Renal Stones

Lecture 50

Urolithiasis

Renal Calculi Nephrolithiasis

Kidney Stones

Renal StonesA kidney stone, is a solid

concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine.

Classification- by location

• Urinary stones are typically classified by their location in the

• kidney (nephrolithiasis),

•ureter (ureterolithiasis),

•bladder (cystolithiasis),

Classification- by chemical composition

1.1. Calcium saltsCalcium salts

2.2. Uric acidUric acid

3.3. Mg ammonium POMg ammonium PO44

4.4. CystineCystine5.5. Other (xanthine, etc.Other (xanthine, etc.))

Causes

Dietary Causes• LOW FLUID INTAKE • HIGH DIETARY INTAKE OF ANIMAL PROTEIN,• SODIUM, • REFINED SUGARS, FRUCTOSE • HIGH FRUCTOSE CORN SYRUP, • OXALATE, • GRAPEFRUIT JUICE• APPLE JUICE

higher Vitamin C

Risk Factors

Risk Factors

Risk Factors• Male sex• Obesity• Family History• H/o stone disease (1/2 will have recurrence)

Risk Factors•Occupation• Small bowel disease (i.b.d.)

• Medical conditions causing hypercalcuria

• Medical conditions causing aciduria

Pathogenesis- Mucoprotein MatRix

• An organic

mucoprotein matrix, making up 1% to 5% of the stone by weight, is present in all calculi.

Pathogenesis- SupERSATURATIon

The most important determinant(Renal stones) is an increased urinary concentration of the stones' constituents, such that it exceeds their solubility (supersaturation).

A low urine volume in some metabolically normal patients may also favor supersaturation.

Supersaturation- Slow urine flow

SOLUBILITY• Solubility is affected by

•Urine pH, •Volume and •Total excretion

Pathogenesis- Calcium Oxalate StonesHypercalcemia & Hypercalciuria

• Calcium oxalate stones are associated in about

5% of patients with

hypercalcemia and hypercalciuria, such as occurs with hyperparathyroidism, diffuse bone disease, sarcoidosis, and other hypercalcemic states.

Pathogenesis 55%Hypercalciuria without hypercalcemia • This is caused by several factors, including:• Hyperabsorption of calcium from the intestine (Absorptive hypercalciuria), • Intrinsic impairment in renal tubular reabsorption of calcium (Renal hypercalciuria),

• Idiopathic fasting hypercalciuria with normal parathyroid function.

Pathogenesis- 20%Hyperuricosuric calcium nephrolithiasis

• 20% of calcium oxalate stones are associated with

• increased uric acid secretion (hyperuricosuric calcium nephrolithiasis),

with or without hypercalciuria. • The mechanism of stone formation in this setting involves• “nucleation” of calcium oxalate by uric acid crystals in the collecting ducts.

Pathogenesis- Hyperoxaluria

• 5% are associated with hyperoxaluria, either

HEREDITARY (primary oxaluria)

or, more commonly,

ACQUIRED by intestinal overabsorption in patients with enteric diseases.

Enteric hyperoxaluria, also occurs in vegetarians, because much of their diet is rich in oxalates.

5%

Pathogenesis- HYPOCITRATURIA

• Hypocitraturia, associated with acidosis and chronic diarrhea of unknown cause, may produce calcium stones.

•

Pathogenesis Idiopathic calcium stone disease

• In a variable proportion of individuals with calcium

stones, no cause can be found

(idiopathic calcium stone disease).

Pathogenesis Magnesium ammonium phosphate stones

• Formed largely after infections by bacteria (e.g., Proteus and some staphylococci) that convert urea to ammonia.

• The resultant alkaline urine causes the precipitation of magnesium ammonium phosphate salts.

Pathogenesis Magnesium ammonium phosphate stones

• These form some of the largest stones,

• as the amounts of urea excreted normally are huge.

• Indeed, so-called staghorn calculi occupying large portions of the renal pelvis are almost always a consequence of infection.

Pathogenesis- URIC ACID stones

• Uric acid stones are common in individuals with hyperuricemia, such as gout, and diseases involving rapid cell turnover, such as

the leukemias.

However, more than half of all patients with uric acid calculi have

neither hyperuricemia nor increased urinary excretion of uric acid.

• In this group, it is thought that an unexplained tendency to excrete urine of pH below 5.5 may predispose to uric acid stones, because uric acid is insoluble in acidic urine. In contrast to the radiopaque calcium stones, uric acid stones are

radiolucent.

Pathogenesis- CYSTINE STONES

• Cystine stones are caused by

• genetic defects in the renal reabsorption of amino acids, including cystine, leading to cystinuria.

• Stones form at low urinary pH.

Pathogenesis• It can therefore be appreciated that 1. increased concentration of stone constituents,

2.changes in urinary pH,3. decreased urine volume, and 4.the presence of bacteria influence the formation of calculi.

Pathogenesis• However, many calculi occur in

the absence of these factors; • conversely, individuals with

hypercalciuria, hyperoxaluria, and

hyperuricosuria often do not form stones.

• It has therefore been postulated that

stone formation is enhanced by

a deficiency in inhibitors of crystal formation in urine.

Inhibitors of Crystal Formation• Pyrophosphate, • Diphosphonate, • Citrate, • Glycosaminoglycans,• Osteopontin, and • Nephrocalcin (Glycoprotein).

Morphology- Gross

• Unilateral 80%Favored sites:

• Renal calyces • Pelves • Bladder.

Morphology- in Renal Mass•Small- 2 to 3 mm.

• May have smooth contours or

• May take the form of an

irregular, jagged mass of spicules.

Morphology• Often many stones are found within

one kidney. • On occasion, progressive accretion of salts

leads to the development of branching

structures known as staghorn calculi,

which create a cast of the pelvic and calyceal system.

Clinical Features

Smaller Stones• In general, smaller stones are most hazardous,

• because they may pass into the ureters,

producing colic, one of the most intense forms of pain, and

• ureteral obstruction.

If stones grow to sufficient size (usually at least 3 millimeters (0.12 in)) they can cause obstruction of the ureter.

• Ureteral obstruction causes • Postrenal azotemia and • Hydronephrosis (distension and dilation of the

renal pelvis and calyces), as well as

• Spasm of the ureter.

Ureteral Obstruction leads to pain, most commonly felt in the flank,

lower abdomen, and groin (a condition

called renal colic).• Renal colic can be associated with nausea,

vomiting, fever, blood in the urine, pus in the urine, and painful urination.

Renal colic typically comes in waves lasting 20 to 60 minutes, beginning in the flank or lower back and often radiating to the groin or genitals (The Hallmark of obstructive ureteral stones).

Larger Stones• Larger stones cannot enter the ureters

and are more likely to remain silent within the renal pelvis.

• Commonly, these larger stones first manifest

themselves by hematuria.

Clinical features cont…

• Stones also predispose to superimposed infection, both by their obstructive nature and by

the trauma they produce.

Diagnosis

HISTORYPHYSICAL EXAMINATION

Renal colic caused by kidney stones is commonly accompanied by:

• Urinary urgency,

• Rrestlessness, • Hematuria,

Sweating, Nausea, Vomiting.

Calcium salt stonesCalcium salt stones 80% of kidney stones contain calcium80% of kidney stones contain calcium

The type of salt depends onThe type of salt depends on– Urine pHUrine pH– Availability of oxalateAvailability of oxalate

General appearance:General appearance:– White, hard, radioopaqueWhite, hard, radioopaque– Calcium POCalcium PO44: staghorn in renal : staghorn in renal

pelvis (large)pelvis (large)– Calcium oxalate: present in ureter Calcium oxalate: present in ureter

(small)(small)

Calcium salt stonesCalcium salt stones

Causes of calcium salt stones:Causes of calcium salt stones:

Hypercalciuria:Hypercalciuria:– Increased urinary calcium excretionIncreased urinary calcium excretion– Men: > 7.5 mmols/dayMen: > 7.5 mmols/day– Women > 6.2 mmols/dayWomen > 6.2 mmols/day– May or may not be due to May or may not be due to

hypercalcemiahypercalcemia

Calcium salt stonesCalcium salt stones• Hyperoxaluria:Hyperoxaluria:

– Causes the formation of calcium Causes the formation of calcium oxalates without hypercalciuriaoxalates without hypercalciuria

– Diet rich in oxalatesDiet rich in oxalates– Increased oxalate absorption in fat Increased oxalate absorption in fat

malabsorptionmalabsorption

• Primary hyperoxaluria:Primary hyperoxaluria:– Due to inborn errorsDue to inborn errors– Urinary oxalate excretion: > 400 Urinary oxalate excretion: > 400

mmols/daymmols/day

Calcium oxalate stones

Calcium salt stonesCalcium salt stones• Treatment:Treatment:

– Treatment of primary causes such as Treatment of primary causes such as infection, hypercalcemia, infection, hypercalcemia, hyperoxaluriahyperoxaluria

– Oxalate-restricted dietOxalate-restricted diet– Increased fluid intakeIncreased fluid intake– Acidification of urine (by dietary Acidification of urine (by dietary

changes)changes)• Calcium salt stones are formed in Calcium salt stones are formed in

alkaline urinealkaline urine

Uric acid stonesUric acid stones• About 8% of renal stones contain uric acidAbout 8% of renal stones contain uric acid• May be associated with hyperuricemia May be associated with hyperuricemia

(with or without gout) (with or without gout) • Form in acidic urineForm in acidic urine• General appearance:General appearance:

– Small, friable, yellowishSmall, friable, yellowish– May form staghornMay form staghorn– Radiolucent (plain x-rays cannot detect)Radiolucent (plain x-rays cannot detect)– Visualized by ultrasound or i.v. Visualized by ultrasound or i.v.

pyelogrampyelogram

Uric acid stonesUric acid stones• Treatment:Treatment:

–Purine-restricted dietPurine-restricted diet–Alkalinization of Alkalinization of urine (by dietary urine (by dietary changes)changes)

–Increased fluid Increased fluid intakeintake

Uric acid stones

Mg ammonium POMg ammonium PO44 stones stones About 10% of all renal stones contain Mg About 10% of all renal stones contain Mg

amm. POamm. PO44

Also called Also called struvitestruvite kidney stones kidney stones

Associated with chronic urinary tract infectionAssociated with chronic urinary tract infection

– Microorganisms (such as from Microorganisms (such as from ProteusProteus

genus) that metabolize genus) that metabolize urea into urea into ammoniaammonia

– Causing urine pH to become alkaline and Causing urine pH to become alkaline and stone formationstone formation

STRUVITE: A crystalline mineral found in guano. It is a hydrous phosphate of magnesia and ammonia.

Guano is the excrement of seabirds, cave-dwelling bats, or birds more generally.

Mg ammonium POMg ammonium PO44 stones stones• Commonly associated with staghorn calculiCommonly associated with staghorn calculi• 75% of staghorn stones are of struvite type75% of staghorn stones are of struvite type

• Treatment:Treatment:– Treatment of infectionTreatment of infection– Urine acidificationUrine acidification– Increased fluid intakeIncreased fluid intake

Mg ammonium phosphate (struvite) stone

Staghorn Stone ( Branching Stone)

Cystine stonesCystine stones• A rare type of kidney stoneA rare type of kidney stone• Due to homozygous cystinuriaDue to homozygous cystinuria• Form in acidic urineForm in acidic urine• Soluble in alkaline urineSoluble in alkaline urine• Faint radio-opaqueFaint radio-opaque

Treatment:Treatment:– Increased fluid intakeIncreased fluid intake– Alkalinization of urine (by dietary Alkalinization of urine (by dietary

changes)changes)– Penicillamine (binds to cysteine to form a Penicillamine (binds to cysteine to form a

compound more soluble than cystine)compound more soluble than cystine)

Cystine stone

Kidney StonesForm in acidic urine• Uric acid Stones• Cystine Stones

Form in alkaline urine• Calcium Salt Stones• Struvite Stones

Kidney StonesRadioopaque• Calcium Salt Stones• Cystine stones

(Faint)• Struvite

Radiolucent• Uric Acid Stones