scholarly journals Fanconi syndrome and nephrogenic diabetes insipidus associated with didanosine therapy in HIV infection: a case report and literature review

2007 ◽  
Vol 22 (12) ◽  
pp. 3656-3659 ◽  
Author(s):  
G. D'Ythurbide ◽  
C. Goujard ◽  
F. Mechai ◽  
A. Blanc ◽  
B. Charpentier ◽  
...  
PEDIATRICS ◽  
1985 ◽  
Vol 75 (3) ◽  
pp. 501-507
Author(s):  
Mario Usberti ◽  
Carmine Pecoraro ◽  
Stefano Federico ◽  
Bruno Cianciaruso ◽  
Bruna Guida ◽  
...  

Indomethacin, a potent prostaglandin synthesis inhibitor, has been proven to be effective in a number of tubular defects characterized by enhanced prostaglandin (namely, prostaglandin E2 (PGE2) production, but its mechanism of action is poorly understood. To elucidate further the mechanism(s) by which indomethacin reverses the abnormal tubular functions, five children with different tubular defects (nephrogenic diabetes insipidus, three cases; Fanconi syndrome, one case; and pseudohypoaldosteronism, one case) were treated with indomethacin. Indomethacin, 1 mg/kg every eight hours, was given for 1 week to all children and then was given chronically to four of the children who responded to the drug. Its use was suspended in a 10 year-old-boy with nephrogenic diabetes insipidus because it proved ineffective. To assess the site along the nephron where indomethacin affects the solute and water excretion, an acute water load study was performed in three responsive children before and during the treatment. Indomethacin did not significantly alter the glomerular filtration rate but was effective in reducing diuresis and levels of urinary sodium and potassium excretion. In the child with Fanconi syndrome, indomethacin was also effective in controlling the urinary loss of phosphate, urate, glucose, and bicarbonate. Results of the water load studies show that indomethacin decreases the delivery of solute from the proximal tubule, reduces the fractional free water clearance, and increases the urine-plasma osmolar ratio. The rate of urinary excretion of prostaglandin E2 was high in all five children; it decreased below normal values in four of them after 1 week of treatment. In the child with nephrogenic diabetes insipidus who did not respond to indomethacin therapy, prostaglandin E2 excretion decreased but the rate remained higher than normal. These results suggest that indomethacin induces retention of solute and water mainly through an enhanced proximal tubular reabsorption.


2000 ◽  
Vol 27 (1) ◽  
pp. 54-56 ◽  
Author(s):  
Jean Kanitakis ◽  
Elisabeth Carbonnel ◽  
Sergio Delmonte ◽  
Jean-Marc Livrozet ◽  
Michel Faure ◽  
...  

2021 ◽  
Author(s):  
Mohamad Ali Hussein ◽  
Bruna Pereira Correia ◽  
Leonardo Valente de Camargo ◽  
Vinicius Aldo Cury ◽  
Juliana Passos ◽  
...  

Context: Guillain-Barré syndrome is a polyradiculoneuropathy of heterogeneous manifestations, necessarily presenting progressive appendicular weakness of variable intensity associated with reduction or abolition of deep reflexes. One of its variants is known as Miller Fisher Syndrome (MFS), characterized by ophthalmoparesis, ataxy and areflexia. It usually has, by etiology, immunomediated reactions induced by acute infections, including HIV. Objectives: This report aims to describe a case of MFS with concomitants HIV infection, attended in a tertiary hospital in northern Paraná and compared it with the literature. [1,7] Case report: A 27-year-old white male patient who presented binocular diplopia, dysarthria, dysphagia, generalized hypotonia, myasfasciculations, sensory ataxia and arreflexia, with a score on the Medical Research Council (MRC) muscle strength scale of 54 points. Treatment with empirical intravenous human immunoglobulina ( IVIG ) was performed pending the result of serologies for etiological screening. He was discharged after eleven days of hospitalization with partial symptomatic improvement and results indicative of acute HIV infection. We compared this case with those described in the published literature Discussion: We compared this case with those described in the published literature and given the low incidence found in the literature of patients with the stage of HIV viremia and the opening of the picture of SMF, the concrete pathophysiology itself is still unknown. The mechanism, however, in which the literature proposes in two theories: (1) an autoimmune action against myelin due to abnormal immunoregulation by HIV; (2) direct action of neurotropic strains of HIV-1. [2.3] Our literature review shows that since 1995, cases of associated guillain barré syndrome have already been reported in the course of HIV viremia. Treatment with immunoglobulin at a dose of 400mg / kg / day for 5 days was done and the symptoms improved. [1,4,6,7] Conclusion: It is exposed, then, a case of HIV-induced MFS whose relationship has consistency, temporality, biological plausibility, coherence and analogy compatible with current literature.


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