Urolithiasis: Renal calculi rsd

Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai
1

Professors:
 Prof. Dr. G. Sivasankar, M.S., M.Ch.,
 Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
 Dr. J. Sivabalan, M.S., M.Ch.,
 Dr. R. Bhargavi, M.S., M.Ch.,
 Dr. S. Raju, M.S., M.Ch.,
 Dr. K. Muthurathinam, M.S., M.Ch.,
 Dr. D. Tamilselvan, M.S., M.Ch.,
 Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai. 2

 Is a common cause of blood in the urine and
pain in the abdomen, flank or groin.
 Occurs 1 in 20 people at some time in life.
 Development of the stones is related to
decreased urine volume or increased
excretion of stone-forming components
such as calcium, oxalate, urate, cystine,
xanthine and phosphate.
 The process of stone formation is also called
nephrolithiasis or urolithiasis.
3
Dept of Urology, GRH and KMC, Chennai.

 Renal tubular acidosis
defective renal tubular H+ secretion and urinary
alkalization – supersaturation of calcium phosphate
 Cystinuria
 Xanthinuria
4

 Saturation - supersaturation – crystal formation –
 Nucleation – crystal growth and aggregation
5

Inhibit crystal growth Promotors
• Citrate, complexes with Ca
• Magnesium, complexes with
oxalates
• Pyrophosphate, complexes with
Ca
• Zinc
• Bacterial Infection
• Matrix
• Anatomic Abnormalities
• Altered Ca and oxalate transport
in renal epithelia
• Prolonged immobilization
• Increased uric acid levels
• Nanobacteria
Inhibit crystal aggregation
• Glycosaminoglycans
• Nephrocalcin
• Tamm- Horsfall Protein
6

Common Stones Uncommon Stones
• Calcium combines with
phosphate or oxalate
• Uric Acid (urate)
• Cystine
• Struvite (magnesium
ammonium phosphate)
• Xanthine
• Dihydroxyadenine
• Silicate
• Matrix
• Triamterene
• Indinavir
• Ephedrine
7

 Matrix : protein like non crystallinematerial . 65% hexosamine 10% water
 Hypercalciuria – absorption
- Renal leak
- resorptive
 Uric acid - gout - excretes less ammoniaand more uricacid
- myeloproliferativedissorder
 Struvite stone -infectionstone, infectionof urine with urease producing
bacteria e.g E.coli, Proteus
Urease splits urea into ammonia
 Silicate – patients taking largwe amt of antacids containingsilicate e.g
magnesium trisilicate
 Indinavir – protease inhibitorfor HIV I . Pts develop kidney stones
8

Stone type Comments
Calcium Ca-Oxalate has sharp projections that lead to hematuria. Ca-
Phosphonate is smooth in appearance with minimum symptoms.
Both are radioopaque.
Uric Acid Appears as irregular plates or rosettes. Radiolucent., ultrasound is
useful for their diagnosis.
Cystine Seen in young girls with autosomal recessive disorder.
Radioopaque.
Struvite Also known as infection or triple-phosphate stones. More often
in women.. Patients may present with flank pain and may have
signs of systemic infection. Failure to treat may lead to risk of
renal loss, sepsis and death. Radioopaque
9

 The incidence was very high, 11.6% of all
general surgery cases.
 The prevalence was minimal among
tribals. Compared to tribals one-and-
one-half times higher among Muslims
and seven times higher among Hindus.
 The incidence was higher in females.
 Calcium and oxalate were present in all
stones.
 Phosphate was present in 194 stones and
uric acid was present in 146 stones.
Am J Clin Nutr. 1978;31(9):1519–1525.
10

 Renal tubular acidosis (RTA) is applied to a group of
transport defects in the reabsorption of bicarbonate
(HCO3-), the excretion of hydrogen ion (H+), or both
 The RTA syndromes are characterized by a relatively
normal GFR and a metabolic acidosis accompanied
by hyperchloremia and a normal plasma anion gap
 hyperchloremic metabolic acidosis ,
bicarbonaturia, reduced urinary excretion of
titrable acid and ammonia and an elevated urinary
pH.
11

 The term incomplete distal RTA has been proposed to
describe patients with nephrolithiasis but without
metabolic acidosis.
 Hypocitraturia is the usual underlying cause
12

SOLUTE DIURESIS
DEFECT IN H+ SECRETION
DECREASED REABSORPTION
OF NA+, K+
NEPHROCALCINOSIS
NEPHROLITHIASIS
CHRONIC MA
LEACHING OF BONE CAUSING
OSTEOPENIA AND
HYPERCALCIURIA
13

Treatment:
 Alkali replacement:
 1-3mmol/kg/day bicarbonate
 Sodium citrate (Shohl’s solution) tolerated better than
sodium bicarb
 Potassium citrate if hypokalemia 2 to 4 mEq/kg/day
 Greater amounts are required in children 8 to 10 mEq/kg
1. the need for base deposition in growing bone
2. bicarbonate wastage in children > in adults.
 Maintenance of alkali therapy for an indefinite period is necessary.
14

 Vitamin D should not be administered initially as it may
precipitate nephrocalcinosis. When rickets persists despite
sustained correction of acidosis, Vitamin D may be given
 Monitoring
- Periodic blood gas estimation to maintain serum HCO3
between 22 – 24 mEq/L
- height monitoring
- Urinary calcium excretion
- Serum Ca, P, Alk phos and Xrays for bone healing
- Annual USG for nephrocalcinosis
15

Type 1 Distal
RTA
Type 2 Proximal RTA
Primary
defect
DCT &
Collecting
Tubule
PCT
Age of onset Infancy and
early childhood
Premature babies
(Immature kidneys)
Pathogenic
mechanism
Defect in acid
secretion
Defect in bicarbonate
reabsorption
Inheritance AR, AD AR
CF –
polyuria,
recurrent
vomiting in
both
impaired growth
and rickets
Growth retardation, feat
of inher dis - cystinosis,
galactosemia, GSD
type1 16

Type 1 Distal RTA Type 2 Proximal RTA
Serum HCO3- 10 – 15mEq/L Usually 15 – 20mEq/L
Features c MA
• Min UpH
• Urine excrn
K+
Ca++
• U anion gap
•%FEHCO3-
> 5.5
Increased
Increased
Positive/normal
< 3 – 5%
< 5.5
N/Increased
Normal
Negative
> 10 – 15%
Nephrocalcinosis ++ -/+
Oral bicarbonate
to correct S pH
(mEq/kg/day)
1 – 3 adult
4 – 15 child
5 – 10
Cysteamine in cystinosis
Diet in galactosemia
17

Risk Factor Mechanism
Bowel disease Promotes low urine volume; acidic urine depletes
available citrate and hyperoxaluria
Excess dietary meat Creates acidic urinary milieu, depletes available citrate
and promotes hyperuricosuria
Excess dietary oxalate Promotes hyperoxaluria
Excess dietary sodium Promotes hypercalciuria
Insulin resistance Ammonia mishandling and alters pH of urine
Gout Promotes hyperuricosuria
Obesity May promote hypercalciuria
Primary hyperparathyroidism Creates persistent hypercalciuria
Prolonged immobilization Bone turnover creates hypercalciuria
Renal tubular acidosis Alkaline urine promotes calcium phosphate
Supersaturation and loss of citrate
Am Fam Physician 2006;74:86-94.
18

 Symptoms usually produced when stones pass from the
renal pelvis to the ureter.
 Pain varies from mild-to-severe, typically waxes and
wanes, and lasts 20–60 minutes.
 Pain is related to movement of the stone in the ureter and
associated uretral spasm.
 Site of obstruction determines the location.
 Hematuria is a single most discriminate predictor of a
kidney stone in patients presenting with unilateral flank
pain.
 May lead to persistent renal obstruction and sepsis.
 Nausea, vomiting, dysuria and urgency.
19

20

Imaging
modality
Sensitivity
(%)
Specificity
(%)
Advantages Limitations
Ultrasonography 19 97 Accessible
Good for diagnosing
hydronephrosis
and renal stones
Requires no ionizing
radiation
Poor visualization of
ureteral stones
Plain radiography 45–59 71–77 Accessible and
inexpensive
Stones in middle
section of ureter,
phleboliths,
radiolucent calculi,
extraurinary
calcifications and
nongenitourinary
conditions
21

Imaging
modality
Sensitivity
(%)
Specificity
(%)
Advantages Limitations
Intravenous
pyelography
64–87 92–94 Accessible. Provides
information on anatomy
and functioning of both
kidneys
Variable-quality
imaging. Requires
bowel preparation
and use of contrast
media. Poor
visualization of
nongenitourinary
Conditions.
Noncontrast
helical
computed
tomography
95–100 94–96 Most sensitive and specific
radiologic test . Indirect
signs of the degree of
Obstruction. Provides
information on
nongenitourinary
conditions
Less accessible and
relatively expensive.
No direct measure
of renal function.
22

KUB: Kidney Ureters and Bladder. Am Fam Physician 2001;63:1329-1338.
23

Clinical indications Suggested diagnosis
Hematuria (microscopic or gross) Urinary calculi, urothelial tumor, UTI,
BPH, renal mass
Abdominal pain Small renal calculi, nonurologic etiology
Flank pain (sharp, extreme pain
with sudden onset)
Urinary calculi, musculoskeletal spasm
Flank tenderness Urinary calculi, musculoskeletal
inflammation, pyelonephritis
Groin pain (scrotal, labial) Ureteral calculi, hernia, testicular mass
Penile or pelvic pain Ureteral calculi, urethritis, prostatitis
Urinary frequency UTI, ureteral calculi, BPH
UTI: Urinary Tract Infection, BPH: Benign Prostrate Hyperplasia. Am Fam Physician 2006;74:86-94.
24

Treatment Indications Advantages Limitations Complicati
ons
ESWL Radiolucent calculi
Renal stones <2 cm
Ureteral stones <1
cm
Minimally invasive
Outpatient
procedure
Requires spontaneous
passage of fragments
Less effective in
patients with
morbid obesity or hard
stones
Ureteral
obstruction by
stone
fragments
Perinephric
hematoma
Ureteroscopy Ureteral stones Definitive
Outpatient
procedure
Invasive
Commonly requires
postoperative ureteral
stent
Ureteral
stricture or
injury
ESWL: Extra-Corporeal ShockWave Lithotripsy Am Fam Physician 2001;63:1329-1338.
25

Treatment Indications Advantages Limitations Complications
Ureterorenoscopy Renal stones <2
cm
Definitive
Outpatient
procedure
May be difficult
to clear
fragments.
Commonly
requires
postoperative
ureteral stent.
Ureteral stricture or
injury.
Percutaneous
nephrolithotomy
Renal stones >2
cm
Proximal
ureteral stones
>1 cm
Definitive Invasive Bleeding
Injury to collecting
system.
Injury to adjacent
structures
26

 Extra-corporeal shock wave
lithotripsy (ESWL)
 Shock wave lithotripsy
(SWL)
 Laser lithotripsy
 Percutaneous lithotripsy
 Endoscopic lithotripsy 27

Shock waves generated under water can travel
through body without any appreciable loss of
energy. When they encounter stones the
changes in density causes energy to be
absorbed and reflected by the stone and this
results in fragmentation of the stones. 28

 ESWL is a completely noninvasive
therapy.
 A computerized X-ray machine is used
to pinpoint the location of the stone
within the kidney.
 A series of shock waves are administered
to the stone.
 Adjustments of both the shock wave
power and the rate at which the shock
waves are delivered can affect treatment 29

 Treatment is restricted in
- Pregnancy,
- Severe skeletal malformations,
- Severe obesity and aorticand/or
- Renal artery aneurysms.
 ESWL should not be carried out in patients with
uncontrolled blood coagulation or uncontrolled
urinary tract infection.
 A pacemaker is not a contraindication.
 For cystine stones with a diameter >15 mm, ESWL
as monotherapy is currently not recommended.
 Patients with chronic kidney infection, as some 30

 Incomplete stone fragmentation and obstruction.
 May reversibly damage all parenchymal
components.
 May raise blood pressure.
 Hematuria (short-term antibiotics are
recommended).
 ‘Stienstrasse’ (stone street) usually due to a large31

 Arifi et al. confirmed that
ESWL is effective in the
treatment of even very
large urinary stones in
children, even in very
young children.
 The highlights of the study
were:
 Three months after the last
lithotripsy session, 30/34
patients presented no
fragments.
Prog Urol. 2006;16(5):594-597.
32

 El-Nahas et al. reported that
obesity and increased stone
density as detected by NCCT
are significant predictors of
failure to fragment renal
stones by SWL.
 Failure of disintegration was
defined as no fragmentation of
the stone after three sessions.
 BMI and stone density >1000
HU were the significant
independent predictors of
failure (p=0.04 and 0.02,
respectively).
Eur Urol. 2006 Dec 4; [Epub ahead of print]
HU: Hounsfield unit
33

 Alpha-blockers (e.g. tamsulosin), relax the ureteral
smooth muscle and hasten the expulsion of
urethral stones.
 Result in painless elimination of stones <8 mm
located in the uretero-bladder junction.
 Patients treated with a-blockers have a 65%
greater chance of spontaneous stone passage than
those not treated with it.
 Decrease the number of ureteral colic episodes and
the intensity of pain during spontaneous passage
at the lower ureteral calculi.
34

 Gravina et al. reported that tamsulosin
therapy, as an adjunctive medical therapy after
ESWL, is more effective than lithotripsy alone
and is equally safe. Moreover, it results in a
decrease in the use of analgesic drugs after the
procedure.
60%
78.50%
76.90%
26.10%
0% 20% 40% 60% 80% 100%
ESWL alone
ESWL with
Tamsulosin
Clinical success Renoureteral colic
Urology. 2005;66(1):24-28.
35

Key findings:
 78.5% of those receiving tamsulosin and 60% of
controls had achieved clinical success at three
months (p=0.037).
 For those with a stone size larger than 10 mm, the
success rate was significantly greater in the
tamsulosin group (p=0.028).
 Renoureteral colic occurred in 76.9% of patients
treated with standard therapy but in only 26.1% of
those receiving tamsulosin (p< 0.001).
Urology. 2005;66(1):24-28.
36

 Autorino et al.
reported
tamsulosin is
efficacious in the
treatment of
distal ureteral
stones up to 1 cm.
They
recommended its
use in
conservative
treatment of
60%
88%
21%
9%
0% 20% 40% 60% 80% 100%
Group A
Group B (plus
Tamsulosin)
Stone expulsion rate Recurrent Colic
Urol Res. 2005;33(6):460-464.
Group A: Diclofenac, Aescin. Group B: Diclofenac, Aescin, Tamsulosin.
37

Key findings:
 The stone expulsion rate was 60% (19/32
patients) for group A and 88% for (28/32) for
group B with a mean expulsion time of 7.4±-2.2
(range 3.5-12) and 4.8±2.7 days (range 1.8-10.5),
respectively.
 Group B showed a significant advantage in terms
of both expulsion rate (p=0.01) and expulsion time
(p=0.005). Urology. 2005;66(1):24-28.
38

39

 Citrate is pathogenetically important in stone
formation, as it retards the crystallization of stone-
forming calcium salts.
 Hypocitraturia, frequently encountered in patients
with nephrolithiasis, is therefore an important risk
factor for stone formation.
 Potassium citrate, calcium citrate and potassium-
magnesium citrate are available.
• Potassium-magnesium citrate is superior to
potassium citrate in the management of stone
disease.
J Urol. 1997;158(6):2069-2073.
40

 Uric acid stone : allopurinol – 300 to 600 mgs per day.
Inactivates xanthine oxidase and decreases uric acid
synthesis
Hydaration and alkalization of urine
 Cystine stone : hydration, alkalization ,.D-
pencillamine – binds cystine forming a complex that is
soluble in urine
41

 Symptoms – intermittent painful voiding
--Ternminal hematuria
-- dull aching or sharp suprapubic pain
-- interruption of urinary stream
 To rule out bladder obstruction – stricture urethra,
BPH, diverticulum of bladder, neurogenic bladder
 X – ray KUB, USG KUB, cystoscopy
 Treatment :
1. Smaller stone < 5cm vesicolithotripsy
2. Larger stone > 5 cm vesicolithotomy
42

 Stone in the prostatic urethra – pusthed back into the bladder –
vesicolithotripsy
 Stone in the anteriorurethra can be milked out
 Stone in the fossa navicularis - meatotomy
 Stone in the urethral diverticulum – diverticulectomyand repair
 Urethral Calculi in women is rare. Usuallyass. With urethral diverticulumO/e
hard mass in the antr. Vaginal wall – excisionof the sac containingcalculus
 Pediatricurolithiasis8 – 10 yrs
 Causes :
 Infection 75%
 Metabolic - hypercalciuria
 Anatomc lesion – PUJ obstruction
-- neurogenic bladder, meningomyelocoele
43

 Stone in the pregnant women – pregnancy as such
doesn’t predispose to calculi.
 Present with vague abdominal pain, unexplained fever,
unresolved bacteriuria , Microscopic hematuria
 Conservative treatment – 85%of pregnant women
spontaneously pass th e stone with hydration.
Analgesics, and antibiotics
 Stent should be placed cystoscopicallly with
sonographic monitoring
44

“I will not cut, even for the stone, but leave such
procedures to the practitioners of the craft.”
Hippocrates.
45

Urolithiasis: Renal calculi rsd

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