Urinary Stone Disease

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URINARY STONE DISEASE

Dr. Jerry Santos

Li, Kingbherly

Lichauco, Rafael

Lim, Imee Loren

Lim, Jason Morven

Lim, John Harold

Lim, Mary

Lim Phoebe Ruth

ETIOLOGY

Polycrystalline aggregates composed of varying amounts of crystalloid and organic matrix

Stone formation requires supersaturated urine

Urinary pH, ionic strength, solute concentration, complexation

Urinary constituents change dramatically during different physiologic states

ROLE OF SOLUTE CONCENTRATION

Greater concentration of 2 ions

The more likely they are to precipitate

Solubility product (K sp

) = as ion concentrations increase, their activity product reaches a specific point

Formation product (K

K sp fp

) = concentration above capable of initiating crystal growth and heterogeneous nucleation

NUCLEATION THEORY

Urinary stones originate from crystals or foreign bodies immersed in supersaturated urine

CRYSTAL INHIBITOR THEORY

• Calculi form owing to absence or low concentration of natural stone inhibitors

– Magnesium, citrate, pyrophosphate, trace metals

A. CRYSTAL COMPONENT

Stones are primarily composed of crystalline component

Crystal formation

Nucleation, growth, aggregation

Theory of mass precipitation

Distal tubules or collecting ducts becomes plugged with crystals, establishing an environment of stasis, for further stone growth

Tubules enlarge as they entire papilla, transit time is only a few minutes

Fixed particle theory

Formed crystals retained within cells or beneath tubular epithelium

B. MATRIX COMPONENT

Noncrystalline matrix component 2-10% by weight

Mainly protein with hexose and hexosamine

Matrix Calculus

 assoc with previous kidney surgery or chronic UTI

Gelatinous texture

May serve as a nidus for crystal aggratation

URINARY IONS

Calcium

Major ion present in urinary crystals

95% calcium filtered at glomerulus is reabsorbed at proximal and distal tubules

<2% excreted in urine

Diuretics – hypocalciuric effect, decrease calcium excretion

Oxalate

Normal waste product of metabolism, relatively insoluble

Enters large bowel, consumed by bacterial decomposition

Excreted by proximal tubule

Supersaturation of calcium oxalate

Hyperoxaluria – bowel disorders

URINARY IONS

Phosphate

Important buffer, complexes with calcium in urine

Filtered cy glomerulus, reabsorbed in proximal tubules

Parathyroid hormone inhibits reabsorption

Uric Acid

By-product of purine metabolism

Any defect in purine metabolism = urinary stone disease

Defect in xanthine oxidase

Xanthine may ppt in urine

URINARY IONS

Sodium

Important role in regulating crystallization of calcium salts in urine

High dietary calcium – increases urinary calcium excretion

Reduces ability of urine to inhibit calcium oxalate crystal agglomeration

Citrate

Pivotal role in citric acid cycle in renal cells

Estrogen increases citrate excretion , factor that decreases incidence of stones in women

Alkalosis increases citrate excretion

URINARY IONS

Magnesium

Lack of magnesium is associated with increased calcium oxalate stone formation

Sulfate

Prevent urinary calculi

Complex with calcium

STONE VARIETIES

STONE VARIETIES

Calcium Calculi

Absorptive hypercalciuric nephrolithiasis

Resorptive hypercalciuric nephrolithiasis

Renal induced hypercalciuric nephrolithiasis

Hyperuricosuric Ca nephrolithiasis

Hyperoxaluric Ca nephrolithiasis

Hypocitraturic Ca nephrolithiasis

Non-Calcium Calculi

Struvite or Magnesium

Ammonium Phosphate

Uric Acid

Cystine

Xanthine

Indinavir

Rare

Silicate

Triamterene

CALCIUM CALCULI

Calcifications accumulate in collecting system 

Nephrolithiasis

(calcareous) elevated urinary calcium elevated urinary uric acid elevated urinary oxalate decreased level urinary citrate

Symptoms secondary to obstruction:

Pain

Infection

Nausea

Vomiting

Asymptomatic hematuria or UTI  urinary stone

ABSORPTIVE HYPERCALCIURIC NEPHROLITHIASIS

Increased calcium absorption from jejunum

Increased calcium filtered from the glomerulus

Suppression of PTH

Decreased tubular reabsorption of calcium

Hypercalciuria

ABSORPTIVE HYPERCALCIURIC NEPHROLITHIASIS

Type I

Type II

Type III

• Most severe type

• Independent of diet

• Elevated urinary calcium level

• Tx: cellulose phosphate, hydrochlorothiazide

• Dietary dependent, Most Common

• Tx: no specific

• returns to normal on calcium restricted diet

• “Phosphate renal leak”

• Decreased serum phosphate  increase

1,25 dihydroxyvitamin D synthesis

• Tx: orthophosphate (inhibit Vit. D synthesis)

RESORPTIVE HYPERCALCIURIC NEPHROLITHIASIS

 typically found in hyperparathyroidism calcium is released from bone in response to the increased activity of osteoclasts caused by excessive and inappropriate serum PTH levels

 causes significant hypercalcemia

PTH causes the kidney to limit calcium excretion, but, with the overwhelming serum calcium load produced with hyperparathyroidism, the kidneys are forced to excrete the extra calcium into the urine, causing the hypercalciuria.

RENAL INDUCED HYPERCALCIURIC

NEPHROLOTHIASIS

• Increased tubular defect in calcium excretion

• Decrease serum calcium

•Increase PTH level

•Increase level of calcium back to kidney,

•renal tubules excrete large amounts of calcium

•elevated fasting urinary calcium level,

•normal serum calcium level, elevated PTH level

HYPERURICOSURIC CALCIUM NEPHROLITHIASIS

Excessive purine

Increased uric acid production

Increased urinary monosodium urates

Management:

Diet modification

DOC: allopurinol 300mg/day

Potassium citrate

HYPEROXALURIC CALCIUM NEPHROLITHIASIS

Increased oxalate levels

Severe dehydration

Malabsorption: increase intraluminal fat and bile

Intraluminal calcium binds to fat  SAPONIFICATION

Tx: calcium supplementation

HYPOCITRATURIC CALCIUM NEPHROLITHIASIS

Increased metabolic demands of mitochondria of renal cells

Decrease excretion of citrate

Tx: potassium citrate supplementation

ACTIONS:

Citrate complexes with calcium decreasing ionic calcium concentration  decrease energy crystallization

Intracellular metabolic acidosis

Hypokalemia

Fasting

Hypomagnesemia

Androgens and gluconeogenesis

UTI

NONCALCIUM CALCULI

STRUVITE

Composed of

Magnesium,

Ammonium, &

Phosphate (MAP)

Most common in women

Frequently present as renal staghorn calculi

Struvite stones are associated with ureasplitting organisms

Proteus

Pseudomonas

Providencia

Klebsiella

Staphylococci

Mycoplasma

Alkaline Urinary pH

Results from the high ammonium concentration derived from the urea-splitting organisms

 pH >7.2 (NV: 5.85)

MAP crystals precipitate

MAP crystals are soluble in the normal urinary pH range

(5-7)

Foreign bodies and neurogenic bladders may predispose patients to urinary infections and subsequent struvite stone formation

Stone removal is therapeutic

Long term management

Optimized with removal of foreign bodies

All stone fragments should be removed with or w/o the aid of follow-up irrigations

Acetohydroxemic acid

Inhibits the action of bacterial urease, thereby reducing the urinary pH and decreasing the likelihood of precipitations

URIC ACID

<5% of all urinary calculi

Usually found in men

High incidence of Uric Acid Lithiasis

Gout

Myeloproliferative disease

Rapid weight loss

Those treated for malignant conditions with cytotoxic drugs

Treatment

Centered on:

Maintaining a urine volume of >2L / dayand a urinary pH of 6

Reducing dietary purines or the administration of allopurinol helps reduce uric acid excretion

Alkalinization

 with oral sodium bicarbonate, potassium citrate, or IV

1/6 normal sodium lactate

May dissolve calculi and is dependent on the stone surface area

CYSTINE

Secondary to an inborn error of metabolism resulting in abnormal intestinal mucosal absorption and renal tubular absorption of dibasic amino acids

Cystine

Ornithine

Lysine

Arginine

Genetic defects of cystinuria has been mapped to chromosome 2p.16 and 19q13.1

Cystine lithiasis

Only clinical manifestation of this defect

1-2% of all urinary stones

Suspected in patients with a (+) FH of urinary stones and the radiographic appearance of a faintly opaque, ground-glass, smooth-edged stone

Urinalysis: hexagonal crystals

Medical Therapy

High fluid intake (>3L/day)

Urinary alkalinization

Penicillamine

Reduce urinary cystine levels

Poorly tolerated by some patients (skin rashes, loss of taste, nausea, vomiting, & anorexia)

Mercaptopropionylglycine

Forms soluble complex with cystine and can reduce stone formation

Surgical

Most stones are recalcitrant to ESWL

XANTHINE

Secondary to a congenital deficiency of xanthine oxidase

Catalyzes the oxidation of hypoxanthine to xanthine and of xanthine to uric acid

Urinary stones develop on 25% of patients with xanthine oxidase deficiency

Stones are radiolucent and are tannish yellow in color

Treatment

Directed by symptoms and evidence of renal obstruction

High fluid intake

Urinary Alkalinization

Stone recurrence

Trial of Allopurinol

Purine-restricted diet

INDINAVIR

Protease inhibitors are a popular and effective treatment in patients with AIDS

Indinavir

6% of patients prescribed had radiolucent stones

Indinavir calculi > only urinary stones to be radiolucent on non-contrast CT scans

Associated with calcium components

Stones are tannish red

Temporary cessation of the medication with intravenous hydration frequently allows thes stones to pass

RARE

Silicate

Associated with long term use of antacids containing silica

Surgical treatment

Triamterene

Associated with anti-hypertensive medications containing triamterene (Dyazide)

Discontinuing the medication eliminates stone recurrence

Glafenine

Antrafenine

PAIN

Colicky

Noncolicky

Usually acute in onset, relatively constant, unexpected and severe

Urinary obstruction due to a direct increase in intraluminal pressure

 stretching nerve endings inflammation, edema, hyperperistalsis, and mucosal irritation

Affected by:

Stone size

Location

Degree of obstruction

Variation of individual anatomy

Patients frequently move constantly into unusual positions in contrast to the lack of movement of someone with peritoneal signs

1.

Renal calyx— deep, dull ache in the flank or back

Mild to severe

Frequently small may be exacerbated after consumption of large amounts of fluid the presence of infection or inflammation in the calyx or diverticulum may contribute to pain perception.

occasionally result in spontaneous perforation with urinoma, fistula, or abscess formation

2.

Renal pelvis

>1 cm in diameter - obstruct the ureteropelvic junction causing severe pain in the costovertebral angle, just lateral to the sacrospinalis muscle and just below the 12th rib dull to excruciatingly sharp, constant, boring

Radiates along the course of the ureter and into the testicle

Partial or complete staghorn calculi- are not necessarily obstructive, few symptoms, “silent” can often lead to significant morbidity, including renal deterioration, infectious complications, or both

3.

Upper and midureter severe, sharp back (costovertebral angle) or flank pain progressing down the ureter – more severe and intermittent

 lodged at a particular site - less pain, especially if it is only partially obstructive

Upper ureteral - lumbar region and flank

Midureteral - radiates caudally and anteriorly toward the mid and lower abdomen in a curved, band-like fashion (initially parallels the lower costal margin but deviates caudal toward the bony pelvis and inguinal ligament)

4.

Distal ureter pain that radiates to the groin or testicle in males and the labia majora in females

(ilioinguinal or genital branch of the genitofemoral nerves)

This pain pattern is likely due to the similar innervation of the intramural ureter and bladder

Bladder – urgency and frequency with burning

(inflammation of the bladder wall around the ureteral orifice)

HEMATURIA

 complete urinalysis : hematuria and crystalluria and documenting urinary pH

 intermittent gross hematuria or occasional teacolored urine (old blood)

Rarely (in 10–15% of cases), complete ureteral obstruction presents without microhematuria.

INFECTION

Magnesium ammonium phosphate (struvite) stones = infection stones

Proteus, Pseudomonas, Providencia, Klebsiella, and Staphylococcus infections

Calcium phosphate stones

 urine pH <6.6 - brushite stones urinary pH >6.6 - infectious apatite stones

All stones, however, may be associated with infections secondary to obstruction and stasis proximal to the offending calculus.

Infection  pain

Uropathogenic bacterial exotoxins and endotoxins may alter ureteral peristalsis

Local inflammation  chemoreceptor activation and perception of local pain

1.

Pyonephrosis—gross pus in an obstructed collecting system extreme form of infected hydronephrosis

Presentation: may range from asymptomatic bacteriuria to florid urosepsis

Renal urine aspiration - definitive diagnosis untreated  renocutaneous fistula

EVALUATION

Differential Diagnosis

 mimic other retroperitoneal and peritoneal pathologic states

Peritoneal signs should be sought during physical examination

History

 onset, character, potential radiation, activities that exacerbate or ease the pain, associated nausea and vomiting or gross hematuria, and a history of similar pain

RISK FACTORS

1.

Crystalluria

The rate of stone formation is proportional to the percentage of large crystals and crystal aggregates.

Crystal production is determined by the saturation of each salt and the urinary concentration of inhibitors and promoters.

Urine samples – fresh, centrifuged and examined immediately

2. Socioeconomic factors

 affluent, industrialized countries

3. Diet

 less energy-dense diet may decrease the incidence of stones

Vegetarians may have a decreased incidence of urinary stones.

High sodium intake is associated with increased urinary sodium, calcium, and pH, and a decreased excretion of citrate;

Fluid intake and urine output

4. Occupation

Physicians and other white- collar workers have an increased incidence of stones compared with manual laborers.

 may be related to differences in diet and physical activity; high temperatures may develop higher concentrations of solutes

5. Climate

—hot climates are prone to dehydration

Increased calcium and oxalate excretion has been correlated with increased exposure time to sunlight

6. Family history

Those with a family history of stones have an increased incidence of multiple and early recurrences

7. Medications

 antihypertensive medication triamterene

Long-term use of antacids containing silica

Carbonic anhydrase inhibitors

Protease inhibitors in immunocompromised patients are associated with radiolucent calculi.

PHYSICAL EXAM

 acute renal colic

Systemic components: tachycardia, sweating, and nausea

Costovertebral angle tenderness abdominal mass may be palpable in patients with longstanding obstructive urinary calculi and severe hydronephrosis

Fever, hypotension, and cutaneous vasodilation: urosepsis thorough abdominal examination should exclude other causes of abdominal pain

RADIOLOGIC INVESTIGATIONS

Computed tomography

 imaging modality of choice in patients presenting with acute renal colic rapid and is less expensive than IVP

It images other peritoneal and retroperitoneal structures and helps when the diagnosis is uncertain

There is no need for intravenous contrast. do not give anatomic details as seen on an IVP

Uric acid stones are visualized no differently from calcium oxalate stones. Matrix calculi have adequate amounts of calcium to be visualized easily by CT.

Intravenous Pyelogram

IV injection of contrast to

 visualize renal collecting systems, ureters and UB gives a comprehensive view of the patient's anatomy

50 ml of a special dye is injected into the bloodstream that is excreted by the kidneys and by its density helps outline any stone on a repeated Xray

X ray images every few minutes to determine if there is any obstruction to the dye as it is excreted into the bladder

Tomography

 useful to identify calculi in the kidney when oblique views are not helpful.

 visualizes the kidney in a coronal plane

 identify poorly opacified calculi, especially when interfering abdominal gas or morbid obesity make

KUB films suboptimal

KUB films and directed ultrasonography

Plain frontal supine radiograph of the abdomen

Visualization of:

Renal shadows

Psoas muscle shadow

Calcification (stones, vascular, lymph node or tumor

UB shadow

Calcium  radiopaque

About 10% of stones do not have enough calcium to be seen on standard X-rays (radiolucent stones)

The distal ureter is easily visualized through the acoustic window of a full bladder. Edema and small calculi missed on an IVP can be appreciated with such studies.

Ultrasound

 presence of hydronephrosis (swelling of the kidney—suggesting the stone is blocking the outflow of urine)

 detect stones during pregnancy when x-rays or CT are discouraged

Retrograde pyelography

 required to delineate upper-tract anatomy and localize small or radiolucent offending calculi.

Visualization of urinary collecting system achieved via cystoscope, ureteral catherization and retrograde injection of contrast

Used when IVU failed to opcacify renal collecting system and ureters

Nuclear scintigraphy

 radioisotopes (here called radiopharmaceuticals) are taken internally, and the emitted radiation is captured by external detectors (gamma cameras) to form two-dimensional images

Bisphosphonate markers can identify even small calculi that are difficult to appreciate on a conventional KUB film

INTERVENTION

INTERVENTIONS

Conservative observation

Dissolution agents

Relief of Obstruction

Extracorporeal Shockwave Lithotripsy (ESWL)

Ureteroscopic stone extraction

Percutaneous Nephrolithotomy

Open stone surgery

Pyelolithotomy

Anatrophic Nephrolithotomy

Radial Nephrotomy

Ureterolithotomy others

Conservative management

Majority of stones pass out within a 6 week period after the onset of symptoms depends on the size of the calculi and its location

Dissolution agents

Use alkalinizing agents

Given oral, IV or intrarenal

Relief of the Obstruction

Emergent drainage in patient with signs of UTI

Extracorporeal Shockwave Lithotripsy (ESWL)

Extracorporeal Shockwave Lithotripsy (ESWL)

CONSIDERATION

 excessive weight (>300 lb) may severely limit or preclude ESWL.

Pregnant women and patients with large abdominal aortic aneurysms or uncorrectable bleeding disorders should not be treated with ESWL.

Individuals with cardiac pacemakers should be thoroughly evaluated by a cardiologist.

URETEROSCOPIC STONE EXTRACTION

Highly effective for lower ureteral calculi

Stone may be extracted using a wire basket

Or lithotrites may be placed through the ureteroscope to fragment the calculi

PERCUTANEOUS NEPHROLITHOTOMY

 the treatment of choice for large (>2.5 cm) calculi; renal and proximal ureteral calculi, those resistant to ESWL, select lower pole calyceal stones with a narrow, long infundibulum and an acute infundibulopelvic angle, and instances with evidence of obstruction

Rapid cure

OPEN STONE SURGERY

Classic way to remove calculi

Mandatory to obtain a radiograph before the incision is made

Not frequently used anymore because of the morbidity of the incision, the possibility of retained stone fragments, and the ease and success of less invasive techniques

PYELOLITHOTOMY

Effective especially with extrarenal pelvis

Transverse pyelotomy - effective and does not require interruption of the renal arterial blood supply

Flexible endoscope – ensures stonefree status

Coagulum – can retrieve multiple, small renal pelvic calculi and difficultto-access caliceal calculi

Cryoprecipitate

Injected into the renal pelvis, endogenous clotting factors result in a

Jelly-like coagulum of the collecting system.

Small stones are entrapped and removed with the coagu- lum.

ANATROPHIC NEPHROLITHOTOMY

1.

2.

3.

4.

Used with complex staghorn calculi

Complete staghorn calculus

Partial staghorn calculus

Incision made on the convex surface of the kidney posterior to the line of Brodel

Occlusion of the renal artery followed by renal cooling with slushed ice

Nerve hook is helpful to tease out calculi

Repair of narrowed infundibula helps reduce stone recurrence rates.

RADIAL NEPHROTOMY

 Allows access to limited calyces of the collecting system

 Frequently used in blown-out calyces with thin overlying parenchyma

 Intraoperative ultrasound to localize the calyx and the calculi

 A shallow incision of the renal capsule can be followed by puncture into the collecting system.

 Stones may be cut with heavy Mayo scissors, and remaining fragments can be retrieved.

OTHER RENAL PROCEDURES

 Partial nephrectomy – for large stones in a renal pole with marked parenchymal thinnin g

 Caution should be taken even with a normal contralateral kidney as stones are frequently associated with a systemic metabolic defect that may recur in the contralateral kidney

 Ileal ureter substitution – to decrease pain with frequent stone passage

 Autotransplantation with pyelocystostomy – for patients with rare malignant stone disease

Partial nephrectomy

Ileal ureter substitution

URETEROLITHOTOMY

Long standing ureteral calculi

1.

2.

3.

4.

5.

Preoperative radiograph to document stone location

Incision lateral to the sacrospinalis muscles to allow medial retraction of the quadratus lumborum; anterior fascicle of the dorsal lumbar fascia must be incised to gain proper exposure

Vessel loop or Babcock clamp placed proximal to the stone to prevent frustrating stone migration

Longitudinal incision over the stone with a hooked blade to expose the calculus

Nerve hook to tease out the stone

PREVENTION

FLUID INTAKE

 About 1.6 L/24 h

 Encouraged during mealtime

 Increased approximately 2 h after meals

 Encouraged to force a nighttime diuresis

METABOLIC INTERVENTION

Stone analysis

Outpatient urine collection during typical activities & fluid intake

Ca stone formers

Initial 24-h urine collection

Include tests for Ca, uric acid, oxalate, citrate,

Na, volume, & pH

Hypercalciuria: most common abnormality

ORAL INTERVENTION

Alkalinizing pH agents

Potassium citrate: oral agent that elevates urinary pH effectively by 0.7–0.8 pH units

Adverse effect: abdominal discomfort

Indications: Ca oxalate calculi 2° to hypocitraturia

(<320 mg/day), including those with renal tubular acidosis; uric acid lithiasis & nonsevere forms of hyperuricosuric Ca nephrolithiasis.

Alternative alkalinizing agents: Na, potassium bicarbonate, orange juice, & lemonade

No effective long-term urinary acidifying agents

ORAL INTERVENTION

Gastrointestinal absorption inhibitor

Cellulose phosphate binds Ca in the gut & inhibits

Ca absorption & urinary excretion

Decreases urinary saturation of Ca phosphate & Ca oxalate

Phosphate supplementation

Indicated for renal PO

4 leak

ORAL INTERVENTION

Diuretics

Thiazides can correct renal Ca leak associated with renal hypercalciuria

Prevents 2° hyperparathyroid state & its associated elevated vitamin D synthesis & intestinal calcium absorption

Hypokalemia  hypocitraturia

ORAL INTERVENTION

Calcium supplementation

Indication: Enteric hyperoxaluric Ca nephrolithiasis

Ca gluconate & Ca citrate

Uric acid-lowering medications

Allopurinol

Urease inhibitor

Acetohydroxamic acid: effective adjunctive treatment in chronic urea-splitting urinary tract infections associated with struvite stones

Prophylaxis after removal of struvite stone

ORAL INTERVENTION

Prevention of cystine calculi

Penicillamine: reduces the amount of urinary cystine that is relatively insoluble

Mercaptopropionylglycine (Thiola)

BLADDER STONES

BLADDER STONES

Manifestation of an underlying pathologic condition, including voiding dysfunction or a foreign body

Most seen in men

Developing countries: frequently found in prepubescent boys

Stone analysis: ammonium urate, uric acid, or Ca oxalate stones

Irritative voiding symptoms, intermittent urinary stream, UTI, hematuria, or pelvic pain

PROSTATIC STONES

Prostatic calculi: found within prostate gland per se & are found uncommonly within the prostatic urethra

Represent calcified corpora amylacea & rarely found in boys

Usually of no clinical significance, rarely they are associated with chronic prostatitis

Large prostatic calculi: may be misinterpreted as a carcinoma

Dx: radiograph or transrectal ultrasound

SEMINAL VESICLE STONES

Smooth & hard

Associated with hematospermia

PE: stony hard gland; multiple stones present with crunching sensation

Confused with tuberculosis of the seminal vesicle

URETHRAL STONES

Originate from bladder

Develop 2° to urinary stasis, urethral diverticulum, near urethral strictures, or at sites of previous surgery

Females: rarely develop urethral calculi due to short urethra & lower incidence of bladder calculi; associated with urethral diverticula

Symptoms : intermittent urinary stream, terminal hematuria, & infection

Dx: palpation, endoscopic visualization, or radiographic study

PREPUCIAL STONES

Occur in adults

Develop 2° to a severe obstructive phimosis or poor hygiene with inspissated smegma

Dx confirmed by palpation

Tx: dorsal prepucial slit or formal circumcision

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