Nephrolithiasis

A process of forming a stone in the

kidney or lower down in the urinary
tract.
Renal Stones
A kidney stone, is a solid
concretion or crystal
aggregation formed in the
kidneys from dietary minerals
in the urine.
iNtroductioN
 Nephrolithiasis is a common, often
recurrent,
and occasionally morbid condition.
 The prevalence of kidney stones
increases with
age such that 11% of men and 5.6%
of women in
the USA will have had a symptomatic
kidney stone
by age 70.
 The first episode of renal colic
related to
nephrolithiasis is most likely to occur
between the
ages of 20 and 30 years for women
and 30–60
years for men.
2
iiNtroductiioN
 Urological intervention is required in
approximately 20% of episodes of
nephrolithiasis.
 Recurrence rates are as high as 50%
within 5
years and 80% within 20 years.
 Many health care providers will
encounter
nephrolithiasis in their clinical
practice, including
primary care physicians,
nephrologists,
urologists, interventional radiologists,
and
emergency department physicians.
3
INTRODUCTION
 Nephrolithiasis, or kidney stone
disease, is a common, painful, and
costly
condition.
 Although nephrolithiasis is rarely
fatal, patients who have had renal
colic report
that it is the worst pain they have
ever experienced.
 Nephrolithiasis is a global disease.
 Data suggest an increasing
prevalence, likely due to
Westernization of Iifestyle
habits (e.g. dietary changes,
increasing BMI) .
 Up to 19% of men and 9% of women
will develop at least one stone during
their lifetime.
 The prevalence is -50% lower
among black individuals than among
Introduction
 Nephrolithiasis is a formation of
stone in the
kidney. Kidney stones are small deposit that
build
up in the kidney made of calcium, phosphate
and
other components.
 Nephrolithiasis represent one of the 3
common
emergency admissions seen on urology
wards (the
other 2 being acute urinary retention and
haematuria).
 Approximately 50% of patients present
between
the ages of 30 and 50 years.
 There is a slight male preponderance.
Nephrolithiasis
Occur throughout the
urinary tract
 pain, infection, obstruction
 Incidence
 typical age range between 30 - 50 years
 sex: male predominance

 race: rare in African Americans

 geographics: “stone belts” and developed

countries
 recurrences are common: 50% in 5 years

 Caused by saturation and

crystallization of stone-
forming
salts in the urine
types of stoNes
Major stone types frequency in
adults
1 Calcium oxalate 40-60%
2 Calcium phosphate 10-20%
3 Uric acid 10-15%
4 Magnesium ammonium
phosphate
((struvite
10-15%
5 Cystine <1%
6 Other: indinavir, triamterene,
xanthine <1%
4
TYPES OF
CALCULI
 It is clinically important to identify
the stone type, which informs
prognosis and selection
of the optimal preventive regimen.
 There are various types of kidney
stones:
 Calcium oxalate stones are most
common(-75%)
 calcium phosphate ( - 1 5%)
 uric acid (-8%)
 struvite (-1 %)
 and cystine (<1 %)
 Many stones are a mixture of crystal
types (e.g. calcium oxalate and
calcium phosphate)
and also contain protein in the stone
Types of urinary stones
 According to site
a. Renal stone.
b. Ureteric stone.
c. Bladder stone.
d. Urethral stone.
 According to
composition
a. Phosphate stone.
b. Oxalate stone.
c. Uric acid stone.
d. Cysteine stone.
e. Xanthine stone.
Types
1. Calcium oxalate (more common)
2. Calcium phosphate (less common)
3. Uric acid, struvite (Mg, Ammonium
Phosphate)
4. Cystine stones
5. Combination of different stones can exist in
single stone
Types of Calculus
 Calcium 75 - 85% radiopaque
 Uric acid 5 - 8% radiolucent
 Cystine 1% radiolucent
 Struvite 10 - 15% radiopaque
McPhee, 2003, p. 468
Classification- by
chemical composition
1. Calcium salts
2. Uric acid
3.Mg ammonium PO4
4. Cystine
5. Other (xanthine, etc.)
Classification- by
location
• Urinary stones are typically classified by their
location in the

• kidney
(nephrolithiasis),
•ureter
(ureterolithiasis),
•bladder
(cystolithiasis
Typical features of some stones
 Phosphate stone
 Also known as triple phosphate stones or
struvite
stones or staghorn stone.
 They tends to grow in alkaline urine
especially
with infection caused by urea splitting
bacteria
(proteus, pseudomonas, staphylococcus).
 They are soft stones with smooth surface.
So,
they causes less pain and presentation will
be
late.
• Oxalate stone
 Irregular sharp projections which cause
bleeding.
Presentation will be early with heamaturia
and
pain.
 Very hard stones.
 Uric acid stone
 Multiple, may be hard or soft. Present in
late stage.
 They are radiolucent that is they are not
seen on
plain xray KUB.
 Uric acid, cysteine and xanthine stones
are known
as metabolic stones.
Calcium Stones
• 70 - 75% of all stones
• Calcium oxalate - brown, gray, or
tan
• Calcium oxalate monohydrate -
dumbbell
• Calcium oxalate dihydrate -
pyramidal
• Calcium phosphate - white or beige
• Calcium phosphate - elongated
(brushite)
Calcium oxalate monohydrate
Calcium oxalate dihydrate
Calcium phosphate brushite
Uric Acid Stones
• Smooth, white or yellow-orange
• Radiolucent
• Crystals form various shapes:
rhomboidal,
needle like, rosettes, amorphous
Uric acid
Struvite Stones - Magnesium
Ammonium
Phosphate
• More common in women than men
• Most common cause of staghorn
calculi
• Grow rapidly, may lead to severe
pyelonephritis
or urosepsis and renal failure
• Light brown or off white
• Gnarled and laminated on X-ray
Struvite
Cystine Stones
• Hexagonal, radiopaque, greenish-
yellow
• Often present as staghorn calculi or
multiple
bilateral stones
Cystine
Pathophysiology
Saturation
Crystal
growth and
aggregation
Supersaturation
Crystal
Retention
Stone
formation
Nucleation
Pathogenesi
s
• 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.
Pathogenesi
s
many calculi
• However,

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
Inhibitors of Crystal
Formation
• Pyrophosphate,
• Diphosphonate,
• Citrate,
• Glycosaminoglycans,
• Osteopontin, and
• Nephrocalcin (Glycoprotein).
Etiology
 Varies with different types of
stones
 calcium stones
 hypercalciuria (50% of stone formers)
Idiopathic (95%) or 1 hyperparathyroidism
(5%)
 uric acid stones
 volume depletion, acidic urine
 struvite stones
 form in high urinary pH (Proteus spp.)
 cystine stones
Defect in the renal tubular absorption of
cystine
 Etiology of Calcium
stones
Idiopathic Hypercalciuria (50%)

Hypercalciuria and Hypercalcemia (10%)

Hyperoxaluria (5%)

Enteric (4.5%)

Primary (0.5%)

Hyperuricosuria (20%)

Hypocitraturia

No known metabolic abnormality (15 to 20%)

 Etiology of other
Stones
Causes
Struvite Proteus
Staphylococcus
Klebsiella
Causes
Uric Acid Gout
Leukemias
Increased dietary
purine
Causesintake
Cystine Calculus Autosomal recessive
defects
PATHOGENESIS
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.
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
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.
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
Pathogenesis-
CYSTINE STONES
• Cystine stones are
caused by
• genetic defects in the
renal
reabsorption of amino
acids, including
cystine, leading to cystinuria.

at low
• Stones form

urinary pH
 Patient Profile
 NAME: XYZ
 AGE: 40 years
 GENDER: Male
 ADDRESS: Saddar Lahore
 MODE OF ADMISSION: OPD
 DATE OF ADMISSION: 22ND June 2018
 Presenting
Complaint

Left flank pain-4 days.

Nausea- 2 days.
History of Present Illness
• Moderate intermittent left flank pain.
• Sudden in onset.
• Colicky in character.
• Radiating to the back.
• Not related to posture
• Worsened after consuming large volumes of
water.
 Cont...

• No fever
• No blood in urine
• No pus in urine
 Medical and Surgical
History

 Diagnosed as Hypertensive one month

ago.

 History of UTI 2 months ago.

 No Significant Surgical History.

Drug History

Taking anti-hypertensive for past 1 month.

PERSONAL HISTORY:
Naswar intake
Non-smoker
No other recreational drug addiction.

FAMILY HISTORY:
Not significant

SOCIOECONOMIC HISTORY:
Satisfactory
 GENERAL
PHYSICAL
EXAMINATIO
N
GPE
A middle aged man of average built lying
comfortably in bed.

VITALS
PULSE: 75 beats/min

BLOOD PRESSURE: 135/80 mmHg

RESPIRATORY RATE: 20 breaths/ min

TEMPERATURE: 98 F
 CLINICAL FINDINGS
•Cyanosis -ve
•Pallor -ve
•Jaundice -ve
•Edema -ve
•Lymph nodes are not palpable
 Abdominal
Examination
• Abdomen is flat
• No visible pulsations, scar marks.
• Umbilicus is central and inverted.
• Moving with respiration.
• No tenderness or rigidity
CVS EXAMINATION:
S1+S2 Normal Intensity
Unremarkable

RESPIRATORY EXAMINATION:
Unremarkable

CNS EXAMINATION:
unremarkable
 Differential Diagnosis
 Renal stones
 Urinary Tract Obstruction
 Musculoskeletal Pain
 Urinary Tract Infection
INVESTIGATIO
NS
 Complete blood
BLOOD COUNTS
picture
Result
Interval
Reference

TLC 7.6 4.0-10.0 X

RBC 10^9 / L
HB 5.17 4.50-6.50 X
PCV 10^12 / L
MCV 13.3 13.5-17.5
MCH g/dl
MCHC 41.1 40-52%
PLATELET COUNT 79.5 80-95 fL
25.9 27-34 pg
DLC 32.6 31.5-34.5 g/dL
253 150-400 X
NEUTROPHILS 10^9 /L
LYMPHOCYTES
MONOCYTES
EOSINOPHILS
49 40-80%
44 20-40%
04 2-10%
03 1-6%
 RFTS
Tests RESULTS REFERENCE
INTERVAL
Urea 3.8 mmol/L 3.3-
6.7mmol/L

Creatinine 102 µmol/L 62-120

µmol/L

Sodium 139 mmol/L 135-150

mmol/L

Potassium 4.1mmol/L 3.3-5.0

 LFTS
TEST RESULT REFERENCE
INTERVAL
Total Bilirubin 8 µmol 0-17 µmol

ALT 41 U/L 0-42 U/L

Alkaline 130 U/L 65-300 U/L

phosphate
Albumin 48 g/L 35-50g/L
 Other Tests
Test Result Reference
Range
Plasma 5.7 mmol/L 5.6-6.9
Glucose mmol/L
(Fasting) (Prediabetes)
Serum Total 3.7 mmol/L <5.2 mmol/L
Cholesterol (Desirable)
Serum 100 µmol/L 62-120
Creatinine µmol/L
Urine 11.6 <15.0
Protein mg/mmol mg/mmol
:Creatinine
Ratio
 Urine R/E
Colour Pale Yellow
Specific Gravity 1.020
pH 6.5
Reaction Acidic
Protein Nil
Glucose Nil
WBCs/HPF 2-4/HPF
Crystal Calcium Oxalate
X-ray KUB

Stone

Artifact

L
Ultrasound KUB
Ultrasound Renal Doppler
Non-Contrast CT KUB
 Diagnosis

Left Pelvic-ureteric
junction Calculus.
(2.9x2cm)
 Treatment Algorithm
for Renal stones:

 Less than 1cm: ESWL, RIRS

 1-2cm: ESWL

 More than 2cm: PCNL, open surgery

 Treatment Plan

Left Percutaneous
Nephrolithotomy (PCNL)
Pre-Op Workup
 Prothrombin Time 13 sec
0-14 sec
 PTTK 32 sec
0-32 sec

 Anti-HCV NEGATIVE
 HBsAg NEGATIVE
Post-Op Medications
Inj.Sulzone (Cephalosporin) 2g BD IV
Inj Campex (Analgesic)100mg SOS IV
Inj Gravinate (Diphenhydramine) SOS
IV
Tab. Artifen (NSAID)50mg BD
Cap Maxflow (Alpha Blocker) 0.4 mg
Hs
Inj Risek (Omeprazole)40mg OD
 Post-Op Care

Vitalsand Urine Output were

regularly monitored.
Post- Surgery Hb levels were
done.
X RAY
 Hydronephrosis is

Renal Recurrent
Failure Infections

Complications

Ureteral Urinary
Obstruction Ureteral Fistula
Perforation
THANK
YOU