Urolithiasis

A- Pathophysiology and etiology:

▬ It is assumed three stages: nucleation (transition from liquid to solid), the concretion as crystals and growth calculation.

The sequence of these steps is determined by the following factors:

* Increasing the urinary concentration of crystallizable substances (hypercalciuria, hyperoxaluria, Hyperuricosuria)

* Lower the crystallization inhibitors (pyrophosphate citrate) influenced by the change in pH.

* Existence of anatomical factors (uropathy) favoring the formation of stones:

• urinary stasis renal (kidney ‘sponge’ ‘the Cacci-Ricci disease scar diverticulum; junction syndrome ureteropelvic) or bottom unit (Neck prostatic obstruction, neurogenic bladder, urethral stricture).

• infected urine (vesicorenal reflux)

• Simple Cyst kidney, polycystic kidney disease, calculation of foreign body.

▬ There are different types of calculations according to their components:

* Calcium lithiasis: very common, usually occurs in young adults and, if untreated, tends to relapse.

The calcium oxalate and calcium phosphate calculated calculations are white radiopaque, gray or black, spiky, forming variable pH, favored by hypercalciuria, hyperoxaluria and the Hyperuricosuria.

* Uric lithiasis: hyperuricemia may be complicated by interstitial nephritis by deposition of uric acid.

The acid urine pH favors the formation of uric acid crystals.

It is common in patients with gout in men (sex ratio = 5-10) after 50 years.

Chronic dehydration and metabolic acidosis (ileostomy resection of the small intestine) favor the concentration of uric acid in urine and ↓ pH.

The increase protein intake => high uricosuria.

It is a calculation brown, smooth and radiolucent.

* Lithiasis cystine: it is a hereditary disease, a rare, transport of amino acids by the intestinal epithelium and renal tubular cells => k cystine excretion.

In the recessive form the calculations appear dan 4th decade.

Some calculations have slightly radiopaque and bilateral.

Recurrence is common.

* Lithiasis phospho-ammniacomagnésienne: it only appears if the urine is infected, alkaline, usually by bacteria producing urease (Proteus, Providentia, sometimes Klebsiella, Serratia, Enterobacter, but not E. coli).

The treatment of infection through the processing of the stone.

The growth of these radiopaque calculations is rapid and recurrence is common.

B- Positive diagnosis:

1- Clinical signs:

▬ colic: sudden onset, favored by a journey, a dietary change, taking a drink plentiful, a period of dehydration.

In very severe intensity (frenzied attack), it sits in the lumbar pit and radiates forward or in the abdominal and inguinal direction but also quadrant …

▬ The associated signs:

* Peritoneal irritation signs: nausea, vomiting, stop transit, bloating.

* Pelvic signs: → bladder urinary frequency, dysuria … or rectal (tenesmus).

▬ Other symptoms: chronic pain, microscopic hematuria (constant) and even macroscopic. Fever indicates a variable importance infection. Sometimes latency.

▬ Kidney failure may reflect stones, if an obstacle on an anatomical or functional solitary kidney.

▬ Physical examination: poor, must look for signs of gravity → hyperemia, hydronephrosis.

2- Radiological examination:

▬ abdominal radiograph without preparation:

• It allows to visualize the radiopaque calculations (90% of stones) and specifies their seats.

• Can show signs of digestive irritation (ileus …)

• But it does not visualize the calculations projected on a piece of bone, the radiolucent stones (uric), non lithiasic obstacles …

▬ Intravenous urography: it highlights the obstacle, the radiolucent calculation (lacunar image) and eliminates extra-urinary calcifications.

She appreciates the impact on the excretory upstream channel and the functional value of the kidneys

▬ Renal Ultrasound:

* Direct signs: hyperechoic picture in the kidney or in the ureter juxtavésical if the bladder is full.

* Indirect Evidence: upstream distension of the obstacle …

* Warning: ultrasound does not explore the ureter due to digestive interposition except sub-pelvic and intramural regions.

▬ practice: ASP and ultrasound are performed in first intention. IVU will be done in case of an invisible obstacle or during surgery or shock wave possible.

3- Laboratory tests:

Basic laboratory tests: blood electrolytes (serum creatinine, serum calcium, uric acid), urinary pH, a urine culture

Treatment C:

▬ Symptomatic treatment:

* NSAIDs through IVL (Profénid®, Indocid®, Voltarène®)

* Antispasmodics (Spasfon®)

* Stop drinks during the crisis and recovery of an abundant hydration after the crisis

▬ Etiological treatment:

* MEDICAL TREATMENT: If uncomplicated renal colic, when the calculation can be dissolved (cystine or uric)

– Uric lithiasis:

• increase in diuresis and urine pH (<6) → Cure diuresis alkalizing (if pH> or = 6.5)

• with limited protein intake …

• We must reduce uricosuria: suppression of uric acid foods.

• Allopurinol if hyperuraturie and / or uric acid levels> 75 mg / l.

– Lithiasis cystine: diuresis cure allows ↓ urinary concentration of cystine, if> 4L / 24h, alkalinization of urine (pH> 7.5).

D-penicillamine in case of recurrence of stones. Thiopronine if remaining cystinuria> 144mg / l.

+ Suppression of eggs rich in cystine.

* SURGICAL TREATMENT: indicated for uncomplicated calculations, from 6 to 10mm, and in case of failure

* Extracorporeal Shock Wave Lithotripsy

* Extraction endoscopically

▬ Preventive treatment of recurrence:

* Water intake: increasing daily fluid intake

* Metabolic abnormality:
hypercalciuria → treatment of etiology (hyperparathyroidism, sarcoidosis, prolonged immobilization …) Idiopathic hypercalciuria absorptive → low calcium diet; Idiopathic hypercalciuria renal → thiazide diuretic; Secondary hyperoxaluria → ↓ intake of foods high in oxalates (tea, chocolate, coffee).

* Treatment of uropathy whenever possible.

IVU and Repercussion:

* IVU appreciate the impact on the urinary tract upstream and on the functional value of the kidneys (hydronephrosis moderate distension or worrying)

– Stasis kidney becomes opaque with behind the opposite kidney.

This delay is not proportional to the stasis;

– The kidney can not excrete (parenchymography but no pyelography).

This is a kidney-called “dumb” by abuse of language;

– The importance of stasis is not necessarily dependent on the size of the calculation (a large staghorn calculus does not result in stasis, unlike a stones wedged in the ureter-bladder meatus).

* Other signs of impact:

– Track inflammatory urinary stricture, difficulty and source of treatment failure (interest antiinflammatory who regress péricalculeux edema);

– Sluggish urinary tract overlying and underlying (ureter visible along its entire length, on one shot, traps). Under physiological conditions, the ureter is driven peristaltic contractions, leading urine bowl, giving a discontinuous aspect of the clichés of IVU;

– Ureteritis pseudo-cystic: radiolucent calculi rosary or edematous stigma of course the stones in the urinary tract;

– Pseudo-tumor périméatique edema (sign Vespiniani) when the stones is enclosed in the intramural portion of the ureter.
All these elements are fundamental to the therapeutic course of action