Cases reported "Nephrocalcinosis"

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1/7. Hypomagnesemia due to renal disease of unknown etiology.

    A young man, investigated because of tetanic convulsions and arthritic pains, was shown to have hypomagnesemia, hypermagnesuria, hypokalemia, hypercalciuria, progressive nephrocalcinosis and chondrocalcinosis. In this syndrome, renal function was normal except for the abnormal excretion of electrolytes. Renal sodium conservation was normal. light and electron microscopic studies of renal biopsy specimens showed the presence of several abnormal tubules. Immunofluorescent staining showed deposits of immunoglobulins in the glomeruli and tubules. magnesium therapy was started under balance study conditions and resulted in decreased calciuria and complete remission of subjective symptoms. The progression of nephrocalcinosis was halted, and there was some decrease in the intra-articular calcium deposits after two years of continuous oral magnesium therapy. The administration of spironolactone decreased urinary magnesium but did not normalize it, whereas triamterene administration was without effect in this respect. The results of the morphologic and electrolyte balance studies are discussed. The patient was found to exhibit several features which have not been described before in connection with hypomagnesemia of unknown origin.
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2/7. The syndrome of renal tubular acidosis with nerve deafness.

    Two brothers with renal tubular acidosis and nerve deafness are described. Studies of the physiopathological characteristics of the renal acidification defect show that the defect is limited to the distal tubule. Renal tubular acidosis with nerve deafness is a distinct nosologic entity that is determined by an autosomal recessive trait.
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3/7. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing.

    nephrocalcinosis is a chronic tubulointerstitial nephropathy characterized by tubular calcium phosphate deposition and slowly progressive renal insufficiency. We report a novel association of acute nephrocalcinosis and acute renal failure (ARF) with colonoscopy preceded by a bowel-cleansing regimen consisting of oral sodium phosphate solution (OSPS). A cohort of 5 patients (mean age, 69.2 years) had normal renal function (mean serum creatininem 0.9 mg/dL) before colonoscopy and presented with ARF (mean serum creatinine, 4.9 mg/dL) from 3 days to 2 months postcolonoscopy. Past medical history included hypertension in all 5 patients. Medications included an angiotensin-converting enzyme (ACE) inhibitor (ACE-I) or angiotensin receptor blocker (ARB) in 4 patients and diuretics in 2 patients. In all patients, colonoscopy was preceded by bowel cleansing with OSPS; OSPS was contraindicated in a single patient with hyperparathyroidism and was used at excessive doses in another. Renal biopsy specimens obtained from all 5 patients revealed diffuse tubular injury and abundant tubular deposition of calcium phosphate. Although the tubular injury involved all tubular segments, lectin and immunohistochemical staining disclosed calcium phosphate deposition confined to distal tubules and collecting ducts. At a mean of 5.8 weeks of postbiopsy follow-up, renal function was unchanged in 4 patients and mildly improved in 1 patient. We conclude that acute nephrocalcinosis is a seemingly rare complication of bowel cleansing with OSPS. The pathophysiology of acute nephrocalcinosis after treatment with OSPS likely involves transient hyperphosphatemia; volume depletion exacerbated by intercurrent ACE-I, ARB, and diuretic use; and elevated distal tubular phosphate and calcium concentrations. Greater awareness of this entity is needed to identify potential risk factors.
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4/7. Renal failure and nephrocalcinosis associated with oral sodium phosphate bowel cleansing: clinical patterns and renal biopsy findings.

    Acute renal failure (ARF) is rarely reported after bowel preparation with sodium phosphate. We report a patient with mild crohn disease (in remission), without history of renal disease, and with normal baseline renal function, who developed ARF 14 days after bowel preparation for colonoscopy with oral sodium phosphate. A renal biopsy showed multifocal calcium phosphate deposition in the renal tubules against a background of diffuse chronic tubulointerstitial injury. review of the literature suggested 2 distinct patterns of ARF in the context of sodium phosphate bowel cleansing. One pattern is characterized by ARF, which develops a few hours or days after sodium phosphate administration, as a component of a systemic syndrome associated with severe hyperphosphatemia and hypocalcemia. Correction of these electrolyte abnormalities was frequently associated with rapid recovery of renal function. The cause of ARF in this context was not clear because the favorable outcome negated the need for renal biopsy. In the second pattern, exemplified by the current patient, ARF was identified incidentally. These patients did not have any features of an acute syndrome immediately after sodium phosphate administration and presented much later (usually weeks) with mild, nonspecific symptoms. At the time of presentation, the serum calcium and phosphate levels were normal. The renal biopsies in each of these patients showed nephrocalcinosis as the possible cause of ARF. The renal failure improved at least partially in most of these patients, but persisted in rare cases.
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5/7. hypokalemia with nephrocalcinosis: a variant of Bartter's syndrome.

    A 28-year-old male presented with profound hypokalemia and was found to have a variant of Bartter's syndrome with nephrocalcinosis, hypercalciuria, normal distal fractional reabsorption of chloride and normal sodium delivery to the distal tubule.
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6/7. medullary sponge kidney associated with congenital hemihypertrophy.

    medullary sponge kidney is a developmental disorder characterized by ectatic and cystic malformation of the collecting ducts and tubules. Clinical manifestations include urinary tract infections, renal stones, and hematuria. It can be associated with other developmental disorders. A case of medullary sponge kidney associated with congenital hemihypertrophy, complicated by nephrocalcinosis and nephrolithiasis, is reported here.
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7/7. Medullary nephrocalcinosis associated with vesicoureteral reflux.

    A case of medullary nephrocalcinosis developing in the course of vesicoureteral reflux is described. It is suggested that the probable mechanism of nephrocalcinosis was the stagnation of urine in collecting tubules favouring precipitation of calcium salts.
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