48 research outputs found

    Nephrocalcinosis in phosphate nephropathy following oral phosphate purgative: a role for underlying subclinical primary hyperparathyroidism?

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    AbstractFull TextImages/Data ReferencesRelated Articles Expand allCollapse all To the Editor: We have 2 questions for Dr Beyea, who described a patient with acute phosphate nephropathy after consumption of oral sodium phosphate solution (OSPS) for colonoscopy. Acute phosphate nephropathy following oral sodium phosphate soution to cleanse the bowel for colonoscopy. Their report belongs to a small group of recently published cases describing coincidence of acute renal failure after bowel cleansing with OSPS and renal heavy deposition of calcium phosphate concretions.First, the authors wrote that phosphate nephropathy differs from nephrocalcinosis by virtue of \u201cdistinct histopathologic findings.We question the accuracy of the distinction between nephrocalcinosis and phosphate nephropathy. Nephrocalcinosis refers to intrarenal deposits of calcium, regardless of whether these deposits occur in the form of phosphate or oxalate salts. In our view, phosphate nephropathy represents an acute nephrocalcinosis.Second, the authors wrote that the patient \u201chas required management for anemia and secondary hyperparathyroidism,but they did not mention the time of follow-up of the chronic renal disease. Is there any possibility that the patient\u2019s hyperparathyroidism was primary? Underlying subclinical primary hyperthyroidism might be a very appealing factor to explain the intriguing puzzle of why only very few patients develop this ominous complication among all the people using OSPS. Primary hyperparathyroidism has been described in one case may be undiagnosed when acute hyperphosphatemia lowers serum calcium levels, and offers the best conditions for nephrocalcinosis in the presence of an oral charge of phosphate, as it is demonstrated in experimental setting

    Ciprofloxacin crystal nephropathy

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    Ciprofloxacin is a widely used fluoroquinolone for the treatment of patients with complicated and uncomplicated infections. With rare exceptions, only immune-mediated interstitial nephritis was described, with direct renal damage reported only in case of overdose. Experimental studies indicated that crystalluria may be associated with the administration of this drug, but the likelihood that ciprofloxacin crystal nephropathy would occur in humans was believed to be very low on the basis of previous data showing that ciprofloxacin crystalluria depended on a urine pH greater than 6.8. However, we report 2 cases of ciprofloxacin crystal-induced nephropathy with a clinical pattern of acute reversible tubular damage and intratubular crystals identical to that previously described in elderly patients treated with ciprofloxacin dosages within therapeutic schedules. Crystals in the tubules were negative for both the von Kossa stain for phosphates and alizarin red stain for calcium
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