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)

After renal transplantation low urinary sodium concentration (UNa) has been used to diagnose acute rejection (AR), for the early phase of AR is often associated with reduced renal perfusion. Early postoperative graft failure without low UNa favors the diagnosis of ischemic tubular damage (ATN). As fractional excretion of filtered sodium (FENa) better reflects glomerulotubular balance in renal sodium handling, FENa was analyzed during the first 2 weeks in 118 renal allografts. From data on 41 transplants with good early renal function (GEF), a temporal profile of FENa was obtained and used to evaluate the behavior of FENa by means of standardized FENa (Z score). Individual subjects followed their own profile with a small deviation (delta Z less than 1.4 for 2 days). In 31 instances, acute rejection was diagnosed. In 14 with AR, the Z score deviated little; 2 responded to methylprednisolone given intravenously. In 17 with AR, the Z score fell significantly (delta Z greater than 1.5 for 2 days), an average of 2.6 days before the first rise in serum creatinine concentration; 15 responded to treatment. The difference between these two groups was significant (P less than 0.001). This functional heterogeneity and different responses to treatment may indicate different immunologic mechanisms which damage different target cells in the graft in AR. In 46 patients with acute tubular necrosis after cadaver kidney transplantation FENa was significantly higher than it was in the GEF group as early as the first posttransplantation day and approached normal as the renal function recovered. This behavior of FENa was clearly different from that in AR.
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PMID:Fractional excretion of sodium after renal transplantation. 39 Feb 18

Fifty-three children, ages one day to 15 years, were treated with hemodialysis for acute renal failure between 1968 and 1977. Twenty-three had acute tubular necrosis. Nine had ATN associated with catastrophic medical illnesses; all died. Fourteen had ATN following major surgical procedures; ten died. Thirty had ARF due to primary nephrologic disorders; 27 survived. Thus it was not the ARF per se but the underlying and concomitant disorders which had the major influences on survival. As prognostic indications of survival in patients with postoperative ATN cannot be clearly defined, these patients almost always deserve aggressive management, including dialysis therapy. Patients with ATN associated with severe medical illness often have fatal underlying conditions which cannot be influenced by presently available technologies.
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PMID:Acute renal failure in infants and children: outcome of 53 patients requiring hemodialysis treatment. 71 76

A total of 209 consecutive neonate and infant autopsies were reviewed with special attention to papillary muscle necrosis (PMN) of the heart. Associated major pathological findings were analysed for the evaluation of significant pathological accompaniments of PMN. PMN was found in 52 cases among 171(30.4%) neonates and major pathological accompaniments were bronchopneumonia, hyaline membrane disease, hypoxic neuronal change, sepsis, subarachnoid hemorrhage, disseminated intravascular coagulation (DIC) and acute tubular necrosis, among which hypoxic neuronal change and ATN had a statistically significant higher incidence when compared with the control group. (p < 0.005). PMN was found in 13 cases among 38(34.2%) infants and accompaniments were congenital heart disease, sepsis, bronchopneumonia, DIC and hypoxic neuronal change, all of which showed no difference from the control group in incidence. The results imply that PMN is a kind of organ damage in stressed subjects regardless of age, that it is not a special form of myocardial injury in any specific age group including the newborn period, and is possibly of different pathogenesis and significance.
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PMID:Papillary muscle necrosis in neonates and infants--analysis of 209 autopsies. 129 38

Postoperative management of kidney allograft recipients requires a reliable and rapid diagnostic method so that proper therapy can be initiated. In this study, we tried to correlate serum neopterin levels with different conditions after transplantation. Serial serum neopterin levels were assessed after operation. Serum neopterin levels of uremic patients were significantly higher than those of healthy persons (239.9 +/- 177.7 nmole/L, n = 33 vs 6.14 +/- 2.78 nmole/L, n = 10, p < 0.001). In recipients with a stable post-transplant course, the serum neopterin level was low. On the contrary, acute rejection episodes were associated with a high level of serum neopterin which declined after successful treatment, although the difference was not significant (96.2 +/- 57.7 nmole/L vs 56 +/- 38.1 nmole/L, p > 0.05). The serum neopterin level was also high in post-transplant acute tubular necrosis (ATN, 256.6 nmole/L), which gradually declined parallel to the resolution of ATN. The neopterin level was low in patients with cyclosporine nephrotoxicity (17.8 +/- 7.6 nmole/L). In summary, the serum neopterin levels were persistently high in uremic and post-transplant ATN patients. Acute rejection episodes were correlated with an increased level of neopterin. It appears that daily measurement of the serum neopterin level may be useful for biochemical detection of immunologic complications in allograft recipients.
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PMID:Monitoring of serum neopterin in renal transplant recipients. 136 46

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

In many studies of renal transplant recipients, acute tubular necrosis has been shown to predispose to a higher rate of graft loss, apparently due to rejection, but the mechanism of this effect is unknown. One possibility is an increased immunogenicity of the graft. To study this possibility, we examined the expression of major histocompatibility complex antigens in kidneys damaged by ischemia, using a mouse model of ischemic ATN. ATN was produced in the left kidney of male CBA mice by temporary clamping of the vascular pedicle for up to 60 min. Class I and II MHC expression was quantified by the extent of binding of monoclonals in radioimmunoassay, after 1 to 35 days in both kidneys. MHC induction was localized by indirect immunoperoxidase staining. Specific steady state mRNA for beta 2 microglobulin and class II were quantified by northern blotting using 32P-labeled probes. Changes in MHC expression were assessed by comparing the ischemically injured left kidney to the control right kidney. By day 1, ATN was evident by histology but there was no change in MHC expression. By day 3, class I was increased in the left kidney by 3-6-fold over the right. In tissue sections, the class I increase was localized to tubular epithelial cells. Starting on day 7 and persisting to day 35, class II was increased by 1.5 to 3 times for the ischemic kidney over the control, primarily in interstitial cells but also in tubular cells. This increase in class II was associated with the appearance of Thy 1.2-positive cells in the interstitial areas. Increased antigen expression was preceded by increased steady state mRNA. Thus unilateral ischemic ATN causes increased MHC expression in tubular cells and the accumulation of an inflammatory infiltrate, both of which may contribute to the increased rate of rejection and graft loss in ischemically injured kidneys.
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PMID:Increased major histocompatibility complex antigen expression in unilateral ischemic acute tubular necrosis in the mouse. 210 46

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

Controversy exists as to the type of cells present in the urine during renal allograft rejection. In order to resolve this controversy as well as to evaluate the value of urine sediment examination as a means of detecting AR, we quantitated the different cells present in urine during AR using an immunoperoxidase technique and monoclonal antibodies reactive with lymphocytes, monocytes, granulocytes, glomerular epithelial, tubular, and urothelial cells. Urine sediment (n = 176) was examined serially over 3 months in 15 transplant recipients. There were 12 episodes of early posttransplant acute tubular necrosis and 21 episodes of AR. It was possible to detect AR as well as to distinguish AR from ATN. Lymphocyte and tubular cell excretions were increased significantly during AR. Excretion of urothelial cells was also significantly increased during most episodes of AR suggesting that rejection of ureters occurs concomitantly with rejection of the kidneys.
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PMID:Urine cytologic profile in renal allograft recipients determined by monoclonal antibodies. Diagnosis of allograft rejection. 264 80

The nephrotoxic effects of cyclosporine (CsA) seem to be augmented by co-existing renal injury. A high rate of prolonged delayed function (acute tubular necrosis [ATN]) and non-function (NF) has been associated with the use of CsA prior to and following renal transplantation. Cyclosporine has also been associated with a slower recovery of allograft function and poor baseline renal function even in allografts that function immediately compared with conventionally treated recipients. In 1983 we hypothesized that the rate of ATN and NF following renal transplantation could be decreased and more normal kidney function achieved if renal injury was resolved before adding the nephrotoxic effects of CsA. A group of 300 nonsplenectomized, uremic recipients have received 304 renal transplants and have been initially immunosuppressed with azathioprine, prednisone, and Minnesota antilymphoblast globulin (ALG) prior to starting maintenance CsA and prednisone. The incidence of NF has been 1.9% and the development of ATN has been 7.6% following transplantation with sequential use of ALG and CsA. Other benefits to the renal recipient have also occurred with use of this immunotherapy protocol. Renal allograft survival for recipients of first, second, and third renal allografts has been higher than that generally reported with cyclosporine and prednisone alone. Rejection episodes have been infrequent during the first six months posttransplant, as 75% and 62% of first and second renal allograft recipients have remained rejection-free. Clinically significant infectious complications were infrequent. No cadaver recipient has developed a lymphoma. Moreover, the initial hospitalization following transplantation with sequential ALG/CsA has been short and generally uncomplicated. We conclude that sequential ALG/CsA following renal transplantation provides excellent early posttransplant immunosuppression while avoiding the nephrotoxic effects of CsA and also provides the steroid and infection-sparing benefits derived from maintenance CsA therapy.
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PMID:Sequential antilymphoblast globulin and cyclosporine for renal transplantation. 354 30

The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation has been assessed by measurement of urinary kallikrein activity in 41 renal transplant recipients. The urinary tosyl arginine methyl esterase assay was used. The urinary kallikrein in these patients appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertension (mean blood pressure 156 +/- 3/98 +/- 2 mm Hg) and excreted less kallikrein (4.0 +/- 1.2 versus 12.5 +/- 4.0 esterase units [EU] per 24 hours, p less than 0.05) than their 18 normotensive counterparts (mean blood pressure 132 +/- 2/77 +/- 1 mm Hg, both p less than 0.01). Subjects with renal complications of transplantation (acute tubular necrosis [ATN], nine patients, or acute rejection [AR], eight patients) also excreted less kallikrein than the 28 subjects without such complications (3.4 +/- 0.9 versus 10.3 +/- 2.7 EU/24 hours, p less than 0.02). Among those with acute renal complications, subjects with ATN excreted less kallikrein than those with AR (1.3 +/- 0.3 versus 5.7 +/- 1.7 EU/24 hours, p less than 0.02). Cadaver graft recipients excreted less kallikrein than living related donor graft recipients (2.1 +/- 0.4 versus 13.0 +/- 3.5 EU/24 hours, p less than 0.01), perhaps reflecting their higher blood pressures (mean systolic pressure 151 +/- 3 versus 140 +/- 3 mm Hg, p less than 0.04), relatively impaired renal function (creatinine clearance values 42 +/- 8 versus 62 +/- 5 ml/min, p less than 0.04), and higher incidence of ATN (nine cases versus none). The kallikrein-kinin system may be involved in the pathogenesis of hypertension and some forms of renal dysfunction after renal transplantation.
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PMID:Urinary kallikrein excretion after renal transplantation: relationship to hypertension, graft source, and renal function. 675 Oct 83


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