University of San Jose-Recoletos

College of Nursing
Cebu City

I. Introduction

A. Definition of the Disease

Nephrolithiasis, the process of forming a kidney stone, a stone in the kidney

(or lower down in the urinary tract). Kidney stones are a common cause of blood in
the urine and pain in the abdomen, flank, or groin. Kidney stones occur in 1 in 20
people at some time in their life.
The 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 stones form in the urine collecting area (the
pelvis) of the kidney and may range in size from tiny to staghorn stones the size of
the renal pelvis itself.
The process of stone formation, nephrolithiasis, is also called urolithiasis.
"Nephrolithiasis" is derived from the Greek nephros- (kidney) lithos (stone) = kidney
stone "Urolithiasis" is from the French word "urine" which, in turn, stems from the
Latin "urina" and the Greek "ouron" meaning urine = urine stone. The stones
themselves are also called renal caluli. The word "calculus" (plural: calculi) is the
Latin word for pebble.

B. Causes

Urinary tract stone disease is likely caused by two basic phenomena:

• The first phenomenon is supersaturation of the urine by stone-forming

constituents, including calcium, oxalate, and uric acid. Crystals or foreign
bodies can act as nidi, upon which ions from the supersaturated urine
form microscopic crystalline structures. The overwhelming majority of
renal calculi contain calcium. Uric acid calculi and crystals of uric acid,
with or without other contaminating ions, comprise the bulk of the
remaining minority. Other, less frequent stone types include cystine,
ammonium acid urate, xanthine, dihydroxyadenine, and various rare
stones related to precipitation of medications in the urinary tract. This is
likely the underlying cause of uric and cystine stones, but calcium-based
stones (especially calcium oxalate stones) likely have a more complex
etiology.

• The second etiology, which is most likely responsible for calcium oxalate
stones, is deposition of stone material on a renal papillary calcium
phosphate nidus, typically a Randall plaque. Evan et al (2007) recently
proposed this model based on evidence accumulating from several
 laboratories. Calcium phosphate precipitates in the basement membrane
of the thin loops of Henle, erodes into the interstitium, and then
accumulates in the subepithelial space of the renal papilla. The
subepithelial deposits, which have long been known as Randall plaques,
eventually erode through the papillary urothelium. Stone matrix, calcium
phosphate, and calcium oxalate gradually deposit on the substrate to
create a urinary calculus. Randall plaques are always composed of
calcium phosphate.

C. Signs and Symptoms

Even large calculi remaining in the renal parenchyma or renal pelvis are
usually asymptomatic unless they cause obstruction. Symptoms, such as severe
pain, often accompanied by nausea and vomiting, and sometimes gross hematuria,
usually occur when calculi pass into the ureter, cause obstruction, or both. Pain
(renal colic) is of variable intensity but is typically excruciating and intermittent,
often occurs cyclically, and lasts 20 to 60 min. Nausea and vomiting is common.
Pain in the flank or kidney area that radiates across the abdomen suggests upper
ureteral or renal pelvic obstruction. Pain that radiates along the course of the ureter
into the genital region suggests lower ureteral obstruction. Suprapubic pain along
with urinary urgency and frequency suggests a distal ureteral, ureterovesical, or
bladder calculus.
On examination, patients may be in obvious extreme discomfort, often ashen
and diaphoretic. Patients with renal colic may be unable to lie still and may pace,
writhe, or constantly shift position. The abdomen may be somewhat tender on the
affected side as palpation increases pressure in the already-distended ureter, but
peritoneal signs (guarding, rebound, rigidity) are lacking. For some patients, the
first symptom is hematuria or either gravel or a calculus in the urine. Other patients
may have symptoms of a UTI, such as fever, dysuria, or cloudy or foul-smelling
urine.

Summary:

Symptoms of kidney stones include:

 Colicky pain: "loin to groin". Often described as "the worst pain ever
experienced". This can also occur in the lowerback.

 Hematuria: blood in the urine, due to minor damage to inside wall of kidney,
ureter and/or urethra.

 Pyuria: pus in the urine.

 Dysuria: burning on urination when passing stones (rare). More typical of

infection.
 Oliguria: reduced urinary volume caused by obstruction of the bladder or urethra
by stone, or extremely rarely, simultaneous obstruction of both ureters by a
stone.

 Nausea/vomiting: embryological link with intestine– stimulates the vomiting

center.

 Hydronephrosis

 Postrenal azotemia: when kidney stone blocks ureter

Localization of kidney stone pain

D. Diagnosis

a. Urinalysis
Macroscopic or microscopic hematuria is common, but urine may be normal
despite multiple calculi. Pyuria with or without bacteria may be present. Pyuria
suggests infection, particularly if combined with suggestive clinical findings, such as
foul-smelling urine or a fever. A calculus and various crystalline substances may be
present in the sediment. If so, further testing is usually necessary because the
composition of the calculus and crystals cannot be determined conclusively by
microscopy. The only exception is when typical hexagonal crystals of cystine are
found in a concentrated, acidified specimen, confirming cystinuria.

b. Imaging tests
Noncontrast helical CT should be done. This study can detect the location of a
calculus as well as the degree of obstruction. Moreover, helical CT may also reveal
another cause of the pain (e.g., aortic aneurysm). For patients who have recurrent
calculi, cumulative radiation exposure from multiple CT scans is a concern. For
those with typical symptoms, ultrasound or plain abdominal x-ray can usually
confirm presence of a stone with minimal or no radiation exposure.
Although most urinary calculi are demonstrable on plain x-ray, neither their
presence nor their absence obviates the need for more definitive imaging, so this
study can be avoided. Both renal ultrasonography and intravenous urography (IVU)
can identify calculi and hydronephrosis, but ultrasonography is less sensitive for
small calculi in patients without hydronephrosis, and IVU is time consuming and
exposes the patient to the risk of IV contrast agents; these studies are generally
used if helical CT is unavailable.

E. Treatment

a. Analgesia
Renal colic may be relieved with opioids, such as morphine and for a rapid
onset, fentanyl. Ketorolac 30 mg IV is rapidly effective and nonsedating. Vomiting
usually resolves as pain decreases, but persistent vomiting can be treated with an
antiemetic (e.g., ondansetron 10 mg IV).

b. Facilitating calculus passage

Although increasing fluids (either oral or IV) has traditionally been
recommended, it has not been proved to speed the passage of calculi. Patients with
calculi with a diameter of < 1 cm who have no infection or obstruction, whose pain
is controlled with analgesics, and who can tolerate liquids can be treated at home
with analgesics and with α-receptor blockers (e.g., tamsulosin 0.4 mg once/day) or
Ca channel blockers to facilitate calculus passage. Calculi that have not passed
within 6 wk typically require removal. In patients with infection and obstruction,
calculi should be removed as soon as possible.

c. Calculus removal
The technique used for removal depends on the location and size of the
calculi. Techniques include extracorporeal shock wave lithotripsy and endoscopic
techniques. Endoscopic techniques may involve rigid or flexible scopes and may
involve direct-vision removal (basketing), fragmentation with some sort of
lithotripsy (eg, pneumatic, electrohydraulic, or laser), or both. For symptomatic
calculi < 1 cm in diameter in the renal pelvis or proximal ureter, extracorporeal
shock wave lithotripsy is a reasonable first option for therapy. For larger calculi or if
lithotripsy is unsuccessful, ureteroscopy (done in a retrograde fashion) with
holmium laser lithotripsy is usually used. Sometimes removal is possible using an
endoscope inserted anterograde through the kidney. For mid-ureteral calculi,
ureteroscopy with holmium laser lithotripsy is usually the treatment of choice.
Shock wave lithotripsy is an alternative. For distal ureteral calculi, endoscopic
techniques, such as direct removal and use of lithotripsy (eg, pneumatic,
electrohydraulic, or laser), are considered by many to be the procedures of choice.
Shock wave lithotripsy can also be used.

d. Calculus dissolution
 Uric acid calculi in the upper or lower urinary tract occasionally may be
dissolved by prolonged alkalinization of the urine with K citrate 20 mEq po bid to tid,
but chemical dissolution of other calculi is not possible.

F. Epidemiology

The incidence of urinary tract stone disease in developed countries is similar

to that in the United States. Stone disease is rare in only a few areas, such as
Greenland and the coastal areas of Japan. In developing countries, bladder calculi
are more common than upper urinary tract calculi; the opposite is true in developed
countries. These differences are believed to be diet-related.
Urinary tract calculi are far more common in Asians and whites than in Native
Americans, Africans, African Americans, and some natives of the Mediterranean
region. Although some differences may be attributable to geography (stones are
more common in hot and dry areas) and diet, heredity also appears to be a factor.
This is suggested by the finding that, in regions with both white and nonwhite
populations, stone disease is much more common in whites.
In general, urolithiasis is more common in males (male-to-female ratio of
3:1). Stones due to discrete metabolic/hormonal defects (eg, cystinuria,
hyperparathyroidism) and stone disease in children are equally prevalent between
the sexes. Moreover, most urinary calculi develop in persons aged 20-49 years.
Patients in whom multiple recurrent stones form usually develop their first stones
while in their second or third decade of life.