Cases reported "Urinary Calculi"

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1/14. hypercalciuria and urolithiasis in a case of costello syndrome.

    costello syndrome is characterized by postnatal growth deficiency, mental retardation, curly hair, coarse characteristic face, and loose skin of hands and feet. patients with this syndrome have a high incidence of cardiac involvement, including arrhythmia, atrial septal defect, and hypertrophic cardiomyopathy. We report a 16-year-old adolescent female with costello syndrome who presents with hypercalciuria and urolithiasis.
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2/14. Recurrent abdominal and flank pain in children with idiopathic hypercalciuria.

    OBJECTIVE: To evaluate the role of idiopathic hypercalciuria (IH) as a cause of recurrent abdominal pain (RAP) in children. patients AND methods: We retrospectively reviewed the medical records of 124 children referred for various complaints who had 24-h urine calcium excretion greater than 2 mg/kg/d or random urine calcium-creatinine ratio greater than 0.18 mg/mg. RESULTS: Fifty-two children with various clinical complaints had RAP or flank pain. These comprised of 22 males and 30 females, 9 mo to 15.9 y of age, mean 6.7 /- 3.5 y. A family history of urolithiasis was present in 50% of all the children. Only 6 of the 52 children with abdominal pain had renal stones. In addition to abdominal pain, 27 children had hematuria and 10 had urinary incontinence. Mild metabolic acidosis was present in three children, parathyroid hormone activity elevated in two and serum vitamin d activity was increased in nine. All children were treated with increased fluid intake and a reduction in dietary sodium and oxalate and some required treatment with thiazide and antispasmodics. Forty-five cases responded to treatment, 5 failed to improve from therapy, and 2, which were not followed up as patients, were not available. CONCLUSION: We describe 52 children with RAP or back pain due to IH and recommend that IH be considered in the differential diagnosis of RAP in childhood.
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3/14. urolithiasis and primary parathyroid adenoma: report of one case.

    A 12-year-old girl was admitted to ward because of persistent left flank pain, vomiting, and hematuria. A stone was located at the ureteropelvic junction of the left kidney, as determined by means of abdominal sonography. Metabolic investigation for a renal stone revealed that she had hypercalcemia, hypophosphatemia, and hypercalciuria. hyperparathyroidism was diagnosed based on the hypercalcemia and inappropriately elevated serum parathyroid hormone level. A parathyroid adenoma was successfully diagnosed by using thallium/technetium subtraction parathyroid scanning. Extracorporeal shock wave lithotripsy was performed to treat the renal stone, and the parathyroid adenoma was successfully removed. The patient's postoperative course was uneventful. This case is presented because urolithiasis and hyperparathyroidism are rare in children. Metabolic evaluation is mandatory in children with a renal stone. Further investigation for the hyperparathyroidism should be performed if hypercalcemia associated with hypercalciuria is documented.
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4/14. Recurrent vesical calculi, hypercalciuria, and biochemical evidence of increased bone resorption in an adult male with paraplegia due to spinal cord injury: is there a role for intermittent oral disodium etidronate therapy for prevention of calcium phosphate bladder stones?

    STUDY DESIGN: Clinical case report with comments by colleagues from sweden, poland, spain, brazil, japan, belgium and switzerland. OBJECTIVES: To discuss the role of disodium etidronate therapy for prevention of calcium phosphate vesical calculi in persons with spinal cord injury, who have hypercalciuria and biochemical evidence of increased bone resorption. SETTING: Regional spinal injuries Centre, Southport, UK. methods: A 21-year-old male sustained paraplegia (T-10; asia scale: A) in a road traffic accident in June 2001. He had an indwelling urethral catheter until the end of August 2001, when he started self-catheterisation. He developed bladder stones and electrohydraulic lithotripsy (EHL) was performed in May 2002. All stone fragments were removed. recurrence of vesical calculi was noted in October 2002. These stones were fragmented by lithoclast lithotripsy in two sessions, in December 2002 and February 2003; all stone fragments were removed at the end of the second session. This patient reverted to indwelling catheter drainage when vesical calculi recurred. In September 2003, X-ray of the abdomen showed recurrence of vesical calculi. By February 2004, the stones had increased in size and number. EHL of vesical calculi was again performed in April 2004. Complete clearance was achieved. RESULTS: A 24-h urinalysis detected hypercalciuria--18.7 mmol/day (reference range: 2.5-7.5). Biochemical analysis of vesical calculus revealed calcium phosphate (85%) and magnesium ammonium phosphate (15%). plasma C-terminal telopeptide (CTX) was increased - 1.06 ng/ml (reference range: 0.1-0.5 ng/ml). Free deoxypyridinoline/creatinine ratio (fDPD/Cr) in urine was also increased - 20.2 (reference range: 2.3-5.4). In April 2004, this patient was prescribed disodium etidronate 400 mg day. Nearly 3 months after commencing therapy with etidronate, plasma CTX decreased to 0.87 ng/ml. fDPD/Cr in urine also decreased to 12.4. After 4 months of etidronate therapy, 24-h urinary calcium excretion had decreased to 6.1 mmol/day. CONCLUSION: Etidronate (400 mg daily) is a very effective inhibitor of calcium phosphate crystallisation. Etidronate decreased urinary excretion of calcium, an important factor in prevention of calcium phosphate bladder stones. Etidronate therapy is not a substitute for other well-established methods for prevention of vesical calculi in spinal cord injury patients, for example, large fluid intake, avoiding long-term catheter drainage. Intermittent therapy with etidronate may be considered in selected patients, in whom hypercalciuria persists after instituting nonpharmacological therapy for an adequate period, for example, early mobilisation, weight-bearing exercises, and functional electrical stimulation. However, possible side effects of etidronate, and the fact that etidronate is not licensed in United Kingdom for prevention of urolithiasis, should be borne in mind.
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5/14. An unusual patient with hypercalciuria, recurrent nephrolithiasis, hypomagnesemia and G227R mutation of Paracellin-1. An unusual patient with hypercalciuria and hypomagnesemia unresponsive to thiazide diuretics.

    A 19-year-old female patient with hypercalciuria and recurrent nephrolithiasis/urinary tract infection unresponsive to thiazide type diuretics is presented. The patient first experienced nephrolithiasis at the age of 4 years. Afterwards, recurrent passages of stones and urinary tract infection occurred. On diagnostic evaluation at the age of 19 years, she also had hypocitraturia and hypomagnesemia. Her serum calcium concentrations were near the lower limit of normal (8.5-8.8 mg/dl; normal range: 8.5-10.5), her serum magnesium concentrations were 1.15-1.24 mg/dl (normal range: 1.4-2.5) and urinary calcium excretion was 900 mg/24 h. PTH concentrations were increased (110-156 pg/ml; normal range: 10-65). We tried to treat the patient with hydrochlorothiazide at a dose of 50 mg/day. During treatment with thiazide diuretics, PTH concentration remained high and the patient had recurrent urinary tract infections and passages of stones. serum magnesium concentration did not normalize even under the parenteral magnesium infusion. Her mother had a history of nephrolithiasis 20 years ago. Severe hypomagnesemia in association with hypercalciuria/urinary stones is reported as a rare autosomal recessive disorder caused by impaired reabsorption of magnesium and calcium in the thick assending limp of Henle's loop. Recent studies showed that mutations in the CLDN16 gene encoding paracellin-1 cause the disorder. In exon 4, a homozygous nucleotide exchange (G679C) was identified for the patient. This results in a point mutation at position Glycine227, which is replaced by an arginine residue (G227R). The mother was heterozygous for this mutation. G227 is located in the fourth transmembrane domain and is highly conserved in the claudin gene family. This case indicates the pathogenetic role of paracellin-1 mutation in familial hypomagnesemia with hypercalciuria and nephrocalcinosis and further underlines the risk of stone formation in heterozygous mutation carriers.
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6/14. Occasional urinary tract infections and urinary depletion effect mask RTA and carbonate-apatite formation in a strong urinary stone former.

    We report on a female patient with severe bilateral urolithiasis. A once-off stone analysis performed in the past revealed Mg-phosphate. Occasional UTIs were considered to be the sole cause of stone formation. To date, this assumption had not been checked thoroughly, while stone formation in the patient steadily increased. An inpatient metabolic and analytical work up was performed and stone-growth related urinary alteration was taken into account in urinalysis interpretation. No UTI. NH4Cl-loading test indicated RTA. CT revealed calculi in both kidneys. Carbonate-apatite (CAP) dominates stone composition. Computed urinary composition proximal to stones indicates hypercalciuria. In this patient, occasional UTIs (pH) masked the causes of urolithiasis. Lack of updated stone analysis (CAP), metabolic work up (RTA) and improved urinalysis interpretation (hypercalciuria) concealed the true causes of stone formation.
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7/14. Irritability and dysuria in infants with idiopathic hypercalciuria.

    Idiopathic hypercalciuria (IH) is being diagnosed with increasing frequency in the pediatric population and occurs in approximately 2.9-6.2% of normal children. The majority of children with IH are asymptomatic; however, the most common clinical presentation is that of isolated hematuria (gross or microscopic). The prevalence, presentation and clinical course of IH is less well established in infants. We have recently seen two young infants with IH who had dysuria on presentation. Their hypercalciuria was difficult to manage and required frequent manipulations of drug therapy and diet restrictions. These cases emphasize the importance of evaluating infants with dysuria and irritability for IH, even in the absence of hematuria. Further studies are needed to establish the prevalence and classical presentation of IH in this population, and to determine the necessary duration of therapy.
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8/14. An acromegalic patient with recurrent urolithiasis.

    A 52-year-old man with an acromegalic appearance of prolonged duration suffered abdominal colic attacks and hematuria during the middle of the course of the disease. The patient was diagnosed as having urolithiasis caused by increased urinary calcium. The calcium metabolic disorder was not considered to be due to hyperparathyroidism because serum calcium and PTH levels were within the normal range and no abnormality was observed in a parathyroidal scintigraph. The serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels (55.0 and 73.0 pg/ml) were higher than the normal range (27.2-53.8 pg/ml). A selective adenomectomy by the transsphenoidal route (Hardy's method) was performed, resulting in an improvement in the hypercalciuria and urolithiasis, and a decrease in the levels of serum 1,25-(OH)2D (23.0 and 23.0 pg/ml). These findings suggest that GH may promote the activation of vitamin d in the kidney in acromegaly, resulting in an acceleration of calcium absorption in the intestine through the action of activated vitamin d and the induction of increased urinary calcium excretion by the urinary excretion of excessive blood calcium.
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9/14. Familial renal hypouricaemia: two additional cases with uric acid lithiasis.

    Two families are reported affected with hereditary renal hypouricaemia associated with uric acid lithiasis. The propositi of both families were found also to have hyperabsorptive hypercalciuria. Based on the study of the effect of pyrazinamide and probenecid on uric acid excretion in both propositi, it is suggested that the defect in uric acid reabsorption is most probably at the pre-secretory site.
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10/14. Pitfalls in parathyroid evaluation in patients with calcium urolithiasis.

    Primary hyperparathyroidism is a major cause of calcium urolithiasis and is easily recognised when it is classically manifested. However, subtle presentations of primary hyperparathyroidism may cause confusion with other causes of calcium stone disease or cause diagnostic difficulty. Several pitfalls of parathyroid evaluation and treatment are illustrated by four cases of calcium urolithiasis. Cases 1 and 2 represent ineffective or useless parathyroid surgery rendered for renal hypercalciuria and absorptive hypercalciuria, respectively. Cases 3 and 4 had mild or intermittent hypercalcaemia. The correct diagnosis of primary hyperparathyroidism was made in Case 3 by parathyroid venous sampling and bone densitometry. In Case 4, the thiazide provocative test was used to establish the diagnosis of primary hyperparathyroidism.
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