Dina Dewi SLI

UROLITHIASIS

KIDNEY STONES
Also known as nephrolithiasis, urolithiasis or renal calculi. Solid concretions ( crystal aggregations) of dissolved minerals in urine found inside the kidneys or ureters. They vary in size from as small as a grain of sand to as large as a grapefruit

Cont.

Kidney stones (calculi) are hardened mineral deposits that form in the kidney. Berasal dari partikel berukuran mikro dan berkembang dlm jangka

Location of Renal stones

A vast majority of stones will contain elements of calcium within them and therefore are easily seen on x-ray having the same density as bone. Depending on the size, number, and the location of the stone(s) as well as it's composition guides initial and then further management can be implemented.

Renal stones
Kidney stones occur in 1 in 20 people at some time in their life. Kebardaan urolithiasis pada anak jarang, bisa terjadi karena ganggguan metabolik atau kelainan konginetaldibawah 5 tahun Remaja cystiuria, hiperparatiroid primer, idiopatic calcium oxalate For precipitation of crystals in urine to occur, the urine must be "supersaturated" for the precipitating crystal.

STONE FORMATION

Kidney stones form when there is a high level of mineral (s) ; i.e. calcium (hypercalciuria), oxalate (hyperoxaluria), or uric acid (hyperuricosuria) in the urine;

Urine normal mengandungcitrate, magnesium, pyrophosphate mencegah pembentukan batu. Kekurangan air dalam ginjal untuk melarutkan bahan metabolit

Cont.

Rendahnya inhibitor menyebabkan pembentukan batu pada ginjal Citrate is thought to be the most important The four most common types of stones are comprised of calcium, uric acid, struvite, and cystine.

CALCIUM STONES:

85 % terdiri dari calcium The most common cause of calcium stone production is excess calcium in the urine (hypercalciuria). In hypercalciuria, excess calcium builds up in the kidneys and urine, where it combines with other waste products to form stones. Low levels of citrate, high levels of oxalate and uric acid, and inadequate urinary volume may also cause calcium stone formation. Terdiri dari oxalate (calcium oxalate) or phosphate (calcium phosphate). Calcium phosphate stones terjadi pada pasien dg ganguan metabolik hormonal spt: hyperparathyroidism dan renal tubular acidosis.

CAUSE OF HYPERCALCIURIA.

Increased intestinal absorption of calcium (absorptive hypercalciuria), excessive hormone levels (hyperparathyroidism), and renal calcium leak (kidney defect that causes excessive calcium to enter the urine) Prolonged inactivity also increases urinary calcium and may cause stones. Renal tubular acidosis (inherited condition in which the kidneys are unable to excrete acid) significantly reduces urinary citrate and total acid levels and can lead to stone formation.

CALCIUM OXALATE MONOHYDRATES

Calcium

oxalate dihydrates

lithotripsy

URIC ACID STONES

Produksi asam urat dari pencernaan. Peningkatan asam dlm urin shg They are not visible on X-rays. Patients with gout often develop these stones. Uric acid stones form in acidic urine and often dissolve when the urine is alkalinized.

URIC ACID

STRUVITE STONES

Disebabkan karena adanya infeksi. Bacteria menetralkan keasaman uri bakteri tumbuhpembentukan batu struvit, They are capable of splitting urea into

ammonia, decreasing the acidity of the urine and resulting in favorable conditions for the formation of struvite stones.

CONT.

Organisms which alkalinize the urine can cause struvite stones to form. Struvite stones are more common in women. The stones usually develop as jagged structures called "staghorns" and can grow to be quite large.

STRUVITE

CYSTINE STONES
Cystine

merupakan asam amino. Kelainan konginetal (herediter) peningkatan produksi cystinecystinuria

CYSTINE

CAUSES AND RISK FACTORS

A low level of citrate is a risk factor for hypocitraturia. Congenital kidney defect that may increase urinary calcium loss and stone formation (medullary sponge kidney) Excessive parathyroid hormone, which causes calcium loss (hyperparathyroidism) Gout (caused by excessive uric acid in the blood) High blood pressure ( hypertension) Inflammation of the colon that causes chronic diarrhea, dehydration, and chemical imbalances (colitis) Sodium (hypernatremia)

Family history, Age of onset, Fluid intake pattern, Diet, medications, History of infections. Certain stone formation has a genetic predisposition Some an autosomal recessive pattern, including cystinuria and primary hyperoxaluria, Some have an autosomal dominant pattern such as renal tubular acidosis (RTA) or the syndrome of idiopathic calcium oxalate urolithiasis.

High doses of vitamin C (i.e., more than 500 mg per day) can result in high levels of oxalate in the urine (hyperoxaluria) and increase the risk for kidney stones. Oxalate is found in berries, vegetables (e.g., green beans, beets, spinach, squash, tomatoes), nuts, chocolate, and tea. Stone formers should limit their intake of cranberries, which contain a moderate amount of oxalate.

CLINICAL MANIFESTATIONS

Signs and symptoms of stones in the urinary tract depend on ob-struction, infection, and edema. When the stones block the ow of urine, obstruction develops, producing an increase in hydro-static pressure and distending the renal pelvis and proximalureter. Infection (pyelonephritis and cystitis with chills, fever, and dysuria) can occur from constant irritation by the stone. Some stones cause few, if any, symptoms while slowly destroying the functional units (nephrons) of the kidney; others cause excruciating pain and discomfort. Stones in the renal pelvis may be associated with an intense, deep ache in the costovertebral region. Hematuria is often present; pyuria may also be noted.

CONT

Pain originating in the renal area radi-ates anteriorly and downward toward the bladder in the female and toward the testis in the male. Pain suddenly becomes acute, with tenderness over the costovertebral area, and nausea and vom-iting appear, the patient is having an episode of renal colic. Diar-rhea and abdominal discomfort may occur. These GI symptoms are due to renointestinal reexes and the anatomic proximity of the kidneys to the stomach, pancreas, and large intestine.

CONT
Stones lodged in the ureter (ureteral obstruction) cause acute, excruciating, colicky, wavelike pain, radiating down the thigh and to the genitalia. Often, the patient has a desire to void, but little urine is passed, and it usually contains blood because of the abrasive action of the stone ureteral colic Colic is mediated by prostaglandin E, a substance that increases ureteral contractility and renal blood ow and that leads to increased intraureteral pressure and pain.

HYDRONEPHROSIS
Dilatation of renal pelvis & calyces with accompanying destruction of the kidney parenchyma Usually due to partial obstruction to the outflow of urine

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PATHOPHYSIOLOGY

Dilatation of the renal pelvis & calyces

Types of hydronephrosis:

Pelvic type Renal type Pelvirenal type: most common type, both the pelvis & calyces are equally dilated

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