PEDIATRICS Vol. 104 No. 3 September 1999, pp. 578-579

Too Little Water Intake Causing Nephrolithiasis, Revealed by Too Much Water!

To the Editor.

In the western world children are generally spared from renal stone disease. However, metabolic diseases, such as primary cystinuria, hyperoxaluria, and renal tubular acidosis, are examples of rare causes of childhood nephrolithiasis seen worldwide. We wish to report an even rarer combination of factors leading to renal stones in a typical adolescent girl.

A 17-year-old Italian girl was followed in our pediatric nephrology outpatient clinic with corticosteroid sensitive minimal change nephrotic syndrome (NS) since 1990. The initial treatment consisted of predisolone in a daily dose of 2 mg/kg for approximately 2 months. Six months later additional corticosteroid treatment was needed for a full-blown relapse of her NS. On remission she was kept for a prolonged period on an every-other-day dose (6 mg) of prednisone.

This good-looking young girl was obviously concerned about her physical appearance and the possible adverse influence of long-term corticosteroid treatment. As it turned out, she had no physical signs or symptoms of continuous alternate-day corticosteroid treatment. Nevertheless, she reacted with what seems to be a healthy form of reduction in food intake (mild, "controlled" anorexia).

On a recent follow-up visit she complained of unexplained, vague abdominal pain, orthostatic hypotension, and admitted to not having had her menstrual period for approximately 4 months. She lost 3 kg in weight during the last months (height: 158 cm, percentile 10-25); BW: 46 kg, percentile 3-10). Because the physical examination was within normal limits, a gynecologic ultrasonography examination was ordered. As usual with such an examination, she was asked to drink at least 1 liter of fluids to fill her bladder for better ultrasonographic contrast. Shortly afterwards she had a typical left-sided renal colic. No gynecologic abnormality was detected, but several stones were found in the lower part of the left ureter. They were later removed endoscopically because extracorporeal lithotripsy was unsuccessful. The stones consisted of calcium-oxalate. An intravenous urographic examination showed a normal urinary tract.

The cause of the renal stones was not immediately obvious. The urinary calcium/creatinine and uric acid/creatinine ratios were normal. In going over her past hospital chart, we, however, suddenly realized (the famed retrospectoscope!) that we had overlooked the fact that for a long period of time she repeatedly had presented with maximally concentrated urines, as evidenced by the finding of urinary creatinine concentrations of 20 000-30 000 µmol/L (226-339 mg/dL), once even 31 060 µmol/L (351 mg/dL) (normal: usually below 12 000 µmol/L, 136 mg/dL) in the second morning urine specimen. Urinary creatinine had been measured to quantitate and standardize urinary protein excretion (U-proteine/creatinine) in the follow-up of NS. This was a case of self-induced chronic dehydration. It now turned out that ES had not only reduced her calorie but probably even more her fluid intake. It thus seemed that the nephrolithiasis was caused not by an abnormal urinary excretion of certain metabolites but by secondary hypersaturation of those metabolites (calcium and oxalate).

The incidence of nephrolithiasis and nephrocalcinosis is known to be increased in NS though still extremely rare, certainly in childhood. Most often the nephrolithiasis in this setting is attributable to hypercalciuria after corticosteroid administration. The latter can cause volume expansion, a rise in renal blood flow, and glomerular filtration with increased urinary excretion of sodium, calcium, and magnesium.¹ No evidence for this course of events was found in our patient. Chronic dehydration sometimes leads to nephrolithiasis, especially uric acid stones.² This probably played an important role in our case. Severe anorexia is known to alter calcium metabolism with decreased oral calcium intake, low estrogene levels, altered vitamin D metabolism, and high levels of serum cortisol. This may lead to osteoporosis and/or fractures.^3,4 Studies on urinary calcium excretion in anorexic patients are controversial.^3,5 Only two previous studies report nephrolithiasis in women with eating disorders.^5,6 This report is probably the third.

The case mentioned above is instructive, be it only by drawing attention to the need to carefully follow urinary concentration indices (easily done and relatively cheap) in young girls with a tendency towards anorexia.

F. Cachat, MD and J-P. Guignard, MD
Department of Pediatrics
Pediatric Nephrology
University Hospital
1011 Lausanne, Switzerland

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