Cases reported "Nephrocalcinosis"

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1/14. nephrolithiasis during pregnancy secondary to primary hyperparathyroidism.

    nephrolithiasis secondary to primary hyperparathyroidism infrequently complicates pregnancy. It can cause severe maternal and fetal complications. We present a case of a pregnant woman with nephrolithiasis and primary hyperparathyroidism. We reviewed the management of nephrolithiasis due to primary hyperparathyroidism during pregnancy. We believe that early recognition and timely intervention can significantly reduce the incidence of complications.
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2/14. hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case.

    hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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3/14. Idiopathic congenital nonobstructive nephrolithiasis: a case report and review.

    We describe a case of congenital nephrolithiasis, which presented with hematuria at birth. No etiopathological factor could be determined for renal stone formation despite extensive investigation. There was a family history of renal stones in both maternal and paternal grandparents and of microscopic hematuria in the mother. There was no associated urinary flow obstruction and the hematuria remitted spontaneously. The infant was treated conservatively. The follow-up studies revealed persistence of renal stone but no hematuria. This case can be considered as idiopathic, or an early presentation of one of the rare genetic disorders associated with renal stones. Congenital nonobstructive nephrolithiasis has not been reported previously and should be considered as a cause of hematuria during this age.
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4/14. nephrocalcinosis in siblings--familial hypomagnesemia, hypercalciuria with nephrocalcinosis (FHHNC syndrome).

    Familial Hypomagnesemia, hypercalciuria with nephrocalcinosis is a rare autosomal recessive inherited disease associated with renal failure. Two girls born of consanguineous parentage aged 16 and 17 presented to us with renal failure, nephrocalcinosis and bone deformities. On evaluation they were found to have hypomagnesemia, hypercalciuria, increased fractional excretion of magnesium, hypocitraturia, renal failure and elevated PTH. Their parental screening was normal. There were no extra-renal features in them. One sibling had nephrolithiasis and the stone analysis revealed calcium phosphate stones. Both were treated with sodium bicarbonate, thiazides, calcitriol and calcium carbonate. They did not require dialysis during hospital stay. Both of them were treated conservatively. They are on regular outpatient follow up. The primary defect in this syndrome is impaired paracellular reabsorption of magnesium and calcium in the medullary thick ascending limb. Mutations in the PCLN-1gene which encodes for the tight junction protein paracellin -1 is identified as the underlying genetic defect. Ocular abnormalities and deafness are the commonly reported associations. End stage renal failure usually occurs in second to third decade. Renal transplantation is the definite treatment.
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5/14. Atypical features of primary hyperoxaluria in end-stage renal disease.

    Two case histories of patients with end-stage renal disease subsequently found to have primary hyperoxaluria are reported. In the setting of renal failure, the diagnosis is both difficult, due to diminished oxalate excretion, and important, because of frequent graft loss due to oxalate deposition after renal transplantation. The diagnosis was obtained by renal and bone biopsies. plasma oxalate levels were normal in one patient and the other patient presented with extensive cystic bone lesions. Primary hyperoxaluria should be considered whenever nephrocalcinosis and/or nephrolithiasis are associated with end-stage renal disease.
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6/14. nephrocalcinosis in sjogren's syndrome: a late sequela of renal tubular acidosis.

    sjogren's syndrome (SS) is an autoimmune exocrinopathy that develops into systemic autoimmune disease in 25% of patients, leading to general complications, one of which is kidney involvement. It presents mainly as interstitial nephritis, disclosed by hyposthenuria, distal renal tubular acidosis (RTA) and diabetes insipidus. We here describe five cases of SS with type-1 RTA (hyperchloraemic metabolic acidosis with an anion gap and alkaline urine pH) who developed nephrolithiasis, nephrocalcinosis and renal insufficiency. hypercalciuria due to acidosis was the main nephrocalcinosis-prone factor in four patients; four subjects displayed diminished renal concentrating capacity, and two had hypokalaemia.
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7/14. Hypocitraturic and hypercalciuric renal tubular acidosis with nephrocalcinosis in a 4-year-old boy.

    A 4-year-old boy suffering from hypocitraturic and hypercalciuric renal tubular acidosis with nephrolithiasis and nephrocalcinosis is reported. Renal function tests indicated that the patient had type 1 renal tubular acidosis. potassium citrate rather than potassium bicarbonate, sodium citrate or bicarbonate is the preferred treatment for stones in RTA-I.
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8/14. Piridoxilate-associated nephrocalcinosis: a new form of chronic oxalate nephropathy.

    Piridoxilate is an association of glyoxylic acid and pyridoxine in which pyridoxine is supposed to facilitate in vivo transformation of glyoxylic acid to glycine rather than to oxalic acid. However, it has recently been shown that long-term treatment with piridoxilate may result in overproduction of oxalic acid and in calcium oxalate nephrolithiasis. We report a patient in whom piridoxilate induced both oxalate nephrolithiasis and chronic oxalate nephropathy with renal insufficiency, an association that has not been previously described. Therefore, piridoxilate should be added to the list of chemicals responsible for chronic oxalate nephropathy.
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9/14. Radiolucent urinary calculus in a transplant patient: an unsuspected cause of ureteropelvic obstruction.

    The occurrence of nephrolithiasis and nephrocalcinosis in the patient who has undergone a renal transplant is rare and is usually related to parathyroid hypersecretion. A case is presented in which the patient had a radiolucent stone that arose as a result of the use of nonabsorbable sutures. It is clear that nonabsorbable sutures. It is clear that nonabsorbable sutures should be avoided in renal allotransplant recipients.
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10/14. Complete distal renal tubular acidosis in systemic lupus: clinical and laboratory findings.

    We report two patients with systemic lupus erythematosus (SLE) who were found to have complete (acidotic) distal renal tubular acidosis (DRTA). One patient had nephrocalcinosis and renal magnesium wasting with tetany; the other patient had nephrolithiasis and nephrotic syndrome secondary to membranous glomerulopathy. Both patients had decreased urinary citrate excretion but neither had hypercalciuria. We discuss the association of DRTA with immunologic disorders and the possible role of hypocitraturia in promoting renal calcification in these patients. We suggest that patients with renal calcification be evaluated for DRTA, and that patients found to have DRTA be further evaluated for signs, symptoms, and laboratory evidence of immunologic disorders.
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