This document summarizes urinary lithiasis (kidney stones). It discusses the epidemiology, including higher rates in men, those aged 40-70, and people in hot climates. Risk factors include obesity, diabetes, family history, low fluid intake, and occupational heat exposure. It also covers the physicochemistry of stone formation including supersaturation, nucleation, crystal growth and retention. Specific stone types like calcium and oxalate stones are examined in depth, outlining related conditions, diagnostic evaluations, and potential treatments.

1. Urinary lithiasis
Dr. Hussein Iman- presenter
Dr. Marvin supervisor

2. • Epidemiology of Renal Calculi
• Physicochemistry and Pathogenesis
• Mineral Metabolism
• Pathophysiology of Upper Urinary Tract Calculi

3. EPIDEMIOLOGY OF RENAL CALCULI
•The lifetime prevalence: 1% to 15%
•varying according to age, gender, race, and
geographic location.
•Gender: men > women.
•Age. uncommon before age 20 but peaks in
incidence in the fourth to sixth decades of life (60 to
69 years) in men.
•women show a bimodal distribution (1st peak 30-39
years), a second peak in the sixth decade of life
corresponding to the onset of menopause and a fall
in estrogen levels.

4. • ??? protective effect of estrogen against stone formation in
premenopausal women, owing to enhanced renal calcium absorption
and reduced bone resorption.

5. • Geography
• a higher prevalence of stone disease is found in hot, arid, or dry climates
such as the mountains, desert, or tropical areas.
• However, genetic factors and dietary influences may outweigh the effects
of geography.
• Occupation
• Heat exposure and dehydration constitute occupational risk factors for
stone disease as well. Cooks and engineering room personnel.

6. •Those exposed to high temperatures:
•exhibited lower urine volumes and pH,
•higher uric acid levels
•higher urine specific gravity,
•All the above lead to higher urinary saturation
of uric acid.

7. • Obesity, Diabetes, and Metabolic Syndrome
• Diet.
• Vegeterians-decreased incindence
• High sodium intake-increased urinary sodium, urinary pH and
calcium with a decreased excretion of citrate.
• Fluid intake
• Urinary output- average urinary output in stone formers is 1.6 l/day.

8. •Family history.

9. PHYSICOCHEMISTRYAND PATHOGENESIS
• The physical process of stone formation comprises a complex cascade
of events that occurs as the glomerular filtrate traverses the nephron.
• It begins with urine that becomes supersaturated with respect to stone-
forming salts, such that dissolved ions or molecules precipitate out of
solution and form crystals or nuclei.
• Once formed, crystals may flow out with the urine or become retained
in the kidney at anchoring sites that promote growth and aggregation,
ultimately leading to stone formation.

10. •Stone formation requires supersaturated urine.
•Supersaturation depends on urinary PH, ionic
strength, solute concentration, and complexation

11. Role of solute concentration.
• A solution containing ions or molecules of a sparingly soluble salt is described by the
concentration product, which is a mathematic expression of the product of the
concentrations of the pure chemical components (ions or molecules) of the salt.
• A pure aqueous solution of a salt is considered saturated when it reaches the point at
which no further added salt crystals will dissolve. The concentration product at the
point of saturation is called the thermodynamic solubility product (Ksp), which is the
point at which the dissolved and crystalline components are in equilibrium for a
specific set of conditions.
• At this point, addition of further crystals to the saturated solution will cause the
crystals to precipitate unless the conditions of the solution, such as pH or
temperature, are changed.

12. • In urine even when the concentration products of ions are greater than
the established solubility product crystals may not form.
I. Other factors play major role in renal calculi formation including
complexation.
II. Complexation influences availability of specific ions.
III. For instance sodium complexes with oxalate reducing its free ionic
form while sulfates can complex with calcium.
IV. Other inhibitors of aggregration.

13. • As concentrations of the salt increase further, the point at which it can no
longer be held in solution is reached and crystals form. The concentration
product at this point is called the formation product (Kf).

14. • The solubility product and the formation product differentiate the three
major states of saturation in urine: undersaturated, metastable, and
unstable .
• Below the solubility product, crystals will not form under any
circumstances and dissolution of crystals is theoretically possible.
• At concentrations above the formation product, the solution is unstable
and crystals will form.

15. • In the metastable range of concentration products, although crystal growth
can occur on existing crystals and heterogenous nucleation., de novo
formation of crystals cannot occur in the length of time it normally takes for
the filtered urine to reach the bladder.
• However, crystal formation can occur in this range under certain
circumstances.
I. -local areas of obstruction or stasis in the upper urinary tract may prolong
urinary transit time and allow crystal formation to occur in metastable
urine.
II. - microscopic impurities or other constituents in the urine can facilitate
the nucleation process by adsorption of the crystal components (
“heterogeneous nucleation”)

17. Nucleation and Crystal Growth, Aggregation, and
Retention
• In normal human urine, the concentration of calcium oxalate is
four times higher than its solubility in water.
• Urinary factors favoring stone formation include low volume and
citrate, while increased calcium, oxalate, phosphate, and uric acid
all increase calcium oxalate supersaturation.
• Nucleation initiates the stone process and may be induced by a
variety of substances including proteinecious matrix, crystals ,
foreign bodies and other particulate particles.

18. • Heterogenous nucleation (epitaxy) which requires less energy and may
occur in less saturated urine is a common theme in stone formation.
• Homogeneous nucleation is the process by which nuclei form in pure
solution.
• Nuclei are the earliest crystal structures that will not dissolve.
• Small nuclei are unstable; below a critical size threshold, dissolution of
the crystal is favored over crystal growth.

19. • If the driving force (supersaturation level) and the stability of the nuclei
are adequate and the lag time to nucleation is sufficiently short compared
with the transit time of urine through the nephron, the nuclei will persist.
• Inhibitors, such as citrate, destabilize nuclei, whereas promoters stabilize
nuclei by providing a surface with a binding site that accommodates the
crystal structure of the nucleus.
• In urine, crystal nuclei usually form through heterogeneous nucleation by
adsorption onto existing surfaces of epithelial cells.

20. • Within the timeframe of transit of urine through the nephron,
estimated at 5 to 7 minutes, crystals cannot grow to reach a size
sufficient to occlude the tubular lumen. However, if enough nuclei
form and grow, aggregation of the crystals will form larger particles
within minutes that can occlude the tubular lumen.
•

21. • Fixed particle growth theory presupposes an anchoring site to which
crystals bind, thereby prolonging the time the crystals are exposed to
supersaturated urine and facilitating crystal growth and aggregation.
• A number of mechanisms have been proposed to account for crystal
fixation.
• One favored theory proposes that oxalate-induced injury to renal tubular
epithelial cells promotes adherence of calcium oxalate crystals

22. Inhibitors and Promoters of Crystal Formation
1.Citrate.
2. Magnesium
3. Polyanion macromolecules, including glycosaminoglycans, acid
mucopolysaccharides
• A. glycosaminoglycan
• -chondrotin sulfate
• B. glycoproteins
• -nephrocalcin
• -Tamm-Horsfall glycoprotein
• -osteopontin or uropontin
• -inter-α-trypsin

23. • Matrix
• Renal calculi consist of both crystalline and noncrystalline components.
• The noncrystalline component is termed matrix, which typically
• accounts for about 2.5% of the weight of the stone.
• In some cases, matrix comprises the majority of the stone (up to 65%), usually in
association with chronic urinary tract infection.
• The exact composition of matrix is difficult to ascertain because only 25% of it is
soluble; however, chemical analysis reveals a heterogeneous mixture consisting
of approximately 65% protein, 9% nonamino sugars, 5% glucosamine, 10%
bound water, and 12% organic ash.
• The exact role of matrix in stone formation, whether as promoter, inhibitor,
orpassive bystander, has yet to be elucidated.

24. Risk factors for people who form stones of calcium oxalate
1. Male sex
2. Low urinary volume
3. Hyperoxaluria
4. Increased urinary pH
5. Hypercalciuria
6. Hyperuricosuria
7. Hypocitraturia
8. Hypomagnesuria

26. Calcium Stones
Read about the physiology of calcium absorption
Hypercalciuria
• Hypercalciuria is the most common abnormality identified in calcium
stone formers
• Hypercalciuria (>200 mg/day)

27. • Absorptive Hypercalciuria.
involves an increase in the amount of calcium absorbed by the
intestinal tract.
normal serum calcium and a normal or reduced level of circulating
intact parathyroid hormone (iPTH).
Type 1. occurs independent of the diet. Excessive urinary calcium
level >150-200mg/24 hours even during calcuim restricted diet

28. • Rx of type 1
• Cellulose phosphate. Non absorbable exchange resin. May cause
seconday hyperoxaluria.
• Thiazide duiretics

29. • Type II. Diet dependent. Is the commonest cause of urinary stone
disease. Calcuim excretion returns to normal on calcium restricted
diet. No specific medical therapy.
• Type III. Phosphate renal leak. Decreased serum phosphate---
increased 1,25 vit D—increased phosphate and calcium absorption.
• Renal phosphate leak, however, is a rare cause of nephrolithiasis,
affecting at most 2% to 4% of patients
• Rx. Replace phosphate. Orthophosphate.

30. • Renal Hypercalciuria (renal leak hypercalciuria)
• is thought to be due to a wasting of calcium by the functioning nephron.
• Intrinsic renal tubular defect in calcium excretion.
• As a result of constant loss of calcium from the distal tubules, these
patients will demonstrate hypercalciuria during all phases of fasting,
loading, or restricting of dietary calcium.
• Elevated fasting urinary calcium, a normal serum calcium, and a mild
elevation of iPTH as the regulatory systems attempt to keep up with the
constant loss of calcium.
• Rx. Thiazide diuretics.

31. Resorptive Hypercalciuria (Primary
Hyperparathyroidism).
•overproduction of parathyroid hormone
•The hallmark of this disorder is the persistence of
increased urinary calcium
•hypercalcemia and elevations of the parathyroid
hormone.

32. •Differentiating primary and secondary
hyperparathyroidism in patient with urinary stone
disease.
•Administer hydrochlorothiazide challenge 50mg for 10
days.
•Primary- normal parathyroid hormone.
•Seconday- elevated parathyroid hormone.

34. Hyperoxaluria
• Hyperoxaluria, defined as urinary oxalate greater than 40 mg/day,
• leads to increased urinary saturation of calcium oxalate and subsequent
promotion of calcium oxalate stones.
• Additionally, oxalate has been implicated in crystal growth and retention
by means of renal tubular cell injury mediated by lipid peroxidation and
the generation of oxygen free radicals.
• Membrane injury facilitates the fixation of calcium oxalate crystals and
subsequent crystal growth.
• Antioxidant therapy has been shown to prevent calcium oxalate

35. • Causes of hyperoxaluria include disorders in biosynthetic pathways
(primary hyperoxaluria); intestinal malabsorptive states associated
with inflammatory bowel disease, celiac sprue, or intestinal resection
(enteric hyperoxaluria); and excessive dietary intake or high substrate
levels (vitamin C) (dietary hyperoxaluria).

36. Primary Hyperoxaluria.
• The primary hyperoxalurias (PHs) are the result of rare autosomal
recessive inherited disorders in glyoxylate metabolism by which the
normal conversion of glyoxylate to glycine is prevented, leading to
preferential oxidative conversion of glyoxylate to oxalate, an end
product of metabolism (Fig. 51-6).
• The markedly high levels of urinary oxalate that ensue (>100 mg/day)
lead to increased saturation of calcium oxalate and formation of
calcium oxalate complexes and crystals in the renal tubular lumen.
• Some crystals attach to the surface of renal tubular epithelial cells
and further aggregate into stones, whereas others are internalized into
tubular cells and then extruded into the renal interstitium, leading to
marked nephrocalcinosis

38. • Three forms of PH have been identified (types 1, 2, and 3) that
• differ in the enzyme and intracellular organelle affected. The primary
• enzyme catalyzing glyoxylate conversion to glycine is the pyridoxal
• phosphate–dependent alanine-glyoxylate aminotransferase (AGT),
• which is synthesized in the liver peroxisome. Mutations in this gene
• (AGXT) result in primary hyperoxaluria type 1 (PH1), and patients
• with this disorder have elevated levels of oxalate and frequently
• glycolate. End-stage renal disease (ESRD) occurs during the second
• to third decade of life in most patients with PH1, making it the
• most aggressive form of the disease

39. • Primary hyperoxaluria type 2 (PH2) is associated with a defect in
glyoxylate reductase/hydroxypyruvate reductase (GRHPR) in the
liver, resulting in hyperoxaluric nephrolithiasis, but with a less
aggressive course with regard to renal failure than PH1

40. • A third type of primary hyperoxaluria has recently been recognized.
• Primary hyperoxaluria type 3 (PH3) is caused by a defective
• mitochondrial enzyme, 4-hydroxy-2-oxoglutarate aldolase (HOGA),
• which is thought to play a role in hydroxyproline metabolism
• (Belostotsky et al, 2010). 4-Hydroxy-2-oxoglutarate derived from
• hydroxyproline is converted to pyruvate and glyoxylate in a reaction
• catalyzed by HOGA. However, the mechanism by which this defect
• leads to hyperoxaluria has not been established. Although PH3 is
• associated with hyperoxaluria and severe hypercalciuria, the recurrent
• calcium oxalate stone formation seen in early childhood may
• become clinically silent later in life, and there are no reports to date
• of progression to ESRD in these patients

41. • Enteric Hyperoxaluria. The most common cause of acquired
hyperoxaluria is enteric hyperoxaluria.
• This abnormality is associated with chronic diarrheal states, by which
fat malabsorption results in saponification of fatty acids with divalent
cations such as calcium and magnesium, thereby reducing calcium
oxalate complexation and increasing the pool of available oxalate for
reabsorption (Earnest et al, 1975).
• The poorly absorbed fatty acids and bile salts may increase colonic
permeability to oxalate, further enhancing intestinal oxalate
absorption

42. • Dehydration, hypokalemia, hypomagnesiuria, hypocitraturia, and low
urine pH also increase the risk of calcium oxalate stone formation in
patients with chronic diarrheal syndrome.
• Malabsorption of any cause can lead to increased intestinal absorption
of oxalate.
• Therefore small bowel resection, intrinsic disease, and jejunoileal
bypass (Cryer et al, 1975) have all been associated with
hyperoxaluria.

43. Dietary Hyperoxaluria.
• Overindulgence in oxalate-rich foods such as nuts, chocolate, brewed
tea, spinach, potatoes, beets, and rhubarb can result in hyperoxaluria
in otherwise normal individuals.
• The contribution of dietary oxalate to urinary oxalate excretion can
range from 24% to 42% (Holmes et al, 2001). In addition, severe
calcium restriction may result in reduced intestinal binding of oxalate
and increased intestinal oxalate absorption.
• Ascorbic acid supplementation has been shown to increase urinary
oxalate levels by in vivo conversion to oxalate (Traxer et al, 2003),
although increased clinical rates of stone formation have not been
unequivocally linked to ascorbic acid use

45. • Recent studies have also implicated O. formigenes, an
oxalatedegrading intestinal bacterium, as a potential modulator of
intestinal oxalate levels (Duncan et al, 2002).
• Stone formers were found to have reduced levels or absent
colonization of O. formigenes compared with non–stone-forming
control subjects, and individuals lacking the bacteria have been shown
to have higher urinary oxalate levels

46. • Cystic fibrosis patients, many of whom are exposed to prolonged
antibiotic use, have also been shown to have absence of O.
formigenes from the intestinal tract and corresponding elevated
urinary oxalate levels

47. • Idiopathic Hyperoxaluria. Several studies have suggested that
• mild hyperoxaluria is as important a factor as hypercalciuria in the
• pathogenesis of idiopathic calcium oxalate stones

48. Hypocitraturia
• Hypocitraturia is an important and correctable abnormality associated
with nephrolithiasis that exists as an isolated abnormality in up to 10% of
calcium stones.
• Citrate is an important inhibitor that can reduce calcium stone formation
by several mechanisms.
I. Reduces urinary saturation of calcium salts by complexing with
calcium.
II. Directly prevents spontaneous nucleation of calcium oxalate.
III. Inhibits agglomeration and sedimentation of calcium oxalate crystals.
IV. Enhance the inhibitory effect of Tamm-Horsfall glycoprotein

49. • Hypocitraturia is defined as a urinary citrate level less than 320 mg/day.
• Acid-base state is the primary determinant of urinary citrate excretion.
• Metabolic acidosis reduces urinary citrate levels secondary to enhanced
renal tubular reabsorption and decreased synthesis of citrate in
peritubular cells.
• Estrogen increases citrate excretion thus preventing against stone
formation.

50. • Low urinary citrate results from a variety of pathologic states associated
with acidosis.
I. Distal RTA.
II. Chronic diarrheal states cause intestinal alkali loss in the stool with
subsequent systemic acidosis and hypocitraturia .
III. Excessive animal protein can provide an acid load, reducing citrate
levels.
IV. Drugs.
 Diuretics such as thiazides induce hypokalemia and intracellular
acidosis.
Angiotensin-converting enzymes.
I. strenuous exercise may induce lactic acidosis.

51. Low Urine pH
• At low urine pH (<5.5), the undissociated form of uric acid
predominates, leading to uric acid and/or calcium stone formation.
• Calcium oxalate stones form as a result of heterogeneous nucleation
with uric acid crystals (Coe and Kavalach, 1974; Pak et al, 1976).
• Any disorder leading to low urine pH may predispose to stone
• formation. Chronic metabolic acidosis can lead to low urine pH,
hypercalciuria, and hypocitraturia. Acidosis increases bone resorption
and produces renal calcium leak (Lemann, 1999; Lemann et al, 2003).
• “Gouty diathesis,” or idiopathic low urine pH, refers to a stone-
forming propensity characterized by low urine pH of unknown
etiology with or without associated gouty arthritis

52. Renal Tubular Acidosis
• RTA is a clinical syndrome characterized by metabolic acidosis
resulting from defects in renal tubular hydrogen ion secretion or
bicarbonate reabsorption.
• There are three types of RTA: 1, 2, and 4. Type 1 (distal) RTA is of
particular significance to urologists not only because it is the most
common form of RTA but also because it is the form of RTA most
frequently associated with stone formation, which occurs in up to
70% of affected individuals (Van den Berg et al, 1983).

53. • Distal and proximal RTA occur as a result of impairment of net
excretion of acid into the urine (distal or type 1) or of reabsorption of
bicarbonate (proximal or type 2).
• Type 1 (Distal) Renal Tubular Acidosis.
• Type 1 RTA comprises a syndrome of abnormal collecting duct
function characterized by inability to acidify the urine in the presence
of systemic acidosis.
• The classic findings include hypokalemic, hyperchloremic non–anion
gap metabolic acidosis along with nephrolithiasis, nephrocalcinosis,
and elevated urine pH (>6.0).

54. • Patients with distal RTA commonly present as adults with symptoms
of nephrolithiasis (Caruana and Buckalew, 1988). However, children
comprise a third of affected individuals, and they often present with
vomiting or diarrhea, failure to thrive, or growth retardation.
• The most common stone composition associated with distal RTA is
calcium phosphate as a result of hypercalciuria, hypocitraturia, and
increased urinary pH (Van den Berg et al, 1983; Pohlman et al, 1984).
• The metabolic acidosis promotes bone demineralization, which leads
to secondary hyperparathyroidism and hypercalciuria.
• Profound hypocitraturia, perhaps the most important factor in stone
formation in this setting, is due to impaired citrate excretion as a
result of metabolic acidosis but may also be related to abnormal renal
tubular citrate transport or migration of citrate into the mitochondria
as a result of intracellular acidosis

55. • Distal RTA occurs as a consequence of dysfunction of the α- type
intercalated cells, which secrete protons into the urine via an apical
H+-ATPase that is coupled to an anion exchanger (AE1) located at the
basolateral membrane

57. • Type 2 (Proximal) Renal Tubular Acidosis. Proximal RTA is
characterized by a defect in HCO3 − reabsorption associated with
initial high urine pH that normalizes as plasma HCO3 − decreases and
the amount of filtered HCO3 − falls (Laing et al, 2005).
• With reduced capacity of the proximal tubule to reclaim filtered
HCO3 −, more HCO3 − is delivered to the distal tubule, which has a
limited capacity for bicarbonate reabsorption.
• Consequently, bicarbonaturia ensues, resulting in reduced net acid
excretion and metabolic acidosis. As the filtered HCO3 − load
declines with progressive metabolic acidosis, less bicarbonate reaches
the distal tubule until eventually the capacity of the distal tubule is
sufficient to handle the load and no further bicarbonate is lost.
• At steady state, serum HCO3 − is low (15 to 18 mEq/L) and urine pH
is acidic (<5.5).

58. • This syndrome is usually associated with generalized defects in
proximal tubule function similar to Fanconi syndrome, with loss of
glycogen, protein, uric acid, and phosphate (Rocher and Tannen,
1986).
• Nephrolithiasis is uncommon in this disorder owing to relatively
normal urinary citrate excretion (Laing et al, 2005). The clinical
manifestations of proximal RTA include growth retardation and
hypokalemia in children resulting from metabolic acidosis.
• Metabolic bone disease is seen more frequently with proximal RTA
because of associated abnormalities in vitamin D metabolism and
hypophosphatemia (Kinkead and Menon, 1995).

59. Hypomagnesiuria
• Hypomagnesiuria is a rare cause of nephrolithiasis, affecting less than
1% of stone formers as an isolated abnormality, although it can be
found in conjunction with other abnormalities in 6% to 11% of cases
(Levy et al, 1995; Schwartz et al, 2001).
• Magnesium complexes with oxalate and calcium salts, and therefore
low magnesium levels result in reduced inhibitory activity.
• Low urinary magnesium is also associated with decreased urinary
citrate levels, which may further contribute to stone formation.

60. Non calcium calculi
Struvite stones.
•Contain magnesium, ammonia and phosphate.
•Found commonly in women and may recur rapidly.
•Are infection stones associated with urea-splitting
organisms including proteus,pseudomonas, klebseilla,
providencia, staphylococci and mycoplasma.
•A history of a foreign body (e.g., forgotten stent, suture
material, staple) or neurogenic bladder may be noted.

61. •Struvite calculi can be quite large and often fill
multiple calyces or even the entire collecting system.
Present frequently as renal starghorn calculi and rarely
present as ureteral stones
•Urine cultures often will reveal a bacterial pathogen,
although the presence of a sterile urine culture does not
preclude the sequestration of bacteria within the
calculus itself.

62. •High ammonium concentration---alkaline urinary pH
(> 7.2). Its only at this pH that MAP crystals ppt.
•MAP crystals are soluble in the normal urinary pH
range (5-7).
•Massive duiresis does not prevent struvite calculi.
•Long term mgt- removal of all FBs including catheters.
•A short ileal loop helps decrease the risk of stones in
patients with supravesical urine diversion.

64. •Acetohydroxamic acid inhibits action of bacterial
urease thereby reducing urinary pH and decreasing
likelihood of ppt. Most patients have a difficult time
tolerating this medicaion.

65. Staghorn Calculi
•Staghorn calculi are large renal stones that
occupy most or all of the renal collecting system.
•The name arises from the fact that these stones
look like the antlers of a deer or stag on imaging.
•The stones frequently involve the renal pelvis and
branch into the surrounding infundibula and
calyces.
•Struvite composes the majority of staghorn
stones, although this configuration of collecting
system involvement can include any type of stone

66. •Untreated, staghorn stones are associated with
recurrent UTIs, urosepsis events, renal functional
deterioration, and a higher likelihood of death.
•Complete renal function loss in 50% of affected
kidneys can occur after 2 years without treatment.

67. Bilateral staghorn calculi

68. Uric acid stones
• Compose <5% of renal calculi
• Found usually in men.
• Hyperuricosuria is defined as urinary uric acid exceeding 600 mg/ day.
• Most patients with uric acid stones do not have hyperuricemia.
• Elevated urine uric acid levels are due to dehydration and purine intake.
• Patient with urate stones have a pH of <5.5.
• As urinary pH increases above the dissociation constant pKa of 5.75, it
dissociates into a relatively soluble urate ion.

69. • The most common cause of hyperuricosuria is increased dietary
purine intake.
• However, acquired and hereditary diseases may also be accompanied
by hyperuricosuria, including gout, myeloproliferative and
lymphoproliferative disorders, multiple myeloma, secondary
polycythemia, pernicious anemia, hemolytic disorders,
hemoglobinopathies and thalassemia, complete or partial HGPRT
deficiency, overactivity of phosphoribosylpyrophosphate synthetase,
and hereditary renal hypouricemia

70. • As urinary pH increases above the dissociation Pka 5.75, it dissociates
into a relatively soluble urate iron.
• Treatment is centered on maintaining urine volume >2l/day and urine
pH>6.
• Reducing dietary purines and administration of allopurinol also help
reduce uric acid excretion.
• Alkalinization of urine ( NaHCO3,KHCO3,Potassium citrate or
sodium lactate) may dissolve calculi.

71. Xanthine stones
• Occurs in congenital deficiency of xanthine oxidase.
• Stones are radiolucent and are tannish yellow in color.
• High fluid intake recommended.

72. Cysteine stones
• Secondary to inborn errors of metabolism resulting in abnormal
intestinal (small bowel) mucosal absorption and renal tubular
absorption of dibasic acids including cysteine, ornithine, lysine and
arginine.
• 1-2% of renal calculi.
• Peak incidence: second or third decade.
• Solubility of cysteine is PH dependent with a Pk of 8.1
• Are frequently associated with calcium calculi.

73. • May present as single, multiple or starghorn stones.
• Medical therapy: high fluid intake (>3l/day) and alkalinization of
urine.
• A low methionine ( precursor of cysteine) has a limited impact as
most of the cysteine is endogenous.
• Glutamine, ascorbic acid and captopril are effective in some patients.
• Penicillamine can reduce urinary cystein levels. It complexes with the
amino acid and this pdt is more soluble.

74. • Many patients poorly tolerate this treatment.
• It may inhibit pyrodoxine which should be supplemented during
treatment (50mg/day).
• Mercaptopropionylglycine (Thiola)- forms a soluble complex with
cysteine and reduce stone formation.

75. drug-induced stones.
• Antiretroviral Agents. Indinavir sulfate.
• Triamterene.
• Guaifenesin and Ephedrine.
• Thiazides cause intracellular acidosis and subsequent hypocitraturia
• Carbonic anhydrase inhibitors such as acetazolamide, Topiramate.

76. Anatomic Predisposition to Stones
• Patients with anatomic anomalies associated with urinary obstruction
and/or stasis have been noted to have a high incidence of associated
stones.
• Ureteropelvic Junction Obstruction
• The incidence of renal calculi is nearly 20%
• Horseshoe Kidneys
• Horseshoe kidneys occur with a prevalence of 0.25% but have an
associated rate of renal calculi of 20%
• Caliceal Diverticula
• Caliceal diverticula are associated with stones in up to 40% of
Patients

77. Medullary Sponge Kidney
• Medullary sponge kidney (MSK) is a disorder characterized by
ectasia of the renal collecting ducts.
• Nephrocalcinosis and renal calculi are frequent complications of
MSK

78. Stones in Pregnancy
• Symptomatic stones during pregnancy occur at a rate of 1 in 250 to 1
in 3000 pregnant women.
• The majority of symptomatic stones occur in the second and third
trimesters of pregnancy, heralded by symptoms of flank pain or
hematuria.
• The diagnosis can be difficult in this patient population; up to 28% of
women are misdiagnosed with appendicitis, diverticulitis, or placental
abruption

79. • Important physiologic changes in the kidney occur during pregnancy
and modulate urinary stone risk factors.
• Renal blood flow increases, leading to a 30% to 50% rise in
glomerular filtration rate, which subsequently increases the filtered
loads of calcium, sodium, and uric acid.
• Hypercalciuria is further enhanced by placental production of
1,25(OH)2D3, which increases intestinal calcium absorption and
secondarily suppresses PTH.
• Hyperuricosuria has also been reported as a result of increased filtered
load of uric acid

80. • Despite increases in a number of stone-inducing analytes, pregnant
women have been shown to excrete increased amounts of inhibitors
such as citrate, magnesium, and glycoproteins.
• Therefore the overall risk of stone formation has been reported to be
similar in gravid and nongravid women.

81. Plain x-ray and intravenous pyelogram

84. Clinical features.
• Upper urinary tract stones usually cause pain.
• The character of the pain depends on the location.
• Calculi small enough to venture down the ureters usually have
difficulty passing throuh the ureteropelvic junction or entering the
bladder at the ureterovesical junction.

85. • A. pain.
• Renal colic- stretching of the collecting system or the ureter. Urinary
obstruction is the main mechanism.
• Non colicky renal pain- distension of the renal capsule.
• Severity and location of the pain can vary from patient to patient due
to stone size, stone location, degree of obstruction, and anatomic
variation ( eg intrarenal versus extrarenal pelvis)

86. • The stone burden does not correlate with the severity of the
symptoms.
• Small ureteral stones frequently present with severe pain while large
starghorn calculi will present with a dull ache or flank discomfort.
• The pain frequently abrupt in onset and severe and may awaken a
patient from sleep.
• Patients move constantly in an attempt to relieve pain.

87. • The symptoms of renal colic depend on the location of the
calculi.
1. Renal calyx. Deep dull ache in the flank or back. Caliceal
calculi occasionally result in spontaneous perforation with
urinoma, fistula or abscess formation.
2. renal pelvis.
Stones >1 cm obstruct UPJ.
Severe pain in costovertebral angle just lateral to sacrospinalis
muscle and just below the 12th rib.

88. 3. Upper and mid-ureter.
Severe back ( costovertebral ) or flank pain.
4. Distal ureter.
Pain that radiates to the groin or testicles in men or
labia majora in female.
Pain in the distribution of the ilioinguinal nerve or
genital branch of the genitofemoral nerve.

89. • B. haematuria. Intermittent gross haematuria or occasional tea colored
urine (old blood). Microhaematuria.
• C. infection.
• -struvite stones
• -phosphate stones
• D. obstruction
• pyonephrosis. Pus in the obstructed collecting system.
• Xanthogranulomatous pyelonephritis.
• Fever.
• Nausea and vomiting.
• Costovertebral tenderness in acute upper urinary tract obstruction.

90. DIAGNOSTIC EVALUATION OF NEPHROLITHIASIS
• Any evaluation should be able to identify associated metabolic
disorders responsible for recurrent stone disease.
• These metabolic problems include distal renal tubular acidosis (RTA),
primary hyperparathyroidism, enteric hyperoxaluria, cystinuria, and
gouty diathesis.
• In many of these relatively uncommon conditions, it is generally
agreed that selective medical therapy is indicated not only to prevent
further stone formation but also to correct underlying physiologic
disturbances that may lead to nonrenal complications

92. • History
• Underlying predisposing conditions (as per Box 52-1)
• Medications (calcium, vitamin C, vitamin D, acetazolamide, steroids)
• Dietary excesses, inadequate fluid intake, excessive fluid loss
• Surgical history: bowel resection.
• Multichannel blood screen
• Basic metabolic panel (sodium, potassium, chloride, carbon dioxide,
blood urea nitrogen, creatinine)
• Calcium
• Intact parathyroid hormone
• Uric acid

93. Urine
• Urinalysis
• pH > 7.5: infection lithiasis or RTA
• pH < 5.5: uric acid lithiasis
• Sediment for crystalluria
• Urine culture
• Urea-splitting organisms: suggestive of infection lithiasis
• Qualitative cystine

94. • The urine sediment should be examined for crystalluria, because
particular crystal types may give a clue as to the composition of
stones the patient is forming.
• Tetrahedral “envelopes” are seen in calcium oxalate lithiasis (Fig. 52-
1), and rectangular, “coffinlid” crystals are often seen in patients with
struvite calculi (see Fig. 52-1). Hexagonal crystals confirm cystinuria
(see Fig. 52-1); uric acid crystals may be seen as amorphous fibers or
as irregular plates.
• The microscopic appearances of common calculi are summarized in
Table 52-1.

96. • Urine cultures are performed if there is a suspicion of infection-
related calculi or if there are signs or symptoms of a UTI. A culture
that is positive for urea-splitting organisms such as Proteus,
Pseudomonas, Klebsiella, Staphylococcus aureus, and Staphylococcus
epidermidis would help explain the formation of a struvite calculus.
• A positive culture also will warrant therapy with appropriate
antibiotics before initiation of any surgical procedure to remove the
stone.
• The surgical management of a calculus during an active infection will
place the patient in great risk for bacteremia or sepsis.
• Unfortunately, many infected calculi will harbor bacteria even after
treatment with broad-spectrum antibiotics.

97. Radiography
• Radiopaque stones: calcium oxalate, calcium phosphate, magnesium
ammonium phosphate (struvite), cystine.
• Radiolucent stones: uric acid, xanthine, triamterene
• Intravenous pyelogram: radiolucent stones, anatomic abnormalities

98. • Abdominal x-ray films (kidney-ureter-bladder [KUB]) should be
obtained to document the existence of any current stones within the
urinary tract.
• The radiopacity of any existing stones may suggest the type of stones
present. Although magnesium ammonium phosphate and cystine
stones are often radiopaque, they are not as dense as calcium oxalate
or calcium phosphate stones.
• A plain abdominal film is also useful in identifying nephrocalcinosis
• (suggestive of RTA).
• A noncontrast computed tomography (NCCT) scan may be obtained
to confirm the presence of radiolucent stones and also identify any
anatomic abnormalities that may predispose the patient to stone
formation.

99. • CT scan.(non contrast). Is the investigationof choice in patients with
renal colic.
• Images other peritoneal and retroperitoneal structures and helps when
diagnosis is uncertain.
• Distal ureteral calculi may be confused with phleboliths.
• Does not give anatomic details as seen in IVP ( a bifid collecting
syatem) that may be important in planning intervention.
• Urate stones are visualised the same as oxalate stones.

100. • Intravenous pyelogram ( IVP).
• Can document both stones and upper tract anatomy.
• Extraosseous calcifications on radiographs may be erroneously
assumed to be urinary calculi.
• Oblique views easily differentiate gall stones from right renal calculi.

101. • Tomography.
• -renal tomography is useful to identify renal calculi when oblique views
are not helpful
• May help identify poorly opacified calculi especially when interfering
abdominal gas or morbid obesity make KUB films suboptimal.
• KUB films and directed ultrasonography.

102. • Retrograde pyelography.
• -delineate the upper tract anatomy
• -localise small or radiolucent calculi.
• MRI
• -Is apoor study to document renal stone disease.
• Nuclear scintigraphy.
• -can identify small stones
• -can not delineate upper tract anatomy in sufficient detail to help
direct a therapeutic plan.

103. • Stone analysis. Finally, available stones should be analyzed to
determine their crystalline composition.
• The presence of uric acid or cystine would suggest the presence of a
gouty diathesis or cystinuria, respectively.
• The finding of struvite, carbonate apatite, and magnesium ammonium
phosphate would suggest infection lithiasis.
• A predominance of a hydroxyapatite component suggests the
presence of RTA or primary hyperparathyroidism and warrants an
assessment of basic electrolytes.
• Stones composed of pure calcium oxalate or mixed calcium oxalate
and hydroxyapatite are less useful diagnostically because they may
occur in several entities, including absorptive and renal
hypercalciuria, hyperuricosuric calcium nephrolithiasis, enteric
hyperoxaluria, hypocitraturic calcium nephrolithiasis, and low urine
volume

104. Treatment modalities
• Conservative observation
• Medical therapy.
• -dissolution agents.
• -oral therapy.

105. intervention
• 1. conservative observation.
• most ureteral calculi pass and do not require intervention
• spontaneous passage depends on stone size, shape,location and
associaed ureteral oedema.
• -ureteral calculi 4-5mm have a 40-50% chance of spontaneous
passage.
• calculi >6mm have <5% chance of passage.

106. • The vast majority of stones that pass do so within a 6 weeks period
after onset of symptoms.
• Calculi at the distal ureter-50% chance of spontaneous passage, mid
ureter (25%) and proximal ureter( 10%)

107. CONSERVATIVE MANAGEMENT
• Fluid Recommendations
• Volume
• One mainstay of conservative management is the forced increase in
fluid intake to achieve a daily urine output of at least 2 liters (Borghi
et al, 1999).
• Increased urine output may have two effects.
• First, the mechanical diuresis that ensues may prevent urinary
stagnation and the formation of symptomatic calculi. It is more likely
that the creation of dilute urine alters the supersaturation of
stonemcomponents.

108. KEY POINTS: FLUID RECOMMENDATIONS
• Patients should be strongly encouraged to consume enough fluids to
produce 2 L/day.
• Water hardness is unlikely to play a significant role in recurrence
risk.
• Carbonated water may confer some protective benefit.
• Soda flavored with phosphoric acid may increase stone risk, whereas
those with citric acid may decrease risk.
• Citrus juices (particularly lemon and orange juices) may be a useful
adjunct to stone prevention.

109. Dietary Recommendations
• Randomized studies have confirmed the advantage of a diet with
reduced animal protein (meat) intake.
• A diet high in fruits and vegetables imparts a reduced risk for stone
formation over diets high in animal protein.
• Randomized trials have demonstrated a benefit of dietary sodium
restriction in both normal volunteers and stone formers.

110. • Protein intake increases urinary calcium, oxalate, and uric acid
excretion and the mathematically calculated probability of stone
formation even in normal subjects

111. • They noted that a high sodium intake not only increased calcium
excretion but also increased urinary pH and decreased citrate
excretion.
• The net effect of a high-sodium diet was an increased propensity for
the crystallization of calcium salts in urine

112. • Dietary calcium restriction actually increases stone recurrence risk.
• Calcium supplementation is likely safest when taken with meals.
• Calcium citrate appears to be a more stone-friendly calcium
supplement because of the additional inhibitory action of citrate.
• Vitamin D repletion is likely safe for stone formers; however, 24-
hour urine calcium should be monitored during vitamin D therapy.
• Bisphosphonates combined with thiazide diuretics appear to reduce
hypercalciuria while protecting the bone.

113. 2. MEDICAL THERAPY OF NEPHROLITHIASIS
• Improved elucidation of the pathophysiology and the formulation of
diagnostic criteria for different causes of nephrolithiasis have made
feasible the adoption of selective treatment programs (Pak et al, 1981;
Preminger and Pak, 1985).
• Such programs should (1) reverse the underlying physicochemical
and physiologic derangements,(2) inhibit new stone formation, (3)
overcome nonrenal complications of the disease process, and (4) be
free of serious side effects.

114. • Dissolution agents
• effectiveness depends on stone surface area, stone type, volume of the
irrigant and mode of delivery
• A) oral alkalinising agents
• -sodium or potassium bicarbonate
• -potassium citrate 60meq in 3-4 divided doses per day. Indicated in
those with calcium oxalate stones secondary to hypocitraturia. It may
also treat uric acid lithiasis.
• Intravenous sodium lactate.
• Orange juice alkalinises urine.

115. B). Thiols for dissolution of cysteine stones
• -penicillamine 0.5% solution
• -n-acetylcysteine 2-5% solution
• Alpha-mercaptopropionylglycine 5% solution.
• C) struvite stone dissolution requires acidifiction.
• -subys G solution.
• -hemiacidrin ( Renacidin)- not approved FDA

117. MISCELLANEOUS SCENARIOS
• Medical Management of Bladder Calculi
• bladder calculi usually occur in men older than 50 years of age and
are usually associated with bladder outlet obstruction.
• The diagnosis of a bladder stone should result in a complete urologic
evaluation for factors that cause urinary stasis, such as urethral
stricture, benign prostatic hyperplasia, bladder diverticulum, and/or a
neurogenic bladder.
• Occasionally, bladder stones may result as a consequence of a
retained foreign body catheter, forgotten double j ureteral stents.

118. • bladder stones are usually composed of uric acid (in noninfected
urine) or struvite (in infected urine).
• The occurrence of calcium oxalate or cystine stones in the bladder
suggests the presence of calculi in the kidney with subsequent ureteral
passage and entrapment in the bladder.

119. • Bladder calculi are usually solitary, but may develop in large
• numbers in the presence of urinary stasis.
• The typical symptoms of a vesical stone are intermittent, painful voiding and
terminal hematuria. Discomfort may be dull, aching, or sharp suprapubic
pain, which is aggravated by exercise and sudden movement. Severe pain
usually occurs near the end of micturition, when the stone becomes impacted
at the bladder neck.
• Relief may be afforded by assuming a recumbent position. The pain
• may be referred to the tip of the penis, the scrotum, or the perineum
• and on occasion to the back or the hip. Besides pain, there may be
• an interruption of the urinary stream from impaction of the stone
• at the bladder neck or urethra.

120. • high component of uric acid and because of overlying prostatic
• tissue. Such stones form negative shadows in the cystogram phase
• of intravenous urography. Ultrasonography is useful for detecting
• radiolucent calculi. Cystoscopic examination is the surest method
• for detecting vesical calculi.

121. • The vast majority of bladder calculi can be removed via endoscopic
techniques.
• Various lithotripters have been used, including ultrasonic handpieces, lasers,
pneumatic devices, and electrohydraulic probes.
• Transurethral and percutaneous approaches have been described with good
success (Dhabalia et al, 2011; Philippou et al, 2011).
• Renacidin may prove beneficial in irrigating indwelling suprapubic or
urethral catheters to decrease and prevent encrustation and occlusion
(Kennedy et al, 1992; Getliffe et al, 2000).
• Twice-daily or thrice-daily irrigation with 0.25% or 0.5% acetic acid solution
also serve as beneficial prophylaxis against recurrent struvite calculi when
catheters must be left indwelling for long periods. Uric acid calculi may be
dissolved by irrigation with alkaline solutions

122. • The mainstay of therapy for the prevention of recurrent
• bladder calculi involves relief of the bladder outlet obstruction.
• This treatment may include the performance of a transurethral
• resection of the prostate or an open prostatectomy if the gland is
• quite large.

123. Neonatal Nephrolithiasis
• Neonates with furosemide-induced nephrolithiasis present with
hematuria, worsening renal function, and calcific densities on
ultrasonography or plain film radiography.
• Nephrocalcinosis is often present on imaging studies.
• This same process has been seen in other infants with severe low birth
weight and/or prematurity and no history of loop diuretic usage.

124. • Management of neonatal nephrolithiasis entails the obvious
optimization of the infant’s overall health.
• Cessation of furosemide diuresis is considered helpful and standard
therapy.
• There has been previous suggestion that treatment with thiazide
diuretics may actually promote the resolution of this process and
reverse the likely parenchymal injury

125. • Children and Adolescents
• the appearance of urinary calculi during childhood should raise the
distinct possibility of an inherited genetic disorder, such as cystinuria,
distal RTA, or primary hyperoxaluria.

126. • Medical Management of Calculi during Pregnancy.
• Radiation exposure to the fetus should be avidly avoided.
• Therefore ultrasonography has become the first-line imaging study to search
for calculi during pregnancy. Although this modality provides adequate
images of the kidneys, it can be difficult to fully discern the ureters and their
contents.
• Additionally, hydronephrosis of pregnancy may be confused for
hydronephrosis from an obstructing calculus. A limited intravenous
pyelogram (IVP) may be obtained that consists of one scout image followed
by one plate taken approximately 30 minutes after the injection of contrast.
• Each plain film exposes the fetus to 0.1 to 0.2 rads, well below the threshold
of 1.2 rads, at which the risk begins to increase.
• Radiation exposure should be particularly avoided durinthe first trimester
during the time of organogenesis and the greatest fetal risk.

127. • Approximately 66% to 85% of pregnant women with ureteral colic
spontaneously pass the calculi when treated conservatively with
hydration, analgesics, and, if infected, antibiotics (Jones et al, 1979;
Stothers and Lee 1992).
• The goal of therapy for the remaining patients is to do the least
required to keep the kidney functioning, the patient free from
symptoms, and the urine uninfected.
• Stents should be placed cystoscopically with minimal radiographic or
sonographic monitoring

128. Strategies for Nonmedical Management of
Upper Urinary Tract Calculi
• Endoscopic. ureterorenoscopy (URS), percutaneous nephrolithotomy (PCNL), and
extracorporeal shock wave lithotripsy (SWL).
• Ureterolithotomy
• Nephrolithotomy
• Retrograde renoscopy—A laser fibre can be introduced through a flexible fibre optic
ureterorenoscope, which is introduced through the urethra and bladder, and up the ureter to
the renal collecting system. Stones 1 cm in diameter can be disintegrated.
• Open surgery—This is needed infrequently. Staghorn stones, in
• which the bulk of the stone lies within calices rather than within
• the renal pelvis, are treated best by open surgery. Kidneys that
• contribute 10% of overall renal function should usually be
• removed. Extensive perirenal fibrosis is usually encountered,
• which makes such a nephrectomy impossible laparoscopically.

129. Ureteral sones
• Conservative management—Most stones 5 mm in maximum diameter are
likely to pass spontaneously and should be allowed to do so. Stones will pass
down the ureter when the ureter peristalses.
• In the presence of an obstruction, diuresis will provoke ureteric dilatation and
reduce peristalsis. Anticholinergic drugs, such as hyosine, similarly will be
ineffective.
• Extracorporeal shockwave lithotripsy—This has been advocated for
ureteric stones, when imaging is possible radiographically or by ultrasound.
• This approach is less successful for ureteric stones than renal stones and is
possible only at urological centres that have a static rather than mobile
lithotripter.
• Endoscopic ureterolithotomy—With or without stone disintegration, this is
a safe and effective method of managing ureteric stones that need
intervention.

130. • Open surgery—This is indicated very rarely for ureteric stones. If
associated ureteric pathology, such as stricture, is present, open
surgery may be the only solution.

132. • Treatment Decision by Stone Burden
• The total kidney stone burden, or total volume of stone(s) requiring
treatment, is arguably the most important factor influencing treatment
decisions.

133. • Kidney Stone Burden up to 1 cm. The majority (50% to 60%) of
solitary kidney stones are 1 cm or less in diameter, and many of them
are asymptomatic (Cass, 1995; Renner and Rassweiler, 1999;
Logarakis et al, 2000).
• Given enough time, however, many will enlarge or become associated
with clinical factors that warrant treatment.
• Almost all renal stones 1 cm or smaller may be treated with SWL,
URS, or PCNL. Laparoscopic or open stone removal is necessary in
exceedingly rare cases, most often when there is underlying aberrant
anatomy.

134. • SWL has been considered first-line treatment for these smaller kidney
stones without complicating clinical or renal anatomic considerations
because it is the least invasive modality, achieves reasonably high
stone-free rates, and requires the least technical skill.
• For kidney stones 1 cm or less in diameter, SWL achievesstone-free
rates of approximately 50% to 90%

137. • Over the last decade, technologic advances in flexible endoscope
design and instrumentation have facilitated the use of URS, also
referred to as retrograde intrarenal surgery, for the treatment of kidney
stones.
• Multiple reports have now clearly established URS as a reasonable
alternative for the treatment of most kidney stones, especially those
smaller than 1 cm.
• Contemporary URS for renal stones 1 cm or smaller offers stone-free
rates of approximately 80% to 90%,

138. • PCNL is reserved for failures of SWL and URS or for patients with
anatomic considerations making PCNL vastly superior, such as lower
pole stones with acute infundibulopelvic angles or calyceal
diverticula.

139. • Kidney Stone Burden between 1 and 2 cm. For renal stones between 1
cm and 2 cm, SWL, URS, and PCNL are the most frequently used
treatments, with laparoscopic and open stone removal seldom
necessary.
• Stone location, composition, and density and patient anatomic factors
become increasingly relevant as stone burden enlarges and have an
important impact on treatment outcomes.
• Larger stone burdens located in lower pole calyces, increasing skin-
to-stone distance, and unfavorable lower renal pole anatomy all
decrease the success rates of SWL and URS but have limited
influence on PCNL outcomes.
• Thus, for renal calculi between 1 cm and 2 cm, stone-specific and
anatomic factors must be carefully considered when weighing the
relative outcomes and invasiveness of each procedure

140. • For stones between 1 cm and 2 cm that are not located in the lower
pole, SWL has traditionally been recommended as first-line therapy,
and remains so in the most updated urolithiasis guidelines from the
EAU (Turk et al, 2013).
• In general, SWL is favored when stones are not located in the lower
pole, stone attenuation is less than approximately 900 HU, skin-to-
stone distance is less than 10 cm, and the patient has no history of
SWL-resistant minerals (cysteine, calcium oxalate monohydrate,
brushite).

141. • Kidney Stone Burden Greater than 2 cm. PCNL should be
considered
• first-line therapy for kidney stone burdens 2 cm and greater.
• Unlike URS and SWL, the success of PCNL is relatively independent
of stone location and stone composition.

142. Staghorn Stones.
• PCNL is the method of choice for treating partial and complete staghorn
kidney stones, with the caveat that poorly or nonfunctioning kidneys and
those associated with xanthogranulomatous pyelonephritis may be best
managed with nephrectomy.

143. • Treatment Decision by Stone Localization
• Stones situated in the lower pole prove more difficult to clear with
URS or SWL, and therefore stones 1 cm or larger within the lower
pole may be most efficiently treated with PCNL.
• Stones in a non–lower pole location tend to respond more readily to
SWL and URS, making those techniques more competitive with
PCNL.

144. • Treatment by Stone Composition
• Stone composition has significant implications with respect to
treatment outcomes primarily with SWL, whereas URS, PCNL, and
laparoscopic and open stone surgery appear to be only minimally
affected.

145. • In general, cystine, calcium phosphate (specifically “brushite”), and
calcium oxalate monohydrate stones are the most resistant to SWL.
• The remainder of the common stone types by order of increasing
fragility are struvite, calcium oxalate dihydrate, and finally uric acid
stones

146. • PCNL is the preferred treatment approach for most matrix renal
stones owing to its high success rates and low recurrence rates.

147. ENDOSCOPIC.
• Ureteroscopic stone extraction.
• -effective for lower ureteral stones
• -complication rate 5-30%
• Ureteral strictures-<5%
• Postoperative vesicoureteric reflux extremely rare.

148. • 1. percutaneous nephrolithotomy.
• -removal of renal and proximal ureteral stones
• -is treatment of choice for large (>2.5cm) calculi, those resistant to
ESWL,lower pole calyceal stones and in evidence of obstruction.
• 2. endoscopic ureterolithotomy.

149. • Open surgery
• -pyelolithotomy- especially with extrarenal pelvis.
• -radial nephrotomy.-
• Partial nephrectomy- large stone burden in a renal pole with marked
parenchymal thinning.
• Ureterolithotomy. Stones inaccessible to endoscopy and resistant to
ESWL.

150. • Other unusual procedures
• Ileal ureter substitution
• Autotransplantation with pyelocystostomy.

151. THANK YOU FOR LISTENING