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)

We have performed 115 "zero-hour" biopsies of transplanted kidneys since 1994. Donor kidneys were divided into five groups, based on the morphological findings of "zero-hour" biopsies. No morphological abnormalities were found in 38.26% of the cases (group 1). Arteriolosclerosis was present in 22.61% of donor kidneys (group 2). Specific morphological alterations, i.e. acute tubular necrosis (24.35%), tubulointerstitial nephritis (5.22%) or glomerulonephritis (9.56%) were detectable in the remaining cases (groups 3-5). During an average of 644 days after transplantation clinical and histological follow-up were performed. According to our observations: 1. Higher creatinine was found in patients with grafts with arteriolosclerosis (group 2). 2. There were more non-viable grafts and longer periods of delayed graft function in patients with acute tubular necrosis (group 3). 3. Higher serum creatinine, more frequent rejections with the need of secondary hemodialysis were observed in patients who received a kidney with "zero-hour" biopsy of tubulointerstitial nephritis (group 4). 4. The only complication observed in patients with glomerulonephritis donor kidneys was delayed functioning of the graft (group 5). Biopsies did not cause complication in any of our patients. In conclusion, "zero-hour" biopsies can be useful and safe tools to predict early graft function. Besides, "zero-hour" biopsies help histological interpretation of consecutive graft re-biopsies.
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PMID:[Clinical value of "zero-hour" biopsy in kidney transplantation]. 1129 59

Acute renal insufficiency (ARI) complicated the course of the underlying process, including primary and secondary glomerulonephritis, interstitial nephritis, pyelonephritis, dysmetabolic nephropathies, urolithiasis, tubulopathies, renal congenitae defects and injuries in 136 of 1695 children with nephrological diseases hospitalized at Republican Pediatric Renal Center during the last decade. In 69.1% cases ARI developed by the renal type, in 23.5% cases was caused by prerenal factors, and rarely (in 7.4% cases) by postrenal factors. Renal ARI in children was caused by 5 causes, including glomerulonephritis (47%), acute tubular necrosis (19%), interstitial nephritis (14%), vascular disorders (11%) resultant from vasculitis, renal vein thrombosis, and acute crystalluria (9%) which developed in the presence of grave dysmetabolic nephropathy. Among three clinical variants of ARI the most severe was observed in renal ARI leading to grave endogenous intoxication and pronounced decompensation of renal function. More benign course of renal ARI caused by acute tubular necrosis or acute crystalluria differed significantly from prerenal ARI by a more pronounced endogenous intoxication, increased fractionated sodium excretion, and renal insufficiency index higher than 1.
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PMID:[Diagnosis of acute renal failure in pediatric nephrology]. 1133 30

It was reported that reactive oxygen metabolites play an important role in the pathogenesis of several renal diseases including glomerulonephritis, ischemia and acute tubular necrosis. However, the effect of oxidants and protective effect of sex steroid hormones on Na+/glucose cotransporter of renal proximal tubular cells is not yet elucidated. In the present study, we examined the effect of sex steroid hormones against tert-butyl hydroperoxide (t-BHP)-induced alteration of Na+/glucose cotransporter activity in primary cultured rabbit renal proximal tubule cells (PTCs). t-BHP inhibited alpha-methyl-D-glucopyranoside (alpha-MG) uptake in a dose-dependent manner. t-BHP-induced inhibition of alpha-MG uptake was due not to Km but to the decrease of Vmax. 0.5 mM t-BHP-induced inhibition of alpha-MG uptake was significantly blocked by estradiol-17beta, but not by progesterone and testosterone. This protective effect was not blocked by estrogen receptor antagonist or transcription and translation inhibitor. In addition, 0.5 mM t-BHP increased [3H]-arachidonic acid (AA) release and Ca2+ uptake. These effects of t-BHP were also significantly blocked by estradiol-17beta, but not by progesterone and testosterone. Protective efficacy of estradiol-17beta on t-BHP-induced inhibition of alpha-MG uptake is exhibited between antioxidants and iron chelators. In conclusion, estradiol-17beta, but not progesterone and testosterone, partially prevented t-BHP-induced inhibition of alpha-MG uptake through its antioxidant activity dependent upon phenol structures and inhibition of AA release and Ca2+ influx.
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PMID:Effects of sex hormones on Na+/glucose cotransporter of renal proximal tubular cells following oxidant injury. 1152 8

This review evaluates the various causes and management of acute renal failure (ARF) in children. ARF is defined as an abrupt decline in the renal regulation of water, electrolytes and acid-base balance, and continues to be an important factor contributing to the morbidity and mortality of critically ill infants and children. The common causes of ARF in children include acute tubular necrosis secondary to various causes (including congestive heart failure and sepsis), haemolytic uremic syndrome, and glomerulonephritis and urinary tract obstruction. Ischaemia, toxins (including drugs) as well as primary parenchymal disease, have to be considered and ARF can also be a complication of systemic disease. The basic principles of management are avoidance of life-threatening complications, maintenance of fluid and electrolyte balance, and nutritional support. Only a few patients require specific management of the underlying disorder, although it is important to diagnose these conditions. Knowledge about the use of drugs for the prevention of ARF is scarce. Mannitol, low-dose dopamine, calcium channel antagonists, atrial natriuretic peptide and albumin have been evaluated and, where possible, meta-analyses are cited. Mannitol treatment appears to be warranted prophylactically after paediatric renal transplantation. Albumin infusion can reverse prerenal ARF in children with nephritic syndrome. For treatment of the complications of hyperkalaemia and volume overload, salbutamol, insulin and glucose infusion and diuretics such as furosemide and sodium bicarbonate, are discussed. All of the major dialysis modalities (peritoneal dialysis, haemodialysis and continuous haemofiltration) can be used to provide equivalent solute clearance and ultrafiltration. The indication for, and the choice of the modality depend on the patient requirements and on local resources, and should involve the care of a paediatric nephrologist. Peritoneal dialysis requires minimal equipment and infrastructure, is easy to perform and remains the favoured modality of renal replacement therapy in children. However, continuous haemofiltration is an excellent alternative to peritoneal dialysis in patients with ARF and severe fluid overload. Dialysis remains the most important tool to bridge the time needed for recovery of renal function. There is increasing evidence that more intense use of dialysis may improve the overall prognosis.
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PMID:Acute renal failure in children: aetiology and management. 1173 64

The differential diagnosis for patients with acute renal failure of their native kidneys, as a result of primary intrarenal disease, includes acute tubular necrosis, glomerulonephritis, and interstitial nephritis. The role of MAG3 renography has not been studied in this setting. The authors describe four patients with acute renal failure in whom MAG3 renal imaging reliably identified acute tubular necrosis, as confirmed by follow-up kidney biopsies. In contrast to the poor parenchymal uptake observed in glomerulonephritis and interstitial nephritis, MAG3 shows a distinctive pattern in patients with acute tubular necrosis. For patients with acute renal failure, a renal scan can facilitate decision-making regarding the initiation of therapy.
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PMID:The role of technetium-99m MAG3 renal imaging in the diagnosis of acute tubular necrosis of native kidneys. 1185 1

A 15-year-old boy developed nephrotic syndrome and acute renal failure 4 years after allogenic bone marrow transplantation (BMT) for lymphoid crisis of chronic myelocytic leukemia. On admission, he presented with clinical features of chronic GVHD including transient exacerbation of cholestatic liver injury. Renal biopsy showed diffuse proliferative glomerulonephritis with cellular crescents. The patient was treated with methylprednisolone pulse therapy (1 g/day, for 3 days) followed by oral prednisolone. Renal function gradually improved but nephrotic state was persistent. A second renal biopsy showed improvement of acute tubular necrosis and endocapillary proliferation and transformation of crescents into a fibrous form. After tapering of oral prednisolone, cyclophosphamide was started, which resulted in a gradual improvement of proteinuria. Several cases of nephrotic syndrome occurring after BMT have already been reported, but most cases had membranous nephropathy. In our case, renal biopsy revealed diffuse proliferative glomerulonephritis with findings of active cellular immunity, and aggressive treatment resulted in attenuation of these findings. Moreover, chronic GVHD-related liver injury was noted at the time of this episode. Our findings suggest that chronic GVHD may be complicated with diffuse proliferative glomerulonephritis through unknown cellular immune mechanism.
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PMID:Diffuse proliferative glomerulonephritis after bone marrow transplantation. 1235 94

Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The potential role of apoptosis ranges from induction and progression to repair of renal injury. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. However, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis on the acute tubular necrosis.
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PMID:Apoptotic cell death in renal injury: the rationale for intervention. 1247 91

Renal diseases unique to the tropics are those that occur in association with infectious diseases including dengue hemorrhagic fever, typhoid fever, shigellosis, leptospirosis, lepromatous leprosy, malaria, opisthorchiasis, and schistosomiasis. These renal complications can be classified on the basis of their clinical and pathologic characteristics into acute transient reversible glomerulonephritis, chronic progressive irreversible glomerulonephritis, amyloidosis, and acute renal failure (ARF) resulting from acute tubular necrosis, acute tubulointerstitial nephritis, and thrombotic microangiopathy. Certain primary glomerular diseases including immunoglobulin (Ig) M nephropathy and focal segmental and global glomerulosclerosis are prevalent in some tropical countries. Renal complications of venomous snakebites also are common in the tropics. This article discusses and summarizes important works in the literature in respect to the clinical syndromes, pathologic features, and pathogenesis of tropical renal diseases both in humans and experimental animal models.
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PMID:Pathology of renal diseases in the tropics. 1256 4

In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.
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PMID:Acute renal failure due to intrinsic renal diseases: review of 1122 cases. 1273 29

We describe three patients with acute renal failure after the onset of gross haematuria. In all patients a presumptive diagnosis of rapidly progressive glomerulonephritis was made and immunosuppressive therapy initiated. A renal biopsy was performed in two patients, which showed evidence of IgA nephropathy. Extracapillary proliferation was seen in a few glomeruli. The most notable abnormality was acute tubular necrosis with intraluminal erythrocytes and cell debris. In the third patient, who was known to have longstanding glomerular haematuria, acute tubular necrosis was considered likely after review of the urinary sediment. Despite the fact that immunosuppressive therapy was stopped, renal function rapidly returned to normal in all these patients. We feel that our patients and additional literature data demonstrate that in patients with glomerular disease a reversible acute renal failure can occur that is caused by acute tubular necrosis mediated by haematuria. Recognition of this entity will prevent unnecessary long-term immunosuppressive therapy.
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PMID:Acute renal failure in patients with glomerular diseases: a consequence of tubular cell damage caused by haematuria? 1285 25


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