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

Continuous peritoneal dialysis (CPD) was performed in 13 children with acute renal failure (ARF) in our intensive care units (ICU). The median age was 6 months (range 3 days to 77 months). Sixty-nine percent of the patients (9/13) were below the age of 12 months. CPD was performed for a median duration of 5 days (range 1-35 days). In 62% of the patients (8/13), the cause of ARF was acute tubular necrosis (ATN) due to cardiac surgery. The outcome of CPD regarding total survival was 54% (7/13). A high mortality was registered (83% of the deaths [5/6]) within the first year of life, which suggests a worse prognosis if ARF occurs at this age. Half of the total deaths (3/6) were among the cardiac surgery patients. Peritoneal equilibration tests (PET) were performed utilizing measurement of urea and glucose transport through the peritoneal membrane at short intervals during a period of 45-60 min from the start of treatment. Short dwell times of 5-20 min were found to be sufficient for adequate uremic control until a satisfactory daily urine production was noted. CPD is a useful and simple treatment modality for ARF in critically ill ICU children. Equilibration tests are useful and should be considered for optimization of CPD treatment in critically ill children with ARF in order to achieve the goal of controlling uremia and fluid overload, and giving nutritional support.
Adv Perit Dial 1994
PMID:Continuous peritoneal dialysis in children with acute renal failure. 799 47

In an attempt to understand the pathogenesis of renal vein thrombosis occurring early after renal transplantation, gene expression of plasminogen activator inhibitor-1 (PAI-1) was investigated by an in-situ hybridization technique. The cases examined were six transplant kidneys complicated by renal vein thrombosis, four 'normal' kidneys and five time-matched transplant kidneys not complicated by renal vein thrombosis but showing acute tubular necrosis, infection, or normal histology. The cell types expressing PAI-1 mRNA were also studied by combined in-situ hybridization and immunohistochemical double staining techniques. Our results showed that PAI-1 mRNA was expressed in transplant kidneys complicated by renal vein thrombosis but there was no detectable expression in 'normal' kidneys, nor in time-matched transplant kidneys not complicated by thrombosis. Double staining showed that PAI-1 mRNA was predominantly expressed by capillary endothelial cells, particularly around large- or medium-sized renal arteries and small nerves. Smooth-muscle cells in the wall of major or medium-sized renal arteries also showed positive expression of PAI-1 in three of six thrombosed transplants. However, endothelium in the major renal vein showed relatively little signal. The pattern was different from that in rejection. The possible relevance of these findings is discussed.
Nephrol Dial Transplant 1994
PMID:Gene expression of plasminogen activator inhibitor 1 in transplant kidneys complicated by renal vein thrombosis: a combined study by in-situ hybridization and immunohistochemistry. 805 38

In the present study we investigated the relationship between secondary hyperparathyroidism in renal graft recipients and post-transplantation acute tubular necrosis (ATN). Patients were divided into two groups according to graft function: group A consisted of 28 patients who had an uneventful postoperative period and did not require haemodialysis. Group B comprised 26 patients with primary non-function of the graft due to biopsy-proven ATN who required continued haemodialysis for the first postoperative week or longer (mean 14.2 +/- 8.7 days). Both groups had comparable donor characteristics, HLA-matching and ischaemia times. All patients were given cyclosporin and low-dose prednisolone for immunosuppression. Pretransplant levels of intact PTH were significantly greater in group B than in group A (203.5 +/- 193.1 pg/ml versus 81.7 +/- 45.2 pg/ml, P < 0.01). Group B patients had more transplant biopsies (50 versus 7) and a longer hospitalization time (33.4 +/- 10.9 days versus 21.9 +/- 11.9 days, P < 0.01), although serum creatinine on the day of discharge was higher in group B (1.77 +/- 0.51 mg/dl versus 1.5 +/- 0.45 mg/dl, P < 0.05). We conclude that patients with secondary hyperparathyroidism as assessed by measuring circulating levels of intact PTH have an increased incidence of ATN.
Nephrol Dial Transplant 1993
PMID:Secondary hyperparathyroidism and acute tubular necrosis following renal transplantation. 838 41

Macroscopic haematuria is common in IgA nephropathy, but its significance and influence on prognosis remains uncertain. We compared the clinical and pathological features of 11 adult patients with primary IgA nephropathy who had had a renal biopsy during or shortly after a bleeding episode. Six patients developed transient acute renal failure (ARF) (group 1) and five did not (group 2). Patients of group 1 had a higher percentage of tubular red-blood-cell (RBC) casts (P < 0.05) and of glomerular crescents (P < 0.001). However, crescents were focal and involved less than 50% of glomeruli. Acute tubular necrosis was only present in patients of group 1, and ARF was attributed to the acute tubular changes rather than to the glomerular lesions. Despite a prolonged duration of ARF (mean: 38 days), further outcome did not differ in patients of both groups. We suggest that acute tubular damage and/or tubular obstruction by RBC casts should be considered in any patient who develops ARF soon after a haematuric episode.
Nephrol Dial Transplant 1993
PMID:Acute reversible renal failure with macroscopic haematuria in IgA nephropathy. 838 83

Intestinal-type alkaline phosphatase (IAP) has been localized to the S3 segment of the renal tubule in previous studies, a site believed to be particularly vulnerable to toxic and ischaemic damage. During a 17-month period a pilot study of the value of urinary enzyme measurements (IAP and tissue non-specific alkaline phosphatase--TNAP, using monoclonal antibody-based immunoassays, and N-acetyl-beta-glucosaminidase--NAG, using colorimetric assay) in 50 prospectively followed cases of acute renal failure (ARF) was performed. Urinary enzymes were measured at initial evaluation ('start'), and then each day for 14 days, with the highest enzyme value ('peak') also used for analysis. Patients were divided into prerenal (n = 16), renal (n = 28), postrenal (n = 6) categories according to standard criteria. Of the renal ARF patients 23 of 28 had acute tubular necrosis (ATN), 3 of 28 acute interstitial nephritis (AIN), and 2 of 28 acute glomerulonephritis (AGN); 18 of 50 had a fatal outcome and 1 of 50 was dialysis-dependent at discharge ('poor' prognosis group), while 31 of 50 survived hospital without becoming dialysis-dependent ('good' prognosis group). Median enzyme concentration were increased in 'poor' compared to 'good' prognosis patients: start IAP 3.2 versus 2.2 U/g creat (NS), start NAG 48.6 versus 13.7 (P < 0.01), start TNAP 3.5 versus 0.9 (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1993
PMID:Urinary enzymes in acute renal failure. 839 30

Twenty-six cases (4.8%) from a total of 540 patients with acute renal failure (ARF) of diverse aetiology had ARF in association with falciparum malaria. Their ages ranged from 15 to 85 years (mean 31.2). Urinary sediment abnormalities and proteinuria (less than 1 g/24 h) were observed in 15 (57.7%) cases. The probable underlying factors leading to ARF were: volume depletion 17 (65.3%), intravascular haemolysis 8 (30.8%), hyperparasitaemia 8 (30.8%), cholestatic jaundice 6 (23%), and hypotension 5 (19.2%). Dialysis therapy was required in 15 patients (57.7%) as they had severe renal failure, and the remaining 11 patients improved with supportive measures. All patients received antimalarial therapy. The clinical course of ARF was consistent with acute tubular necrosis in 20 patients. Six cases were subjected to percutaneous renal biopsy. One patient showed histological features of necrotizing glomerulonephritis along with acute tubulointerstitial nephritis. The biopsies in the other five patients showed features of acute tubular necrosis in three, and acute interstitial oedema with patchy tubular necrosis in two. The mortality rate was 30.8%. Thus falciparum malaria, which has been an important cause of ARF in certain highly endemic zones of India, is showing an increasing prevalence in other parts such as Eastern Uttar Pradesh due to an imbalance between the increasing population and inadequate sanitary facilities, which further worsen during floods.
Nephrol Dial Transplant 1996 Dec
PMID:Acute renal failure in falciparum malaria--increasing prevalence in some areas of India--a need for awareness. 930 75

Urinary excretion of aluminium after a successful transplant can reverse pre-transplant aluminium intoxication. We have evaluated the time course of urinary aluminium excretion and its correlation with several parameters of renal function and mineral metabolism in 49 patients (33 men and 16 women) with a wide range of pre-transplant serum aluminium concentrations, performing sequential determinations at pre-transplant time and at 7, 30, 60, and 90 post-transplant days. Mean serum aluminium at pre-transplant was 54.5+/-46.8 microg/l decreasing progressively to 28.7+/-24.4 microg/l at 90 days (P<0.0002), paralleling the decrease in serum creatinine. Urinary aluminium decreased from 63.0+/-77.9 to 52.4+/-55.9 microg/l at 90 days (P<0.0001). The maximum urinary aluminium/creatinine was 1.8+/-2.7 at 7 days and was associated with the greatest fractional excretion of sodium (4.7+/-5.1%), and the lowest tubular reabsorption of phosphate (55.7+/-25.1%). The fractional excretion of aluminium was also greatest at day 7 (1.1+/-0.9%) when serum creatinine was still elevated (3.6+/-2.3 mg/dl). At each period of time after transplantation fractional excretion of aluminium was similar in all patients despite disparate serum aluminium concentrations. Fractional excretion of aluminium was highest in those patients who developed post-Tx acute tubular necrosis (0.7+/-0.5 vs 1.5+/-1.0%, P=0.008). We found a direct positive correlation (r=0.43; P<0.002) between urinary aluminium and urinary phosphate. Basal levels and sequential changes in serum PTH, calcium, and phosphate did not correlated with fractional excretion of aluminium. These findings suggest: (i) urinary aluminium remains elevated during prolonged periods after transplant and is probably a marker of pre-transplant tissue aluminium accumulation; (ii) post-transplant fractional excretion of aluminium seems to correlated positively with other evidences of renal tubular dysfunction. Early post-transplant tubular malfunction could significantly enhance urinary aluminium elimination.
Nephrol Dial Transplant 1998
PMID:Time course and functional correlates of post-transplant aluminium elimination. 956 31

The present report addresses the status of the renal dopaminergic system activity in patients afflicted with different renal disorders and in the remnant kidney of uninephrectomized (UNX) rats, based on the urinary excretion of L-DOPA, dopamine and amine metabolites. In renal transplant recipients with good recovery of graft function (group 1, n=11), the daily urinary excretion of DOPAC, but not that of HVA, was found to increase progressively throughout the first 12 days post-transplantation from 698+/-57 nmol in the first day to 3498+/-414 nmol on day 9, and then remained constant until day 12. This resulted in a 6-fold increase in the urinary DOPAC/dopamine ratios. In renal transplant recipients with acute tubular necrosis (group 2, n=8), the urinary levels of dopamine, DOPAC and HVA were approximately 30% of those in group 1. In a group of 28 patients with chronic renal parenchymal disorders, the daily urinary excretion of L-DOPA, free dopamine and dopamine metabolites (DOPAC and HVA) correlated positively with the degree of deterioration of renal function (P<0.01). However, the U(Dopamine/(L)-DOPA) and U(DOPAC/Dopamine) ratios in patients with chronic renal insufficiency were found to be similar to those observed in patients with normal renal function. In 14 IgA nephropathy (IgA-N) patients with near normal renal function, the changes in 24 h mean blood pressure when going from 20 to 350 mmol/day sodium intake correlated negatively with the daily urinary excretion of dopamine (r(2)=0.597, P<0.01). The urinary excretion of L-DOPA and dopamine in IgA-N patients with salt-sensitive (SS) blood pressure was lower than in salt-resistant (SR) patients (P<0.05), irrespective of their daily sodium intake. However, the rise in urinary dopamine output during salt loading (from 20 to 350 mmol/day) was greater (P<0.05) in IgA-N SS patients (21.2+/-2.5% increase) than in SR patients (6.3+/-1.4% increase). Fifteen days after the surgery, uninephrectomy (UNX) in the rat was accompanied by an enhanced (P<0.05) urinary excretion of dopamine (36+/-3 vs 26+/-2), DOPAC (124+/-11 vs 69+/-6) and HVA (611+/-42 vs 354+/-7) (nmol/g kidney/kg body weight). This was accompanied by an increase in V(max) values for renal aromatic L-amino acid decarboxylase in the remnant kidney of UNX rats (P<0.05). Sch 23390, a D1 dopamine receptor antagonist, produced a marked reduction in the urinary excretion of sodium in UNX rats, whereas in sham-operated rats the decrease in urinary sodium did not attain a significant difference. It is concluded that the study of the renal dopaminergic system in patients afflicted with renal parenchymal disorders should address parameters other than free urinary dopamine, namely the urinary excretion of L-DOPA and dopamine metabolites (DOPAC and HVA). It is also suggested that in SS hypertension of chronic renal parenchymal diseases, renal dopamine produced in the residual tubular units may be enhanced during a sodium challenge, thus behaving appropriately as a compensatory natriuretic hormone.
Nephrol Dial Transplant 2001
PMID:Renal dopaminergic mechanisms in renal parenchymal diseases and hypertension. 1136 22

Tacrolimus is a cornerstone immunosuppressive agent in renal transplantation and compared with cyclosporin, its use is associated with a reduced incidence of acute rejection. Optimizing immunosuppressive management in the early post-transplant period is important for achieving long-term graft function and survival. In attempts to improve the long-term outcomes of renal transplantation further, tacrolimus has been combined with two novel immunosuppressive agents, mycophenolate mofetil (MMF) and sirolimus, with encouraging results in terms of patient and graft survival, acute rejection rates and renal graft function. Tacrolimus in combination with MMF adjunctive therapy showed significantly better graft survival in patients with delayed graft function, fewer episodes of corticosteroid-resistant rejection and better renal function at the 3-year follow-up compared with cyclosporin microemulsion plus MMF immunosuppression. A tacrolimus plus MMF regimen was also effective for renal transplant recipients at our centre in Pennsylvania, resulting in excellent survival and rejection rates at 1 year post-transplantation. The 3-month results of a US multicentre study comparing tacrolimus in combination with either MMF or sirolimus showed these two treatment regimens to be equivalent in terms of patient and graft survival, delayed graft function, the incidence of biopsy-confirmed acute rejection and renal graft function, although differences were apparent in terms of acute tubular necrosis and hyperlipidaemia. In conclusion, the development of a new immunosuppressive regimen in renal transplantation should take account of factors that influence graft function, both in the short and long term, as a way of optimizing individual maintenance therapy.
Nephrol Dial Transplant 2003 May
PMID:Tailoring tacrolimus-based immunotherapy in renal transplantation. 1273 59

Despite the importance of endothelial injury and healing for primary and secondary renal disease and the availability of genetically engineered mouse models, to date no generally applicable murine disease model with site-specific renal endothelial injury has been established. We induced specific microvascular renal injury via selective renal arterial perfusion of the lectin concanavalin A (Con A) followed by sheep anti-concanavalin A and harvested tissues after 4 h, 24 h, days 3 and 7. Compared to control kidneys, histological evaluation demonstrated endothelial cell injury with subsequent complement, and platelet activation and thrombosis by light and electron microscopy. Mouse kidneys showed histologic evidence of severe glomerular and peritubular microvascular thrombosis with acute tubular necrosis, proteinuria, increased BUN and presence of schistocytes. Initial cell death of intrinsic renal cells resulted in a decrease of the glomerular cell count by 50% after 4 h followed by a proliferative response of glomerular (day 3, P < 0.05), interstitial (day 3, P < 0.05) and tubular cells leading to increased total glomerular cell count by day 7. This study establishes the Con A anti-Con A model as specific endothelial injury model in the mouse kidney providing a novel tool for investigating endothelial injury and repair mechanisms as well as elucidating the role of platelets in genetically engineered mice.
Nephrol Dial Transplant 2008 Apr
PMID:A murine model of site-specific renal microvascular endothelial injury and thrombotic microangiopathy. 1804 20


<< Previous 1 2 3 4 Next >>