tract infections

Urinary tract infections are extremely common diseases of childhood, especially early childhood, and are especially common in girls due to anatomical predisposition to infection of the urethra. Urinary tract infection is especially dangerous for children with altered motility of the urinary tract, primarily vesicoureteral reflux. The presence of reflux creates the prerequisites for infection to penetrate into the upper urinary tract, renal pelvis and calyx and long-term persistence of infectious inflammation both in the urinary tract and in the renal interstitium. The latter characterizes the occurrence of chronic pyelonephritis. The symptoms of urinary tract infection can be very non-specific and create difficulties for rapid recognition of the disease. Thus, in infancy or in a newborn, the symptoms of infection may be limited to anxiety, poor weight gain, vomiting, frequent "breakdowns" in stool (diarrhea), and fevers of the wrong type. Only urine analysis, its cultures and quantitative characteristics of the existing bacteriuria provide the key to recognizing the nature of acute and severe febrile disease. Etiological factors are most often intestinal microorganisms.

Neurogenic bladder dysfunction syndrome

The syndrome of impaired motor coordination of the bladder, its muscles, the muscles of the afferent and effluent urinary tract, leads to disorders of both the retention and excretion of urine (urination). Urodynamic disorders at the bladder level are the cause of subjective disturbances in well-being, complaints and restrictions on the lifestyle or education. Along with this, neurogenic dysfunction can be a component of more common motor disorders that aggravate obstructive and reflux manifestations, contributing to the emergence of ascending infection. The cause of discoordination can be changes in higher levels of regulation of the autonomic nervous system of both segmental and suprasegmental sections.

There are two different types of neurogenic dysfunction - hyporeflexive and hyperreflexive. In the second type, pollakiuria is predominant, increased urge to urinate with small amounts of urine. In the first type, the tone of the bladder is reduced, urination is rare with a large volume of urine, and the act of urination itself is prolonged. There is also a type of neurogenic dysfunction that manifests itself only in a vertical position - "postural" bladder.

Urinary tract obstruction syndrome

Disruption of the normal outflow of urine formed in the kidneys through the urinary tract is a common cause of chronic diseases of the urinary system. Obstruction, even unilateral and partial, creates conditions for dystrophic and infectious-inflammatory lesions of the kidneys themselves and the underlying parts of the urinary system. The final result of any obstructive syndrome is an ascending infection - pyelonephritis - and ascending dysfunction of the kidney on the side of the obstruction - from partial tubular disorders to combined dysfunction of the tubules and glomeruli.

The causes of obstruction may be organic causes, in particular anomalies in the structure of the kidneys or calculus of the urinary tract, as well as functional features of the urine outflow tract associated with pathological phenomena of their motility, such as reflux.

Anatomical obstruction leading to the formation of hydronephrosis of the kidney is most often observed at the level of the ureteropelvic junction. Here, internal stenosis of the ureter or its external compression by an aberrant renal artery and its branches can be observed. Often, such obstruction is caused by the presence of a horseshoe kidney in a child.

Obstruction at the level of the vesicoureteral junction initially causes gradual dilation of the ureter or development of a megaureter. This type of obstruction may be seen in the presence of a duplicated ureter, which is complicated by vesicoureteral reflux.

Obstruction associated with the presence of a posterior urethral valve in boys is very common. It causes dilation in the prostatic urethra, hypertrophy of the muscular wall of the bladder with a relatively small bladder size, and, as a rule, vesicoureteral reflux.

Vesicoureteral reflux and reflux nephropathy in children

Backflow of urine from the bladder to the ureter and kidney is usually associated with congenital insufficiency of the vesicoureteral junction, less often this insufficiency occurs as a complication or consequence of a previous urinary tract infection. Reflux can occur in several family members. A factor predisposing to the occurrence of reflux is a change in the anatomical relationship between the length and diameter of the ureteral "tunnel" in the wall of the bladder - the normal ratio is (4... 5): 1. Reflux is accompanied by a ratio of 2: 1 and less. A similar violation of protection against backflow of urine is observed in case of anatomical disorder of the ureteral triangle, duplication or diverticulum of the ureter. Neurogenic bladder, especially in combination with myelomeningocele, is complicated by reflux in almost half of the cases. The main pathogenic effect of reflux on the structures and function of the kidney is associated with increased hydrostatic pressure of urine on the pelvis and the substance of the kidney during urination, when this hydrostatic pressure is highest. In addition, stasis of urine or its reverse injection are the most "favorable" for the transmission of ascending infection. In the classification of vesicoureteral reflux, several of its degrees are distinguished. At degree I, only the presence of a reflux of a radiopaque substance into the ureter is noted. At degrees IV and V of reflux severity, expansion and tortuosity of the ureter, dilation of the pelvis and calyces of the kidney are already visible. Clinical manifestations of even severe reflux can be minimal, often limited to isolated urinary syndrome. If reflux of one type is detected, one can expect the presence of other forms of reflux in the child, including several types of intrarenal reflux.

Reflux nephropathy is a complication of reflux syndromes of the urinary system, leading to the development and progression of minimal and purely local interstitial nephritis - nephrosclerosis and subsequent expansion of its area with the final outcome in chronic renal failure already in young people. The presence of reflux nephropathy can also be one of the factors leading to the early formation of arterial hypertension in children and adolescents. Reflux nephropathy progresses especially quickly in children with renal hypoplasia. The causes and mechanisms of reflux nephropathy include ischemia of the renal parenchyma, the cytotoxic effect of leukocytes infiltrating ischemic tissue, and the possible formation of autoimmune reactions.

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Renal failure syndrome

The term "renal failure" includes the entire set of clinical and laboratory-functional manifestations of the disorder of homeostatic functions inherent to the kidney. The main manifestations of renal failure are increasing azotemia, diselectrolytemia, metabolic acidosis, insufficient or, much less frequently, excessive excretion of water.

Renal failure can be partial or total. Partial renal failure is understood as a persistent decrease in any renal function (for example, acidogenesis, etc.). In total renal failure, disorders of all renal functions are observed. It usually develops when only 20% of nephrons retain their function. According to the course, renal failure is divided into acute and chronic.

Acute renal failure (ARF)

Its essence is determined by the fact that the existing capabilities of glomerular filtration and tubular functions cannot provide the necessary removal of nitrogenous and other waste products, as well as water. This leads to a profound disruption of water and electrolyte homeostasis.

Acute renal failure in children can be observed in glomerulonephritis, hemolytic uremic syndrome, renal necrosis, various severe diseases (sepsis and other infections), as well as at the onset of acute glomerulonephritis and pyelonephritis. ARF most often occurs with accidental transfusion of incompatible blood, poisoning with barbiturates, nephrotoxic poisons (mercury, lead compounds) and antibiotics. From what has already been said, it is clear that very common causes of ARF are non-renal causes. It is customary to distinguish

In this group of causes as "prerenal". They are all similar in one thing - the occurrence of impaired blood supply to the kidneys, which is possible with any shock, poisoning, blood loss or general disease (heart failure), leading to a decrease in arterial pressure or effective blood flow in the kidneys. From this moment, the actual damage to the kidneys begins.

The main symptom of acute renal failure is oliguria, turning into anuria, which is accompanied by headache, anorexia, convulsions, thirst, nausea and vomiting. Body weight increases rapidly, peripheral edema appears. Skin itching, refusal to eat, sleep disorders occur, bowel disorders and abdominal pain are added. Breathing becomes acidotic, blood pressure may temporarily increase, then arterial hypotension and hemodynamic decompensation with pulmonary or cerebral edema with coma and convulsions occur. Blood tests reveal azotemia, hyperkalemia, hypocalcemia.

In the case of benign acute renal failure, the polyuric phase usually occurs after 3-4 days, during which a large amount of salts and nitrogenous wastes are excreted in the urine. After this, the function of the tubules is restored to some extent.

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Chronic renal failure in children

Chronic renal failure (CRF) is sometimes diagnosed in children with kidney diseases that have developed quite acutely but then become chronic. The distinction between acute and chronic renal failure is based on significant differences in both the clinical picture and the dynamics of impaired renal function. Such criteria are:

• decrease in endogenous creatinine clearance by 20 ml/min or less by 1.73 m2;
• an increase in serum creatinine levels over 177 μmol/l;
• decrease in endogenous creatinine clearance to 20 ml/min or less per 1.73 m2;
• an increase in serum creatinine levels of more than 177 μmol/l for 3 months or more.

Most often, CRF develops gradually. At first, its clinical manifestations are not observed, then patients develop moderate thirst and polyuria. Their manifestations can slowly increase, often accompanied by pallor associated with anemia and, often, increased blood pressure, nocturia, hyposthenuria occur. Subsequently, the density of urine becomes equal to the density of blood plasma, electrolyte disturbances (hypokalemia, hyponatremia) occur. Patients lag behind in growth, become significantly exhausted, they have increasing general muscle weakness, drowsiness, headache, loss of appetite, dry mouth, weak muscle twitching (hypocalcemia), uremic breath odor. Later, a critical picture of uremia occurs with loss of consciousness, significant disorders of various body systems (cardiovascular, digestive, etc.) and metabolism.

Currently, more and more importance in the development of the clinical picture of true uremia is given not to the content of residual nitrogen (retention of slags in the body), but to disturbances of electrolyte metabolism and acid-base balance. Both with ARF and with true uremia, a significant increase in the magnesium content in the blood is detected (up to 2.5 mmol / l). With hypermagnesemia, phenomena similar to hyperkalemia occur: a disorder of the central nervous system, up to a comatose state and paralysis; on the ECG - an elongation of the atrioventricular complex, a high and peaked T wave, a widening of the QRS complex. With dialysis, during which excess magnesium ions are removed from the body, uremic phenomena also disappear. With uremia, there is also a retention of oxalic, sulfuric and phosphoric acids in the body.

In children, the development of renal failure, both general and isolated, is observed more often, and the rate of increase is usually more significant than in adults. This is explained by the lower compensatory capabilities of the kidneys due to the peculiarities of their structure, as well as the immaturity of the regulatory mechanisms carried out by the nervous system and endocrine glands. The permeability of cell membranes in children is higher than in adults. This leads to the fact that metabolites more easily penetrate the central nervous system and other organs, causing toxic damage to them.

In recent decades, CRF has ceased to be a synonym for doom for children with kidney disease. Systematic use of hemodialysis, including outpatient and home peritoneal dialysis procedures, treatment with genetically engineered erythropoietin preparations, scrupulous dietary and functional-biochemical monitoring of the disease can significantly improve their quality of life and ensure its extension. Even more striking immediate and remote results can be obtained with kidney transplants from relatives or other compatible donors.

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Bedwetting in Children

One of the most common diseases in preschool and primary school children, often moving on to adolescence and adulthood, determining significant limitations in a person's life opportunities during these periods. In essence, enuresis is not a single disease, but is the result of the implementation, or syndrome, resulting from the course of many other constitutional features and diseases. With different diseases, the leading role in the genesis of nocturnal enuresis is played by different factors, conditions and characteristics of the child as a whole or his urinary, nervous or endocrine systems. The components of the syndrome can be diseases of the lower urinary tract such as neurogenic bladder, cervical cystitis or urethritis, infravesical obstruction, ureteral anomalies. These components are leading in 7-10% of cases of nocturnal enuresis.

Disorders at the level of spinal centers are responsible for 20-25% of cases of nocturnal enuresis. A direct role is played by residual organic insufficiency of spinal centers, their ischemia in regional lesions of spinal cord vessels and associated neurogenic dysfunctions of hyporeflexive or hyperreflexive type. One can also talk about a significant role of residual organic insufficiency or dysfunction of cerebral higher centers of urination regulation. The connection of urinary incontinence with the depth and phasic nature of night sleep, with the features of the electroencephalogram of sick children both at rest and during falling asleep has been convincingly proven. Urination occurs during the period of the deepest "slow" sleep against the background of some signs of age-related immaturity according to the ratios of EEG frequency characteristics. This group accounts for up to 50% or more of the entire group of children with enuresis.

Mental illnesses or accentuations may play a certain role, where enuresis reflects reactions of active and passive protest (up to 5-7%), but systemic neuroses are much more significant, accounting for up to 15% of all cases of enuresis.

The connection between nocturnal enuresis and maturation factors is confirmed by a significant decrease in the frequency of nocturnal enuresis in senior school and adolescence.

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Diseases of the genital organs in boys. Disorders of testicular descent

The testicles develop as structures within the abdominal cavity and move toward the entrance to the inguinal canal during the 7th month of intrauterine development. By the time of birth, the testicles are usually already in the scrotum, but often the transition to the scrotum occurs in the first 2 weeks of life or even a little later. Regulation of the testicle's movement is carried out by hormonal stimuli: gonadotropins, androgens, and the inhibitory factor of the paramesonephric duct. Spontaneous descent of the testicle after one year of life becomes unlikely.

Often, the doctor or parents mistakenly state that the testicle is not descended. The reason for this is an increased cremasteric reflex and the testicle(s) being pulled up to the outlet of the inguinal canal at the time of their palpation.

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Incomplete descent of the testicles (testicle)

It can be stated if it is detected in some area of its normal migration on the way to the scrotum. If they (it) are in the abdominal cavity or inside the inguinal canal, then palpation of the testicles is impossible. During surgical treatment, they often attract attention by their small size, soft consistency, separation of the testicle and its appendage. The presence of a large hernial sac is characteristic. Spermatogenesis is usually grossly impaired.

Ectopia of testicles

In ectopia, the testicles pass through the inguinal canal, but upon exiting it, their normal movement is disrupted, and they can be located in the perineum, thigh, or pubic symphysis. Ectopic testicles are easily detected by palpation, and during surgery they look normal. The hernial sac is often absent.

Phimosis

The foreskin is tightly connected to the head of the penis in boys in the first year of life, and attempts to open the head at this time should not be made. Spontaneous separation occurs in the interval from 1 to 4 years of life. Repeated balanitis and trauma to the foreskin during attempts to open the head lead to the appearance of scars and stenosis of the outlet of the foreskin - phimosis.

Hypospadias

One of the most common congenital anomalies of the male genital organs. In this case, the opening of the urethra opens much more proximally than normal.