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)

Renal involvement in Hansen's disease was evaluated in 94 Portuguese patients, average age and duration of disease of 47.6 and 6.8 years respectively. Sixty-seven were studied retrospectively and 27 prospectively; renal biopsy was obtained in 4, fat-tissue needle aspiration for amyloidosis in 20, and tubular function was tested in ten. Mild proteinuria and/or haematuria was found in 33 patients, the severity increasing during erythema nodosum leprosum reactions, but without overt nephritic or nephrotic syndrome. Two patients had renal amyloidosis on biopsy and two more were confirmed by fat biopsy, a 10.5% incidence in those studied prospectively; all but one were of the lepromatous type, with frequent bouts of erythema nodosum leprosum. The two other renal biopsies showed mesangial glomerulonephritis, and one unexplained acute tubular necrosis; none had immune deposits by immunofluorescence. Proximal acidification was always normal, distal acidification tested by bicarbonate infusion was abnormal in one of nine patients, and six of nine patients had concentration defects. Leprosy causes frequent urinary sediment changes and concentration defects, usually without clinical expression; proteinuria and/or glomerular involvement is mainly due to amyloidosis.
Nephrol Dial Transplant 1989
PMID:Renal involvement in leprosy. 249 59

This study records our experience with 40 infants who developed acute renal failure in a tropical environment over a period of 2 years. All the patients required intermittent peritoneal dialysis. Septicaemia (88%) and acute gastroenteritis (55%) constituted the leading causes of acute renal failure. Haemolytic uraemic syndrome was present in six (18%) patients. An elevated serum creatinine (85%), metabolic encephalopathy (75%), uncompensated metabolic acidosis (75%) and hyperkalaemia (48%) were the major indications for dialysis, while fluid overload was present in only 18% of the infants. Intermittent peritoneal dialysis was used in all the patients and was found to be effective. Procedural complications were minor and infrequently encountered. The clinical course and laboratory data consistent with haemolytic uraemic syndrome was observed in six patients, and acute tubular necrosis was the predominant renal lesion in the remainder. Mortality was 75%. The aetiology of acute renal failure in infants in the tropics differs significantly from that in the West, and even within a given country marked regional variations exist.
Nephrol Dial Transplant 1989
PMID:Acute renal failure in infants in the tropics. 250 74

Erythropoiesis has been examined in relation to kidney function in 38 patients during the 3-month period following successful renal transplantation, using serial determinations of erythropoietin, haemoglobin, and creatinine. Two peaks of serum erythropoietin were observed: an early peak that occurred within 2 days of transplantation and was observed in ten patients, and a late one between 8 and 30 days, observed in 28 patients. The early peak did not produce an increase in haemoglobin and occurred only in the presence of delayed onset of graft excretory function when serum creatinine was greater than 1000 mumols/l. The ineffectiveness of the early peak may be due to the uraemic environment, which is probably a sequel of the tubular damage associated with postoperative acute tubular necrosis. The late peak followed a decrease in serum creatinine to less than 200 mumols/l and was associated with an increase in haemoglobin of 3-4 g/dl during the next 2-6 weeks.
Nephrol Dial Transplant 1989
PMID:The initiation of erythropoiesis following renal transplantation. 251 29

A sandwich ELISA assay has been formatted from two commercially available murine monoclonal antibodies, URO-4 and URO-4a, directed against a 120,000 dalton glycoprotein, the adenosine deaminase binding protein (ABP), found on the brush border of the renal proximal tubular epithelial cell. Untimed urine samples from 37 normal individuals and urinary ABP less than 0.1 AU; 37 patients with pure glomerular disease had ABP less than 0.4 AU (with 29, or 76% less than 0.2 AU); 10 patients with pre-renal azotaemia had ABP less than 0.6 (with 8, or 80% less than 0.3 AU). In contrast, 79 patients with post-ischaemic acute tubular necrosis had ABP greater than 0.6 AU. Acute renal failure due to myoglobinuria, contrast dye, and aminoglycoside toxicity were all associated with urinary ABP greater than 1.0 AU. In addition, all six patients with acute bacteraemic pyelonephritis had ABP greater than 0.7 AU, as opposed to ABP less than 0.2 AU in the urines of 12 women with acute cystitis. We conclude that this monoclonal antibody based urinary assay is a sensitive measure of renal proximal tubular injury, reliably distinguishes acute tubular from glomerular disease, and may be helpful in differentiating forms of urinary tract infection.
Nephrol Dial Transplant 1987
PMID:Diagnosis of renal proximal tubular injury by urinary immunoassay for a proximal tubular antigen, the adenosine deaminase binding protein. 288 57

In a prospective study the diagnostic value of urinary thromboxane B2 (TXB2) and beta 2-microglobulin (beta MG) in renal allograft rejection was studied in 34 patients after transplantation. Twenty-four episodes of rejection were diagnosed by clinical symptoms. The clinical diagnosis of rejection was confirmed by an increase of urinary TXB2 in 21 (88%) cases. The augmented renal excretion of TXB2 proceded the clinical signs of rejection for 2.0 +/- 0.75 days. The symptoms in the remaining three (12%) cases of supposed allograft rejection without increased urinary TXB2 were caused by non-immunological events (urinary tract infection, acute tubular necrosis). No elevated TXB2 excretion was observed during urinary tract infection, sepsis, and acute tubular necrosis whereas urinary beta MG increased during these events as during transplant rejection. Urinary TXB2 was found to be an early, specific, and sensitive marker of renal allograft rejection with greater reliability than beta MG excretion or clinical signs of rejection.
Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985
PMID:Thromboxane B2 and beta 2-microglobulin as early indicators of renal allograft rejection. 388 70

We have serially measured serum beta 2 M microglobulin in a series of transplant recipients along with other standard clinical parameters. Independent comparison of the beta 2 M results leads to the following conclusions: 1. Beta 2 M is superior to the Scr in detecting acute rejection, with diagnostic elevations occurring 2 to 7 days before Scr increase. The observation is valid for all rejection episodes. 2. Beta 2 M decreases prior to or simultaneously with the Scr following successful rejection therapy or beginning resolution of acute tubular necrosis. 3. Abnormal beta 2 M following rejection therapy invariably heralds another rejection episode within 10-20 days, despite the Scr having returned to baseline. 4. Beta 2 M remains normal in high grade ureteral obstruction despite increased Scr. 5. Beta 2 M is remarkably increased in patients with viremia, despite minimal change in Scr. Beta 2 M remains normal in lower UTI from bacterial origin. Beta 2 M appears to be a major contribution in the monitoring of the renal transplant recipient which may have significant impact on therapeutic decisions in the future. In addition, it provides a reliable in vitro parameter which can be used to further assess specific treatment variables in a prospective controlled protocol approach.
Proc Clin Dial Transplant Forum 1980
PMID:Serum beta-2-microglobulin: an adjunctive monitoring test in renal transplantation. 618 Apr 32

Post transplant acute tubular necrosis (ATN) is responsible for approximately 90% of acute renal failure episodes occurring within the first few weeks following renal transplantation. This phenomenon is observed in 34% of cadaver transplant recipients and 9% of those with live donor kidneys. Although the exact cause of post transplant ATN remains unknown, the following factors are thought to be associated with a higher incidence of ATN: 1) donor hypotension, 2) prolonged "warm ischemia time", 3) increased vascular resistance with poor perfusate flow, 4) presence of "ligandin" or excess lactate in the renal perfusate, 5) reduced allograft blood flow, 6) cold lymphocytotoxins in the patient's serum and 7) administration of nephrotoxic drugs particularly to the hypovolemic graft recipients. Therapeutic maneuvers such as hydration of the donors and recipients, harvesting the kidneys from heart beating cadavers, donor pretreatment with massive doses of corticosteroids and alpha-adrenergic blocking agents and warming of the graft immediately after vascular anastomosis, seem to reduce the incidence of ATN. Since the management differs significantly, post transplant ATN has to be distinguished from other causes of acute renal failure such as the renal artery thrombosis, hyperacute rejection and obstruction of the urinary tract. The tests which are of use in the differential diagnosis include, 131-I Hippuran renogram, transplant ultrasound, renal angiogram, retrograde pyelogram and renal transplant biopsy. Patients with established ATN should undergo every other day dialysis, under low dose or regional heparinization, until the creatinine clearance improves to 20 ml/min. The dose of azathioprine has to be reduced to prevent bone marrow toxicity. Even though there are short term disadvantages, the post transplant ATN does not appear to exert any detrimental effects in the long run. However, this issue remains controversial in the published reports.
Clin Exp Dial Apheresis 1983
PMID:Post transplant acute renal failure: a review. 634 76

In this study the hippuran uptake capacity (HUC) in 32 patients with an acute deterioration of renal function was measured. The HUC2 is the ratio between the activity accumulated in the kidneys in the first two minutes, divided by the injected dose, which was measured by the gammacamera, during standardised renography. Thirteen patients had an acute glomerular disease (AGD) and 19 patients had acute tubular necrosis (ATN). During the acute deterioration of renal function, the HUC2 values ranged between 0 and 3.0 in the AGD group and between 1.9 and 8.7 in the ATN group. In only one patient of this latter group was the HUC2 value below three. Measurement of HUC2 is useful in the differential diagnosis of acute renal failure. It can be performed in the absence of urine production and indicates renal blood perfusion despite complete absence of filtration. When the HUC2 value is higher than three, ATN is the most probable aetiology of the acute renal failure and recovery of renal function can be expected. Values below this limit most probably indicate AGD.
Proc Eur Dial Transplant Assoc 1983
PMID:The predictive value of hippuran uptake in acute renal failure. 665 84

The sonographic changes occurring during post transplant acute tubular necrosis and rejection are discussed. Seven patients with proven ATN are shown to maintain normal sonographic features and exhibit normal hypertrophy. In contrast during acute rejection the findings in 21 patients included in order of frequency the following 1) sudden increase in renal volume, 2) prominent medullary pyramids, 3) abnormal echogenicity, 4) decreased amplitude of the central sinus echoes, 5) increased cortical thickness, 6) crescent shaped fluid collections and 7) indistinct corticomedullary boundary.
Proc Eur Dial Transplant Assoc 1980
PMID:Sonographic features of ATN and of acute rejection in renal allografts. 701 82

Acute tubular necrosis is the most common cause of acute renal failure making up two-thirds of such cases. Mortality is best correlated to basic disease. Surgery, particularly in the abdomen, carries an unusually sinister prognosis. The influence of age on outcome is controversial. Intensified dialysis, early reoperations, hyperalimentation, and possibly continuous dialysis and antibiotic barrage deserves close investigation as tools of improving survival. Almost all surviving patients recover renal function within 30 days and beyond two months recovery almost never occurs. Approximately 3% of the patients initially suspected of having acute tubular necrosis will need chronic hemodialysis indefinitely or have a transplant to regain renal function. The older patient seems to be more susceptible to this problem. Delayed recovery and chronic renal failure is unusual. High dose loop diuretic therapy and hyperalimentation with intravenous amino acids may shorten the time for recovery, although considerable controversy exists.
Clin Exp Dial Apheresis 1981
PMID:Recovery from acute renal failure. 733 33


<< Previous 1 2 3 4 Next >>