seminar renal stone on 24.10.16

EVALUATION OF RENAL STONE IN CHILDREN

Presented By-DR. AZMERY SAIMA

DR. RAKHI MAITRAYEE BHOWMIC

PHASE A ( NEONATOLOGY)

Bangabandhu Sheikh Mujib Medical

University (BSMMU), Dhaka.

Case scenario• A 15 year old boy admitted in hospital with the complaints of severe left flank pain , haematuria for 10 days. But patient has no fever, gave history of inadequate fluid intake. Family history of nephrolithiasis positive.

INTRODUCTION Kidney Stones, also known as renal

calculus or nephrolith, are small, hard deposits of mineral and acid, salts on the inner surfaces of the kidneys.

If stones grow to sufficient size they can cause blockage of the ureter.

• Urolithiasis- stone in urinary tract.• Nephrolithiasis- stone in renal tissue.• Nephrocalcinosis- deposition of calcium in the substance of the kidney.

EPIDEMIOLOGY• Urinary lithiasis in children is related to genetic, climatic, dietary & socioeconomic factors.

• The incidence is increasing : in 1996 the rate of symptomatic nephrolithiasis was 7.9 in 10000, whereas in 2007 it was 18.5 in 10000 .

• Approximately 7% of urinary calculi occur in children younger than 16 year of age.

EPIDEMIOLOGY

• The prevalence of pediatric urolithiasis in developed countries had fallen following improved socioeconomic condition, but currently is increasing. This may be explained by an increase in diagnosis secondary to improved diagnostic technique.

INCIDENCE Urinary calculi are more common in men than in

women. (3:1) Incidence of urinary calculi peaks between the 3rd

and 5th decades of life. 80% of stones under 2mm in size 90% of stones pass through the urinary system

spontaneously There is seasonal variation with stone occurring

more often in the summer months.

STONE FORMATION

Highly concentrated urine constituents crystallize and harden to form calculi.

Kidney stones form when urine contains more crystal-forming substances - such as calcium, oxalate and uric acid.

At the same time, urine may lack substances that prevent crystals from sticking together, creating an ideal environment for kidney stones to form.

The crystals get deposited on the nucleus and continue to grow. These can some times adhere to the renal papillae.

Inhibitors and promotors of stone formationINHIBITORSInhibits crystal Growth - Citrate Magnesium Pyrophosphate ZincInhibits crystal Aggregation Glycosaminoglycans Tamm- Horsfall Protein

PROMOTERS Bacterial Infection Anatomic Abnormalities – PUJ obst. Altered Ca and oxalate transport in renal

epithelium. Prolonged immobilisation. Increased uric acid levels - taking

increased purine subs– promotes crystalisation of Ca and oxalate

Stone formation• Stone formation depends on four factors:1. Matrix2. Precipitation-crystallization3. Epitaxy 4. Absence of inhibitors of stone

formation in the urine

TYPES OF KIDNEY STONES Calcium oxalate

Calcium phosphate

Struvite

Uric acid

Cystine

Fig: staghorn calculi

Calcium stones: Most kidney stones are calcium stones, usually in the form of calcium oxalate and calcium phosphate. Oxalate is a naturally occurring substance found in food. Some fruits and vegetables, as well as nuts and chocolate, have high oxalate levels.

Uric Acid: This type of kidney stone is more common in men than in women. They can occur in people with gout or those going through chemotherapy.

Struvite: This type of stone is found mostly in women with urinary tract infection. These stones can be quite large and cause urinary obstruction.

Cystine: Cystine stones are rare. They occur in both men and women who have the genetic disorder cystinuria.

Other: Other, rarer types of kidney stones also can occur. Such as xanthine, dihydroadenine stone, indinavir etc.

RISK FACTORSHIGH MINERAL CONTENT IN DRINKING WATER

DEHYDRATION

FAMILY OR PERSONAL HISTORY

DIETARY INTAKE

BEING OBESE

PATHOPHYSIOLOGY• Slow urine flow, resulting in super saturation of the urine.

• Damage to the lining of the urinary tract

• Decreased inhibitor substances in the urine that would otherwise prevent super saturation and crystalline aggregation.

Approach to diagnosis of renal stone

Approach to renal stone1. Detailed history 2. Clinical examination3. Relevant Investigations

HISTORY

• Age – uncommon in children.• Sex- more common in male (3:1)• Geography -More in southeast Asia.• Climatic & geographic factors• Occupation – sedentary lifestyle.

HISTORY… Presentation is variable.• Children may present initially with- loin pain (50%),abdominal pain haematuria features of UTI, N, V dysuria, urgency, frequency may be asymptomatic

• Birth history- PT (12-64%), LBW, diuretics, duration of oxygen therapy.

• Family history of nephrolithiasis, consanguinity• Past illness – similar type illness, IBD, Cystic

fibrosis, malignancy.• Dietary history-Fluid intake, vitamin & mineral

suplementation, tea, coffee, dairy products, spinach, beet, peanuts.

• Personal history- immobility, bowel habit (cr. Diarrhoea).

• Drug history-Loop diuretics, corticosteroid, is geeting chemotherapy.

• An underlying metabolic abnormality –

symptoms of thirst polyuria, anorexia, muscle cramps,

abdominal & bone pain• Evaluation of growth & development, bone structure, blood pressure.

Presentation• Factors

–Size of stone–Location of stone–Degree of obstruction–Presence of infection–Presence/absence of normal contralateral kidney

Clinical feature:

Renal stone:• 1.Recurrent flank pain or renal colic

occurs in 40-75% of children or Abdominal pain

• 2.Gross or Microscopic hematuria in 33-90% of children

• 3.Repeated attack of UTI

• 4.Occasionally the stone may be silent & leads to obstructive uropathy .

Ureteric Calculus

1.Always of Renal Origin

2.Commonly of elongated shape

3.Can get impacted at 3 constrictions of ureter

4.Can cause: ObstructionHydronephrosisInfectionUreteral Stricture

5.C/F:Colicky Pain (from loin to tip genitalia)

Hematuria, dysuria, frequency, strangury

Tenderness in iliac fossa

Bladder Calculus1.Primary vesical calculus:

• occurs in sterile urine

• Comes down from kidney through ureter and gets enlarged in bladder (usually oxalate stone).

• Can irritate bladder mucosa causing hematuria

2.Secondary vesical calculus:

• Occurs in presence of infection (commonest bladder stone)

• Usually phosphate stone, occurs in bladder only

Urethal stone:• Dysuria

• Inability to void/difficulty voiding.

• Present with terminal hematuria

• It is uncommon to pass urethral calculus

without symptoms

Investigations for Urolithiasis:• 1.Imaging

Plain X-ray

Ultrasonography

IVU

CT abdomen

• URINE for

Routine analysis(including & specific gravity)

Culture

Spot specimen: Ca, protein, uric acid, oxalate, citrate ,Mg, creatinine.

24hr urine:

Volume, protein, creatinine, Na, Ca, Mg, oxalate, phosphorus, uric acid, citrate, cystine.

• Stone analysis.

PH

BLOOD for• Urea

• Creatinine

• Electrolytes

• PH

• HCO3

• Ca

• Phosphorus

• Uric acid

• Citrate

• Cystine

• CBC

Imaging: Plain X-ray KUB• Not useful

– Radioluscent stone– Stone <4mm– Lies over sacrum/bony structures

• Bowel gas can obscure its efficacy

• Cannot differentiate– Stones– Calcified LN

• Sensitivity: 50-70%

X-ray findings:

75% radiopaque

Imaging: KUB Ultrasound• Sensitivity to detect renal calculi ~95% (complement

KUBXR)

• Very sensitive to detect obstruction and radioluscent stone,Hydronephrosis

• Non-invasive

• May miss small stone (<5mm) and ureteral stone

Imaging: IVU• Provide anatomical and functional informations

• Size and location of the stone

• Presence and severity of obstructions

• Renal and ureteral abnormalities

IVU:

CT Scan Renal StoneOn CT almost all stones are opaque(has 96% sensitivity& specificity), but vary considerably in density.  

1. calcium oxalate +/- calcium phosphate: 400-600HU

2. struvite (triple phosphate): usually opaque but variable

3. uric acid: 100 - 200HU

4. cysteine: opaque

5. HIV medication related stones (indinavir) difficult to visualize

Urine analysis:

Normal urinary excretion of important constituents:Constituent

24hrs excretion

Ca Less than 4mg/KgProtein Less than 100mg/m2

Oxalate

Less than 2mg/Kg

Mg More than 0.8mg/KgUric acid

Less than 35mg/kg

Cystine

Below 10yrs :less than 13 mg/1.73m2

Above 10yrs :30-50 mg/1.73m2

Citrate More than 320 mg/1.73m2

Creatinine

Newborn: 8-10mg/KgChild: 15-20mg/Kg

Na More than 3000mg/1.73m2

Phosphorus

Less than 1100mg/1.73m2

Method of stone analysis

Test Procedure Observation 

1- pH

Sample + 1 drop of universal

indicator

Yellow- red:

Acidic

Green: Neutral

Blue: Alkaline

2-Carbonate Sample + 2 drops of 2N HCL Effervescence

3-Oxalate Sample mixed with equal

portion of resorcinol +1 drop

of conc. Sulphuric acid

Dark blue green

color

4-Phosphate Sample + mixture of [2 drops

of cobalt chloride + 2 drops

of Na CN ]+ 1 drop of 10N

NaOH

Blue color

5-Calcium Sample + 2 drops of H2O + 2

drops of 2N HCL + 5 drops

of 10N NaOH add gradually.

Gelatinous PPt.

6- Cystine

Sample + 2 drops of NaOH

10% + 1 drop of amm.

Hydroxide 25% + 2 drops

of Na CN allow to stand for

5 min. + few crystals of

sodium nitroprusside

Red color

7-

Ammonium

salts

Sample+ 2 drops NaOH

10% + 5 drops of cobalt

chloride

Blue color

8-Uric acid Sample + 2 drops of NaOH

mix. + 3 drops of

phosphotungestic acid

Blue color

9-

Magnesium

Sample + 2 drops of

NH4OH 25% + 2 drops

Na2 PO4 0.1M

Gelatinous

white PPt.

How to Investigate Urolithiasis??Urine- RME- 24 hour

urine collection

- Urine C+S

Blood- CBC- Renal

Profile

Imaging- KUB X-

ray- KUB

Ultrasound

- IVU

Plan for Intervention- DTPA

If IVU contraindicated- CTU

Algorithm for the investigation of renal calculi:

Stone

HypercalciuriaHyperoxaluria(primary/

enteric)Hypocitraturia

Increased urinary cystine(cystinuria)

Hyperuricaemia(IEM,Diuretic)

Hyperuicosuria(IEM,TLS,Chr.diarrhea)Infection

Passed

In urina

ry tract

MgNH4 PO4

Paediatric urologist

HypercalcemiaMetabolic

acidosis(DRTA,PRTA)Hypokalaemia(RTA,Bartt

er’s)Hypochloremia

Hypomegnesaemia

Captured

Ca phospha

teCa

OxalateCystine

Uric acid

Not captured

Metabolic evaluation

Not captured

Algorithm for investigation of Hypercalciuria:Hypercalcae

mia

Hypophosphatasia

vit D excessImmobilization

malignancyhyperparathyroid

ism

Yes

No

No

Metabolic acidosis

Metabolic alkalosis

No

Yes

Yes

Rickets,GF,

aminoaciduria,

glycosuria,

acidosisHyperchloraemia,urinary pH

6

Proximal RTA,Fanconi’s

Syndrome,Tubulo-interstitial disorder

Distal RTA

Bartter’s syndrome,loop diureticsIdiopathic

hypercalciuria, immobilization ,Juvenile chronic

arthritisDent’s diseaseMedullary sponge

kidneyHaematuria,UTI,dilated

tubules on IVP

Low mol. Wt.

proteinuria,fam his

Electrolytes,

urinalysis NAD

Case:Siam,6months old boy presented with passage of sand like substance during micturition and not growing well since his 2months of age.

Nephrocalcinosis• Refers to renal parenchymal calcification. The

calcification may be dystrophic or metastatic.

1.With dystrophic calcification, there is deposition of calcium in necrotic tissue. This type of parenchymal calcification occurs in tumors, abscesses, and hematomas.

2.Metastatic nephrocalcinosis occurs most often with hypercalcemic states caused by hyperparathyroidism, renal tubular acidosis, and renal failure.

Metastatic nephrocalcinosis can be

• further categorized by the location of calcium deposition as cortical or medullary.

Causes of Nephrocalcinosis• Causes of cortical nephrocalcinosis include

1.Acute cortical necrosis

2.Chronic glomerulonephritis

3.Chronic hypercalcemic states

ethylene glycol poisoning, sickle cell disease, and rejected renal transplants

• Causes of medullary nephrocalcinosis include

1.Hyperparathyroidism (40%)

2.Renal tubular acidosis (20%)

3.Medullary sponge kidney

bone metastases, chronic pyelonephritis, cushing’s syndrome, hyperthyroidism, malignancy, renal papillary necrosis, vitamin D excess, and Wilson’s disease.