The Relationship Between Urinary Calcium, Sodium, and Potassium
Excretion and the Role of Potassium in Treating Idiopathic Hypercalciuria
Alexies V. Osorio, MD, and Uri S. Alon, MD
ABSTRACT. Objectives. 1) To evaluate the relation-ships between urinary sodium (UNa), potassium (UK), and calcium (UCa) excretion in the pediatric population; and 2) to determine the effect of increasing potassium intake in patients with idiopathic hypercalciuria and in-vestigate whether this intervention can be offered as another mode of therapy in this patient population.
Design. Prospectively, we determined UNa, UK, UCa, and creatinine (Cr) concentrations in randomly collected urine samples from children on initial evaluation for urinary frequency, dysuria, hematuria, enuresis, or kid-ney stones to identify children with hypercalciuria.
Setting. The outpatient renal clinic of an academic hospital.
Participants. Twenty-three black children (13 girls and 10 boys) and 77 white children (44 girls and 33 boys) 3.92 to 16.67 years of age.
Interventions. Eleven children with hypercalciuria were given potassium supplementation or placed on a high-potassium diet for at least 2 weeks.
Outcome Measures. UNa to UK, UNa to Cr, UK to Cr, and UCa to Cr ratios were calculated from measured levels of urinary minerals. These were repeated in 11 hypercalciuric patients after 2 weeks of increased potas-sium intake.
Results. A total of 100 urine samples were analyzed. The UCa/Cr ratio in blacks 0.0460.06 (mean6standard deviation) was significantly lower than in whites 0.166 0.12. There were 21 hypercalciuric white children versus only 1 black child. Linear regression analysis revealed a positive direct correlation between UNa/Cr and UCa/Cr in all 100 subjects and in whites alone but not in blacks. An inverse relationship existed between UK/Cr and UCa/Cr in all subjects and in whites and showed a strong trend in blacks. A marked direct relationship was found between UNa/K and UCa/Cr in all subjects (r25.43) as well as in whites (r2 5 .59) and blacks (r2 5 .49). One black child and 10 white hypercalciuric children were treated with “extra” K for at least 2 weeks. The UNa/K decreased from 4.7362.28 to 1.9861.09, and the UCa/Cr decreased from 0.3160.10 to 0.1460.07, with resolution or improvement of the patients’ symptoms.
Conclusions. In our patient population with urinary symptoms, the UCa/Cr ratio in black children is lower and hypercalciuria less common than in white children. In both white and black populations, the UNa/K ratio had the strongest association with the UCa/Cr ratio,
in-dicating an opposing role of UNa and UK on the UCa/Cr ratio. Increased potassium intake was found to be bene-ficial for hypercalciuric children by decreasing the UNa/K ratio and, consequently, the UCa/Cr ratio. Pediatrics 1997;100:675– 681; calcium, diet, hypercalciuria, potassium, sodium.
ABBREVIATIONS. UCa/Cr, urinary calcium to creatinine ratio; UNa/K, urinary sodium to potassium ratio; UNa/Cr, urinary sodium to creatinine ratio; UK/Cr, urinary potassium to creati-nine ratio.
H
ypercalciuria during childhood is defined as.4 mg/kg/24 hours1–3 while on a regular
diet. Because of the difficulty of timed urine collection, the ratio of urinary calcium to creatinine (UCa/Cr) has been used extensively as a means for screening and diagnosis of hypercalciuria (UCa/ Cr.0.21 in mg/mg).1,4Approximately 2% to 5% of
children with hypercalciuria have renal stones1;
however, the more frequent clinical manifestations of hypercalciuria include dysuria, frequency, back and abdominal pain, enuresis, and hematuria.1,5,6
Initial management of hypercalciuric children con-sists of a high fluid intake and dietary salt restric-tion.1,6 The latter is based on the well-established
observations that dietary sodium is an important modulator of UCa excretion7–9 and that close
corre-lation exists between urinary sodium (UNa) and UCa excretion in 24-hour urine collections in both healthy adult subjects and patients who form renal stones.7–9
Despite the above interventions, a significant num-ber of these patients remain hypercalciuric, requiring the addition of a thiazide diuretic.6,9
Thiazide diuretics lower UCa excretion by increas-ing its reabsorption by the distal renal tubule. The hypocalciuric effect of thiazide therapy depends markedly on sodium intake, because it is fully ex-erted when combined with salt restriction and is blocked by excessive dietary sodium.9 Hence, the
prescription of thiazides does not free the patient from the need for maintaining a low-salt diet, a task with which many pediatric patients find it difficult to comply. Furthermore, treatment with thiazide di-uretics has been found to be associated with a rise in total serum cholesterol and in low-density lipopro-tein cholesterol.10
Calcium is the most important element in the for-mation of kidney stones,2,3,11 and UCa excretion
cor-relates directly with prevalence of renal stone dis-ease.2,3,11,12A recent epidemiologic study by Cirillo et
al12has shown that adults with a high random UNa From the Section of Pediatric Nephrology, Children’s Mercy Hospital,
University of Missouri at Kansas City, Missouri.
This work was presented in part at the Pediatric Academic Societies Annual Meeting, Washington, DC, May 6 –10, 1996.
Received for publication Dec 16, 1996; accepted Feb 20, 1997.
Reprint requests to (U.S.A.) Children’s Mercy Hospital, 2401 Gillham Rd, Kansas City, MO 64108.
to potassium (UK) ratio (UNa/K) caused by high sodium and/or low potassium excretion are at higher risk of developing urinary stone disease. This finding most likely reflects a relation between dietary sodium and potassium intake with hypercalciuria and urolithiasis. This hypothesis is based on the known effects of increased dietary sodium7,8and
de-creased dietary potassium13–15on UCa excretion and
the fact that UNa and UK excretion parallel their dietary intake.7,8,13–15
The purpose of our study was first to evaluate whether the interrelationships between urinary ex-cretion of sodium, potassium, and calcium in the pediatric population follow the pattern observed by Cirillo et al in adults.12 If such a relationship was
found to exist between UNa/K and UCa/Cr, we intended to examine whether intervention to in-crease UK excretion would affect UNa/K and con-sequently UCa/Cr ratios in children with hypercal-ciuria.
PATIENTS AND METHODS
From November 1994 to December 1995, we prospectively en-rolled in the study children and adolescents 4 to 18 years of age seen at the Children’s Kidney Center for evaluation of possible hypercalciuria (presenting with symptoms of dysuria, hematuria, enuresis, frequency) or kidney stones. Children with known kid-ney disorders or with secondary causes of hypercalciuria, or who were undergoing treatment with medications that affect UCa ex-cretion were excluded from the study.
Random urine specimens were collected from these children, who were on a nonrestricted diet during clinic visits in the early afternoon hours. The UNa and UK levels were measured by ion-specific electrodes using a Beckman (Beckman Instruments, Brea, CA) E4A electrolyte analyzer. Using the Gilford Impact 400E automated analyzer, the calcium concentration in the urine was measured by the cresolphthalein complexone spectrophotometric procedure, and the urine Cr was determined by kinetic Jaffe reaction. Ratios between UNa/Cr (mEq/mg), UK/Cr (mEq/mg), UCa/Cr (mg/mg), and UNa/K (mEq/mEq) were calculated for each subject.
Eleven children with idiopathic hypercalciuria (UCa/Cr ra-tio.0.21), all but one symptomatic (Table 1, patient 11), who were under our direct care were given potassium supplementation (K citrate, K gluconate, or KCl at 1 mEq/kg/day divided, b.i.d.) or placed on a high-potassium diet (Table 2). Urine chemistries in these patients were repeated after 2 to 4 weeks of therapy. In six of these children, blood chemistries were examined as well. No attempt was made to quantify dietary sodium, potassium, cal-cium, and fluid intake on any of the patients. All children were advised to increase fluid intake to about 1.5 times maintenance. Salt and calcium restrictions were not recommended during
po-tassium therapy. Compliance was verified verbally with the fam-ily at follow-up for children placed on a high-potassium diet.
Using Statmost for Windows (Datamost Corporation, Salt Lake City, UT),x2tests, Student’s unpaired and paired t tests
(two-tailed), and linear regression analyses were performed. A P value, .05 was regarded as significant. Data are presented as mean 6 standard deviation. The study was approved by the institutional review board.
RESULTS
At baseline, 100 urine samples were collected from 23 black and 77 white children. The median age of black children was 7.83 years (boys, 6.50 to 11.92 years; girls, 4.00 to 13.33 years) and of white children was 8.50 years (boys, 5.08 to 16.67 years; girls, 3.92 to
TABLE 1. Clinical Characteristics and Pre- and Post-potassium Supplementation Values of UNa/K and UCa/Cr Ratios in 11 Children With Idiopathic Hypercalciuria
Patient Age (y) Sex Race Symptoms UNa/K (mEq/mEq) UCa/Cr (mg/mg)
Pre Post Pre Post
1* 8.8 F C Frequency, urgency, abdominal pain 5.44 1.89 0.32 0.08
2* 8.9 M C Frequency, urgency, incontinence 4.88 1.14 0.24 0.12
3† 5.5 F C Recurrent UTI, bladder spasms, microhematuria 1.45 0.61 0.22 0.14
4‡ 12.3 M C Gross hematuria 2.99 2.77 0.25 0.05
5‡ 7.7 F C Dysuria, enuresis 5.33 2.32 0.50 0.12
6‡ 5.3 F C Microscopic hematuria 8.08 2.31 0.50 0.30
7‡ 9.9 F C Frequency 7.36 1.57 0.37 0.18
8‡ 13.3 F B Day/night enuresis 6.46 3.20 0.24 0.10
9‡ 5.2 M C Microscopic hematuria 2.09 1.13 0.28 0.09
10‡ 6.2 F C Abdominal pain, microhematuria, dysuria 6.00 4.10 0.25 0.16
11§ 8.0 M C Status postureteral stone 1.94 0.69 0.23 0.18
* Treated with K citrate; † K gluconate; ‡ KCl; § high K diet.
TABLE 2. High-potassium (Low-oxalate) Foods*
Serving
Fruits and fruit juices
Apricots 3 raw or 3 halves canned
Avocado 1/8 inch slice
Banana 1/2 small
Cantaloupe 1/4 small
Grapefruit juice 1/2 cup
Honeydew 1/4 cup
Kiwi 1 medium
Nectarine 1 medium
Orange 1 medium
Orange juice 1/2 cup
Pear raw 1 medium
Prune juice 1/2 cup
Raisins 1 tbs
Tangerine juice 1/2 cup
Tomato juice 1/2 cup
V-8 juice 1/2 cup
Vegetables
Broccoli 1 stalk
Brussel sprouts 5 pieces
Carrots 1 raw
Corn on the cob 4-inch ear Lettuce, romaine and butterhead 1/2 cup
Mushrooms 5 raw or 1/2 cup canned
Potato 1/2 cup
Squash 1/2 cup
Succotash 1/2 cup
Tomato 1/2 cup
Dairy
Cottage cheese 1 cup
Ice cream 1 cup
Milk 8 oz
Yogurt 8 oz
15.50 years) with no difference between the two groups. The distribution of boys/girls was similar in both groups: 10/13 in blacks and 33/44 in whites, respectively.
As shown in Fig 1, the UCa/Cr ratio was lower in blacks compared with whites (0.0460.06 vs 0.16 6 0.12; P,.001). Of the 22 hypercalciuric children, 21
were white and only 1 was black (P 5 .04). The
UNa/Cr correlated directly with UCa/Cr in all 100 subjects combined (P 5.016). The relationship held true also in whites alone (P5.030), but not in blacks alone (P5.166).
The UK/Cr had an inverse relationship with UCa/Cr in all subjects combined (P5.018), as well as in whites alone (P 5 .011), and showed a strong trend in blacks (P5 .059) (Fig 2).
A direct relationship was found between UNa/K and UCa/Cr in all subjects combined (r250.43, P,
.001) as well as in white (r250.59, P, .001) and in
black children (r250.49, P5.002) (Fig 3). There was
no difference in the UNa/K ratio between blacks and whites. Using a UNa/K ratio.4.5 as a cutoff value in predicting the occurrence of hypercalciuria in whites, its sensitivity was found to be 61.90% and its specificity 100%. The positive predictive value was 100% and the negative predictive value 87%. In all subjects combined, the sensitivity was 63.64% and specificity was 96.15%. The predictive value of a positive test was 82.35% and that of a negative test was 90.36%.
In the 11 children with hypercalciuria treated with potassium supplementation or a high-potas-sium diet, the UNa/K ratio decreased from 4.736 2.28 to 1.9861.09 (P5.003) (Fig 4). This decrease was primarily attributed to the increase in UK/Cr
ratio from 0.5360.36 to 1.036 0.47 (P, .01) at a time when the UNa/Cr ratio declined only slightly and insignificantly from 1.9261.22 to 1.7260.74. With treatment, UCa/Cr declined from 0.3160.10 to 0.14 6 0.07 (P , .001), and 10 of the children became normocalciuric (Table 1). None of the 6 children tested developed hyperkalemia (serum potassium range, 3.6 to 4.5 mEq/L; mean, 4.1 mEq/L) or other mineral or electrolyte abnormal-ities. Of the 10 symptomatic children, 9 became asymptomatic, and in 1 (patient 3) a satisfactory improvement was observed.
In two of the treated children (patients 2 and 10), discontinuation of potassium supplementation re-sulted in relapse of symptoms. UCa/Cr and UNa/K ratios in patient 2 became 0.25 and 4.05, respectively, and in patient 10, 0.37 and 4.12, respectively. Both children responded to reinstitution of potassium supplementation with resolution of their symptoms. UCa/Cr and UNa/K ratios in patient 2 became 0.06 and 2.47, respectively, and in patient 10, 0.06 and 2.80. In a third patient (patient 3), the family reported recurrence of symptoms whenever the child did not adhere to the high-potassium diet; however, no doc-umentation of urine electrolytes during these epi-sodes was made.
The last hypercalciuric patient who entered the study (patient 11) was started on a high-potassium diet from the beginning and four others (patients 1, 4, 6, and 9) who were started initially on a pharmaco-logic potassium preparation were later switched to the high-potassium diet. Three patients (patients 2, 3, and 10) were maintained on potassium supplemen-tation. A trial to switch patient 2 to the high-potas-sium diet was unsuccessful, because the child did not
tolerate it and complained of abdominal discomfort, and the parents of the two other patients elected to keep them on the potassium preparation. After up to 10 months of observation (mean, 5.57 months; range, 2 to 10 months), all eight patients who continued follow-up in our facility remained normocalciuric and asymptomatic.
DISCUSSION
Originally, idiopathic hypercalciuria was thought to be comprised of two entities, absorptive and renal (fasting) hypercalciuria, depending on whether the excessive renal loss of calcium is the result of pri-mary intestinal hyperabsorption of calcium or an Fig 2. Relationship between UK and UCa in 100 children with urinary symptoms.
impairment in the renal tubular reabsorption of cal-cium.16,17 Oral loading and deprivation tests have
been used to distinguish between children with renal and absorptive hypercalciuria.16,18 However, it has
become apparent that absorptive hypercalciuria and renal hypercalciuria may constitute a continuum rather than separate entities, representing a spectrum of a single disorder.1,3,11,16Consequently, in practical
terms the management of the child with idiopathic hypercalciuria of either type is the same without the necessity of defining the type of hypercalciuria.1,6,16
Therefore, in the present study, we did not attempt to differentiate between absorptive and renal hyper-calciuria.
Sodium intake is a main factor influencing urinary excretion of calcium. Daily excretion of calcium in the urine increases on average by 0.8 to 1.5 mmol/ day per 100 mmol/day increase in UNa excre-tion.7,13,20As with our observation (Fig 1), the
corre-lation between UCa and UNa excretion has been demonstrated previously in children by others.16,21,22
With increased salt intake, the coupling of UNa and UCa excretion results in an increase in UCa excre-tion. This leads to a decrease in serum calcium con-centration, stimulating increased secretion of para-thyroid hormone and, consequently, calcitriol. The latter augments intestinal calcium absorption, result-ing in increased UCa excretion.19,21
A few articles on adults23–25 had alluded to an
inverse relationship between UK and UCa excretion, as reported by the present investigators (Fig 2). An increase in dietary potassium reduces UCa excretion and causes calcium balance to become more positive, suggesting that potassium either directly or
indi-rectly promotes renal calcium retention and inhibits net bone resorption.13,15,23,26 Another subtle effect of
potassium is to cause renal phosphate retention, which inhibits renal synthesis of calcitriol and, sub-sequently, intestinal calcium absorption.27 The only
previous investigation of the correlation between UK and UCa in children also found inverse correlation between the two, but concluded that it is UCa con-centration that affects UK expression.23The authors,
however, did not examine the effect of induced changes in UK or UCa.
Our finding in children of a linear correlation be-tween UNa/K and UCa/Cr ratios (Fig 3) confirmed the similar observation in adults.12 Compared with
either UNa/Cr (Fig 1) or UK/Cr (Fig 2) alone, the UNa/K ratio had the strongest relationship with UCa/Cr. Whether this is the result of physiologic factors or the arithmetic of sodium and potassium acting in opposite directions remains to be eluci-dated. The fact that in our black population, data demonstrated only a trend for correlation between UNa/Cr and UCa/Cr ratio and between UK/Cr and UCa/Cr ratio most likely can be attributed to the small sample size.
The normal UNa/K ratio in children generally have been reported as ,2.28 Indeed, in our patient
dietary or physiologic factors. The possible genetic role is demonstrated by the black population studied by us, in which hypercalciuria was found to be un-common even though the UNa/K ratio was similar to that of whites (Fig 3). This observation is consis-tent with our previous experience6and the reports by
others of the rarity of kidney stone disease in blacks29
and the finding that bone mineral density is greater in blacks than in whites.30At least two other studies
suggested a lower UCa/Cr in black children than in white children.31,32 These phenomena might be
re-lated to differences in vitamin D metabolites, recep-tors, rate of calcium absorption, or other factors re-lated to genetic make-up.33
It is well established that UCa excretion is affected by the individual’s acid-base homeostasis. Metabolic acidosis increases calciuria, whereas alkali treatment decreases calcium excretion.34,35Therefore, to exclude
the possible effect of the anion in the supplemental potassium salts on UCa excretion, we used different potassium preparations in a stepwise manner. After the first three patients received an alkali salt (citrate or gluconate), the next seven children received KCl. The hypocalciuric effect was well preserved in those seven children treated with KCl (Table 1). This study was not designed to investigate the mechanism by which potassium supplementation decreased the UCa/Cr ratio; however, analysis of pre- and post-treatment UNa/Cr and UK/Cr ratios revealed that whereas the change in the UNa/Cr ratio was insig-nificant, the UK/Cr ratio doubled. These findings of the therapeutic effect of potassium per se initiated dietary modifications, a more desired intervention than the use of pharmacologic agents. A diet rich in potassium is basically a “healthy” diet (Table 2) com-posed largely of fruits, vegetables, and milk (but that also permits ice cream and yogurt). In cases in which a high-potassium diet fails, potassium citrate may be the preferred preparation over KCl, because citrate provides other advantages in treating hypercalciuria such as increased UCa solubility.6,22As we and others
have observed, the treatment of hypercalciuria by potassium preparations was not associated with changes in serum chemistry.23
In summary, the present investigation demon-strated that in our area, UCa/Cr is generally lower and hypercalciuria uncommon in black children compared with white children. The strength of the correlation between UNa/K and UCa/Cr ratios ex-ceeded the direct correlation between UNa/Cr and UCa/Cr and the inverse correlation between UK/Cr and UCa/Cr. Potassium supplementation of all types had a beneficial effect on UCa/Cr ratio and patients’ symptoms. Potassium supplementation and a high-potassium diet may play an important role in the management of hypercalciuria. A randomized, controlled study comparing the efficacy of different modes of therapy such as a low-salt diet, thiazide therapy, and potassium therapy would be worth-while. Similarly, the mechanism by which potassium supplementation operates needs to be further inves-tigated.
ACKNOWLEDGMENTS
This work was supported by the Sam and Helen Kaplan Re-search Fund in Pediatric Nephrology.
We thank Nancy Wilson, MT (ASCP), and Sylvia DiMaggio, LT II, for their expert laboratory assistance, and Mrs Tammy Johnson for her valuable secretarial support.
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“The process of scientific discovery is, in effect, a continuous flight from wonder.”
DOI: 10.1542/peds.100.4.675
1997;100;675
Pediatrics
Alexies V. Osorio and Uri S. Alon
and the Role of Potassium in Treating Idiopathic Hypercalciuria
The Relationship Between Urinary Calcium, Sodium, and Potassium Excretion
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DOI: 10.1542/peds.100.4.675
1997;100;675
Pediatrics
Alexies V. Osorio and Uri S. Alon
and the Role of Potassium in Treating Idiopathic Hypercalciuria
The Relationship Between Urinary Calcium, Sodium, and Potassium Excretion
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