to the editor: A 37-year-old black woman with poorly controlled type 1 diabetes and a history of urinary tract infections (UTIs) presented with a three-week history of increasing sharp right flank pain, tactile fever, chills, nausea, anorexia, and a single episode of hematuria. She denied dysuria, frequency, urgency, vomiting, or abdominal pain. Four days earlier, she had been placed on trimethoprim-sulfamethoxazole for a UTI at another hospital. Her past surgeries included tubal ligation, three cesarean sections, and removal of an ectopic pregnancy. Her medical history included hypertension, iron deficiency anemia, depression, and hypercholesterolemia.

Six weeks before admission, she was treated with ciprofloxacin for a UTI by her personal physician; however, urine culture ultimately grew group B streptococcus (GBS) not sensitive to ciprofloxacin. Initial follow-up with her physician indicated she was improving.

Physical examination revealed a slender, uncomfortable woman. Her pulse was 114 and blood pressure was 142/91 mm Hg. She exhibited pale mucosa and a soft cardiac flow murmur, a benign abdominal examination, but significant right flank tenderness. Pelvic examination and wet preparation revealed yeast and trichomonal vaginitis. A bilateral distal peripheral neuropathy was present.

White blood cell count was 10,000 per mm3 (10 X 109 per L), with a differential of 73 percent neutrophils, 10 percent lymphocytes, and 16 percent monocytes; hemoglobin level, 8.6 g per dL (86 g per L); and platelet count, 272 X 103 per mm3 (240 X 109 per L). Urinalysis revealed glucosuria, mild proteinuria, excretion of six to 10 red blood cells and one to five white blood cells per high-powered field, with negative leukocyte esterase and nitrate. Chemistry panel was normal except for a glucose level of 317 mg per dL (17.6 mmol per L). Hemoglobin A1c was 16.3 percent.

A computed tomography scan revealed a 4- to 6-cm right perinephric abscess and nonspecific enlargement of both kidneys. This patient recovered with percutaneous drainage of the abscess and intravenous antibiotics directed against GBS, which grew from the abscess drainage.

GBS is a cause of fatal puerperal sepsis. In addition to colonization of the pregnant female genital tract with the risk of early or late onset of neonatal sepsis, GBS causes approximately 2 percent of cystitis, pyelonephritis, and nongonococcal urethritis in adults. Other invasive GBS infections include pneumonia, endocarditis, arthritis, osteomyelitis, skin and soft tissue infections, and, rarely, unusual abscesses and device-related infections.1 These illnesses are more common in blacks and elderly persons.

One report2 describes a 17-year-old black girl with poorly controlled diabetes mellitus and duplication of her upper right ureter- who exhibited signs and symptoms similar to our patient. There also have been case reports of GBS perinephric abscess in a 47-year-old woman,3 a young adult man with diabetes,4 a male newborn,5 and a 61-year-old woman with diabetes who was treated for renal abscess caused by "beta-hemolytic streptococcus."6

GBS may cause perinephric abscess and other types of invasive infections, particularly in persons with underlying medical problems. It is important that this organism be treated with antibiotics active against GBS when found to be the etiologic agent of UTI.

DENNIS J. BAUMGARDNER, M.D.
Department of Family Medicine
University of Wisconsin Medical School
Milwaukee Clinical Campus
Aurora Health Care, Inc.
2801 W. Kinnickinnic River Pkwy., Ste. 155
Milwaukee, WI 53215

REFERENCES

1. Edwards MS, Baker CJ. Streptococcus agalactiae (Group B Streptococcus). In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and practice of infectious diseases. 5th ed. Philadelphia: Churchill Livingston, 2000:2156-67.

2. Woods CR, Edwards MS. Renal abscess caused by group B Streptococcus. Clin Infect Dis 1994; 18:662-3.

3. Ishizu K, Yamaguchi S, Naito K. A case of multiloculated retroperitoneal abscess successfully treated by percutaneous drainage with a Malecot catheter [in Japanese]. Hinyokika Kiyo 1999;45:103-5.

4. Jernelius H, Tollig H. Renal abscess caused by Streptococcus group B [in Swedish]. Lakartidningen 1982;79:3832.

5. Walker KM, Coyer WF. Suprarenal abscess due to group B streptococcus. J Pediatr 1979;94:970-1.

6. Morse FP 3d, Bennett AH. Unusual renal infections. Urology 1973;2:405-8.

Hypercalcemia in Infants Williams syndrome Autosomal recessive hypophosphatasia Secondary hyperparathyroidism from maternal hypocalcemia Blue diaper syndrome Jansen metaphyseal chondrodysplasia Subcutaneous fat necrosis Dietary phosphate deficiency

to the editor: I read with interest the article, "A Practical Approach to Hypercalcemia,"1 in the May 1, 2003, issue of American Family Physician. In addition to the causes of hypercalcemia that were listed in the article, family physicians who take care of infants also may want to consider other etiologies (see accompanying table).2

I also would be interested to know whether the authors think that substituting a spot urine calcium/creatinine ratio for a 24-hour urine calcium level is acceptable for evaluation of these infants. Timed urine collections can be difficult, especially in children.

JAMES E. SPRINGATE, M.D.
251 Old Lyme Dr.
Amherst, N.Y. 14221

REFERENCES

1. Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician 2003;67:1959-66.