Cases reported "Kidney Diseases"

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1/18. Neutral phosphate-induced renal tubular metabolic alkalosis.

    A severely burned patient receiving neutral phosphate supplement developed renal tubular alkalosis. This phenomenon is compared with the results of experimental observations on animals, reported in the literature. The physiologic mechanism, including the possible role of parathyroid hormone, is illustrated.
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2/18. copper deficiency anemia and nephrosis in zinc-toxicity: a case report.

    zinc is a ubiquitous element that is essential for normal enzymatic function in multiple metabolic pathways. Chronic excessive zinc ingestion causes severe reversible anemia in humans. In animals, zinc toxicity leads to anemia as well as physiologic and morphologic damage to the pancreas, kidneys, and often, multisystem failure and death. In this case, a young female ingested approximately 2000 mg of zinc gluconate daily for 12 months. She subsequently developed anemia consistent with zinc-induced copper deficiency and severe nephrosis. After cessation of zinc ingestion, her anemia and nephrosis resolved. This case study underscores the importance of an accurate and thorough investigation of nutritional supplements during the history and physical examination. Given the promulgation of zinc for the treatment of skin disorders and the common cold, along with the commercialization of nutritional supplements, unimpeded by regulatory guidelines, it is imperative that primary care physicians be attuned to the potentially dangerous consequences of excessive zinc ingestion.
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3/18. Examination of megalin in renal tubular epithelium from patients with dent disease.

    dent disease is characteristic for the urinary loss of low-molecular-weight proteins and calcium, leading to renal calcification and, in some patients, chronic renal failure. This disorder is caused by loss-of-function mutations in the renal chloride channel gene, CLCN5. The animal model of this disease has demonstrated the possible role of disturbed megalin expression, which is a member of the low-density lipoprotein receptor family and is associated with renal reabsorption of a variety of proteins, in dent disease. We examined the expression of megalin in the renal tubular epithelium of two unrelated patients with dent disease. One patient, whose CLCN5 gene was completely deleted, showed significantly decreased staining of megalin compared with controls, while there was no change in another patient with partial deletion of the gene. These results demonstrated that mutation of CLCN5 in some patients with dent disease may impair the expression of megalin, resulting in abnormal calcium metabolism, manifested as hypercalciuria and nephrocalcinosis.
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4/18. Retinoic acid may increase the risk of bone marrow transplant nephropathy.

    bone marrow transplant nephropathy (BMTN) classically presents more than 100 days after transplantation as an acute nephritis with hypertension, azotaemia and anemia that usually results in end stage renal failure (ESRF). The risk of developing BMTN may be greater with the use of more intensive chemotherapy and higher total body and tumor bed irradiation. Cis-retinoic acid (RA) may further increase the risk of developing BMTN. Here, we report the cases of two children who developed typical clinical and biochemical features of BMTN. They were both treated for stage IV neuroblastoma with chemotherapy, bone marrow transplant (BMT) conditioning that included total body irradiation and RA therapy after BMT, although the patient in case 1 had established renal insufficiency prior to the commencement of RA. Renal biopsy of these children showed classical BMTN histology, and the renal manifestations progressed quickly; the patient in case 1 became dialysis dependent by 1 year post-bone marrow transplant. Recently, RA has been added to the post-BMT therapy in children with stage IV neuroblastoma. The occurrence of BMTN in two children treated with RA in our unit is unlikely to be coincidental. Although RA has been shown to confer a significant survival advantage in this disease, animal studies and a previous case report have suggested it could increase the toxic effects of chemotherapy and renal irradiation. It is likely that RA contributed to the deterioration in renal function in these patients.
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5/18. Salt handling in the distal nephron: lessons learned from inherited human disorders.

    The molecular basis of inherited salt-losing tubular disorders with secondary hypokalemia has become much clearer in the past two decades. Two distinct segments along the nephron turned out to be affected, the thick ascending limb of Henle's loop and the distal convoluted tubule, accounting for two major clinical phenotypes, hyperprostaglandin E syndrome and Bartter-gitelman syndrome. To date, inactivating mutations have been detected in six different genes encoding for proteins involved in renal transepithelial salt transport. Careful examination of genetically defined patients ("human knockouts") allowed us to determine the individual role of a specific protein and its contribution to the overall process of renal salt reabsorption. The recent generation of several genetically engineered mouse models that are deficient in orthologous genes further enabled us to compare the human phenotype with the animal models, revealing some unexpected interspecies differences. As the first line treatment in hyperprostaglandin E syndrome includes cyclooxygenase inhibitors, we propose some hypotheses about the mysterious role of PGE(2) in the etiology of renal salt-losing disorders.
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6/18. Carboxyatractyloside poisoning in humans.

    OBJECTIVE: Cocklebur (xanthium strumarium) is an herbaceous annual plant with worldwide distribution. The seeds contain the glycoside carboxyatractyloside, which is highly toxic to animals. We describe nine cases of carboxyatractyloside poisoning in humans which, to our knowledge, has not previously been reported. The clinical, laboratory and histopathological findings and our therapeutic approach are also discussed. SUBJECTS AND methods: The patients presented with acute onset abdominal pain, nausea and vomiting, drowsiness, palpitations, sweating and dyspnoea. Three of them developed convulsions followed by loss of consciousness and death. RESULTS: Laboratory findings showed raised liver enzymes, indicating severe hepatocellular damage. BUN and creatinine levels were raised, especially in the fatal cases who also displayed findings of consumption coagulopathy. CPK-MB values indicative of myocardial injury were also raised, especially in the fatal cases. Three of the patients died within 48 hours of ingesting carboxyatractyloside. Post-mortem histopathology of the liver confirmed centrilobular hepatic necrosis and renal proximal tubular necrosis, secondary changes owing to increased permeability and microvascular haemorrhage in the cerebrum and cerebellum, and leucocytic infiltrates in the muscles and various organs including pancreas, lungs and myocardium. CONCLUSIONS: Carboxyatractyloside poisoning causes multiple organ dysfunction and can be fatal. Coagulation abnormalities, hyponatraemia, marked hypoglycaemia, icterus and hepatic and renal failure are signs of a poor prognosis. No antidote is available and supportive therapy is the mainstay of treatment.
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7/18. Tubulointerstitial macrophage infiltration in a patient with hypokalemic nephropathy and primary sjogren's syndrome.

    We report a case of hypokalemic nephropathy associated with primary sjogren's syndrome (SS). The patient presented with profound and persistent hypokalemia secondary to distal renal tubular acidosis (RTA). A renal biopsy exhibited tubular degeneration, marked interstitial fibrosis and intense macrophage infiltration. hypokalemia has been reported to induce macrophage infiltration in experimental animal models but not in humans. This is the first report of intense tubulointerstitial macrophage infiltration in a patient with hypokalemic nephropathy associated with SS.
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8/18. A non-invasive test for receptor binding applied to nephrogenic diabetes insipidus.

    Studies in animals have determined the importance of specific receptors to the action of many hormones and drugs. In man, a non-invasive external counting technique has been used and absence of receptor function has been demonstrated in a patient with nephrogenic diabetes insipidus using radioactively labelled arginine vasopressin. This is in contrast to the findings in a patient with pituitary diabetes insipidus and a normal control. These results suggest a model for the study of hormone and drug kinetics in man avoiding multiple samplings of biological fluids.
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9/18. Experience with digoxin immune Fab (ovine) in patients with renal impairment.

    Digibind is a purified antigen binding fragment (Fab) of immunoglobulin g antibodies raised to bind digoxin. Studies in animals suggest renal excretion accounts for a substantial portion of Fab's elimination. Thus it is expected that elimination of antidigoxin Fab fragments would be prolonged in patients with renal impairment; it remains unclear whether digoxin might be released with possible recurrence of toxicity. To shed light on this potential for recrudescent digitalis toxicity following release of bound digoxin, the author scrutinized the records of patients with impaired renal function who were treated with Digibind. Data are available from three sources: the original multicenter investigation of Digibind in 150 patients with life-threatening digoxin or digitoxin toxicity, a postmarketing surveillance study of 745 patients treated with Digibind, and all other reports in the literature or to Burroughs Wellcome Co of physician experience with any antidigoxin Fab. Sixty percent of patients in the multicenter trial and 80% of patients in the postmarketing surveillance trial had some degree of renal impairment. patients with poor renal function had no evidence of decreased effectiveness or safety either in terms of percent of patients responding, onset of effect or evidence of recrudescence. From all sources the authors identified 28 patients treated with Fab who were functionally anephric. Twenty-seven of these patients had no evidence of recrudescent toxicity. One patient was reported to have complete resolution of digoxin-induced third-degree atrioventricular (AV) block, but AV block recurred 10 days after Fab treatment and persisted for 10 days thereafter. Although this case offers the only clinical evidence suggesting recrudescence can occur, there were no likely alternative explanations for the clinical findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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10/18. Comparison of Tc-99m MAG3 and Tc-99m DTPA in renal transplant patients with impaired renal function.

    Tc-99m mercaptoacetyltriglycine (MAG3) is a new Tc-99m renal agent that compares favorably to I-131 Hippuran in animal models, normal volunteers, and patients. Based on the fact that Tc-99m MAG3 has a much more rapid clearance than Tc-99m DTPA and a smaller volume of distribution, it was postulated that the image quality of Tc-99m MAG3 studies should be superior to scans obtained using Tc-99m DTPA, particularly in patients with impaired renal function. To test this hypothesis, Tc-99m DTPA and MAG3 images were obtained in three transplant patients during periods of stable but impaired renal function. In one study, the Tc-99m DTPA study was potentially misleading, whereas the Tc-99m MAG3 examination assessed the clinical situation correctly. In all three cases, the Tc-99m MAG3 images were superior.
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