Renal Stone

urosurgery

Renal stone
Renal stone are polycrystalline aggregates of varying amount of crystalloid and organic matrix and require supersaturated urine which depend on ( urinary PH, ionic strength and solute concentration). Calcium is a major ion present in urinary crystal, oxalate is a waste product of metabolism and is relatively insoluble. Phosphate complexes with calcium in urine lead to formation of calcium phosphate stone. Uric acid is the product of purine metabolism and undissociated in acidic urine. Increase citrate concentration in urine decrease incidence of calcium urolithiasis.
Calcium calculi
85% of all urinary stone are calcareous.
Absorptive hypercalciuria: type 1: is independent of diet, treated by cellulose phosphate and hydrochlorothiazide. Type 2: is dietary depended. Type 3: is secondary to phosphate

renal leak, lead to increase 1,25 dihydroxy vitamin D synthesis.

Resorptive hypercalciuria: occur in primary hyperparathyroidism.
Renal induced hpercalciuric nephrolithiasis: intrinsic renal tubular defect in calcium excretion, lead to decrease serum calcium and subsequent secondary hyperparathyroidism. Treated by hydrochlorothiazide.
Hperuricosuric calcium nephrolithiasis: excessive dietary intake of purine or an increase in endogenous uric acid production. PH of urine >5.5 treated by decrease purine intake.
Hperoxaluric calcium nephrolithiasis : is secondary to increase urinary oxalate excretion as a result of chronic diarrhea state.

Non calcium calculi

Struvite : composed of magnesium, ammonium and phosphate (MAP), commonly occur in women, it is infectious stone associated with urease splitting microorganism( proteus, pseudomonas and klebsiella).
Uric acid stone : 5% of all urinary stones, usually found in acidic urine, PH < 5, myeloproliferative disease, gout increase risk, treated by dietary modulation and allopurinol.
Cystine stone : inborn error of metabolism lead to abnormal intestinal absorption and renal tubular absorption of cystine, autosomal recessive need acidic media, medical therapy like pencellamine and high fluid intake one of the treatment option.
Xanthine stones: congenital deficiency of xanthine oxidase, it normally catalyzed the oxidation of xanthine to hypoxanthine and then to uric acid.
Symptoms
Pain: either colicky or non-colicky , 1st due to stretching of the pelvicaliceal system and the 2nd due to stretching of the renal capsule, renal colic does not always come in wax and wane like biliary or intestinal colic. In the ureter local pain referred to the distribution of the ilioinguinal and genitofemoral nerve. Stone in the renal calyx usually cause dull ache pain , stone in the renal pelvis more than 1 cm
Commonly cause obstruction and so severe pain radiate to the costovertebral angle, stone in the upper third of the ureter cause pain radiate to the flank , mid ureteric stone pain radiate to the bony pelvis and stone in the intramural ureter cause symptoms mimic cystitis( frequency, urgency, dysuria and gross hematuria).
Fever: urinary stone and fever is relative medical emergency. Fever with urinary tract obstruction require prompt decompression.
Nausea and vomiting: usually occur in the upper tract obstruction.
Hematuria
Risk factor:
Crystalluria, socioeconomic factors(high incidence in industrialized countries), diet (increase stone incidence in people with high intake of fatty acid, animal protein and sugar). Occupation (high incidence in in people who exposed to high temperature). Hot climate increase incidence of urolithiasis, family history and some medication increase incidence of urinary stone, antihypertensive (triamterene), long term of antacid.
Physical sign : tenderness at costovertebral angle, palpable mass in patient with severe hydronephrosis.
Radiological examination :
CT scan : non contrast spiral CT scan are now the imaging of choice in patient with urolithiasis.
IVP: simultaneously document nephrolithiasis and upper tract anatomy.
KUB and directed ultrasonography .
Intervention :
Conservative observation : spontaneous passage of ureteric calculi depend on (size, shape and location ), 4-5 mm had chance f 40-50% of spontaneous passage, 6 mm had chance of <5% of spontaneous passage , this does not mean that 1 cm stone will not pass or that of 1-2 mm will always pass uneventfully.
Dissolution agent : either alkalinization , or acidification of urine depend on stone size.
Relief of obstruction : presence of obstruction and urinary tract infection require emergent drainage either by JJS or percutaneous nephrostomy.
ESWL failure of conservative treatment of ureteric stone or stone impaction (>6 ws stone not progress).
Ureteroscopic stone extraction: is highly efficacious for lower ureteric calculi.


In general management of renal or ureteric stone is to control the pain and manage the obstruction .
Pain control : NSAID 1st choice in patient with acute renal colic it act directly on prostaglandin.
Opioids 2nd choice when there is contraindication to NSAID (morphine, pethidine, tramadol, …etc.).
Alpha blocker : reduce recurrent renal colic attack and decrease the time for the ureteric stone to pass , especially in the lower ureteric stone < 1cm .
So treatment of the renal stone except lower pole stone :
>2cm : percutaneous nephrolithotomy.
1-2cm : a. ESWL, B. retrograde renal surgery.
1<1cm: ESWL or retrograde renal surgery.
Lower pole stone : 1-2 cm either retrograde renal surgery, ESWL or PCNL.
For ureteric stone :
Proximal ureter:
1cm : ESWL or ureteroscope.
<1cm : 1st choice : ureteroscope , 2nd choice : ESWL.
Distal ureteric stone :
>1 cm : 1st choice ureteroscope , 2nd choice :ESWL
< 1cm : either ESWL or ureteroscope.

Hydronephrosis

Dilatation of the renal calyx and the pelvis with urine , may be acute or chronic , unilateral or bilateral , congenital or acquired.
Most common cause incidence in women (pregnancy, cervical or uterine cancer), in men the main cause is prostatic disease. Congenital cause may be pelviureteric junction obstruction , ureterocele, retrocaval ureter, obstructed megaureter,…
Macroscopic changes in the upper urinary tract:
Pooling of urine, decrease ureteral contractility cause back in the pressure lead to hydronephrosis, flat renal papillae , edema of the renal parenchyma by 7 days , cortical and medullary thinning of the renal parenchyma by days 21-28.
Microscopic changes in the upper urinary tract:
Massive tubular dilatation, renal tubular cell stress then apoptotic cell death and progressive tubulointerstitial fibrosis, late the glomeruli change to glomerulosclerosis.
Renal haemodynamic , glomerular filtration rate and intrarenal pressure in upper urinary tract obstruction:
Normal resting pressure of the renal pelvis 0-10cm H2O, during peristalsis varies between 20-60cm H2O. in unilateral obstructive nephropathy there is 3 separate phases:
Initial phase: last 90 minutes, tubular pressure high, GFR decrease, lead to compensatory increase in PGE2 mediate decrease afferent arteriolar resistant and maintain GFR 80% of normal.
Second phase: lasting 1.5 -4 hrs. , decline in renal blood flow , persistent increase renal pelvic pressure, GFR reduced to 20% f the normal.
Final phase : decrease in the renal pressure and blood flow and loss of kidney function.

Effect of obstruction on the kidney
Obstruction lead to atrophy of the renal parenchyma, the principle effect of this obstruction on the papillae, tubule, then ultimately on glomeruli.
Post obstructive diuresis
Following relief of the ureteral obstruction, functional recovery is depended on the degree and the duration of the obstruction. After 6 ws of complete unilateral obstruction , no GFR recovery at all.
Complication of hydronephrosis:
Infection , stone , trauma , hypertension.