Pathologic & other aspects

1. Renal Stones
Lecture 50
Urolithiasis
Renal Calculi
Nephrolithiasis
Kidney Stones

2. Renal Stones
A kidney stone, is a solid
concretion or crystal
aggregation formed in the
kidneys from dietary minerals
in the urine.

3. Classification- by location
• Urinary stones are typically classified by their
location in the
•
kidney (nephrolithiasis),
•ureter (ureterolithiasis),
•bladder (cystolithiasis),

4. Classification- by chemical composition
1.1. Calcium saltsCalcium salts
2.2. Uric acidUric acid
3.3. Mg ammonium POMg ammonium PO44
4.4. CystineCystine
5.5. Other (xanthine, etc.Other (xanthine, etc.))

5. Causes

6. 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

7. Risk Factors

8. Risk Factors

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

10. Risk Factors
•Occupation
• Small bowel disease (i.b.d.)
• Medical conditions causing hypercalcuria
• Medical conditions causing aciduria

11. Pathogenesis-
MucoProtein Matrix
• An organic
mucoprotein matrix,
making up 1% to 5% of the stone
by weight, is present in all
calculi.

12. 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.

13. Supersaturation- Slow urine flow

15. SOLUBILITY
• Solubility is affected by
•Urine pH,
•Volume and
•Total excretion

16. Pathogenesis- Calcium Oxalate Stones
Hypercalcemia & 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.

17. 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.

18. 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.

19. 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%

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

21. Pathogenesis
Idiopathic calcium stone disease
• In a variable proportion of
individuals with calcium
stones, no cause can be
found
(idiopathic calcium stone disease).

22. 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.

23. 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.

24. 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.

25. 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.

26. 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.

27. 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.

28. Pathogenesis
• However, many calculi occur in
the absence of these factors;
• conversely, individuals with
hypercalciuria, hyperoxaluria, and
hyperuricosuria often do not form
stones.

29. • It has therefore been postulated that
stone formation is enhanced by
a deficiency
in
inhibitors of
crystal

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

31. Morphology-
Gross• Unilateral 80%
Favored sites:
•Renal calyces
•Pelves
•Bladder.

32. 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.

33. 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 castof the pelvic and
calyceal system.

35. Clinical Features

36. 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.

37. 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.

38. 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).

39. 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.

40. Clinical features cont…
• Stones also predispose to
superimposed infection, both by
their obstructive nature and by
the traumathey produce.

41. Diagnosis
HISTORY
PHYSICAL
EXAMINATION

42. Renal colic caused by kidney stones is
commonly accompanied by:
• Urinary
urgency,
• Rrestlessness,
• Hematuria,
Sweating,
Nausea,
Vomiting.

43. Calcium saltCalcium salt
stonesstones 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 pelvis: staghorn in renal pelvis
(large)(large)
– Calcium oxalate: present in ureter (small)Calcium oxalate: present in ureter (small)

44. 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 hypercalcemiaMay or may not be due to hypercalcemia

45. Calcium salt stonesCalcium salt stones
• Hyperoxaluria:Hyperoxaluria:
– Causes the formation of calcium oxalatesCauses the formation of calcium oxalates
without hypercalciuriawithout hypercalciuria
– Diet rich in oxalatesDiet rich in oxalates
– Increased oxalate absorption in fatIncreased oxalate absorption in fat
malabsorptionmalabsorption
• Primary hyperoxaluria:Primary hyperoxaluria:
– Due to inborn errorsDue to inborn errors
– Urinary oxalate excretion: > 400Urinary oxalate excretion: > 400
mmols/daymmols/day

46. Calcium oxalate stones

47. Calcium salt stonesCalcium salt stones
• Treatment:Treatment:
– Treatment of primary causes such asTreatment of primary causes such as
infection, hypercalcemia, hyperoxaluriainfection, hypercalcemia, hyperoxaluria
– Oxalate-restricted dietOxalate-restricted diet
– Increased fluid intakeIncreased fluid intake
– Acidification of urine (by dietaryAcidification of urine (by dietary
changes)changes)
• Calcium salt stones are formed inCalcium salt stones are formed in
alkaline urinealkaline urine

48. 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 (with orMay be associated with hyperuricemia (with or
without gout)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. pyelogramVisualized by ultrasound or i.v. pyelogram

49. Uric acid stonesUric acid stones
• Treatment:Treatment:
–Purine-restricted dietPurine-restricted diet
–Alkalinization of urineAlkalinization of urine
(by dietary changes)(by dietary changes)
–Increased fluid intakeIncreased fluid intake

50. Uric acid stones

51. Mg ammonium POMg ammonium PO44 stonesstones
 About 10% of all renal stones contain Mg amm.About 10% of all renal stones contain Mg amm.
POPO44

Also calledAlso called struvitestruvitekidney stoneskidney stones
 Associated with chronic urinary tract infectionAssociated with chronic urinary tract infection
– Microorganisms (such as fromMicroorganisms (such as from ProteusProteus genus)genus)
that metabolizethat metabolize urea into ammoniaurea into ammonia
– Causing urine pH to become alkaline and stoneCausing urine pH to become alkaline and stone
formationformation
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.

52. Mg ammonium POMg ammonium PO44 stonesstones
• 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

53. Mg ammonium phosphate (struvite) stone
Staghorn Stone ( Branching Stone)

54. 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 changes)Alkalinization of urine (by dietary changes)
– Penicillamine (binds to cysteine to form aPenicillamine (binds to cysteine to form a
compound more soluble than cystine)compound more soluble than cystine)

55. Cystine stone

57. Kidney Stones
Form in acidic urine
• Uric acid Stones
• Cystine Stones
Form in alkaline urine
• Calcium Salt Stones
• Struvite Stones

58. Kidney Stones
Radioopaque
• Calcium Salt Stones
• Cystine stones
(Faint)
• Struvite
Radiolucent
• Uric Acid Stones