URINARY SYSTEM Anatomical & physiological features Mass, size & form Mass & size of kidneys in children

ren of early age are relatively larger than older children & adults Kidney size : body mass for newborns 1:100 , adults 1:200 Children till 1 year old , upper & lower pole of each kidneys are close and resemble a round organ, later bean shape.

Topography

1st y o life : Upper pole at T9-T12, lower pole at lvl upper margin of L4 vertebra, below iliac crest. This feature disappears at 7 y.o.

Paranephron Kidneys of children are more mobile than adults due to the weak development of pre & retronephric fascia. Formation of the fixation mechanism ends at 5-8 y.o. Structure Displacement of kidney in normal during respiration does not exceed 1.8% of the length of child.

1st y o life : Lobular structure (disappears 2-5.y.o), thickness of medullary layer predominates cortical Quantity of nephrons in one volume of tissue in newborns are more than adults. Diameter is less. 2 y o , nephrons are insufficiently differentiated

Morphological maturation of cortical substance ends at 3-5 yo, kidney maturation during school age.

Functional features Filtration abilities LOW due to 1. 2. 3. Histological structure of visceral layer of nephron capsule ( cubic epithelium ) Small nephron ( general filtration surface of nephron 5 x > in adults ) Low hydrostatic P (blood V, flowing through kidney/min , adults 25% AVG output, newborn 5% )

GFR increased and becomes close to adult level at the end of 1st y. o. life. Tubular reabsorption & secretion(different stages of formation in newborn)

1. 2.
3.

Tubular reabsorption of electrolytes & LMW lower , > higher excretion of uric amino acid, phosphates & bicarbonates. Reabsorption of glucose in 1st week of life is = / > adults. Reabsorption of Na+ intensive, during loading of NaCl the newborn kidney continues reabsorbing Na+, as adults it depresses Newborns not able to adequately excrete H20 & NaCl, the kidneys can excrete it in fractions over 24 hrs , simultaneous loading can be accompanied by lack of diuretic effect

4.
5.

Decreased excretion of K+,Ca2+, Mg2+. Regulation acid-base at birth is immature, produces 2 x < acid radicals. Due to immature tubules, low enzyme activity limits production & secretion of H+ & NH3. Base mechanism dont function.

6.

Concentration function Low (early age children) insufficient formation of ADH, immature regulation of mechanism, small long nephron loops, functional incomplete distal tubule epithelium, low GFR . Low specific gravity. Concentration ability = adults 9-12 months.

Optimal homeostatic function 10 11 y.o

1. Due to immature osmo & volume regulation, childrens kidneys cannot rapidly & effectively normalize H20 & elecrtrolyte dysbalance leaving them with high probability of developing edema & dehydration. 2. Diet disorder, early switching to artificial feeding due to low secretory ability in postnatal period can have unfavourable results for children tendency to concentrate in blood / ion, that acquire symptommocomplex ( hyper/hypocalcemia, hyper/hypokalemia) 3. Low & slow excretion of kidney needs to be taken into consideration when prescribing drugs antibiotics/salt solutions
4. Switching to artificial feeding, especially 1st year of life , acid-base stability

may shift to acid direction, causing increased protein load, subsequently, product quantity, subject to eliminating from organism in case of physiological low GFR & tubular ability to eliminate H+. 5. Immature mechanism or regulation of acid-base balance, leads to rapid
URINARY TRACT Early age children have underdeveloped muscle wall & elastic tissue of urinary tract.\

PELVIS : wider than adults, mostly located intrarenal (till 5 y.o), renal sinus expressed weakly. Ureters come out from it at right angles URETERS : Long, wide, hypotonic, relatively low contractility, > coiled, has bends. Distal part (lie directly on wall & submucous layer of UB) very short, with age it lengthens , reaches max 10-12 y.o UB : higher in children, with age descends into small pelvis. Anterior wall not covered with peritoneum, lie against ant abdominal wall. Oval form, mucous membrane thick, friable, good blood supply. Muscle fibers in the hiatus area weakly developed, thats why the orifice is gaping. Physiological capacity of UB of newborn 50 ml 1 yo 5-9 yo 12-14 -100 ml -150-200 ml -300-400 ml

URETHRA : always shorter n wider than . Its curvature in children > expressed than adults. ( attention when cathetherization )

No urination for 24 hours pathological

Daily urine in children till 10 y.o =

Frequency of urination in a day

600 + 100 x (n-1)

Age Newborn(except 1st day of life) 6 mths 1 yr 2-3 y.o Schoolchildren

Times 20-25 15-16 7-8 5-6

Anatomical features of urinary tract in early age Relatively short Hypotonic pelvis Coiling Hypotonic ureters coming out from pelvis at R angles, larger than adult Mobile kidney

Predisposed to disturbance of urodynamics, causing MICROBIAL INFLAMMATORY PROCESS Short intravesical segment of ureter, weakly developed muscle fiber in orifice earea predispose to VESICO-URETER REFLUX Structure of urethra in females, near to anus gives condition for penetrative infection from periureteral region of urinary tract. DIURESIS Newborn 1st 3 days of life Transitory Oliguria / not at all (1st 12 hours) Cause : Little fluid received, extrarenal loss & special haemodynamics. Urination act Reflectory No voluntary urinary retention Conditional reflectory braking of urge to urinate in the process of upbringing. Ability to voluntarily regulate urination develop at end of 1st year of life. By 2nd y.o.l stabilize. Sometimes, emotions play a role in involuntary urination up till 3 y.o , during sleep 5 y.o.

METHOD OF INVESTIGATION 1.When symptoms appear 2.Analysis results 3.Analyse treatment & its effectiveness 4.Presence of disease of urinary tract in close relatives

NSPECTION Symptoms of organs of urinary system SYMPTOM Paleness COMMENTARIES Cause : Arteriole spasm/ anemia.

Waxy paleness : AMYLOIDOSIS of kidney Pale with icteric shade : UREMIA (scratches,ecchymoses, dry coated tongue, ammonia odour from oral cavity/skin)

Edema(pastous) face& extremities

2 types : a)General / anasarca b)Fluid in cavities : ascites,hydrothorax,hydropericardium. Puffy face, periorbital edema, narrow eye fissure ( facies nephritica ), smooth joint contours, lumbar lordosis, clothes indentation When suspect edema : 1.McClure-Aldrich test 2.Daily weighing child 3.Daily measure diuresis

Changes of size & form of abdomen, contour of suprapubic, lumbar region

Abdomen enlarges in volume in ascites a)Vertical : hanging down with sac in the umbilicus (due to increased i/abd P) b)Horizontal : Flattened with distended sides (frog belly) Distended suprapubic region is due to filling of overfilled UB in acute urinary retention. Newborn & child of 1st mth of life filling of UB protrude above pubis. Swelling of lumbar region in affected side paranephritis

Stigma dysmorphogenesis Changes behaviour of child during urination

Genetic nephropathy defect of kidney & urinary tract 1.Breastfeeding age cries during pain urination, either at the time/after urination 2.Hyporeflectory form neurogenic dysfunction of UB, prolonged urination act continues, to relieve urination, children apply P on ant abd wall.

GENERAL BLOOD ANALYSIS Analyse fresh morning urine (midstream) after thoroughly cleaning external genitals.

Symptom Colour

Normal Straw-yellow (depend on main content : urochromes,urobilin, uroerythin,urorosein)

Features of urine in children Amber brown : 1st wk o life, due to production of uric acid , mild crystallization & residue of brick-red nappy stain (kidney infarct of newborn acidic urine). Brickred due to destruction of cells causing release of purine and pyrimidine bases, end products of its metabolism is uric acid Breastfeeding age urine > striking than older children & adults varying from straw yellow- amber yellow

Transparency pH

Full Weak-acid / neutral

As adults Newborn 5.4-5.9

2-4th DOL : pH increase & depends on feeding -breastfeeding pH : 6.9-7.* -artificial 5.4-5.9(physiological acidosis) SG Protein 1002-1030 (depend on H20 load) Till 0.033g/L Lowers SG in 1st WOL , =/< 1016-1018 1st DOL Transitory proteinuria permeable nephron,tubular & capillary epithelium Mature babies it disappears in 4-10th DOL (premature-later) Organic elements of urine sediment : a)RBC b)WBC 0-2 in FOV c)Cylinders 0-4 in FOV d)Epithelial cells None One Non organic sediment(salt) Depends on colloid condition, pH, other urine contents & condition of epithelium of urinary tract Newborn characteristic sediment from uric acid Older age uric acid is from abundant intake of meat, physical exertion, fever, starving, cytostatics, GC, increased catabolism. Oxalates present when excess consumption of products rich in oxalic() acid has 5-6 in FOV Same as adults

Results of quantitative tests in healthy children Sediment elements WBC RBC Nechiporenko method Till 2000 Till 1000 - Test Till 2 000 000 Till 1 000 000

Bacteriological investigation of urine Pathological bacteria = > 10 (a=4) microbial bodies / 1 L of urine in newborns & early age children, > 0.5-1.0 x 10 (a=5) in children of older age Functional Renal Tests Investigated function GFR Tubular reabsorption Concentration function Method Clearance of endogenous creatinine(modified Reberg test), according to quantity of plasma/mL , full release of substance / min Rebergs Test Zimnitsky Test Normal Newborn 30-50 mL/min/1.73m 1 year 80-120 mL/min/1.73m 97-99% SG=1018 /> (N) Difference btwn max & min SG = 0.010-0.012 proves preserved ability of concentration fxn Daily dieresis = 2/3-3/4 of 24 hours To evaluate function of a)prox tubule evaluate clearance of free amino acid & phosphates b)distal tubule excretion of H+ & electrolytes (Na+,K+,Cl-,phosphor, Ca2+)

SEMIOTICS Anomalies of kidney development

Quantity changes

Accessory kidney Doubling kidney (2 pelvis in one mass of kidney parenchyma) Agenesis(full absence) Aplasia(absence of oorgan with presence of vascular stalk)

Form changes

Horse-shoe (union of lower / upper poles) Ring (both ends unite) L-form S-form

Position changes Hypoplasia of kidney

Dystopia in embryonal fold, anomalies of rotation Simple (decrease relative mass of organ > than for unilateral, >1/3 for bilateral , decrease quantity of calyxes) Dysplastic (decrease relative mass of kidney with disorder of its structures)

Dysplasia Congenital hydronephrosis

group of congenital kidney defects with disturbance of differentiation of renal tissue & presence of embryonal structures progressive widening of pelvis & calyces due to disturbance in urine flow. Most often cause is stenosis of pelvic-ureter segment, due to recanalization of ureters in embryogenesis.

Anomalies of ureter development 1. 2. 3. 4. 5. 6. 7. Doubling uni/bilateral Splitting at cranial/caudal part Strictures Ectopia (atypical position) of orifice Diverticula Megaloureter Retrocaval ureter

Anomalies of UB 1. 2. 3. Agenesis Extrophy (congenital crevice of UB & abdominal wall) Diverticula

Anomalies of urethra: 1. Agenesis

2.

Atresia/stenosis Hypospadia (birth defect of the urethra in the male that involves an abnormally placed urinary meatus (opening). Instead of opening at the tip of the glans of the penis, a hypospadic urethra opens anywhere along a line (the urethral groove) running from the tip along the underside (ventral aspect) of the shaft to the junction of the penis and scrotum or perineum.)

3.

4.

Epispadia (type of malformation of the penis in which the urethra ends in an opening on the upper aspect (the dorsum) of the penis)

Urinalysis Changes URINARY SYNDROME Proteinuria Haematuria Leucocyturia Cylinduria Salt sediment changes

Isolated/Different combinations

URINE COLOUR CHANGES due to different pathological process,durg intake and also healthy children after consumption of food with certain substances Colour Straw-yellow Colourless Dark-yellow Red (meat soak in H20) Dark-brown Orange Green Green-brown (beer colour) Cause Normal Diuretics, infusion therapy, CRF Increased [bile pigments] Oliguria-exrarenal loss fluid,fever,ascorbic acid consumption Erythrocyturia,haemoglobinuria,myoglobinuria,porphyrinuria,beetroot intake, cherries, blackberries, phenolphthalein Urobilinogen(haemolytic anemia) Uraturia(acidic urine infarct of newborn), consumption rifampicin, nitrofurantoin,furazidine Bilirubinemia (mechanical jaundice) Bilirubinemia & urobilinogenuria ( parenchymatous jaundice)

\ LEUCOCYTURIA

Neutrophilic : Microbial-inflammatory dis of genitourinary tract (pyelonephrities,cystitis,urethritis,tuberculosis etc) Mononuclear & lymphocytic : Tubulointerstitial tissue Glomerulonephritis,interstitial & lupus nephritis

HAEMATURIA Revealed in urine > 2 RBC FOV Macrohaematuria Microhaematuria Renal Extrarenal

Macrohaematuria acquire red/brown tone, <<meat wash>> is evidence of Hb/destroyed RBC

DEGREE

Microhaematuria under microscope (no visual colour change)

Insignificant 10-15 RBC FOV Moderate 20-50 RBC FOV (no visible colour changes)

Haematuria
Renal pathological process in kidney tissue Glomerular Non glomerular Prerenal Postrenal

CAUSE

Extrarenal

DEGREE

Traces 0.03g/L protein in general urinalysis Insignificant till 1.0 g/day Moderate 1.0-3.0 g/day Selective LMW protein (<65000)albumins Non selective Increased clearance Glomerular damage/change of medium & HMW proteins 2 basal membrane macroglobulin, -lipoprotein, Tubular disorder of ability of tubule to reabsorb protein from primary urine Mixed

PROTEINURI A

CONTENT OF PROTEIN IN PLASMA

CAUSE

EXTRARENAL RENAL

Prerenal Increased formation of LMW protein(light chains of Ig, Hb, myoglobin) that is filtrated normally by glomerulus, increased tubular ability to reabsorb Postrenal

URINALYSIS CHANGES Form Transparency pH

Cause Incomplete transparency cellular elements & mucous Urine turbid bacteria, salt, fat droplets Acidic overconsume meat, GN, diabetic coma Alkalic-vege diet, overconsume alkali mineral H20, vomit(loss Cl-), inflammatory process in urinary tract, hypokalemia, phosphaturia, edema, bacterial fermentation in intestine

SG

Fluctuation of specific gravity <1010 indicates disturbance of concentration function HYPOSTHENURIA Constant SG, corresponding to SG of 1 urine (1008-1010) ISOSTHENURIA Decreased SG disturbed concentration present in chronic GN with severe tubulointerstitial tissue damage, interstitial nephritis, congenital & inherited kidney disease, chronic pyelonephritis in sclerosing interstitial stage.

Increased SG HYPERSTHENURIA (>1030) glucose,protein,salts

Cylinduria

Associated with sedimentation of protein in lumen of tubules. Hyaline : physical exertion,fever, orthostatic proteinuria, nephrotic syndrome Granular : Severe degenerative tubular damage Waxy : Damaged tubular epithelium, nephrotic syndrome Epithelial degenerative changes of tubules in GN, nephrotic syndrome Erythrocytic Haematuria renal genesis Leucocytic Leucocyturia renal genesis

Glucosuria Ketonuria Urobilinogenuria, urobilinuria Epithelial cells

Excess consumption of sugar, infusion glucose solution, DM, disorder of glucose reabsorption in proximal part of nephron (tubulopathy, interstitial nephritis) Acetonemic vomiting, DM Haemolysis, liver damage, constipation, enterocolitis, intestinal obstruction Squamous epithelium ( upper layer epith of UB) Acute & chronic cystitis Cynlindric & cubic epithelium (epithelial tubule, pelvis, ureter)-inflammatory disease, dysmetabolic nephropathy

Crystalluria

Residues from uric acid & its salts in children with acidic urine diathesis, disturbed formation of ammonia in tubular epithelium. Triplephosphate & amorphic phosphate - microbial-inflammatory disease , 1 & 2 tubulopathy in the background of hyperphosphaturia & disturbance of acido& ammoniogenesis.

DISTURBED URINE PRODUCTION Form of disturbance Polyuria Definition Increase daily dieresis > 2 x in comparison to N (children older age > 1500 mL/m/ d) Cause Oliguria Decrease daily diuresis from 1/3-1/4 of normal according to age

Massive water exertion. Edema. Osmotic diueritcs Severe kidney dysfxn(renal insuff in polyuric phase) Diabetes insipidus GN, pyelonephritis, uremia. Extrarenal :

-limited fluid intake -increased sweating -profuse diarrhea -repeated vomiting -growing cardiac edema Transitory oliguria in newborn : 1st 3 days of life Anuria Decrease dieresis (6-7% from normal / full absence) No urine from kidney to UB True anuria / obstruction True anuria ARF, impaired blood supply to kidney(shock,acute blood loss), toxicity, acute infln of renal parenchyma(acute pyelonephritis) Ischuria Acute urinary retention Disturbed outflow of urine from UB. Acute/Total traumatic rupture / obturation by stone of urinary tract / prolonged retention due to atonia UB. Frequent retention (incomplete emptying, residual urine) obstacle at UB neck / urethra (cervix fibrosis, valvular, stricture urethra, stone & tumour of UB ureterocele)

Incomplete chronic retention Interrupted stream, late urination, carried out in 2 stages,diverticula or UB , urethrohydronephrosis, vesico-ureter reflux

Nicturia EDEMA

Predominatn urination at night

CRF

Decreased oncotic P plasma decreased protein concentration (albumin), in blood Increased permeability of capillaries as a result of hyaluronidase activity Activation of RAAS increased Na & H20 reabsorbtion

Decreased GFR ACUTE / CHRONIC GN, AMYLOIDOSIS, UREMIA, HEAVY METAL POISONING

NEPHROTIC SYNDROME Edema

Severe proteinuria (>50mg/kg/d)

Hypoproteinemia (hypoalbuminemia)

Hyperlipidemia

Clinical form Total all symptommocomplex Partial - absence of edema / one of the lab symptoms Clean Not accompanied by haematuria , no high BP Mixed with haematuria / high BP

PRIMARY NEPHROTIC SYNDROME Congenital & infantile nephrotic syndrome GN: Minimal glomerular changes Focal-segmented glomerulosclerosis Membranous Mesangioproliferative Mesangiocapillary Extracapillary with semilunar Fibroplastic

SECONDARY NEPHROTIC SYNDROME Intrauterine infection (toxoplasmosis, CMV, congenital syphilis( Infectious dis (Hep B & C, TB, HIV, syph) Systemic dis of CT & systemic vasculitis Structural dysembriogenesis of renal tissue Metabolic disease Thrombosis of renal vein Inherited dis & synd Chromosomal dis

NEPHRITIC SYNDROME

Extrarenal symptom (edema, high BP, changes of CVS, CNS) Renal symptom (oliguria,haematuria,proteinuria,cylinduria)

Acute nephritic syndrome is most char for GN.

DYSURIC SYNDROME disturbed act of urination Disturbance Reduced urination Frequent urination (pollakiuria) Characteristics Hyporeflectory UB, significant fluid loss due to intensive sweating, repeated vomiting,diarrhea, growing edema, oliguria, uremia In healthy children during cold Pollakiuria is combined with pain during urination Cystitis Pollakiuria > in daytime , increase during movement UB stones. Also in : urethritis, prostitits, reflectory influence in intestinal direction(anal fissue) Incontinence without urgency, dont depend on act of urination Ture/false. True : Characteristic for damage SC, SC hernia. False :ectopy of ureter orifice in urethra canal & vagina, extrophy of UB, vesico-rectal & urethrorectal fistula Eneuresis incontinence during sleep Urinary incontinence- cannot retain during urges to urinate Stranguria pain during urination NS pathology, psychic disturbance / patho in inf urinary tract Cystitis, neurogenic dysfunction of UB, diverticulitis in UB stone Inflammation of UB, urethra. Cystitis pain & sharpness at end of urination Urethritis during urination & remains for a while after it.

PAIN SYNDROME 1. Stretching of renal capsule parenchymatous dis(GN,amyloidosis), in patients with CHF. Pain is not intensive, dull, constant.

2. 3.

Inflammatory edema of mucous membrane/stretched renal calyx (pyelonephritis) Intensive & increasing pain

Spasm of urinary tract acute, attack-like, very intensive in lumbar/along ureter (renal colic) kidney stone disease

Pain during urination in lumbar region bi / uni lateral side vesico-uretero reflux. Pain in UB are cystitis, stones, urinary retention Pain in urethra inflammation ARTERIAL HYPERTENSION Due to damage of renal parenchyma/constriction of renal vessels RAAS activated increase periph R retention of Na+ & H20 increase CO & circ bld V

Parenchymatous renal HPT diffuse renal parenchyma damage : acute & chronic GN, interstitial nephritis, congenial renal anomalies, amyloidosis, renal tumour, renal trauma Vasorenal HPT stenosis of renal aa, multiple renal aa, anomalies of renal vv, thrombosis/aneurysms, aortoarteritis, juvenile polyarteritis with damage of renal aa