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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of rhabdomyolysis and acute renal failure associated with cytomegaloviral infection is rare. A 27-year-old housewife was admitted to our hospital with complaints of thirst, muscle weakness, abdominal pain and oliguria. There was no past history of diabetes, drinking, fever or drug habituation and a negative family history. Laboratory tests revealed myoglobinuria, hyper-pancreatic type amylaseuria, hyperglycemia, azotemia and highly increased creatine phosphokinase in the plasma. She was treated with hemodialysis and insulin therapy. Serological studies showed a 4-fold increase in cytomegalovirus antibody titers 4 weeks after admission. Muscle biopsy specimens showed hyaline degeneration and infiltration of T cell lymphocytes in the muscle. Renal biopsy specimens showed acute tubular necrosis and some myoglobin casts. No cytomegalovirus antigen was found in renal specimens by immunofluorescence study. From these results, it was determined that a systemic cytomegalovirus infection triggered pancreatitis which caused diabetic ketoacidosis, rhabdomyolysis and acute renal failure.
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PMID:Cytomegalovirus infection associated with acute pancreatitis, rhabdomyolysis and renal failure. 131 48

Exocrine secretions of 16 of 22 pancreas allografts were drained into the urinary tract. Seven of these 16 patients have functioning allografts, six with pancreaticocystostomies and one with duct-to-ureter anastomosis. A notable problem has been a chronic metabolic acidosis, along with weight loss and hypotension, secondary to chronic bicarbonate loss and volume depletion through the urinary pancreatic fistula. This occurred as early as one week posttransplant, and intermittently thereafter up to four years. The syndrome was aggravated by episodes of renal dysfunction (acute tubular necrosis or rejection), and febrile syndromes. An inverse relationship between serum and urine bicarbonate concentrations existed, with a correlation coefficient, r = -0.746, (P less than 0.05). A negative correlation was also noted between serum bicarbonate and serum creatinine, r = 0.726, (P less than 0.05). Hyperchloremic metabolic acidosis with normal anion gap occurred despite periods of marginal pancreas allograft function resulting from ongoing rejection. Treatment consisted of intravenous and/or oral bicarbonate supplementation, and bicarbonate dialysis for uremic patients. In addition, one patient was first seen with severe balanitis and urethritis due to documented activation of trypsinogen and chymotrypsinogen, presumably caused by recurrent episodes of urinary tract infection. Urinary assay revealed a 10(2-3) increase in activated trypsin and chymotrypsin in comparison with other asymptomatic allograft recipients. Conversion to ductal enteric drainage led to resolution of both the balanitis and bicarbonate wasting. Measurement of urinary amylase levels were gross indicators of graft viability since no correlation could be found between these levels, onset of hyperglycemia, and eventual graft rejection confirmed by pathological examination.
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PMID:Pancreatic allograft exocrine urinary tract diversion. Pathophysiology. 243 6

Rats with untreated diabetes mellitus are protected from gentamicin-induced nephrotoxicity. In order to evaluate the role of hyperglycemia, glycosuria, and polyuria in this phenomenon, miniosmotic pumps filled with insulin were implanted for 15 days in seven female Sprague-Dawley rats with streptozotocin-induced diabetes mellitus. Plasma glucose levels were successfully maintained under 126 mg/dl. To serve as the control group, eight age-matched diabetic (plasma glucose > 400 mg/dl) rats had miniosmotic pumps placed delivering only Ringer's solution. Six days after placement of the pumps, gentamicin (40 mg/Kg/day) was administered to all animals for 9 days. The insulin-treated diabetic rats exhibited clear signs of nephrotoxicity by Day 6 of gentamicin, whereas the diabetic control group remained free from any functional or morphological evidence of proximal tubular damage throughout the 9 days of the aminoglycoside administration. At the end of the experiment, the creatinine clearance in the insulin-treated diabetic group was 45% lower than in the untreated diabetic group (P < 0.005). In addition, there was a rise in plasma creatinine (P < 0.02), muramidase appeared in the urine, and mild patchy acute tubular necrosis of the renal cortex was observed by light microscopic examination. The insulin-treated group also accumulated more gentamicin in the renal cortex than the untreated animals (P < 0.005). It is concluded that protection against the nephrotoxic effects of gentamicin is a feature of untreated experimental diabetes mellitus in the rat and that correction of the hyperglycemic state with insulin reverses this resistance.
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PMID:Insulin reverses the protection given by diabetes against gentamicin nephrotoxicity in the rat. 807 55

Hyperglycemia amplifies the inflammatory state after ischemia/reperfusion (I/R), and activated neutrophils have been implicated in the development of I/R-induced renal injuries. D-ribose is a naturally occurring monosaccharide found in all living cells. In this study, we examined whether D-ribose attenuates I/R-induced renal injury by reducing neutrophil activation in rats with transient hyperglycemia. Male Wistar rats were divided into sham (n = 24), control (n = 64), and D-ribose (n = 32) groups. Rats received intraperitoneal injection of glucose (3 g/kg) 30 min before induction of ischemia to induce transient hyperglycemia. Anesthetized rats underwent right nephrectomy and subsequent occlusion of the left renal artery and vein for 45 min. D-ribose (400 mg/kg) was intravenously administered 30 min before induction of ischemia. D-ribose significantly reduced the degree of the I/R-induced increases in renal concentrations of cytokine-induced neutrophil chemoattractant-1 (a chemotactic factor for the activation of neutrophils and chemotaxis to the site of injury) and myeloperoxidase (an indicator of neutrophils infiltration). D-ribose also reduced the I/R-induced increases in serum levels of blood urea nitrogen and creatinine, and improved histological changes, including acute tubular necrosis in the corticomedullary junction fields. These results indicate that D-ribose reduces the I/R-induced acute renal injury in rats with transient hyperglycemia, probably by reducing neutrophil activation. D-ribose might thus be useful for surgical procedures, such as renal transplant surgery, under hyperglycemia.
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PMID:Protective action of D-ribose against renal injury caused by ischemia and reperfusion in rats with transient hyperglycemia. 1985 Oct 50

Sepsis is a common and important cause of mortality in critically ill patients. Acute kidney injury (AKI) is one of the most important factors determining morbidity and mortality in the prognosis of sepsis. Recent studies have indicated that the pathogenetic mechanism in septic AKI is totally different from that in non-septic AKI. Our understanding of sepsis-associated AKI pathophysiology is shifting from renal vasoconstriction, ischemia, and acute tubular necrosis to heterogeneous vasodilation, hyperemia, and acute tubular apoptosis. Especially, apoptosis is gradually gaining importance in the understanding of the development of renal injury. The frequency of renal tubular apoptosis on biopsies of septic patients has been pointed out in recently published studies. Apoptosis can be triggered by ischemia, exogen toxins, or endogen mediators. It has been shown in some animal models that hyperglycemia, which is common in critically ill patients, causes apoptosis in renal tubular cells. New treatment options have emerged in the light of recent findings. Ghrelin that inhibits pro-inflammatory cytokines, caspase inhibitors that block the apoptotic pathway, and suppression of anti-inflammatory reactions are under study. Among the existing methods of treatment, usage of arginine, which is a vasopressor agent, ventilation with a low tidal volume, and hemofiltration methods cleaning toxic mediators from the circulation should be considered in the first place. Hyperglycemia treatment is of major importance, since, besides its anti-inflammatory effect, it has a protective role on the kidney. Regarding pathogenesis, rates of morbidity and mortality are aimed to be reduced through the new agents of therapy that have been studied on.
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PMID:Renal cell apoptosis and new treatment options in sepsis-induced acute kidney injury. 2318 51