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)

A renal transplant patient in whom acute pancreatitis developed 2 1/2 years after surgery is presented. Pancreatisis was accompanied by hyperlipaemia, diabetes mellitus and acute renal failure possibly due to acute tubular necrosis. Pancreatic abscesses necessitated subtotal pancreatectomy 2 months later. Because of generalized tuberculosis finally the patient succumbed 6 weeks thereafter. As aetiological factors cytomegalovirus disease, disorders in lipid metabolism and immunosuppressive therapy must be discussed. It is concluded that prophylactic measures as well as early diagnosis, intensive care and therapy are necessary for reducing the high risks of pancreatis in renal transplant recipients.
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PMID:[Pancreatitis after renal transplantation (author's transl)]. 20 57

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

Although it has been suggested that cytomegalovirus (CMV) infection of the kidney might facilitate the development of human immunodeficiency virus-associated nephropathy (HIVAN) or other morphologic renal changes in patients with AIDS, no systematic study has been performed on kidneys from AIDS patients. We examined 75 autopsy kidneys, two renal biopsy specimens, and a nephrectomy specimen from 78 HIV-infected patients (five with HIVAN) for the presence of CMV. Immunocytochemistry (ICC) utilizing a monoclonal antibody against the late antigen of CMV and in situ hybridization (ISH) with a biotinylated DNA probe for CMV sequences were used. The detection system for both ICC and ISH was streptavidin-conjugated alkaline phosphatase with Fast Red TR chromogen. CMV was detected in only 10 of the 78 kidneys examined (12.8%): eight by both methods, one by ISH only, and another by ICC only. All 10 positive kidneys were obtained from autopsies of patients with AIDS. The average number of positive cells (in approximately 15 x 10 mm sections) was 22 with ICC and 10 with ISH. Glomerular intracapillary cells (possibly endothelial cells) were the most commonly stained, followed by positive cells in the interstitium and peritubular capillaries. Relatively few tubular epithelial cells were stained. The majority of positive cells by either ICC or ISH did not show nuclear or cytoplasmic inclusions; however, only two of the 10 positive kidneys did not contain cells with typical Cowdry type-A intranuclear CMV inclusions. The most frequent pathologic finding in the kidneys positive for CMV by either ICC or ISH was acute tubular necrosis (in six of 10, 60%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is cytomegalovirus associated with renal disease in AIDS patients? 132 3

The monitoring of plasma soluble interleukin-2 receptor (S IL-2R) concentrations has been proposed in organ transplantation, especially to detect early manifestations of rejection. In organ transplantation, immune activation occurs in various circumstances such as rejections and infections. We performed S IL-2R determination 3 times a week in the sera of 106 patients undergoing kidney and/or pancreas transplantation. In kidney transplantation, S IL-2R was increased before the transplant. It also increased under prophylactic and especially under curative anti-rejection OKT3 or ATG therapy. In 90% cases, S IL-2R increased 2 to 4 days before creatininemia rise. In the other 10% cases, no correlation could be found with any clinical status modification. S IL-2R concentrations never increased in isolated acute tubular necrosis or in cyclosporine A (CsA) nephrotoxicity. In pancreas transplantation, the correlation between S IL-2R concentrations and possible pancreas rejection, was very poor. During cytomegalovirus (CMV) infection, only 50% patients with clinical CMV manifestations had high concentrations of S IL-2R. During Dihydroxy Propoxy Methyl Guanine (DPHG = Ganciclovir) treatment, S IL-2R still increased at the beginning, then it decreased progressively when therapy was efficient on CMV infection. The monitoring of S IL-2R concentrations may be useful in the weeks following organ transplantation provided that results are interpreted in the context of clinical and other laboratory findings, particularly with the renal function status and creatininemia.
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PMID:Soluble interleukin-2 receptor (S IL-2R) in renal and pancreatic transplantation. 165 83

The role of platelet transfusion as a preparative method for kidney transplantation is still a matter of debate. Two groups of 28 male patients transplanted between 1983 and 1988, paired for age, date of transplant, absence of anti-HLA antibody and immunosuppressive therapy have been compared. Group I was given 5 purified platelet transfusions at 1-week intervals before transplantation. Each transfusion contained 7.6 x 10(6) platelets contaminated by less than 1 leukocyte in 10(5) platelets. Group II received from 3 to 5 whole blood transfusions. In all cases it was a first transplant from cadaveric donors and previously untransfused patients before entering the protocol. No patient in group I developed cytotoxic antibodies. Acute tubular necrosis occurred with the same incidence in group I and in group II but was more severe and longer in group I, requiring hemodialysis in 62.5% and only 22% in group II. ATN was significantly associated with graft loss in group I (P less than 0.05). The total number of rejections and the number of patients undergoing rejection were not significantly different in both groups. However, the intensity of rejection was significantly higher in group I with 41% (21/51) of severe or irreversible rejections versus 9/46 (19.5%) in group II (P less than 0.05). The first rejection occurred significantly earlier in group I than in group II since 75% of the first rejection episodes occurred in the first 10 days versus 38% in group II (P less than 0.02) with a mean delay of 12.8 +/- 3.2 and 19.10 +/- 3.3 days, respectively. Although platelet transfusions are devoid of leukocytes the incidence of CMV infection was not significantly different in both groups: 57% in group I and 68% in group II. Purified platelet transfusions did not induce humoral immunization but lack of sensitization does not imply indefinite graft prolongation. Because platelets do not carry class II antigens, purified platelets transfusions represent a useful model to analyze the role of class I antigens alone in the induction of unresponsiveness in organ transplantation.
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PMID:The value of platelet transfusions as preparation for kidney transplantation. 184 72

Thirty four patients with advanced renal insufficiency and after kidney transplantation have been prospectively studied using pulsed wave doppler. The doppler flows were evaluated using an index of resistance. The index of resistance varies proportionally with the peripheral resistances. This study showed in 14 patients without symptoms a mean index of resistance equal to 0.71 +/- 0.087. During acute rejection, the mean index of resistance increases to 0.91 +/- 0.12 (p less than 0.01). Seven patients with acute tubular necrosis and an index of resistance equal to 1 (p less than 0.01). There is no increase of the indices of resistance in patients with cytomegalovirus infection or with overdosed cyclosporin treatment. The pulsed wave doppler has a very good sensitivity to diagnose the acute rejection (90%) and acute tubular necrosis (100%) but cannot differentiate them. However, the repetition of systematic examinations allows the early diagnosis of acute rejection and the follow-up of the vascularization of anuric kidneys related to tubulopathy.
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PMID:[Diagnosis of early complications of the transplanted kidney by pulsed Doppler]. 206 79

To evaluate changes in T-lymphocyte subsets and DR expression on tubular cells, 74 fine-needle allograft aspirates (FNAB) were evaluated in 31 patients with cadaver kidney transplants. Monoclonal antibodies against T helper CD4+, cytotoxic/suppressor CD8+, and HLA-DR were used with an indirect alkaline-phosphatase-staining technique. Cases with acute rejection (n = 11) showed a significant increase of CD8+: CD4+ ratio versus those with stable function (n = 21), acute tubular necrosis (n = 10) or CsA toxicity (n = 7) (ANOVA F = 10; P less than 0.01). Cases with chronic rejection or CMV infection showed no differences in the CD8+: CD4+ ratio with the other groups. DR expression on tubular cells was frequently found in cases of acute rejection, chronic rejection and CMV (73%, 66%, and 43% respectively), occasionally found in CsA toxicity (14%), but never seen in controls or ATN. Both tests, the CD8+: CD4+ ratio and the DR expression on tubular cells, had a high sensitivity and specificity in differentiating acute rejection versus controls, acute tubular necrosis, and CsA toxicity. When both tests are taken together no case without rejection showed a CD8+:CD4+ ratio greater than 1.6 and DR expression on tubular cells. Cases with acute rejection who lost the graft (n = 6) had a CD8+:CD4+ ratio significantly greater than those who responded to antirejection therapy (n = 5) (t = 2.9; P less than 0.05).
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PMID:Monoclonal analysis of fine-needle aspiration biopsy in kidney allografts. 212 91

This prospective study was conducted in 34 consecutive renal transplant patients. Pulsed doppler was used to evaluate the peripheral resistance (PR) in the transplant vessels. Under normal conditions, the PR of the graft is low, resulting in a continuous diastolic blood flow. The intensity of this blood flow was evaluated by means of a resistance index (RI), Pourcelot's index, calculated as follows: RI = systolic peak - end-diastolic peak/systolic peak This study demonstrated values for RI of 0.71 +/- 0.087 in 14 totally asymptomatic patients. In 10 cases of acute rejection, the RI increased to 0.91 +/- 0.12. The 7 patients with acute tubular necrosis had an RI equal to 1. In patients with cytomegalovirus infection of suffering from cyclosporin overdose, the RI was not modified in relation to asymptomatic subjects. This study demonstrates the existence of a rise in the PR in cases of acute rejection and acute tubular necrosis with a sensitivity of 90% and 100% respectively for these two diagnoses. However, this method cannot be used to distinguish between acute rejection and acute tubular necrosis.
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PMID:[The value of pulsed Doppler for the follow-up of the transplanted kidney in the first 3 months of transplantation]. 216 33

In a longitudinal study, 53 renal allograft recipients were investigated for changes in serum creatinine and neopterin levels and in the neopterin/creatinine (N/C) ratio which makes it possible to disregard the glomerular filtration level. The patients were divided into 5 groups according to their clinical situation: stability, acute renal failure due to acute tubular necrosis, acute graft rejection, bacterial or viral infection and cyclosporin overdosage. Only N/C discriminated between these situations, being normal (less than 200.10(-6) in groups 1 and 2, significantly elevated in groups 3 and 4 and low in group 5. The highest N/C value was observed in patients with primary cytomegalovirus infection. It is concluded that the N/C ratio is a good biochemical parameter to be used in the follow-up of renal allograft recipients.
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PMID:[Monitoring of renal grafts. Value of the determination of serum neopterin and neopterin versus creatinine ratio]. 253 67

Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 +/- 3.3 mumol/l and the mean increase was 190 +/- 28.3 mumol/l (range 80-1,000). Peak serum creatinine was higher than 200 and 300 mumol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 +/- 4 mumol/l) and at the end of the treatment (83 +/- 4 mumol/l) was significantly lower (p less than 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Foscarnet nephrotoxicity: mechanism, incidence and prevention. 255 31


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