1/3. Analysis of urinary sediment by transmission electron microscopy. An innovative approach to diagnosis and prognosis in renal disease.Urinary sediment TEM is capable of unequivocally demonstrating renal tubule cells and distinguishing them from urinary tract epithelial cells. The renal tubule cells and the accompaniments including myeloid bodies, inflammatory cells, or fibrin permit, in a particular clinical setting, synthesis of a meaningful renal diagnosis. Sequential TEM sediment studies can clarify ambiguities in diagnosis. Precisely, when much difficulty is experienced in distinguishing ATN from aminoglycoside nephrotoxicity in a patient with sepsis who has received aminoglycoside, urinary sediment TEM can facilitate the differential diagnosis with confidence. In another clinical setting, such as hypersensitivity acute interstitial nephritis, TEM urinary sediment has an irrevocable place by exhibiting the characteristic eosinophil granules that will confirm the above diagnosis, or deny it when they are absent. The morphologic features in the renal tubule cells in the sediment reflect similar changes in the tubular cells in renal tissue. Therefore, the severity of tubular changes are commensurate with the clinical outcome in terms of renal function recovery, need of dialysis, and mortality. The degree of correlation is significant. Thus, slight or no TEM sediment tubular changes signifies a good prospect for renal function recovery and low or no mortality. Conversely, severe tubular changes in the TEM sediment denote persistent renal failure accompanied by high mortality. Furthermore, the most severe tubular changes, found in hepatorenal syndrome, are consistent with its dismal prognosis.- - - - - - - - - - ranking = 1keywords = hepatorenal syndrome, hepatorenal (Clic here for more details about this article) |
2/3. Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study.This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.- - - - - - - - - - ranking = 7keywords = hepatorenal syndrome, hepatorenal (Clic here for more details about this article) |
3/3. Acute anuric renal failure in nonfulminant hepatitis a infection.Acute renal failure has recently been recognized as a rare complication of nonfulminant hepatitis a infection. The availability of a specific test for IgM antibody to hepatitis a should permit prompt diagnosis of the disease and a better evaluation of its association with acute renal failure. The exact mechanism for acute renal failure in hepatitis a is uncertain but glomerulonephritis, acute tubular necrosis and hepatorenal syndrome have been postulated. We report a patient with hepatitis a infection and acute renal failure most likely due to acute tubular necrosis.- - - - - - - - - - ranking = 1keywords = hepatorenal syndrome, hepatorenal (Clic here for more details about this article) |