A Case Report

Nephrolithiasis

PRECEPTOR:
dr. GinandaSiregar, Sp.U

COMPOSERS:
CarvinHerryanto 110100204
KynaTroeman 110100115
Devandran Mahendran 110100403
Pieter Lumbanraja 110100366
Try YudiaRamadhany 110100118
Choky Lumban Gaol 110100338
Angelia Sitanggang 110100277
Regina Tambunan 110100097
PuvanaSubramaniam 110100503
Hemakanen Nair 110100413

CLINICAL SENIOR WORK

GENERAL REFERENCE CENTRE HOSPITAL HAJI ADAM MALIK
SURGERY DEPARTMENT
MEDICAL FACULTY OF SUMATERA UTARA UNIVERSITY
MEDAN
2016
 TABLE OF CONTENT

Title ............................................................................................................... 1
Table of Content .......................................................................................... 2
Chapter 1 Preliminary ................................................................................ 3
1.1. Background ...................................................................................... 3
Chapter 2 Literature Review ..................................................................... 4
2.1. Urinary Stone Formation Process ................................................... 4
2.2. Type Stone Tract ............................................................................. 6
2.3. Clinical Manifestations and Evaluation ............................................ 11
2.4. Management of Urinary Tract Stone............................................... 13
Chapter 3 Case Report ............................................................................... 18
Chapter 4 Discussion .................................................................................. 23
Chapter 5 Conclusion ................................................................................. 25
Reference ...................................................................................................... 26

2
 CHAPTER 1
PRELIMINARY

CHAPTER 1
PRELIMINARY

1.1. Background
Nephrolithiasis is a multi-factorial disorder resulting from the combined
influence of epidemiological, biochemical and genetic risk factors. Kidney stones
are of four types. The overall probability of forming stones differ in various parts
of the world and is estimated as 1-5% in Asia, 5-9% in Europe, 13% in North
Americaand the recurrence rate of renal stones about 75% in 20 years span
(Sutherland et al 1985). It occurs both in men and women but the risk is generally
high in men and is becoming more common in young women1.
Nephrolithiasis remains a chronic disease and our fundamental
understanding of the pathogenesis of stones as well as their prevention and cure
still remains rudimentary .Kidney stone are a form of polycrystalline aggregates
thatformed by a variety of crystalloid and the organic matrix. There several types
of urinary tract stones are the main basis of the components constituent namely:
calcium oxalate stones, calcium phosphate stones, struvite stones, Uric acid stones
and cystine stones 2.
Stone formation is influenced by the concentration of urine depends the
urine pH, ion content in the urine, the solute concentration and others.Some other
factors that affect the formation of stones inhuman factors such as age, sex, race,
geographic location, diet andfluid consumption, use of drugs and the presence or
absence of diseasebroadcaster. Family history is also one of the factors which
25%patients have a family with a history of urinary tract stone disease2.
In Indonesia, kidney stone disease still occupies portionsthe largest
number of patients in the urology clinic. From the data everpublished found an
increasing number of patients with kidney stonesgot action in RSUPN-

3
CiptoMangunkusumo from year to yearstarted 182 patients in 1997 to 847
patients in 2002.3

CHAPTER 2
LITERATURE REVIEW

2.1. Defination
The formation of crystal aggregates in the urinary tract results in kidney
stones, the clinical condition referred to as nephrolithiasis 4.Nephrolithiasis
specifically refers to calculi in the kidneys, but renal calculi and ureteral calculi
(ureterolithiasis) are often discussed in conjunction. The majority of renal calculi
contain calcium5 .

2.2 Aetiology and Risk factor6

1. Crystalluria: Stone formers, especially those with calcium oxalate
stones,frequently excrete more calcium oxalate crystals, and those crystals
are larger than normal >12 mm).Crystal production is determined by the
saturation of each salt and the urinary concentration of inhibitors and
promoters.
2. Socioeconomic factors: Renal stones are more common
in affluent, industrialized countries.
3. Diet : Increase of fatty and animal protein diet results in stone
formation.High sodium intake is associated with increased urinary sodium,
calcium, and pH, and a decreased excretion of citrate increases urinary
saturation thus leads to stone formation.
4. Occupation: This factor related todifferences in diet but also may be
related to physical activity,physical activity may agitate urine and dislodge
crystalaggregates.
5. Climate: Individuals living in hot climates are proneto dehydration, which
results in an increased incidence ofurinary stones.Although heatmay cause

4
 a higher fluid intake, sweat loss results in loweredvoided volumes. Hot
climates usually expose peopleto more ultraviolet light, increasing vitamin
D3 production which easily causes the stone formation.
6. Family history: Family historyA family history of urinary stones
isassociated with an increased incidence of renal calculi.Those with a
family history of stones have an increased incidence of multiple and early
recurrences.
7. Medication:There are few medication are the risk to form kidney stone for
example theantihypertensive medication triamtereneis found as a
component of several medicationsand has been associated with urinary
calculi.Long-term use of antacids containingsilica has been associated
with the development of silicatestones.

2.3 Classification Of Stones7

Urinary stones can be classified according to size, location, X-ray characteristics,
aetiology of formation, composition, and risk of recurrence
Stone size7
Stone size is usually given in one or two dimensions, and stratified into
those measuring up to 5, 5-10, 10-20, and > 20 mm in largest diameter.
Stone location7
Stones can be classified according to anatomical position: upper, middle or
lower calyx; renal pelvis; upper, middle or distal ureter; and urinary bladder.

X-ray characteristics7
Stones can be classified according to plain X-ray appearance [kidney-ureter-
bladder (KUB) radiography], which varies according to mineral composition.
Non-contrast-enhanced computer tomography (NCCT) can be used to classify
stones according to density, inner structure and composition, which can affect
treatment decisions.

5
Aetiology of stone formation7
Stones can be classified into those caused by: infection, or non-infectious
causes (infection and non-infection stones); genetic defects; or adverse drug
effects (drug stones).

Stone composition7
Metabolic aspects are important in stone formation, and metabolic
evaluation is required to rule out any disorders. Analysis in relation to metabolic
disorders is the basis for further diagnostic and management decisions. Stones are
often formed from a mixture of substances.
Calcium Stone8
Calcifications can occur and accumulate in the collecting system, resulting
in nephrolithiasis. Eighty to eighty-five percent of all urinary stones are
calcareous.
Nephrocalcinosis may result from a variety of pathologic states. Ectatic
collecting tubules, as seen with medullary sponge kidney, are common. This is
frequently bilateral process. Increased calcium absorption from the small bowel is
common with sarcoidosis, milk-alkali syndrome, hyperparathyroidism, and
excessive vitamin D intake. Disease processes resulting in bony destruction,
including hyperparathyroidism, osteolytic lesions, and multiple myeloma, are a
third mechanism. Finally, dystrophic calcifications forming on necrotic tissue may
develop after a renal insult.

6
Absorptive Hypercalciuric nephrolithiasis8
Normal calcium consumption on average per day is 900-1000 mg.
Approximately 150-200 mg to be excreted through the urine. Absorptive
hypercalciuria is secondary to increased calcium absorption from the small bowel,
predominantly from the jejunum. Absorptive hypercalciuria is secondary to
increased calcium absorption from the small bowel, predominantly from the
jejunum. The result is suppression of parathyroid hormone, leading to decreased
tubular reabsorption of calcium, culminating in hypercalciuria (>4 mg/kg This
physiologic cascade is in response to the primary defect, an increased absorption
of calcium from the small bowel. AH is divided into three types: type I, II, and
III. Type I AH is independent of diet and represents 15% of all cases of calcium
stones. There is an elevated urinary calcium level (>150200 mg/24 h) even
during a calcium-restricted diet. Type II absorptive hypercalciuria is dietary
dependentand is a common cause of urinary stone disease. Type III absorptive
hypercalciuria is secondary to a phosphate renal leak and accounts for 5% of all
urinary calculi. Decreased serum phosphate leads to an increase in 1, 25-
dihydroxyvitamin D synthesis. Physiological cascade will increase the absorption
of phosphate and calcium in the intestines and increasing calcium excretion from
the kidneys, resulting in hypercalciuria.

Resorptive Hypercalciuric nephrolithiasis8

About half of the patients with primary hyperparathyroidism experience
urinary tract stone diseases. Patients with calcium phosphate stones, women with
recurrent calcium stones should be suspected to have hyperparathyroidism.
Hypercalcemia is a common sign of hyperparathyroidism. Parathyroid hormone
can cause elevated levels of phosphorus in the urine and decreased levels of
phosphorus in plasma, followed by rising plasma and urinary calcium levels.

7
Renal-induced hypercalciuric nephrolithiasis8
Hypercalciuria of renal origin is due to an intrinsic renal tubular defect in
calcium excretion. Excessive urinary calcium excretion results in a relative
decrease in serum calcium, which leads to a secondarily increased parathyroid
hormone level that mobilizes calcium from the bone and increases calcium
absorption from the gut. This step completes the pathologic cycle by delivering
increased levels of calcium back to the kidney, whereby the renal tubules excrete
large amounts of calcium.

Hyperoxalouric calcium nephrolithiasis8

Hyperoxalouric calcium nephrolithiasis is caused by increased levels of
oxalate in the urine which is above 40 mg in 24 hours. Usually it is found in
patients with inflammatory bowel disease,chronic diarrhea and severe dehydration
and rarely caused by an excess intake of oxalate. Free oxalates are readily
absorbed and not affected by inhibitors. Increased absorption of oxalate results in
an increased formation of calcium oxalate product. This resulted in the potential
for the occurrence of nucleation and crystal growth .

Struvite Stone8
Struvite stones are composed of magnesium,ammonium, and phosphate
(MAP). They are found most commonly in women and may recur rapidly.
Struvite stones are infection stones associated with urea-splitting organisms,
including Proteus, Pseudomonas, Providencia, Klebsiella, Staphylococci, and
Mycoplasma. The high ammonium concentration derived from the urea-splitting
organisms results in an alkaline urinary pH. It is only at thiselevated urinary pH
(>7.19) that MAP crystals precipitate.

8
 Schematic formation of struvite stones
Source: Source: Campbell-Walsh Urology 10th Edition. Urinary lithiasis.

Uric Acid Stones8

Uric acid stones compose <5% of all urinarycalculi and are usually found
in men. Patients with gout, myeloproliferative diseases, or rapid weight loss, and
those treated for malignant conditions with cytotoxic drugs have a high incidence
of uric acid lithiasis. Elevated uric acid levels are frequently due to dehydration
and excessive purine intake.

Scheme of uric acid stone formation

Source: Campbell-Walsh Urology 10th Edition. Urinary lithiasis.

9
.

2.4. Urinary Stone Formation Process8

Urinary stones are no exception; they are polycrystalline aggregates
composed of varying amounts of crystalloid and organic matrix. Theories to
explain urinary stone disease are incomplete. Stone formation requires
supersaturated urine. Supersaturation depends on urinary pH, ionic strength,
solute concentration, and complexation. The role of solute concentrations is clear:
The greater the concentration of 2 ions, the more likely they are to precipitate.
Low ion concentrations result in undersaturation and increased solubility. As ion
concentrations increase, their activity product reaches a specific point termed the
solubility product (Ksp). Concentrations above this point are metastable and are
capable of initiating crystal growth and heterogeneous nucleation. As solutions
become more concentrated, the activity product eventually reaches the formation
product (Kfp). Supersaturation levels beyond this point are unstable, and
spontaneous homogeneous nucleation may occur.

Stages saturation of urine

Source: Campbell-Walsh Urology 10th Edition. Urinary lithiasis. Pearle, M.

10
 Nucleation theory asserts that urinary tract stones are formed fromcrystals
or foreign objects from urine levels are saturated. However,stones are not always
formed from a high patient or excretion rate at risk of dehydration. The theory of
crystal inhibitor is another theory on stone formation. According to this theory,
the stone was formed because of the low the concentration of ions into a natural
inhibitor of the stone like magnesium, citrate and pyrophosphate. However, the
validity of this theory is still questionable, because many people are deficient ions
are not impaired urinary tract stones.8
Complexation influences the availability of specific ions. For instance,
sodium complexes with oxalate and decreases its free ionic form, while sulfates
can complex with calcium. Crystal formation is modified by a variety of other
substances found in the urinary tract, including magnesium, citrate,
pyrophosphate, and a variety of trace metals. These inhibitors may act at the
active crystal growth sites or as inhibitors in solution (as with citrate). The crystal
inhibitor theory claims that calculi form owing to the absence or low
concentration of natural stone inhibitors, including magnesium, citrate,
pyrophosphate, and a variety of trace metals. This theory does not have absolute
validity since many people lacking such inhibitorsmay never form stones, and
others with an abundance of inhibitors may, paradoxically, form them.8
Causes of stone formation. The raised concentration of stone-forming
substances can be the result of prerenal, renal, and postrenal factors: Prerenal
causes produce the increased filtration and excretion of stone-producing
substances via a raised plasma concentration . Thus, prerenal hypercalciuria and
phosphaturia are the result of raised intestinal absorption or mobilization from
bone, for example, if there is an excess of PTH or calcitriol (A2).9
Hyperoxalemia can be brought about by a metabolic defect in amino acid
breakdown or by increased intestinal absorption (A3). 9
Hyperuricemia occurs as a result of an excessive supply, increased new
synthesis, or increased breakdown of purines (A3). 9
Xanthine stones may occur when the formation of purines is greatly
increased and the breakdown of xanthines to uric acid is inhibited. However,

11
xanthine is much more soluble than uric acid and xanthine stones are therefore
much less common. 9
Release of ADH (in volume depletion, stress, etc) leads to a raised
concentration of stone-forming substances via enhanced urine concentration (A4).
The solubility of some substances depends on the pH of urine. Phosphates
are easily dissolved in an acidic urine, but poorly in an alkaline one. Phosphate
stones are therefore, as a rule, only found in alkaline urine. Conversely,uric acid
(urate) is more soluble when dissociated than undissociated, and uric acid stones
are formed more readily in acidic urine. If the formation of NH3 is reduced, the
urine has to be more acidic for acid to be eliminated, and this promotes the
formation of urate stones. 9
A significant factor is also how long crystals that have already formed
actually remain in the supersaturated urine. The length of time depends on the
diuresis and the flow conditions in the lower urinary tract that can, for example,
lead to crystals getting caught (postrenal cause). 9

12
 Pathogenesis Of Stone Formation
Source: Color Atlas Of Pathophysiology 2nd Edition. Silbernagl, S, et al.

2.5. Clinical Manifestation

Many of the symptoms and signs can accompany urinary stone

disease.However, there are also some stones will not show any special symptoms
or signs but found radiological examinations. The symptoms often occur in
patients with stone are pain, hematuria, nausea, vomiting, fever and small bowel
disorders such as frequency, urgency and dysuria. 10

Renal colic and noncolicky renal pain are the 2 types of pain originating
from the kidney. Renal colic usually iscaused by stretching of the collecting
system or ureter caused by obstruction which causes increased intraluminal
pressure, stretched nerve endings, and local mechanisms at the site of obstruction
such as inflammation, oedema, and irritation of the mucous.While noncolicky
renal pain is caused by distention of therenal capsule. These symptoms may
overlap, making a clinicaldifferentiation difficult or impossible. Urinary
obstructionis the main mechanism responsible for renal colic.6

Obstruction in renal calyx will cause in the flank or back area with varying
intensity. Pain can arise if excessive fluid consumption. Obstruction renal
pelvic stones with a diameter of above 1 cm, the pain will appear on
costovertebra corner. Pain can arise in the form of pain that dim until a sharp pain
that is constant and unbearable, and can spread to the flank and abdominal
quadrant area ipsilateral 6.

Obstruction in the proximal ureter causes pain on the costovertebral angle

and can propagate along the dermatomes of affectedspinal nerves. In the upper
ureteral obstruction, pain spread to the lumbar region, while the obstruction
midureter pain spread to the lower abdomen area. Obstruction in the distal part of
the ureter likely to cause pain spread to the groin and testes in men or labia majora

13
in women. The pain conducted through the ilioinguinal nerve or genital branch of
the nerve genitofemoral 6.

The incidence of hematuria in patients with urinary tract stones is

estimated 90% based on theory. However, the absence hematuria is not a
guarantee that urinary stones do not occur. An estimated 10% of patients had
negative results on the examination microscopy and dipstick .Complete urinalysis
is required to ensure diagnosis of urinary tract stones by hematuria and
crystalluria and pH urine. Patients usually complain of urine colour like dark
tea. On 10-15% of cases, microhematuria not happen due to a complete
obstruction of ureter 11.

Fever associated with urinary tract stones shows aemergency

condition.Signs of clinical sepsis are variable and include fever, tachycardia,
hypotension, and cutaneous vasodilation.Whileupper-tract obstruction is
frequently associated with nausea and vomiting.Magnesium ammonium
phosphate (struvite) stones are
synonymous with infection stones. They are commonly associated with Proteus,
Pseudomonas, Providencia, Klebsiella,andStaphylococcus infections.All stones,
however, may be associated with infections secondary to obstruction and stasis
proximal to the offending calculus.Infection may be a contributing factor to pain
perception 6 .

Diagnose

1. Medical History

In the diagnosis of these patients, systemic and environmental influences must be

carefully identified. Systemic abnormalities include intestinal disease, disorders of
calcium homeostasis such as primary hyperparathyroidism, conditions
accompanied by extra renal 1,25 (OH)2D production such as granulomatous
diseases, obesity, type II diabetes, recurrent urinary tract infection, bariatric

14
surgery, medullary sponge kidney, and various drug treatments. Diet plays a
crucial role in the formation of kidney stones. High dietary salt and protein
consumption are the two most common dietary aberrations that increase the risk
of nephrolithiasis. Aside from dietary risk factors, it has been suggested that
kidney stone risk increases in hot climates as well as with frequent and/or intense
exercise, largely due to extra renal fluid loss as a result of perspiration, resulting
in a significant fall in urine volume.12

The characteristic cramping and intermit- tent abdominal and flank pain occur as
kidney stones travel within the urinary tract. The pain is often accompanied by
hematu- ria, nausea or vomiting, and malaise; fever and chills may also be
present.13

2. Laboratory Diagnosis

Laboratory diagnosis includes stone analysis, imaging studies, blood

profiles, and a urine metabolic evaluation. In a complete blood count test, mild
leukocytosis often accompanies a renal colic attack, a high index of suspicion for
a possible renal or systemic infection should accompany any serum WBC count of
15,000/L or higher in a patient presenting with an apparent acute kidney stone
attack, even if afebrile. A depressed RBC count suggests a chronic disease state or
severe ongoing hematuria.13,14

Measurements of serum electrolyte, creatinine, calcium, uric acid,

parathyroid hormone (PTH), and phosphorus are needed to assess a patients
current renal function and to begin the assessment of metabolic risk for future
stone formation. A high serum uric acid level may indicate gouty diathesis or
hyperuricosuria, while hypercalcemia suggests either renal-leak hypercalciuria
(with secondary hyperparathyroidism) or primary hyperparathyroidism. If the
serum calcium level is elevated, serum PTH levels should be obtained. Serum
creatinine level is the major predictor of contrast-induced nephrotoxicity. If the
creatinine level is higher than 2 mg/dL, use diagnostic techniques that do not

15
require an infusion of contrast, such as ultrasonography or helical CT scanning.
Hypokalemia and decreased serum bicarbonate level suggest underlying distal
(type 1) renal tubular acidosis, which is associated with formation of calcium
phosphate stones.14

3. Urinalysis

Microscopic examination of the urine for evidence of hematuria and

infection is a critical part of the evaluation of a patient thought to have renal colic.
Gross or microscopic hematuria is only present in approximately 85% of patients
with urinary calculi. The lack of microscopic hematuria does not eliminate renal
colic as a potential diagnosis. In addition to a dipstick evaluation, always perform
a microscopic urinalysis in these patients. Degree of hematuria is not predictive of
stone size or likelihood of passage. No literature exists to support the theory that
ureterolithiasis without hematuria is indicative of complete ureteral obstruction.
Attention should also be paid to the presence or absence of leukocytes, crystals,
and bacteria and to the urinary pH. In general, if the number of white blood cells
(WBCs) in the urine is greater than 10 cells per high-power field or greater than
the number of RBCs, suspect a UTI. Pyuria (>5 WBCs/hpf on a centrifuged
specimen) in a patient with ureterolithiasis should prompt a careful search for
signs of infected hydronephrosis. Urine cultures are crucial if the patient is febrile
or leuko- cytes are detected in the urine. Determining urinary pH also helps. A
urine pH greater than 7 suggests presence of urea-splitting organisms, such as
Proteus, Pseudomonas, or Klebsiella species, and struvite stones. A urine pH less
than 5 suggests uric acid stones.12,14

4. Radiologic Evaluation

Renal ultrasonography by itself is frequently adequate to determine the

presence of a renal stone. The study is mainly used alone in pregnancy or in
combination with plain abdominal radiography to determine hydronephrosis or
ureteral dilation associated with an abnormal radiographic density believed to be a

16
urinary tract calculus. A stone easily identified with renal ultrasonography but not
visible on the plain radiograph may be a uric acid or cystine stone, which is
potentially dissolvable with urinary alkalinization therapy. On some stones,
ultrasonography works quite well; however, it has been found to be less accurate
than IVP or CT in diagnosis of ureteral stones, especially those in the distal ureter.
Diagnostic criteria include direct visualization of the stone, hydroureter more than
6 mm in diameter, and perirenal urinoma suggesting calyceal rupture. 3 Plain
abdominal radiography (also referred to as flat plate or KUB radiography) is
useful for assessing total stone burden, as well as the size, shape, composition,
and location of urinary calculi in some patients. Calcium-containing stones
(approximately 85% of all upper urinary tract calculi) are radiopaque, but pure
uric acid, indinavir-induced, and cystine calculi are relatively radiolucent on plain
radiography. When used with other imaging studies, such as a renal
ultrasonography or, particularly, CT scanning, the plain film helps provide a better
understanding of the characteristics of urinary stones revealed with these other
imaging studies. This may also be helpful in planning surgical therapy. The flat
plate radiograph uses the same orientation and anatomical presentation that is
observed on fluoroscopy images and retrograde pyelograms or during endoscopic
ureteral surgery, such as ureteroscopy or intracorporeal lithotripsy. Not all urinary
calculi may be visible on the KUB radiograph, whether because of their small
size, stone radiolucency, or overlying gas, stool, or bone. The stones that are
observed can be correlated with opacities found on other studies for identification
and tracking progress. If a stone is not visible on a flat plate radiograph, it could
be a radiolucent uric acid stone that can be dissolved with alkalinizing medication.
Such a stone is more likely if the urine pH indicates very acidic urine. In practice,
any patient with symptoms of acute renal colic who demonstrates a urine pH
lower than 6.0 should be considered at risk for a possible uric acid stone. If a
stone of adequate size is visible on a CT scan but not visible on KUB, then uric
stones should be considered.14

17
At most institutions that offer this examination, CT scanning has replaced IVP,
the historic criterion standard, for the assessment of urinary tract stone disease,
especially for acute renal colic. CT scans are readily available in most hospitals
and can be performed and read in just a few minutes. Numerous studies have
demonstrated that CT has a sensitivity of 95-100% and superior specificity and
accuracy when compared with IVP. A renal colic study consists of a noncontrast
or unenhanced CT scan of the abdomen and pelvis, including very narrow cuts
taken through the kidneys and bladder areas, where symptomatic stones are most
likely to be encountered.14

Management and Therapy

Conservative Management

High oral fluid intake must be considered in all stone formers. A prospective
controlled study has shown that increasing water intake to ensure a urinary
volume of ap- proximately 2.5 liters/d was associated with reduced uri- nary
supersaturation with CaOx and a significant reduc- tion in stone recurrence.
Another study suggests that fluid intake as fruit juice, specifically orange juice, is
also effective in reducing urinary CaOx saturation and increas- ing urinary citrate
excretion.12

The only other general dietary guidelines are to avoid excessive salt and protein
intake. Moderation of calcium and oxalate intake is also reasonable, but great care
must be taken not to indiscriminantly instruct the patient to reduce calcium intake.
Patients with calcium stones and relatively low urinary citrate should increase
their intake of fruits and vegetables. Dietary calcium should not be restricted
beyond normal unless specifically indicated on the basis of on 24-hour urinalysis
findings. Urinary calcium levels are normal in many patients with calcium stones.
Reducing dietary calcium in these patients may actually worsen their stone
disease, because more oxalate is absorbed from the GI tract in the absence of
sufficient intestinal calcium to bind with it. This results in a net increase in oxalate

18
absorption and hyperoxaluria, which tends to increase new kidney stone formation
in patients with calcium oxalate calculi. An empiric restriction of dietary calcium
may also adversely affect bone mineralization and may have osteoporosis
implications, especially in women. This practice should be condemned unless
indicated based on a metabolic evaluation. As a rule, dietary calcium should be
restricted to 1000-1200 mg/d in patients with diet-responsive hypercalciuria who
form calcium stones. This is roughly equivalent to a single high-calcium or dairy
meal per day.14

Pharmacological Treatment

Thiazide diuretics and their analogs are commonly used medical treatments for
lowering calcium excretion in recurrent calcium stone formers. In several
randomized controlled trials, thiazide diuretics were effective in significantly
reducing kidney stone recurrence. The optimal effect of thiazides is achieved with
a low-salt diet that attenuates urinary calcium excretion and the provision of
sufficient potassium supplementation to avoid hypocitraturia. Potassium citrate
holds an advantage over potassium chloride. Potassium citrate is used either alone
or in combination with thiazide treatment in recurrent calcium or UA stone
formers. Alkali treatment is effective in lowering urinary calcium ex- cretion,
raising urinary citrate, and reducing urinary CaOx, CaP, and undissociated UA
supersaturation.12

2.6. Prevention

The most common causes of kidney stones are hypercalciuria, hyperuricosuria,

hyperoxaluria, hypocitraturia, and low urinary volume. Each of these major
factors can be measured easily with a 24-hour urine sample using one of several
commercial laboratory packages now available. Kidney stone preventive therapy
consists of dietary adjustments, nutritional supplements, medications, or
combinations of these.14

19
Strongly encourage patients who have a stone at a young age (ie, < 25 y), multiple
recurrences, a solitary functioning kidney, or a history of prior kidney stone
surgery to obtain a 24-hour urine collection for stone prevention analysis,
especially if they are motivated to comply with a long-term stone prevention
program. These 24-hour urine collection kits can be obtained from a number of
commercial medical laboratories.14

20
 CHAPTER 3
PATIENT STATUS

3.1. Identity
Name : NuardinSimatupang
Age : 50 years-old
Sex : Male
Occupation : Fisherman
Address : Lk.IILubukTukaPandan, Tapanuli Tengah
Admission Date : 15th December 2016

3.2. Anamnesis
Chief Complain : Flank Pain
History of Present Illness :
The patient has been suffering from the pain for 3 months before he got
admitted to the hospital. The pain was localized on the left flank, but sometimes
migrating to the umbilical region. No history of passing stone, haematuria (+),
nausea, vomiting and sweating was found. There was no fever and cloudy urine.
Patient also claims that there is pain on his supra pubic region and dysuria at the
end of micturition. Incomplete emptying (+), frequency (+).
Post Medical History : Hypertension (-) DM (-) Hyperuricemia (-)
Previous Medication : Unclear

3.3. Present Status :

Consciousness : Compos Mentis
Blood Pressure : 120/70 mmHg
Pulse : 84 times / minute
Respiratory Rate : 20 times / minute
Temperature : 36.9oC
General Status : Malaise
Nutritional Status : Good

21
3.4. Physical Examination
General Survey
Head
o Eyes : Inferior Conjunctiva Palpebrae: Anaemia (-/-)
o Ears : Normal
o Nose : Normal
o Mouth : Normal
Neck : Lymph Node Enlargement (-/-)
Thorax
o Inspection : Symmetrical Thorax
o Palpation : Stem Fremitus Right = Left
o Percussion : Sonor
o Auscultation : Vesiculer on both sides
Abdomen
o Inspection : Symmetrical Abdomen
o Palpation : Soepel
o Percussion : Tympani
o Auscultation : Normoperistaltic

Urologic Status
Flank Area
o Inspection : Normal
o Palpation : Pain (+)
Supra Symphysis Area
o Inspection : Normal
o Palpation : Pain (-)
Genital : Male, OUE Normal
Digital Rectal Exam : Tight Sphincter Ani, Smooth Mucous, Bulging
Prostate (-), Glove: Clean

22
3.5. Support Examination
1. Laboratory Examination

Type Examination Result Normal

HAEMOTHOLOGY

Hemoglobin (HGB) 14,7 1318

Red Blood Cells 5.39 4,50-6,50

White Blood Cells 11.770 411x103

Hematocrit 44 3954%

Platelet 353.000 150450x103

RENAL FUNCTION TEST

Urea 45 18-55 mg/dL

Creatinine 3.95 0,71,3 mg/dL

ELECTROLITE

Natrium (Na) 136 135155 mEq/L

Potassium (K) 4,7 3,65,5 mEq/L

Chloride (Cl) 106 96106 mEq/L

BLOOD GAS ANALYSIS

pH 7,300 7.35 7.45

pCO2 28,0 38 42 mmHg

pO2 186,0 85 100 mmHg

Bicarbonate 13,8 22 26 mmol/L

Base Excess -11,2 (-2) (2) mmol/L

23
2. Chest X Ray
Conclusion :
There is no heart and lung abnormalities
3. Ultrasonography

Left Kidney : Acoustic Shadow (-), Hydronephrosis (+)

Right Kidney : Acoustic Shadow (-), Hydronephrosis (-)
Urinary Vesika : Acoustic Shadow (+), Mass (-)
Conclusion :
Bladder Stone + Moderate Hydronephrosis (L)

24
 4. CT Scan

Conclusion :
Left Nephrolithiasis + Left Hydronephrosisdue to ureter stone at proximal
+ Vesicolithiasis

3.6. Diagnose :
Proximal Ureter Stone (L) + Moderate Inferior Calyx Hydronephrosis (L)
due to ureter stone + Bladder Stone

3.7. Management :
1. IVFD NaCl 0.9% 20 gtt/i
2. Injection Ketorolac 30 mg/8 jam
3. Injection Ranitidine 50 mg/12 jam
4. Planning Open Ureterolithotomi (L)

25
 CHAPTER 4
DISCUSSION

THEORY CASE
Many of the symptoms and signs that From the patient we found:
can accompany stone disease urinary Flank and supra pubic pain
tract. However, there are also some Hematuria
stones that are not show symptoms or Nausea
signs of special but found in results Vomiting
radiological examinations. Dysuria
The symptoms often occur in patients
can of pain, hematuria, nausea,
vomiting, fever and bowel disorders
small such as frequency, urgency and
dysuria
In addition to ultrasound, radiological Ultrasonography
examination otherwise be done is Left Kidney : Acoustic Shadow (-),
plain radiography examination. Plain Hydronephrosis (+)
film (KUB) may use to look at the Right Kidney : Acoustic Shadow (-),
position of stones in the kidney, ureter, Hydronephrosis (-)
and bladder. KUB has 90% sensitivity Urinary Vesika: Acoustic Shadow
in the detection of urinary tract stones, (+), Mass (-)
and 92% of stone can be determined Conclusion :
through this action. Bladder Stone + Moderate
Non-Contrast computed Hydronephrosis (L)
tomography (NCCT) has become the
standard in diagnosing acute pain CT Scan
replace intravenous urography (IVU) Conclusion :
which has become the gold standard Left Nephrolithiasis + Left
for many years. NCCT also can used Hydronephrosis due to ureter stone at
for diagnosis of peritoneal and proximal + Vesicolithiasis

26
retroperitoneal disorders and help
when the diagnosis is uncertain.

27
 CHAPTER 5
CONCLUSION

5.1. Conclusion
Mr. NS, male, 50 years old, came to Emergency Unit General Reference
Centre Hospital Haji Adam Malik Medan with chief complain pain in left plank
and diagnosed by Proximal Ureter Stone (L) + Moderate Inferior Calyx
Hydronephrosis (L) due to ureter stone + Bladder Stone. Then, he was planned to
do open uterolithotomi.

28
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