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226 Schenkman and Henderson

Preoperative localization allows the surgeon to accurately plan the operation. Tumor

localization may help prevent complications by allowing for a unilateral neck or chest

exploration. Operating-room time and cost may be reduced. If diffuse hyperplasia is seen

on localization studies, a more complex operation is planned involving exposure of all

four parathyroid glands. This may dissuade the surgeon from operating in a frail patient

with significant comorbidities (18,29). Despite improved localization studies, most

parathyroid surgeons still insist on bilateral neck explorations. Mixed results are

reported as to whether preoperative localization reduces operating room time (30,31). In

borderline patients the localization may help in the decision to operate or not to operate.

In patients with urolithiasis, a clear-cut indication to operate is almost always present

(32). Therefore, the presence of urolithiasis in a patient with 1HPT should prompt the

urologist to make the appropriate referral.

Secondary Hyperparathyroidism

The diagnosis of secondary hyperparathyroidism is made when normal serum cal-

cium is found on serial examinations with an elevated PTH. Parathyroid hormone is

appropriately elevated in this condition as a response to a low serum calcium from

chronic renal failure, intestinal malabsorption (of vitamin D or calcium), or renal leak

of calcium. In terms of nephrolithiasis, secondary hyperparathyroidism is most often

seen with renal leak hypercalciuria. Serum calcium is normal and PTH levels are mini-

mally elevated, or normal.

VITAMIN D

Both diet and synthesis in the skin are important sources of vitamin D

. In the skin,

ultraviolet light causes a photosynthetic conversion of 7-dehydrocholesterol to previtamin

(Fig. 3). This heat labile previtamin is isomerized to vitamin D

(cholecalciferol).

Vitamin D

is carried to the liver and is converted to 25-hydroxycholecal-

ciferol [25-(OH)

] (33,34). In the kidney’s proximal tubule, PTH stimulates 1 α-

hydroxylase in the mitochondria to convert 25-(OH)

to 1,25(OH)

which is the

active form of the vitamin. Decreased serum phosphate levels also activate the enzyme.

Decreased serum calcium indirectly stimulates 1-α-hydroxylase production via stimu-

lation of PTH production. 1,25 (OH)

production is also stimulated by estrogen,

growth hormone and prolactin (2).

Vitamin D functions to increase serum calcium and phosphorus levels to enhance

bone mineralization. 1,25 (OH)

stimulates absorption of calcium and phosphate from

the brush border of the intestinal mucosa (33). The hormone increases calcium-binding

protein synthesis in the kidney, which leads to renal calcium reabsorption.

Hypervitaminosis D

Hypercalcemia occurs in patients taking greater than 50,000 units of vitamin D daily

(35). These patients may be self-administering excessive doses of vitamin D or are

prescribed medical replacement for hypoparathyroidism. Infrequently, patients may

develop urolithiasis and become symptomatic. Stones are typically calcium phosphate.

More commonly, patients present with other signs and symptoms of hypercalcemia

without nephrolithiasis (Table 1). Treatment is withdrawal of the vitamin D and calcium

supplements, increased fluids and high-dose corticosteroid therapy (23).

Chapter 11 / Hormonal Influences on Nephrolithiasis 227

CALCITONIN

Calcitonin is a 32-amino acid polypeptide produced by thyroid parafollicular cells. Its

half-life in circulation is less than one hour, and it is inactivated in the kidney (36).

Calcitonin acts on bone and in the kidney to decrease serum calcium and phosphate. In

bone, it inhibits bone resorption by blocking osteoclast activity and osteoclast precursor

differentiation (2). In the human kidney, calcitonin produces increased natriuresis and

kaliuresis (37). High dose infusion in humans acts to inhibit inorganic phosphate and

calcium reabsorption (2,19,37–39). The effects on calcium and phosphate handling at

physiologic doses are controversial; some authors suggest a minimal role for this hor-

mone in calcium homeostasis (2,37). The actions of calcitonin are mediated by adenylate

cyclase and c-AMP (37). Calcitonin may stimulate 1α-hydroxylase activity in the proxi-

mal straight tubule of the kidney and have a role in vitamin D synthesis. Calcitonin

secretion is stimulated by increased serum calcium. Gastrointestinal hormones such as

gastrin, glicentin, secretin, and cholecystokinin-pancreozymin, may also stimulate cal-

citonin release.

There exists little objective evidence for a defined role for calcitonin in nephrolithi-

asis. Plasma concentration of calcitonin is significantly higher in children with idio-

pathic hypercalciuria (40–42). D’Angelo et al. concluded that “calcitonin plays a

contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to

be strictly correlated with dietary calcium intake; thus higher production and sensitivity

to calcitonin could be related to persistent hypercalciuria” (43).

Fig. 3. Biosynthesis of 1,25-dihydroxycholecelciferol. (From ref. 2 with permission.)

228 Schenkman and Henderson

SEX HORMONAL INFLUENCES

Significant sex-related differences exist in the rate of stone formation and types of

stones formed. Soucie and associates determined the prevalence rate of all types of stone

formation between men and women to be 2.64 to 1 (44). Idiopathic calcium stones are

even more common in men, with a 4–5 to 1 male to female ratio (45,46). The risk in men

peaks at age 35; women display a bimodal peak at ages 30 and 55 (45). Men tend to have

smaller stones made of pure calcium oxalate, whereas women have relatively larger

stones with a higher relative percentage of calcium phosphate (47). The risk of stone

formation in men is influenced by testosterone. In adult women three different hormonal

milieus exist: nonpregnant, pregnant, and postmenopausal.

Male Factors

The cause of the high rate of calcium oxalate stones in men has not been explained on

the basis of limited clinical studies. Urinary oxalate levels have been implicated, and

hyperoxaluria is up to three times more common among men than women (48). Hammar

et al. found no significant change in urinary citrate excretion or the calcium to citrate

ratios of men before and after orchiectomy (49). Van Aswegen et al. studied urinary

testosterone in 14 calcium oxalate stone formers and 21 healthy subjects. Urinary tes-

tosterone levels in stone formers were lower than in the controls. They concluded that

urinary testosterone was needed to help prevent calcium oxalate stone formation (50).

This finding seems counterintuitive, because it is assumed that testosterone is respon-

sible for increased male calcium urolithiasis.

The clinical evidence does not affirm laboratory animal models investigating sex

related differences in stone formation. The most practical and most commonly used

animal model is ethylene glycol induced nephrolithiasis in the rat. Ethylene glycol (EG)

consumption results in significant hyperoxaluria, which leads to stone formation in an

animal that is not normally prone to renal stones. In the EG-induced rat model, a com-

mon trend is noted: calcium oxalate crystallization and stone formation are generally

increased in the presence of testosterone and decreased in the presence of female hor-

mones.

Many studies have focused on the effects of testosterone on oxalate excretion. Lee et

al. fed EG to intact and castrated male and female rats and noted that intact male rats had

the highest rates of hyperoxaluria, although urinary oxalate was increased in all rats fed

EG. Furthermore, urolithiasis occurred most commonly among intact male rats and did

not occur in female rats. Castrated males were noted to have a 14.3% rate of stone

formation compared to 71.4% for intact males (51).

A follow-up study showed that administration of testosterone to castrated males

resulted in increased stone formation compared to castrated males without testosterone

replacement. Castrated females given testosterone also exhibited urolithiasis much

more frequently than intact females (52). In another EG rat model, Fan et al. used a series

of male and female rats, both intact and castrate, implanted with preparations of test-

osterone and estradiol. The groups with testosterone implants had much higher daily

oxalate excretion than the groups with estradiol implants. No estradiol-implanted rats

had calcium oxalate crystal deposition in the kidneys, whereas 15 of 22 rats implanted

with testosterone had crystal deposition (53).

Yagisawa et al. used an EG rat model to look in depth at sex hormone effects by

focusing on osteopontin, a protein that plays a complex and incompletely elucidated role

Chapter 11 / Hormonal Influences on Nephrolithiasis 229

in stone formation. Osteopontin may act as a stone promoter by forming the matrix

portion of stones; however it has also been shown to inhibit calcium oxalate crystalliza-

tion in vitro. Twenty-four-hour urinalyses and osteopontin expression in renal tissue

were studied in intact and castrated rats of both sexes. Testosterone promoted stone

formation by suppressing osteopontin expression in the kidneys and increasing oxalate

excretion. Estrogen appeared to inhibit stone formation by increasing osteopontin and

decreasing urinary oxalate levels (54).

In another EG induced urolithiasis rat model, the effects of castration and finasteride

were investigated. Urinary oxalate levels were highest in EG-treated intact male rats and

significantly lower in castrated rats and those treated with finasteride. The effect of

finasteride led to the conclusion that some of the hyperoxaluria seen in the EG rat model

was caused by the effect of dihydrotestosterone (55).

Although vasectomy has no direct hormonal effects clinically, it has been associated

with an increased incidence of urolithiasis. A study of over 11,000 men found an age-

adjusted relative risk of urolithiasis of 1.67 in vasectomized men compared to men who

did not undergo vasectomy. The highest relative risk was 2.6 for men age 30–34 (56).

To study the effect of vasectomy in the laboratory, Scherieber and Schwille divided rats

into vasectomy, vasosvasotomy, and sham-operated groups. Two rats out of 12 in the

vasectomy group developed nephrolithiasis, whereas no stones developed in the other

two groups. Although serum and urinary testosterone levels were unchanged, serum

magnesium was decreased and urine phosphate levels were increased in the vasectomy

group. Tissue levels of phosphorus, calcium, and magnesium in the renal papillae were

higher in the vasectomy group than the other groups. They concluded that vasectomy has

subtle metabolic effects and hypothesized this may be related to a disturbance in auto-

nomic tone resulting from vasectomy (57).

Female Factors

Other than epidemiologic evidence, clinical evidence is scant concerning the low rate

of calcium stone disease found in women. A survey of 1302 women in Scandinavia

revealed a history of stone disease in 5% of all age groups, with the highest rate noted

at 46 yr of age and the lowest at 62 yr of age. The incidence of stone disease in this study

was 3.7 per 1000 women per year (58).

The higher levels of urinary citrate in women compared to men have been cited as a

likely cause of lower rates of calcium oxalate lithiasis. In a study of 173 stone formers,

no differences could be found in urinary inhibitors (citrate, magnesium, pyrophosphate,

and glycosaminoglycans) between men and women (59). Another study focused on

citrate, the most well characterized inhibitor of calcium lithiasis, in 24-h urine samples

from three groups: pregnant women, postmenopausal women on hormonal replacement

therapy, and castrated men. The urinary citrate levels were not altered significantly in

any of these groups (49).

A different study noted that postmenopausal women had significantly higher calcium

excretion than groups of young women and groups of young and old men. Citrate levels

were lowest in young men compared to either young women or old men. Older women

had citrate levels not significantly different from young men. Magnesium excretion was

higher in postmenopausal women than in young subjects of either sex (60).

Iguchi et al. studied a female rat EG model to determine the effect of female hormones

on stone formation. They noted that oophorectomized rats given EG had the highest rates

230 Schenkman and Henderson

of oxalate excretion and the highest rates of crystal deposition in the renal tissues.

Osteopontin mRNA expression was highest in the oophorectomized group. Administra-

tion of female hormones reversed each of these elevated parameters. In contrast to the

previously cited study by Yagisawa, et al., this study concluded that increased osteopontin

levels were consistent with stone promotion. Citrate levels in the oophorectomized rats

did not differ significantly from controls (61).

ENOPAUSE

Menopause results in lower circulating levels of female hormones. Use of hormonal

replacement therapy is variable and individualized. Many women in this stage of life are

at risk for osteoporosis and are encouraged to take calcium supplements. This has raised

concern among researchers about promotion of calcium urolithiasis in this group of

women. Of added concern is that many stone formers have lower bone density than age

matched controls, and thus, stone formers may be at greater risk for osteoporosis and

more likely to require calcium supplementation (61). Female stone formers age 36–68

placed on 1 gm/d calcium citrate were found to have increased urinary calcium excretion

over a 6-mo study period. Citrate and oxalate excretion as well as calcium oxalate

saturation were not significantly changed from baseline. Serum levels of parathyroid

hormone and 1,25 (OH

) vitamin D concentration decreased significantly over the course

of the study (62).

A study of postmenopausal women given either calcium carbonate or calcium carbon-

ate and calcitriol did not demonstrate increased calcium oxalate saturation (63).

A study by the same team investigated the effects of calcium carbonate supplemen-

tation vs calcium carbonate plus estrogen replacement in healthy nonstone forming

women. After 3 mo of treatment, no changes were noted in urinary excretion of calcium,

citrate, or oxalate. Neither the calcium/creatinine ratio nor the calcium oxalate saturation

in the urine was changed significantly from baseline (64).

In 1454 adult calcium oxalate stone formers, Heller et al. compared outpatient meta-

bolic evaluations of the men and postmenopausal women. Lower urinary calcium in

women was noted until the age of 50 yr, whereas a reduction of urinary citrate below that

observed in men occurred at the age of 60 yr. Postmenopausal women treated with

estrogen had lower 24-h urinary calcium, 2-h fasting urinary calcium, and calcium

oxalate saturation compared with untreated postmenopausal women. These data suggest

that the lower risk of stones in women may be caused by lower urinary saturation and that

estrogen replacement in postmenopausal women may reduce the risk of stone recurrence

(65).

REGNANCY

Pregnancy induces anatomic and physiologic changes in the kidneys which have a

bearing on urolithiasis. The kidney increases in weight and in length (about 1 cm) during

pregnancy. These changes are caused by pregnancy related increases in renal interstitial

and intravascular volume (66). In the renal collecting system, the calices, pelvis, and

ureters dilate and show hypertrophy of the ureteral smooth muscle and hyperplasia of

connective tissue as well. Dilatation of the collecting system begins at 6–10 wk of

gestation, is more prominent on the right renal unit, and occurs in 90% of women at term

(66–70). The etiology of this dilatation has not been fully elucidated but is related to

anatomic obstruction of the distal ureter by the uterus as well as some effect from the

hormone progesterone. Two findings give credence to the hormonal influence on preg-

Chapter 11 / Hormonal Influences on Nephrolithiasis 231

nancy related hydronephrosis: (1) the ureters dilate before uterine enlargement; (2)

prolonged ureteral catheterization does not reverse the collecting system dilatation

during pregnancy (66). Several factors argue for the influence of ureteral obstruction by

the gravid uterus. The ureteral pressure when monitored in the third trimester of preg-

nancy is noted highest in the standing and supine positions; the pressure decreases in the

lateral decubitus and knee–chest position. Ureteral pressures decrease immediately after

caesarean section, and pressures are noted to decrease only above the pelvic brim (66).

In addition to anatomic changes, the kidney undergoes functional changes that may

influence the formation of urinary calculi. Both the glomerular filtration rate (GFR) and

the renal plasma flow (RPF) increase markedly by 35–50% during pregnancy. The

reasons may include increased cardiac output and increased extracellular volume. This

is countered by a decrease in systemic vascular resistance and blood pressure. Pregnancy

related changes in circulating hormones include increases in aldosterone, desoxycorti-

costerone, progesterone, prolactin, and chorionic gonadotropin, but these increases alone

cannot explain the increase in GFR. GFR is increased because of an increase in RPF

resulting from a decrease in renal vascular resistance. Values of plasma blood urea

nitrogen and creatinine are also lower in pregnancy. The pregnant woman experiences

an increase in glucosuria and aminoaciduria caused by increased filtered load of these

substances. Uric acid excretion increases, and the serum levels of urate fall by 25%.

The incidence of urolithiasis in pregnancy has been estimated at 1 in 1500, with a

range of 1 in 188 to 1 in 3821 pregnancies and an incidence rate of 0.026–0.53% (71,72,

74). There is no increase in either the incidence of urolithiasis or numbers of recurrences

of stones in pregnant women compared with nonpregnant women (75). Pregnant women

form the same types of stones same as nongravid stone formers (75,76)80–90% of stones

present clinically in the second or third trimester of pregnancy (76,77).

Pregnant women have marked hypercalciuria and an increased urinary supersatura-

tion ratio for calcium oxalate and brushite. Howarth et al. studied 1034 normal women

in the third trimester and found 20% excreted >350 mg of calcium in 24 h, which

exceeded the 95% limit for nonpregnant women (78). These investigators felt increased

calcium excretion was related to increased filtered load of calcium secondary to higher

GFR (78). In addition to increased GFR causing hypercalciuria, increases in levels of

1,25 vitamin D during gestation cause increases in the intestinal absorption of calcium,

bone mobilization, and hypercalciuria.

Hypercalciuria and supersaturation of urinary salts is accompanied by an increase in

inhibitors. Although the inhibitors citrate and magnesium are elevated in the urine

during pregnancy, they are not elevated proportionally to the increase in supersaturation

of stone constituents found in the urine (79). This “inhibitor gap” has given investigators

cause to search for other stone inhibiting substances. Pregnant women exhibit increased

production of the inhibitory glycoprotein Tamm–Horsfall protein which decreases crys-

tal aggregation and growth (67,81–83). Another glycoprotein inhibitor of calcium

oxalate lithiasis, nephrocalcin, has been found to increase significantly throughout

pregnancy which may counterbalance the hypercalciuria (82,83).

OTHER HORMONAL INFLUENCES

Other hormones not directly involved in calcium homeostasis or sexual function may

also play a limited role in urolithiasis. These hormones may include insulin, growth

hormone, thyroid hormone, glucocorticoids, and mineralocorticoids.

232 Schenkman and Henderson

Insulin

Insulin acts at the proximal tubule of the kidney to increase urinary calcium excretion.

Diabetes and glucose ingestion are associated with hypercalciuria (37,85,86). Iguchi and

associates showed that increases in plasma glucose levels following a glucose tolerance

test were similar in stone formers and controls. Urinary calcium excretion increased in

stone formers and controls in response to oral glucose, but the effect was greater in stone

patients than in the control subjects (86). Many investigators believe that diets high in

refined sugars are partially responsible for the high rates of stone formation seen in

Western countries (87–89).

Growth Hormone

Urolithiasis may affect 12–39% of patients with acromegaly (89–91). Animal studies

show no acute effects of growth hormone on urinary excretion of calcium or phosphate;

however patients with acromegaly and normal persons taking growth hormone exhibit

increased levels of urinary calcium and magnesium. In one study 72% of the patients

demonstrated hypercalciuria (89). In addition, growth hormone may affect calcium

balance by increasing renal calcitriol synthesis in a process mediated by insulin-like

growth factor- I.

Thryoid Hormone

Thyroid hormone’s renal effects include enhancing free water excretion, increasing

urinary calcium and magnesium excretion and increasing renal tubular absorption of

phosphate. Hyperthyroidism may cause hypercalcemia caused by a direct effect of thy-

roid hormone on bone resorption. Serum calcium may be elevated in 10–20% of patients

with hyperthyroidism. Increased filtered load of calcium, resulting from increased GFR

and mobilization of calcium from bones with suppression of PTH secretion, causes

hypercalciuria. Nephrocalcinosis and nephrolithiasis may result from this abnormal

calcium excretion (16,37,93).

Adrenocortical Hormones

The long-term administration of exogenous mineralocorticoid results in increased

levels of urinary calcium and magnesium in response to increased plasma volume.

Serum calcium remains stable, possibly because of secondary parathyroid hormone

secretion. Several case reports have documented nephrocalcinosis and nephrolithiasis

associated with mineralocorticoid excess. Treatment with sprionolactone reverses the

metabolic abnormalities and controls the nephrolithiasis (93,94).

Glucocorticoid administration has been associated with hypercalciuria and hyper-

magnesiuria. The bone demineralizing effects of glucocorticoids may lead to nephrocal-

cinosis and calcium lithiasis (16).

CONCLUSION

Hormonal effects play a role in most cases of stone disease. This role may range from

a direct role in the case of hyperparathyroidism to a more subtle role in men and aging

women. A significant amount of clinical and laboratory research will be needed to

illuminate the specific contribution of hormonal influences on nephrolithiasis.

Chapter 11 / Hormonal Influences on Nephrolithiasis 233

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