Main kidney diseases in children

In the study of kidney disease in children, it is very important to carefully question the mother or the child (if he is older) about those or other disorders of urination and the timing of their appearance. It is necessary to find out what amount of urine the patient allocates. Is there no frequent urination (pollakiuria), pain when urinating?

It is important to find out how much the child drinks, whether there is thirst. When she appeared; which preceded the present disease; whether the child was sick before with acute respiratory diseases, angina, scarlet fever; whether any vaccinations were made to the child; after how many days there were violations of urination after a disease or vaccination.

From the anamnesis it is possible to find out a number of complaints typical for kidney diseases: headaches, back pain, and the appearance of swelling and skin discoloration (pallor in nephritis, especially with nephrotic component, pale gray in pyelonephritis, etc.) ).

When examined for kidney disease, children have a discoloration of the skin - pale, puffy face - facies nephritica.

The characteristic "renal" or "marble" pallor is caused either by spasm of blood vessels (with an increase in blood pressure) or by compression of the vessels due to edema. Less pale is determined by anemia.

Edema syndrome also has several clinical options. With a small expression of edematous syndrome, there is an increase in body weight, a decrease in diuresis, an acceleration of the resorption of the blister with a cutaneous water sample, and occasionally the pasty of the eyelids can be noted. Explicit edema (peripheral, hydrothorax, ascites, up to anasarca) develop with diffuse kidney disease. Their formation can be very fast.

Edema in kidney disease is initially located on the face, less - on the trunk and extremities. To reveal the latent edema of the patient, the patient is systematically weighed and the hydrophilicity of the tissues is determined by the McClure-Aldrich "Blister Test" method. A syringe with a thin needle is injected intradermically in the forearm with 0.2 ml of an isotonic solution of sodium chloride, after which a blister forms on the skin, which in a healthy child of the first year of life dissolves in 15-20 min, from 1 year to 5 years - for 20-25 min , 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.

In the pathogenesis involved an increase in the volume of circulating blood and extravascular fluid, the development of hypoalbuminemia and blood giponkii. Later there is an increase in hypovolemia with an increase in the production of renin, aldosterone. The secretion of natriuretic peptide of the atria decreases and the secretion of sodium in the urine decreases.

Pain syndrome is often combined with dysuric and is determined by the organic (abnormal development of the urinary system) or functional obstruction of the urinary tract and dilated capsule of the kidney. The pain is localized in the lower abdomen and in the lumbar region, irradiating along the ureter and into the inguinal region. Pain syndrome is especially characteristic for microbial-inflammatory processes in the kidney and urinary tract (cystitis, urethritis).

The hypertensive syndrome usually develops with an increase in the content of vasoconstrictors such as biogenic amines and the activation of the "renin-aldosterone-angiotensin" systems, which lead to an increase in arterial pressure in both systolic and diastolic blood pressure. This is accompanied by pallor and a headache. Especially characterized by hypertensive syndrome for acute and chronic nephritis, abnormalities and diseases of the renal arteries, acute and chronic renal failure. The reverse picture - lowering of arterial pressure - can be observed with dismetabolic nephropathies and tubulopathies before the formation of chronic renal failure.

With diffuse lesions of the kidneys, hypertension is noted, which can be transient or lasting for a long time. In connection with hypertension, nephritis often changes the boundaries of the heart (widening to the left), strong tones are heard, especially I on the tip, and in the second intercostal space on the right (aorta) - the accent of II tone.

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

Acute glomerulonephritis (post-streptococcal)

Acute glomerulonephritis (post-streptococcal) occurs most often in school-age children, naturally after a certain period after a streptococcal infection of the nasopharynx or respiratory tract. Much less often, nephritis occurs after infection with another localization. The interval after infection with beta-hemolytic streptococcus group A may be 7-14 days. Symptomatology manifests as general malaise, headache and weakness with the gradual addition of pallor and small puffiness of the skin with the predominant localization of edema on the eyelids, behind the hands and feet. The color of urine can change, up to the color of "meat slops", its amount is somewhat reduced. In urine tests, erythrocytes are detected in large numbers, the amount of protein, leukocyte and erythrocyte cylinders is increased. Relatively rare and as a sign of a serious form of the disease, blood pressure may rise and seizures of encephalopathy with convulsive syndrome occur. A sudden and sharp increase in blood pressure creates the risk of cardiac decompensation.

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

Nephrotic syndrome

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

The basis for the emergence of the primary nephrotic syndrome are the immunopathological processes and the immediate effect of pro-inflammatory cytokines, which create a high permeability of the glomerular structures for the protein.

Congenital nephrotic syndrome is inherited autosomally and recessively. In essence, it is fundamentally different from the acquired forms of the disease, since the leading cause here is microdisplasia of the kidneys by the type of their microcystosis. Sometimes the swelling of the placenta is noted at birth. At the child the expressed edematic syndrome is revealed in the first year of life in parallel with proteinuria and hypoalbuminemia.

Nephritis with hemorrhagic capillarotoxicosis (Shenlaine-Henoch disease) accompanies some of the cases of this disease and is manifested almost exclusively by hematuria during periods of enhancement of cutaneous hemorrhagic syndrome. Only in some patients there is relatively rapid chronization of kidney damage, sometimes with a predominance of nephrotic syndrome.

Interstitial nephritis

Interstitial nephritis is an acute or chronic nonspecific inflammatory disease with inflammation localized primarily in the interstitial tissue of the kidneys. The disease reflects the reaction of the kidneys to toxic effects, viruses, hypoxia, medication damage, circulation of vasotropic interleukins and immune complexes. For acute interstitial nephritis, necrosis of the papillae and signs of hypoxia of the cortex are characteristic. Possible development of acute renal failure.

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

Urinary tract infections

Urinary tract infections are extremely common diseases of childhood, especially early childhood, and are especially characteristic of girls because of an anatomical predisposition to infection of the urethra. Especially dangerous is the infection of the urinary tract for children with the presence of altered motility of the urinary tract, especially vesicoureteral reflux. The presence of reflux creates the prerequisites for infection to enter the upper parts of the urinary tract, pelvis and kidney cups and perennial persistence of infectious inflammation in both the urinary tract and in the interstitium of the kidney. The latter characterizes the emergence of chronic pyelonephritis. Symptoms of urinary tract infections can be very nonspecific and create difficulties for rapid recognition of the disease. Thus, in infancy or in a newborn, the symptoms of infection can be limited only by anxiety, poor body weight gain, vomiting, frequent stools (diarrhea), and fever of the wrong type. Only the study of urine, its culture and the quantitative characteristics of the bacteriuria present give the key to recognizing the nature of acute and severe febrile illness. Etiological factors are most often microorganisms of the intestinal group.

Syndrome of neurogenic dysfunction of the bladder

Syndrome of impaired motor coordination of the bladder, its muscles, musculature of the leading and escaping urinary tract, leads to violations of both preservation and excretion of urine (urination). Violations of urodynamics at the level of the bladder are the cause of subjective disorders of well-being, complaints and limitations of the regime of life or training. Along with this, neurogenic dysfunction can be a component of more common motor disorders, exacerbating obstructive and reflux manifestations, contributing to the emergence of an ascending infection. The cause of discoordination may be changes in the overlying levels of regulation of the autonomic nervous system of both segmental and supragmentary divisions.

There are two different variants of neurogenic dysfunction - hyporeflective and hyperreflective. At the second, the phenomena of pollakiuria predominate, intensified urge to urinate with small portions of excreted urine. At the first, the tone of the bladder is reduced, urination is rare with a large volume of urine, the act of urination is prolonged. There is also a variety of neurogenic dysfunction that manifests itself only in the vertical position - a "postural" bladder.

Syndrome of urinary tract obstruction

Violation of the normal flow of urine formed in the urine by the urinary tract is a frequent cause of the formation of chronic diseases of the urinary system. Obstruction, even one-sided and partial, creates conditions for dystrophic and infectious-inflammatory lesions of the kidneys themselves and the underlying parts of the urinary system. The end result of any obstructive syndrome is an ascending infection - pyelonephritis - and an upset violation of kidney functions on the side of the obstruction - from partial tubular disorders to combined dysfunction of the tubules and glomeruli.

As reasons for obstruction, both organic causes, in particular abnormalities in the structure of the kidneys or urinary tract calculi, and the functional features of the urinary outflow pathways associated with pathological phenomena of their motor function, for example reflux, can act as causes of obstruction.

Anatomical obstruction leading to the formation of kidney hydronephrosis is observed most often at the level of the lobic-ureteral joint. Here it is possible to ascertain the internal stenosis of the ureter or its external compression by the aberrant renal artery and its branches. Often, such an obstruction leads to the presence of a horseshoe kidney in the child.

Obstruction at the level of vesicoureteral connection causes first a gradual expansion of the ureter or the development of a megaureter. Obstruction of this type can be observed in the presence of a doubled ureter, which is complicated by vesicoureteral reflux.

Obstruction associated with the presence of a posterior urethral valve in boys is very widespread. In this case, there is an enlargement in the prostatic part of the urethra, hypertrophy of the muscular wall of the bladder with relatively small dimensions of the bladder itself and, as a rule, vesicoureteral reflux.

Bladder and ureter reflux and reflux nephropathy in children

Reverse urine flow from the bladder to the ureter and kidney is usually associated with a congenital failure of the vesicoureteral junction, less often this failure occurs as a complication or consequence of a previous urinary tract infection. Reflux may occur in several family members. The factor predisposing to the onset 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 impairment of protection against reverse urine flow is observed when the anatomy of the urinary bladder triangle is disturbed, doubling 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 structure and function of the kidney is associated with increased hydrostatic pressure of urine on the pelvis and kidney matter during urination, when this hydrostatic pressure proves to be the highest. In addition, urinary stasis or its reverse injection is the most "favorable" for the transmission of an ascending infection. In the classification of vesicoureteral reflux, several degrees are distinguished. At the first degree, only the presence of an X-ray contrast agent in the ureter is detected. At IV and V degrees of expressiveness of reflux, the enlargement and tortuosity of the ureter, dilatation of the pelvis and kidney cups are already visible. Clinical manifestations of even expressed reflux may be minimal, often limited only to isolated urinary syndrome. If one type of reflux is detected, it may be expected that the child and other forms of reflux, including several varieties of intrarenal ones.

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

[14], [15], [16], [17]

Syndrome of kidney failure

The concept of "renal failure" includes the whole set of clinical and laboratory-functional manifestations of the disorder of homeostatic functions peculiar to the kidney. The main manifestations of renal insufficiency are increasing azotemia, diselectrolithy, metabolic acidosis, insufficient or, rarely, excessive water release.

Renal failure can be partial and total. Under partial renal failure is understood as a persistently expressed decrease in any function of the kidneys (eg, acidogenesis, etc.). With total renal failure, disorders of all kidney functions are observed. It usually develops when only 20% of nephrons are preserved. The course of 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 the functions of the tubules can not provide the necessary excretion of nitrogenous and other slags, as well as water. This leads to a profound disturbance of the homeostasis of water and electrolytes.

Acute renal failure in children can be observed with glomerulonephritis, hemolytic-uremic syndrome, kidney necrosis, with various severe diseases (sepsis and other infections), as well as in the onset of acute glomerulo- and pyelonephritis. ARF occurs more often with accidental transfusion of incompatible blood, poisoning with barbiturates, nephrotoxic poisons (mercury compounds, lead) and antibiotics. Already from the above it is clear that very frequent causes of acute renal failure are non-primary causes. Accepted

In this group of reasons as "prerenal". They are all similar in one - 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 blood pressure or effective blood flow in the kidneys. From this moment begins actually defeat of kidneys.

The main symptom of OPN is oliguria, turning into anuria, which is accompanied by headache, anorexia, convulsions, thirst, nausea and vomiting. Rapidly increasing body weight, there are peripheral edema. There is skin itching, refusal to eat, sleep disorders, joins stool disorders and abdominal pain. Breathing acquires the nature of acidotic, arterial pressure may temporarily increase, then arterial hypotension and decompensation of hemodynamics with edema of the lung or brain with coma and convulsions occur. The blood test reveals azotemia, hyperkalemia, hypocalcemia.

In benign OPN, usually 3-4 days later, the polyuric phase occurs, in which a large number of salts, nitrogenous slags are released with urine. After this, the function of the tubules is restored to some extent.

[18], [19], [20], [21], [22]

Chronic kidney failure in children

Chronic renal failure (CRF) is sometimes diagnosed in children with kidney disease, which is quite acute, but acquires a chronic course. The distinction between acute and chronic course of renal insufficiency is based on significant differences in the clinical picture and dynamics of impaired renal function. Such criteria are:

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

More often chronic renal failure develops gradually. Initially, its clinical manifestations are not observed, then patients develop moderate thirst and polyuria. Their manifestations can slowly increase, and often pallor associated with anemia and, often, an increase in blood pressure, there is nocturia, hypostenuria. Subsequently, the density of urine becomes equal to the density of the blood plasma, electrolyte disturbances occur (hypokalemia, hyponatremia). The patients lag behind in growth, are significantly depleted, they have general muscle weakness, drowsiness, headache, loss of appetite, dry mouth, weak muscle twitching (hypocalcemia), uremic odor from the mouth. Later, a critical picture of uraemia with loss of consciousness, significant disorders of the activity of various body systems (cardiovascular, digestive, etc.) and metabolism occurs.

At present, increasing importance in the development of the clinical picture of true uremia is attached not to the content of residual nitrogen (slag retention in the body), but to disturbances in electrolyte metabolism and acid-base state. As with ARF, and with true uraemia, a significant increase in the magnesium content in the blood (up to 2.5 mmol / l) is found. With hypermagnesia, phenomena such as hyperkalemia occur: a disorder in the central nervous system, including coma and paralysis; on the ECG - elongation of the atrioventricular complex, high and pointed tip T, broadening of the QRS complex. In dialysis, during which excess magnesium ions are removed from the body, uremic phenomena also disappear. With uremia, there is also a delay in the body of oxalic, sulfuric and phosphoric acids.

In children, the development of renal failure, both general and isolated, is observed more often, and the rate of increase is usually greater than in adults. This is due to the smaller compensatory possibilities of kidney function 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 penetrate more easily into the central nervous system and other organs, causing toxic damage to them.

In recent decades, chronic renal failure has ceased to be synonymous with the doom of children with kidney damage. Systematic use of hemodialysis, up to outpatient and home procedures of peritoneal dialysis, treatment with genetically engineered preparations of erythropoietin, scrupulous dietary and functional-biochemical control over the course of the disease can significantly improve the quality of their life and ensure its prolongation. Even more vivid immediate and long-term results can be obtained from kidney transplants from relatives or other compatible donors.

[23], [24],

Bedwetting in children

One of the most frequent illnesses in preschool and primary school children, often turning into adolescent and adult periods of life, while defining during these periods significant limitations in the life opportunities of a person. At its core, enuresis is not a single disease, but represents the outcome of the implementation, or syndrome, resulting in many other constitutional features and diseases. With different diseases, the leading factors in the genesis of nocturnal incontinence are various factors, conditions and characteristics of the child as a whole or his urinary, nervous or endocrine systems. The components of the syndrome can be lower urinary tract diseases such as a neurogenic bladder, cervical cystitis or urethritis, an infravesical obstruction, an abnormality of the ureters. These components are leading in 7-10% of cases of nocturnal enuresis.

Violations at the level of spinal centers are responsible for 20-25% of cases of nocturnal enuresis. Immediate role is played by residual-organic deficiency of spinal centers, their ischemia in regional lesions of the spinal cord and related neurogenic dysfunctions of the hyporeflective or hyperreflex type. It can also be said about the significant role of residual-organic insufficiency or dysfunction of cerebral higher centers of urination regulation. The connection between urinary incontinence and the depth and phaseiness of night sleep has been convincingly proved, with the peculiarities of the electroencephalogram of sick children both at rest and during asleep. Urination occurs in the period of the deepest "slow" sleep against a background of some signs of age immaturity by the ratio of the frequency characteristics of the EEG. This group accounts for up to 50% or more of the entire group of children with enuresis.

Some role can play mental illness or accentuation, where enuresis reflects the reaction of active and passive protest (up to 5-7%), but much more significant systemic neuroses, which account for up to 15% of all cases of enuresis.

The association of nocturnal enuresis with maturation factors is confirmed by a significant decrease in the frequency of nocturnal enuresis in the senior school and adolescent years.

[25], [26], [27], [28], [29], [30]

Diseases of the genital organs in boys. Symptoms of lowering of testicles

The testicles develop as formations within the abdominal cavity and advance to the entrance to the inguinal canal during the 7th month of intrauterine development. At 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 somewhat later. Regulation of the progress of the testicle is carried out by hormonal stimuli: gonadotropins, androgens and the inhibitory factor of the parameconephral duct. The self-lowering of the testicle after one year of life becomes unlikely.

Often, the implication of a testicle is ascertained by the doctor or parents erroneously. The cause of this is an increased cremaster reflex and pulling of the testicle (testicles) to the outlet of the groove channel at the time of their palpation.

[31], [32], [33]

Incomplete lowering of testicles (testis)

It can be stated if it is found in some part 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 revealing of the testicles is impossible. When surgical treatment is often attracted attention by its small size, soft consistency, disconnection of the testis and its appendage. Characteristic of a large hernial sac. Spermatogenesis is usually grossly impaired.

Testicle Ectopy

When an ectopic testis passes through the inguinal canal, but upon exiting from it the normal progression of them is disturbed, and they can be located in the perineum, hip or pubic symphysis. Ectopic testicles are easily detected palpation, and during surgery look as normal. The hernial sac is more often absent.

Phimosis

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

Hypospadias

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