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STONE DISEASE

STONE DISEASE...tract, second heterogeneous nucleation presence of abnormal substance favor the crystal formation pathogenesis •In normal urine the solubility of calcium oxalate

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  • STONE DISEASE

  • Calculi are typically composed of urinary chemicals that are usually soluble in urine but occur in amounts too high to stay dissolved

    Stones could be described according to the site (kidney, bladder, ureter, urethra) or radiodensityon KUB (radio opaque, radiolucent, relatively radiolucent) or the size and composition

  • • Calcium oxalate ..80%

    • Uric acid …5-10%

    • Calcium phosphate …10% mostly mixed

    • Struvite …2-20%

    • Cystine…1%

    • Others as drug induced

  • pathogenesis

    • The solution is considered saturated when reach the point at which the added salt crystals will not dissolve

    • The concentration at this point is called saturation product,

    • In urine despite the concentration of stone forming component exceed the solubility product crystallization not necessary happen because of presence of inhibiters

  • • In this state of saturation the urine is considered metastable

    • concentration at which no longer mount of crystal be dissolved and crystallization will happen is called formation product

    • the urine above formation product is considered unstable

  • • If urine is under saturated (below the solubility product )crystals will not form

    • If urine is unstable (above formation product) crystals will form

    • If urine is metastable (between the both product ) inhibiters will prevent crystallization in most of time

    • Under certain circumstances crystal will form if urine is metastable , first if there is obstruction in upper urinary tract, second heterogeneous nucleation presence of abnormal substance favor the crystal formation

  • pathogenesis

    • In normal urine the solubility of calcium oxalate is 4 times higher than it’s solubility in water

    • This is because various inhibiters of crystallization (citrate,GAG,Tamm-Horsfallprotein)

    • The earliest phase of crystal formation is nucleation ,then aggregation process will start

  • Epidemiology

    • The lifetime prevalence of kidney stones is 8.8% in USA

    • The peak incidence of stone disease is between (20-50) years

    • Gender: male to female ratio 1.4:1

    • Race: the highest prevalence of stone disease is between the whites

    • Prevalence: proportion of persons who have a condition in particular time

    • Incidence: proportion of person who develop a condition in particular time

  • Geography: stone disease has higher prevalence in hot and dry climate, however the genetic and dietary influences outweigh the effect of geography

    Occupation: workers who exposed to high temperature have higher risk of stone disease, also individual with sedentary occupation has higher risk of unknown reason.

  • • Obesity: obesity associate with increase excretion of oxalate and uric acid, also associate with lower urine PH.

    • Diet: high protein intake (high urinary oxalate),high salt intake cause hypercalciuria, low calcium diet ??

    • Water: high water intake decrease the incidence of stone disease

  • Calcium oxalate stone

    • Calcium oxalate : dehydration, hypercalciuria, hyperoxaluria, hypernatrituria, hypocitraturia and hyperuricosuria

    • Hypercalciuria : increase absorption from GI like in high level of VIT D,

    • renal hypercalciuria : impaired renal reabsorption of calcium and so increase renal excretion of calcium, lasix(furosmide) inhibit calcium reabsorption and so hypercalciurea

    • Resorptive hypercalciuria: primary hyperparathyroidism lead to excessive bone resorptionand so high level of calcium

  • • Drugs: steroid increase bone resorption and reduce bone formation

    • Hyperoxaluria: primary oxaluria which is rare autosomal recessive disorder associate with high level of oxalate

    • Enteric hyperoxaluria : fat malabsorption leads to increase the attachment of fat with calcium and so more free oxalate and increase it,s absorption like in IBD and enteric bypass

    • Dietary hyperoxaluria: like chocolate and nuts, VIT C intoxication

  • • Hypocitraturia: metabolic acidosis reduce urinary citrate level

    • Hyperuricosuria: is associate with calcium oxalate stone by unknown mechanism and associate with uric acid stone , the most common cause is high dietary intake (meat) , gout and multiple myeloma, post chemotharapy

  • Uric acid stone

    • The three main determinant of uric acid formation low PH, low volume, hyperuricosuria

    • Urin PH is a critical factor in determining uric acid solubility, uric acid is less soluble in acidic urine (low PH), DM and obesity is associated with low urinary PH

  • Cystine stone

    • cystinuria is inherited autosomal recessive disorder characterized by decrease renal reabsorption of cystine amino acid

  • Infection stone

    • Struvite =infection=triple phosphate stone: is composed of magnesium ammonium phosphate

    • Bacterial urease convert urea into ammonia and carbon dioxide

    • This will result to alkaline urine which favor conversion of ammonia into ammonium

    • The alkaline condition also increase concentration of phosphate

  • • Proteus is the most common organism associate with infection stone

    • E coli rarely secretes urease

    • Infection stone is more in female

  • Calcium phosphate stone

    • Distal renal tubular acidosis(type 1): inability to acidify the urine inspite of metabolic acidosis, due to abnormal collecting duct secretion of acid

    • Characterize by hypokalemia and hyperchloremia, metabolic acidosis and alkaline urine , calcium phosphate stone and nephrocalcinosis, hypocitraturea, hypercalciurea

    • Acetozolamide (carbonic anhydrase inhibiter diuretic): block bicarbonate absorption and so alkaline urine wthe calcium phosphate stone

  • • Urinary obstruction such as PUJS and hors shoe kidney associate with stasis and infection and so increase incidence of stone

    • Medullary sponge kidney: ectasia of renal collecting duct which associate with distal RTA and hypercalciurea

  • Kidney stones

    • May present with symptom or found incidentally

    • Symptoms include pain, hematurea,

    • Infection stone present with recurrent UTI, or infection complication

  • • Radiological assessment of kidney stone:

    • KUB: exposure from level of diaphragm to inferior pubic ramus, stone is classified according to appearance on KUB into:

    • Radio opaque: calcium phosphate and calcium oxalate

    • Relatively radiolucent: struvite, cystine

    • Radiolucent: uric acid , indinavir

  • Radio-opaque

  • Semi-radiolucent

  • • stones can be characterised by their size and shape on KUB

    • Stone that occupy the renal pelvis and one or more renal calyces is called staghorn stone, which mostly composed of infection stone stone

    • Limitation : stones could be obscured by overlying gas or bone, pelvic calcification could confused with ureteral stone, radiolucent stone does not appear on KUB

  • 3-size, staghorn stone…

    .

  • Renal ultrasound : sensitivity to identify renal stone is variable, operator dependent

    CT scan without contrast: the modality of choice to detect renal stone

    It is more sensitive than KUB and provide anatomical information about the kidney and degree of HN

  • radiolucent

  • • Small asymptomatic stone in older age group could be managed by watchful waiting

    • Struvite stone is not suitable for watchful waiting because the risk of RI and sepsis.

    • The minimally invasive modality for stone fragmentation include SWL,URS,PCNL

    • Deciding the best treatment option depends on stone related factors, anatomical factors, clinical factors

  • Treatment

    1- ESWL: extracorporeal fragmentation of stone

    effects depend on stone size, location, anatomy of collecting system, and stone composition

    ESWL is less effective in stone>1 cm ,lower pole stone or calyceal diverticulum stone and cystinestone and obese patient

    Side effect of ESWL include hematurea or perirenal hematoma

  • • ESWL is contraindicated in:

    • Pregnancy

    • Bleeding tendency

    • Arterial aneurysm near the stone

    • Obstruction distal to the stone

    • Skeletal malformation

  • ESWL

  • 3- Flexible ureteroscopy and laser :- in ESWL failure,or contraindicated , in lower pole stone less than 1 cm with unfavourable factors such as obesity, and hard stone ( cystine stone)

  • 2- PCNL:- in stone more than 2 cm, failed other modalities and anatomic abnormality

    The first line treatment in staghorn and stone more than 2 cm or lower pole stone more than 1 cm

  • PCNL

  • Flexible ureteroscopy

  • 4-laparoscopic or open pyelolithotomy rarely done

  • medical therapy ( dissolution therapy):-

    uric acid stone are suitable for dissolution therapy

    Dissolution therapy is based on hydration, urine alkalinization with potassium citrate, and allopurinol

    Allopurinol inhibit xanthine oxidase and so decrease the level of uric acid

  • Ureteric stone

    • Presents with ureteric colic, fever, hematuria, and RF

    • Acute management of ureteric colic is analgesia with narcotic or NSAID better analgesic effect because it reduce the GFR and so the dilatation

    • Conservative management involve analgesia for pain exacerbation and medical expulsive therapy and waiting the stone to pass spontaneosly.

    • Example of MET alpha 1 blocker and calcium channel blocker.

  • • Factors that favor the passage of stone

    • Stone less than 5 mm

    • Lower ureteric stone

    • Less duration of symptom

    • Less degree of HN

  • • Indication of urgent intervention to releiveobstruction or remove the stone :

    • Pain not responding to analgesia

    • Fever (obstructive pyelonephritis): jj stent vsnephrostomy

    • Impaired renal function: single kidney or bilureteric obstruction

    • Prolonged unrelieved obstruction: more than 4 weeks

  • • Methods to releive the obstruction:

    • Jj stent

    • nephrostomy

  • JJ stent

  • Nephrostomy

  • Upper ureteric stone

  • Middle ureteric stone

  • Lower ureteric stone

  • CTKUB

  • Treatment

    Treatment option for ureteric stone

    ESWL: good option for upper ureteric stone less than 1 cm in size

    Ureteroscopy : semi rigid URS with intra corporeal fragmentation of the stone

  • 4-if more than 5mm according to size and sites:-

    - More than 10 mm whatever site best TX ureteroscopy and intracorporal lithotripsy

    - Less than 10 mm upper ureter.. Best Tx ESWL

    - Less than 10 mm mid ureter .. Best Tx URS

    - Less than 10 mm lower ureter .. Best Tx URS

  • Intracorporal lithotripsy

    1- pneumatic lithotripsy :- bursts of compressed air, safe, but stone migration

    Ultrasonic lithotripsy:- break and suck stones, used in PCNL

    3-Laser lithotripsy:- by photo thermal mechanism so stone vaporization, less stone migration

    4-Electrohydraulic lithotripsy:-

    Narrow safety margin,

  • Evaluation of stone former

    low risk stone former:

    History about underlying condition, medication, diet and fluid intake

    CBC and KFT with electrolyte, calcium, PTH, uric acid, urin test for infection and PH

    Radiography

    Stone analysis

  • • High risk stone former:

    • Recurrent stone former

    • Strong family history

    • Gout

    • Osteoporosis

    • Single kidney

    • Inflammatory bowl disease

    • Infection, cystine, uric acid stone

  • • Workup for high risk stone former include: 24 hour urinary collection for calcium, oxalate, uric acid, cystine, and evaluation for RTA with the basic work up for low risk

  • • Dietary recommendation of stone former:

    • Increase in fluid intake( urine output at least 2 liters

    • Protein and salt restriction

    • Avoidance of oxalate( chocolate and nuts)

    • Moderate calcium intake

  • Bladder stone

    -mostly struvite ( infected) or uric acid (non infection)

    -Tx according to size :- if less than 3cm .. Cystolitholapaxy, if more than 3 cm .. Cystolithotomy

    - Occure in chronically catheterize patient or in BPH