Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study sought to determine the procedure of choice for kidney retrieval for transplantation by comparing open donor nephrectomy to laparoscopic donor nephrectomy and modified laparoscopic donor nephrectomy and by analyzing intraoperative donor and recipient graft function parameters. In this single-center, controlled, sequential analysis, 100 consecutive donor-recipient pairs were recruited, grouped according to surgical procedure, and operated upon between 1997 to 2004, as follows: group 1, open donor nephrectomy (n = 30), performed from 1997 to 2000; group 2, laparoscopic donor nephrectomy (n = 28), performed from 2000 to 2002; and group 3, modified laparoscopic donor nephrectomy (n = 42), performed from 2002 to 2004. Data were analyzed by type of operative procedure, graft function, length of hospital stay, and donor recovery time. Operative time was similar for all three surgical approaches. Warm ischemia times for open donor nephrectomy and modified laparoscopic donor nephrectomy were similar. Acute tubular necrosis occurred in 7% of patients in all groups. Donor recovery and lengths of hospital stay were significantly shorter for laparoscopic approaches. Donor complications were similar in numbers, differing only in complication type. Graft function and survival were similar for all three surgical approaches. We conclude that modified laparoscopic donor nephrectomy is the procedure of choice for living kidney retrieval.
Transplant Proc 2005 Sep
PMID:A controlled sequential evaluation of open donor nephrectomy versus classical and modified laparoscopic donor nephrectomy: an update. 1621 69

Spontaneous renal allograft rupture is one of the most dangerous complications of kidney transplantation, which can result in graft loss. This condition needs immediate surgical intervention. Conservative management has dismal results. Its prevalence varies from 0.3% to 3%. Rupture occurs in first few weeks after transplantation. Predisposing factors for graft rupture are acute rejection, acute tubular necrosis, and renal vein thrombosis. There are growing reports about successful results of repairing these ruptured kidneys. In this study, we reviewed the medical records of 1682 patients who received kidney allografts from living donors from 1986 through 2003. There were six (0.35%) cases of renal allograft rupture. All were preceded by acute graft rejection. They were treated with antirejection medications. In first three cases, the kidney allografts were removed because the procedure of choice in this situation is graft nephrectomy; but in three next cases we repaired the ruptured grafts with good results in two of them. In conclusion, the procedure of choice for kidney allograft rupture is graft repair.
Transplant Proc 2005 Sep
PMID:Spontaneous kidney allograft rupture. 1621 11

Acute renal failure is a very rare complication seen during the course of non- fulminant hepatitis A. Several mechanisms have been postulated in the pathogenesis of renal failure. Firstly, there is insufficiency of renal blood flow due to developing endotoxemia or cryoglobulinemia, secondly mesangial proliferative glomerulonephritis or interstitial nephritis occurs due to immune complexes and finally there is acute tubular necrosis caused by the direct cytopathic effect of the virus or due to immune complexes. The following case report describes a 17 year old male patient admitted with complaints of appetite loss and severe weight loss due to anorexia nervosa. During the second week of admission, he developed hepatitis A infection which was complicated by acute renal failure requiring hemodialysis therapy. Hepatorenal parameters returned to normal values by the fifth week of admission in this case of biopsy proven acute tubular necrosis. In this case, the possible negative effects of malnutrition on the liver and kidneys were not observed. The present authors emphasize that during the course of non- fulminant hepatitis A, renal functions should be closely monitored and renal biopsy should be performed if acute renal failure occurs.
Turk J Gastroenterol 2002 Sep
PMID:Acute oligo-anuric renal failure during the course of non-fulminant hepatitis A in a patient with anorexia nervosa. 1637 99

The complement system is one of the important mediators of renal ischemia-reperfusion injury (IRI). We hypothesized that efficient silencing of C3, which is the central component on which all complement activation pathways converge, could be achieved using small interfering RNA (siRNA), and that this would result in overall inhibition of complement activation, thereby preventing IRI in kidneys. A series of experiments was conducted, using a mouse model of IRI and vector-delivered C3-specific siRNA. We demonstrated the following: (1) renal expression of C3 increases as a result of IRI; (2) by incorporation into a pRNAT U6.1 vector, siRNA can be delivered to renal cells in vivo; (3) systemically delivered siRNA is effective in reducing the expression of C3 in an experimentally induced mouse kidney model of IRI; (4) similarly, siRNA reduces complement-mediated IRI-related effects, both in terms of renal injury (as evidenced by renal function and histopathology examination) and mouse mortality and (5) silencing the production of C3 diminishes in vivo production of TNF-alpha. This study implies that siRNA represents a novel approach to preventing IRI in kidneys and might be used in a variety of clinical settings, including transplantation and acute tubular necrosis.
Am J Transplant 2006 Sep
PMID:Preventing renal ischemia-reperfusion injury using small interfering RNA by targeting complement 3 gene. 1679 25

Contrast-induced nephropathy (CIN) is the third leading cause of acute kidney injury in hospitalized patients and is associated with significant patient morbidity. The pathogenesis of CIN is complex and not fully understood, but iodinated contrast agents induce intense and prolonged vasoconstriction at the corticomedullary junction of the kidney. Moreover, high-osmolar dyes directly impair the autoregulatory capacity of the kidney through a loss of nitric oxide production. These effects, coupled with direct tubular toxicity of contrast media, lead to overt acute tubular necrosis and the syndrome of CIN.
Am J Cardiol 2006 Sep 18
PMID:Pathophysiology of contrast-induced nephropathy. 1694 76

Acute renal failure is a known complication during hemolytic crisis in paroxysmal nocturnal hemoglobinuria (PNH). However, chronic renal failure is rare despite the well-known spectacular hemosiderosis of the kidneys due to chronic hemolysis. Here, we report about a 74-year-old man with PNH who developed acute on chronic renal failure after an episode of intercurrent urinary tract infection and subsequent hemolytic crisis. Mild chronic hemolysis, well-documented over the past decade, had long been considered the cause of a constantly declining glomerular filtration rate. Accordingly, magnetic resonance imaging during admission demonstrated marked siderosis of both kidneys, supporting the hypothesis that chronic renal failure (CRF) was likewise related to PNH. However, a renal biopsy revealed acute tubular necrosis and distinct renal siderosis, as expected. Additionally, tubulointerstitial injury and global glomerular sclerosis, best classified as arterionephrosclerosis, were present. In retrospect, these findings were explained by a 15-year history of hypertension and a 4-year medication with cyclosporine. Careful diagnostic workup including a renal biopsy is mandatory, given a misleadingly suggestive correlation between chronic hemolysis and CRF. Chronic renal failure in PNH is a diagnosis of exclusion, even if radiologic evidence of heavy siderosis draws off the physician's attention.
Clin Nephrol 2006 Sep
PMID:A blue kidney--chronic renal failure as a consequence of siderosis in paroxysmal nocturnal hemoglobinuria? 1699 44

HIV-infected patients may undergo renal damage related to the HIV infection itself, to the presence of co-infections, arterial hypertension, diabetes or to the exposure to nephrotoxic drugs. Tenofovir has been associated with the development of acute renal failure with Fanconi syndrome and acute tubular necrosis and, albeit rarely, with chronic liver disease. Patients with low CD4 cell count, low body weight and with concomitant diseases such as arterial hypertension and diabetes or co-infections with HCV, HBV or Treponema pallidum seem at higher risk of tenofovir-related nephrotoxicity. Other risk factors include previous exposure to nephrotoxic drugs and the association of tenofovir with boosted protease inhibitors or with didanosine. However, from the analysis of published papers the incidence of tenofovir-related renal toxicity seems low, as confirmed also by our personal casuistry (SCOLTA Project). Thus, a careful selection of patients including the evaluation of existent renal disease before starting an antiretroviral regimen including tenofovir is necessary to prevent renal damage. Furthermore, frequent monitoring of renal function in patients at higher risk of renal damage is strongly recommended, as well as a tenofovir dose adjustment if an alteration of renal function is detected.
Infez Med 2006 Sep
PMID:[Renal toxicity in HIV-infected patients receiving HAART including tenofovir]. 1712 26

Renal dysfunction is common in patients with end-stage liver disease. Etiological factors include conditions as diverse as acute tubular necrosis, immunoglobulin A nephropathy and hepatorenal syndrome. Current standard tests of renal function, such as measurement of serum urea and creatinine levels, are inaccurate as the synthesis of these markers is affected by the native liver pathology. This article reviews novel markers of renal function and their potential use in patients with liver disease.
Hepatol Res 2007 Sep
PMID:Novel approaches to assessing renal function in cirrhotic liver disease. 1750 36

Clostridium perfringens type D isolates cause enterotoxemia in sheep, goats, and probably cattle. While the major disease signs and lesions of type D animal disease are usually attributed to epsilon toxin, a class B select agent, these bacteria typically produce several lethal toxins. Understanding of disease pathogenesis and development of improved vaccines are hindered by the lack of a small-animal model mimicking natural disease caused by type D isolates. Addressing this need, we developed an oral challenge mouse model of C. perfringens type D enterotoxemia. When BALB/c mice with a sealed anus were inoculated by intragastric gavage with type D isolates, 7 of 10 type D isolates were lethal, as defined by spontaneous death or severe clinical signs necessitating euthanasia. The lethalities of the seven type D isolates varied between 14 and 100%. Clinical signs in the lethally challenged mice included seizures, convulsions, hyperexcitability, and/or depression. Mild intestinal gas distention and brain edema were observed at necropsy in a few mice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of most challenged mice that developed a clinical response. When the lethality of type D isolates in this model was compared with in vitro toxin production, only a limited correlation was observed. However, mice could be protected against lethality by intravenous passive immunization with an epsilon toxin antibody prior to oral challenge. This study provides an economical new model for studying the pathogenesis of C. perfringens type D infections.
Infect Immun 2007 Sep
PMID:Development and application of an oral challenge mouse model for studying Clostridium perfringens type D infection. 1756 65

Over a ten year period (1979 to 1989), 200 patients have undergone live donor nephrectomy through a flank extraperitoneal approach without rib resection. The average hospital stay was short and the major complications were negligible. Early graft function was seen in 97% of the cases. Delayed function due to acute tubular necrosis developed in 3%. Urinary leak was seen in 3%. Two kidneys were lost due to infection related to urinary fistulate. In 70 donors, 37 +/- 13 month's follow-up was available. Hypertension developed in two patients three and three and one-half years post donation. Significant proteinuria (>300 mg/day) was noted in one patient. No significant renal functional abnormalities were observed. Creatinine clearance was about 70% of the initial measurement at the observation time. We conclude that extraperitoneal flank live donor nephrectomy is generally safe and associated with minimal perioperative and long-term morbidity. Moreover, the procedure provides an excellent allograft function.
Ann Saudi Med 1993 Sep
PMID:Experience with living related donor nephrectomy: Evaluation of 200 cases. 1759 Jul 20


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