Drug-induced liver injury: Relation between the R ratio and histopathology.

INTRODUCTION AND AIM: Drug-induced liver injury (DILI) is a diagnosis based on the ruling out of potential liver diseases and consolidated by establishing causality through the temporal relation between a potentially hepatotoxic substance and altered liver biochemistry. Incidence fluctuates greatly worldwide, with very few reports of causal agents of DILI in Colombia. A retrospective study on patients treated at the Centro de Estudios en Salud (CES), within the time frame of January 2015 and June 2020, was conducted to document the causal substances of DILI in patients with liver biopsy and to correlate the types of histologic patterns with the biochemical pattern of liver injury (R ratio). RESULTS: Of the 254 adult patients with liver biopsy and no tumor etiology, 20 patients were identified as cases of DILI (7.87%). The two most frequently found causal substances were efavirenz, in three HIV-positive patients, and Moringa oleifera (moringa), in two patients. There was a statistically significant association between cholestatic patterns (p = 0.037) and mixed patterns (p = 0.031), in the comparison of the histopathologic categories and the R ratio. CONCLUSION: To the best of our knowledge, there are no reports on DILI secondary to Moringa oleifera (moringa). The R ratio could be a useful tool, in relation to the histologic pattern of injury, in cases of mixed and cholestatic patterns.

[Expression of nephrin, podocin and a-actinine-4 in renal tissue of patients with proteinuria]. / Expresión de nefrina, podocina y alpha-actinina-4 en tejido renal de pacientes con proteinuria.

INTRODUCTION: Slit diaphragm and/or podocyte's cytoskeleton alterations are related to proteinuria and nephrotic syndrome. In our population, focal and segmental glomerulosclerosis causing nephrotic syndrome is the more frequent biopsy demonstrated glomerulopathy. Our aim was search for alterations in some slit diaphragm-associated proteins in patients with nephrotic range proteinuria. METHODS: Renal tissue from 40 patients with nephrotic range proteinuria, 10 patients with non-nephrotic proteinuria, 3 with isolated hematuria, and 10 samples of normal renal tissue (deceased donors) were studied, by indirect immunofluorescence, for expression of nephrin, podocin, and alpha-actinin-4. RESULTS: Expression of these proteins was lineal, homogeneous, in the glomerular capillary walls in normal renal tissue and in patients with isolated hematuria. In nephrotic proteinuria this normal appearance was altered and immunostaining showed a fine granular appearance. In 18 cases (45%) of patients with nephrotic proteinuria and 3 cases (30%) of patients with non-nephrotic proteinuria there was loss of at least one of these proteins (p = 0.49). These alterations were found in the diverse glomerulopathies more frequently causing nephrotic syndrome. CONCLUSIONS: In nephrotic range proteinuria redistribution or loss of expression of slit diaphragm-associated proteins is very frequent. In many of our cases this fact could be more a consequence than a cause of proteinuria. These alterations can be also evidenced in patients with non-nephrotic proteinuria.