1/41. magnesium deficiency in children with urolithiasis.In a group of 57 children with urolithiasis hypomagnesaemia was found in 15 cases (26.3%). All children but one with abnormally low serum magnesium levels had recurrent or bilateral nephrolithiasis or nephrocalcinosis. prevalence of hyperoxaluria and hypercalciuria, marked severity of the clinical features, abnormality of Ca metabolism and its responsiveness to MgO treatment were demonstrable in Mg deficiency.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
2/41. hypercalciuria preceding IgA nephropathy in a child with haematuria.We describe a child with isolated haematuria who was diagnosed and successfully treated for idiopathic hypercalciuria for 6 months, after which IgA nephropathy was demonstrated on renal biopsy performed due to the relapse of haematuria in spite of low calciuria levels. To our knowledge, this is the first case evaluated systematically in the literature shown to have IgA nephropathy while being followed up for idiopathic hypercalciuria.- - - - - - - - - - ranking = 2keywords = hypercalciuria (Clic here for more details about this article) |
3/41. Zonisamide - induced urinary lithiasis in patients with intractable epilepsy.We report here three patients with intractable epilepsy who developed urinary lithiasis during zonisamide (ZNS) treatment. abdominal pain due to left-sided hydronephrosis was the initial symptom in the first patient, and it was resolved after the excretion of a stone. The second patient, who had no specific symptoms, was found to have a thick sludge of calcium phosphate in the bladder when he suffered from aspiration pneumonia and dehydration. The third patient, who had a history of recurrent urinary obstruction, was also found to have a thick sludge of calcium oxalate in the bladder. The urinalysis of the three patients revealed alkaline urine and hypercalciuria. Although their urinary lithiasis was resolved by discontinuation of ZNS and supportive therapy, routine examination of urine parameters such as pH and sediments, and daily urine-output checks are thought to be necessary during treatment with ZNS, especially for patients who are bedridden for a long time and receive multiple antiepileptic drugs.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
4/41. Identification of two novel mutations in the CLCN5 gene in Japanese patients with familial idiopathic low molecular weight proteinuria (Japanese Dent's disease).Two Japanese patients, belonging to unrelated families, with idiopathic low-molecular-weight proteinuria (LMWP; Japanese Dent's disease) showed novel mutations of the gene encoding renal-specific chloride channel 5 (CLC-5). proteinuria was first noticed at the ages of 2 and 3 years in patients 1 and 2, respectively. During follow-up, marked increases in urinary ss(2)-microglobulin levels, hypercalciuria, and high levels of urinary excretion of growth hormone were observed in both patients. nephrocalcinosis was detected in patient 2. Renal biopsy specimens from both patients showed minimal alterations in glomeruli and tubulointerstitium, except for mild mesangial proliferation in patient 2. dna sequence analysis of the entire 2,238-bp coding region and exon-intron boundaries of the CLCN5 gene showed the presence of two novel mutations in exon 10, consisting of one missense mutation (I524K) in patient 1 and one nonsense mutation (R637X) in patient 2. dna analysis and measurement of urinary ss(2)-microglobulin levels in family members indicated an X-linked mode of inheritance in patient 1 and sporadic occurrence in patient 2. These results have expanded our understanding of the association between idiopathic LMWP (Japanese Dent's disease) and mutations of the CLCN5 gene.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
5/41. medullary sponge kidney.medullary sponge kidney is a benign asymptomatic developmental anomaly of the kidney mostly seen in adult females. Presentation in childhood is uncommon. urinary tract infection, nephrolithiasis, hematuria and hypercalciuria are the common complications. We report a eleven-year-old female child who presented with recurrent urinary tract infection and nephrolithiasis and was found to have bilateral medullary sponge kidney.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
6/41. Thiazide therapy for ACTH-induced hypercalciuria and nephrolithiasis.A one-year-old boy presented with hypercalciuria and nephrolithiasis following a course of ACTH therapy for infantile spasms. After a successful cystolithotripsy, therapy with chlorothiazide was followed by regression of the hypercalciuria within 42 months. Neither nephrolithiasis nor nephrocalcinosis recurred. Therapy with thiazides to prevent hypercalciuria caused by ACTH is proposed.- - - - - - - - - - ranking = 7keywords = hypercalciuria (Clic here for more details about this article) |
7/41. Studies of glucose turnover and renal function in an unusual case of hereditary fructose intolerance.Examination of glucose kinetics, pancreatic alpha and beta cell function, plasma lipids, urinary acidification and calcium excretion has been undertaken in a patient with hereditary fructose intolerance. This case was unusual as it was associated with insulin-requiring diabetes, type IV hyperlipemia, hypercalciuria and renal calculi. He also demonstrated the previously described fructose-induced defect of urine acidification. glucagon and c-peptide assays showed that the pancreatic alpha cells were stimulated by fructose and that the beta cells did not respond to fructose. It is not known whether the latter was due to his diabetes or to the lack of a beta cell response to this sugar. Primed 14C-glucose infusions were used for the first time to study nonsteady state glucose kinetics in man. They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. However, after the administration of sorbitol the plasma glucose concentration decreased because glucose production decreased. After the administration of sorbitol there was no change in the metabolic clearance of glucose. This reflects the lack of a peripheral insulin effect and is consistent with the lack of any measurable c-peptide. glucose utilization also decreased, but this decrease was less than the decrease in glucose production. Because the metabolic clearance of glucose remained unchanged, it was concluded that the change in glucose utilization was solely due to the decrease in glucose concentration. The absence of c-peptide in the plasma indicated that changes in glucose turnover were not related to any changes in endogenous plasma insulin. Furthermore, the plasma glucagon concentration increased and, hence, changes in this hormone could not account for the decrease in glucose production. Therefore, it was concluded that the sorbitol-induced decline in glucose production was due to a direct effect on hepatic metabolism.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
8/41. hypercalciuria and kidney calcifications in terminal 4q deletion syndrome: further evidence for a putative gene on 4q.We report a newborn girl with a de novo terminal 4q deletion (q31.3 --> qter) and a characteristic phenotype of minor facial anomalies, cleft palate, congenital heart defect, abnormalities of hands and feet, and postnatal onset of growth deficiency. Laboratory studies showed excessive urinary calcium excretion on standard milk formula and on oral calcium load. blood measurements of parathyroid hormone, calcitonin, bicarbonate, calcium, phosphorus, magnesium, sodium, chlorine, potassium, and urinary measurements of phosphorus, magnesium, sodium, chlorine, potassium were normal for age. At 2 months of life, ultrasonography showed kidney calcifications. Clinical and laboratory data support the diagnosis of absorptive hypercalciuria or abnormal regulation of calcium-sensing receptors in the renal tubules. The evidence of hypercalciuria and kidney calcifications associated with 4q terminal deletion strengthens the hypothesis that a putative gene for hypercalciuria is located on the terminal segment of chromosome 4q.- - - - - - - - - - ranking = 3keywords = hypercalciuria (Clic here for more details about this article) |
9/41. Recurrent calcium nephrolithiasis associated with primary aldosteronism.Typical manifestations of hyperaldosteronism include salt retention, hypokalemia, and metabolic alkalosis. However, a consequence infrequently recognized and described is hypocitraturia. In combination with hypercalciuria, aldosterone-induced hypocitraturia can trigger calcium nephrolithiasis. The authors report a case of an individual with primary hyperaldosteronism from an adrenal adenoma that resulted in hypocitraturia. The patient had severe recurrent renal calcium calculi that corrected with adrenalectomy. The clinical physiology of renal calcium and citrate handling in hyperaldosteronism is reviewed.- - - - - - - - - - ranking = 1keywords = hypercalciuria (Clic here for more details about this article) |
10/41. Rare presentation of Wilson's disease: a case report.A female presented with pain in left flank, detected to have bilateral renal calculi with deranged liver functions. On investigation found her to have Wilson's disease with hypercalciuria and incomplete distal renal tubular acidosis. Patient was started on penicillamine following which her hepatitis improved but hypercalciuria persisted after 10 weeks of follow up. The rarity of such presentation and literature review for the same is discussed.- - - - - - - - - - ranking = 2keywords = hypercalciuria (Clic here for more details about this article) |
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