C h a p t e r 2 5
Disorders of Renal Function
633
surgical treatment of structural defects may be indicated.
Treatment of complicating urinary tract infections due
to urinary stasis is also important.
Kidney Stones
The most common cause of upper urinary tract obstruc-
tion is urinary calculi. Although stones can form in any
part of the urinary tract, most develop in the kidneys.
Kidney stones, also known as
nephrolithiasis
or
renal
calculi
, are the third most common disorder of the uri-
nary tract, exceeded only by urinary tract infections and
prostate disorders.
28
Kidney stones are polycrystalline aggregates composed
of materials that the kidneys normally excrete in the
urine.
4,5,28–31
The etiology of urinary stone formation is
complex. It is thought to encompass a number of factors,
including increases in blood and urinary levels of stone-
forming components and interactions among the com-
ponents; anatomic changes in urinary tract structures;
metabolic and endocrine influences; dietary and intestinal
absorption factors; and urinary tract infections. Added to
the mystery of stone formation is the fact that although
both kidneys are exposed to the same urinary constitu-
ents, kidney stones tend to form in only one kidney.
Two factors implicated in kidney stone formation are a
supersaturated urine and an environment that allows the
stone to grow. The risk for stone formation is increased
when the urine is supersaturated with stone components
(e.g., calcium salts, uric acid, magnesium ammonium
phosphate, and cystine). Supersaturation depends on uri-
nary pH, solute concentration, ionic strength, and com-
plexation. The greater the concentration of two ions, the
more likely they are to precipitate. Complexation influ-
ences the availability of specific ions. For example, oxa-
late complexes with sodium and decreases the availability
of free sodium ions to participate in stone formation.
In addition to supersaturated urine, kidney stone for-
mation requires a nidus or nucleus that facilitates crystal
aggregation. In supersaturated urine, stone formation
begins with small clusters of crystals such as calcium
oxalate. Most small clusters tend to disperse because
the internal forces that hold them together are too weak
to overcome the random tendency of ions to move
apart. Larger ion clusters form nuclei and remain sta-
ble because the attraction forces balance surface losses.
Once they are stable, nuclei can grow at levels of super-
saturation below that needed for their creation. Organic
materials, such as mucopolysaccharides derived from
the epithelial cells that line the tubules, are also thought
to act as nuclei for stone formation by lowering the level
of supersaturation required for crystal aggregation.
The fact that many people experience supersatura-
tion of their urine without developing kidney stones
is believed to be due to the presence of natural stone
inhibitors, including magnesium, citrate, and the Tamm-
Horsfall mucoprotein. To date, the measurement and
manipulation of stone inhibitors has not been part of
clinical practice, with the exception of citrate.
28,29
Urine
citrate reduces supersaturation by binding calcium and
inhibiting nucleation and growth of calcium crystals.
Citrate is a normal by-product of the citric acid cycle in
renal cells. Metabolic stimuli that consume this product
(as with metabolic acidosis due to fasting or hypokale-
mia) reduce the urinary concentration of citrate. Citrate
supplementation (potassium citrate) may be used in the
treatment of some forms of hypocitraturic kidney stones.
Types of Stones
There are four basic types of kidney stones: calcium
(i.e., oxalate or phosphate), magnesium ammonium
phosphate, uric acid, and cystine stones.
4,5,28–30
The
causes and treatment measures for each of these types
of renal stones are described in Table 25-2. Most kidney
TABLE 25-2
Composition, Contributing Factors, andTreatment of Kidney Stones
Type of Stone
Contributing Factors
Treatment
Calcium (oxalate and
phosphate)
Hypercalcemia and hypercalciuria
Treatment of underlying conditions
Immobilization
Increased fluid intake
Thiazide diuretics
Hyperparathyroidism
Vitamin D intoxication
Diffuse bone disease
Milk-alkali syndrome
Renal tubular acidosis
Hyperoxaluria
Dietary restriction of foods high in
oxalate
Intestinal bypass surgery
Magnesium ammonium
phosphate (struvite)
Urea-splitting urinary tract infections
Treatment of urinary tract infection
Acidification of the urine
Increased fluid intake
Uric acid (urate)
Formed in acid urine with pH of
approximately 5.5
Increased fluid intake
Gout
Allopurinol for hyperuricosuria
High-purine diet
Alkalinization of urine
Cystine
Cystinuria (inherited disorder of
amino acid metabolism)
Increased fluid intake
Alkalinization of urine
