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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

Acute renal failure in liver disease includes prerenal renal failure, acute tubular necrosis (ATN) and hepatorenal syndrome (HRS). Patients with liver cirrhosis are susceptible to prerenal renal failure because of gastrointestinal bleeding, diuretics and paracentesis etc. ATN is more common in patients with obstructive jaundice but it also develops as a result of prolonged prerenal renal failure. HRS is a functional form of oliguric acute renal failure, occurring in patients with advanced liver disease in the absence of known cause of renal failure. Intrarenal vasoconstriction, attributable to a decrease in effective arterial blood volume, induced by peripheral arterial vasodilation, is proposed to play a causative role. Central hemodynamic monitoring is useful to distinguish HRS from other reversible conditions with renal failure in liver disease.
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PMID:[Renal damage in liver cirrhosis: pathophysiology and management]. 811 86

During the first month after bone marrow transplantation, approximately 15% of patients develop acute renal failure (ARF). This usually occurs in the setting of hepatic veno-occlusive disease (VOD). Prior clinical data have suggested that this form of ARF has a hemodynamic basis, analogous to the hepatorenal syndrome (HRS). If so, then proximal tubular injury would not be expected. To directly test this hypothesis, enzymuria (N-acetyl-beta-D-glucosaminidase [NAG]) was quantitated in the following groups of patients within the first 35 days after BMT: (1) VOD+ARF (serum creatinine level > 1.5 mg/dL; N = 10); (2) VOD with relatively normal renal function (serum creatinine level < 1.5 mg/dL; N = 11); and (3) patients without hepatic or renal complications (BMT controls; N = 12). For comparison, NAG was also quantitated in the following groups of non-BMT patients: (1) toxic/ischemic acute tubular necrosis (ATN) (N = 10); (2) jaundice without azotemia (N = 5); and (3) HRS (N = 6). Urine samples from eight healthy subjects established normal NAG concentrations (2.5 +/- 0.5 microU/mg urinary creatinine; mean +/- SE). All non-BMT patients with ATN had markedly elevated NAG levels (61 +/- 12; P < 0.001), validating the test as a marker of tubular damage. NAG concentrations were significantly elevated in all of the control BMT patients (24 +/- 3; P < 0.01), and the presence of VOD was associated with further striking increments (approximately 50 times normal). However, the degree of enzymuria was virtually identical for VOD patients with (125 +/- 27) and without (122 +/- 17) ARF. Jaundice in a non-BMT setting was associated with only mild NAG elevations (11 +/- 2). However, striking enzymuria was noted in all HRS patients (61 +/- 20), equaling the levels seen with ATN. The following conclusions were derived: (1) subclinical tubular injury, as defined by enzymuria, appears to be ubiquitous after BMT; (2) VOD dramatically increases the extent of enzymuria; (3) the degree of enzymuria in VOD patients is not correlated with renal dysfunction, implying that the associated ARF has a large hemodynamic component; and (4) HRS and ATN manifest comparable degrees of enzymuria, suggesting that substantial tubular damage exists in both of these forms of ARF.
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PMID:Marked enzymuria after bone marrow transplantation: a correlate of veno-occlusive disease-induced "hepatorenal syndrome". 874 94

A specific medical therapy for 'the hepatorenal syndrome' (HRS) is not available. However, the increasing knowledge of the mechanisms involved in the development of HRS leads to new therapeutic approaches to this syndrome of functional renal failure. Recognition and prevention of precipitating factors, the correction and treatment of prerenal failure and acute tubular necrosis are particularly important in the treatment of patients with liver cirrhosis, ascites and hepato-renal failure. Vasoconstrictor agents (ornipressin, dopamine) are administered to achieve an improvement of the systemic circulation. Definitive therapy of HRS is liver transplantation.
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PMID:[Therapy of hepatorenal syndrome]. 906 19

Acute renal failure has recently been recognized as a rare complication of nonfulminant hepatitis A infection. The availability of a specific test for IgM antibody to hepatitis A should permit prompt diagnosis of the disease and a better evaluation of its association with acute renal failure. The exact mechanism for acute renal failure in hepatitis A is uncertain but glomerulonephritis, acute tubular necrosis and hepatorenal syndrome have been postulated. We report a patient with hepatitis A infection and acute renal failure most likely due to acute tubular necrosis.
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PMID:Acute anuric renal failure in nonfulminant hepatitis A infection. 965 39

In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis.
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PMID:Acute renal failure in patients with cirrhosis: perspectives in the age of MELD. 1254 Jul 70

Pretransplant renal failure is a well-known risk factor which adversely affects the prognosis after liver transplantation. We report a case with pretransplant renal failure and discuss the perioperative management of such patient. The patient was 62 year-old-woman who was diagnosed with end-stage liver disease due to primary biliary cirrhosis, for which living donor liver transplantation (LDLT) was indicated. Her pretransplant serum creatinine was 9.4 mg/dl due to combination of drug-induced (antibiotics) acute tubular necrosis and hepatorenal syndrome. The management of renal failure consisted of the avoidance of calcineurin inhibitor as an induction immunosuppression and the use of perioperative continuous hemodiafiltration (CHDF). The postoperative course of the patient was complicated with CMV pneumonia and acute rejection, however she recovered and discharged on 94 POD with well-preserved graft function and normal renal function without any adverse sequela. LDLT for patients with renal failure can be performed successfully by careful management.
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PMID:[Living donor liver transplantation for a patient with renal failure]. 1263 31

The use of folk remedies is widespread throughout Africa. Acute renal failure (ARF) is one of the most severe, but under-recognized, complications of folk remedy use. This report aims to describe the clinical presentation, outcomes, and nature of renal injury in patients with folk-remedy-associated ARF. Clinical data were evaluated retrospectively in 78 patients with ARF associated with recent folk remedy use. ARF was defined as elevated serum urea and creatinine above the age-appropriate normal ranges, persistent oligoanuria, worsening renal function with time, or need for dialysis. Overall mortality in patients with ARF was 41%. Mortality was higher in adults (45.5%) than in infants (36.6%), in patients with both renal and liver dysfunction (62.5%) than in those with renal dysfunction alone (22.6%), and in HIV-positive (44.4%) versus HIV-negative (34.6%) patients. Vomiting (51.3%) and diarrhea (43.6%) were the most frequent presenting symptoms. Metabolic acidosis (80.8%) and volume depletion (62.8%) were the most frequent clinical findings. The definable causes of ARF were pre-renal (26.9%), acute tubular necrosis (ATN; 26.9%), hepatorenal syndrome (6.4%), urinary tract infection/sepsis (7.7%), and primary renal disorders (7.7%). Twenty-seven patients had concomitant medical conditions unlikely primarily related to folk remedy ingestion. In conclusion, ARF occurring after use of folk remedies in South Africa is associated with significant morbidity and mortality. The most common contributors to ARF in this setting are volume depletion and ATN. Significantly, although a proportion of patients have underlying systemic or renal conditions that may contribute to renal dysfunction, in the majority of patients, folk remedy use appears to be the most likely proximate cause. In view of the large numbers of Africans living abroad, more widespread awareness of this important clinical problem needs to be raised.
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PMID:Acute renal failure associated with the use of traditional folk remedies in South Africa. 1571 33

Imaging techniques, especially ultrasonography and Doppler, can give an effective assistance in the differential diagnosis of acute renal failure (ARF). An resistance Index (RI) value >0.75 is reported as optimal in attempting differential diagnosis between acute tubular necrosis (ANT) and prerenal ARF. In hepatorenal syndrome (HRS) RIs is very increased. In some renal vasculitis, as nodose panarteritis (PN), hemolytic-uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), parenchymal perfusion is reduced and RI increased. In lupus nephritis the RI values are correlated with creatinine level and normal RI are considered as a good prognostic tool. In acute primitive or secondary glomerulonephritis (GN), RI value is normal, with diffuse parenchymal hypervascularization. In acute crescentic and proliferative GN and tubulo-interstitial disease, color Doppler (CD) and power Doppler (PD) reveal a decreased renal parenchymal perfusion, which correlates with increased RI values. In acute thrombosis of renal artery, US color Doppler (DUS) reveals either an absence of Doppler signal or a tardus-parvus pulse distal to the vascular obstruction. In this situation it is possible to visualize hyperthropic perforating vessels that redirect their flow from the capsular plexus to the renal parenchyma. In acute thrombosis of the renal vein Doppler analysis of parenchymal vessels reveals remarkable RI values, sometimes with reversed diastolic flow. In postrenal ARF an adjunct to the differentiation between obstruction and non obstructive dilatation can be found through RIs. Diagnostic criteria of obstruction as reported by literature are: RI>0.70 in the obstructed kidney and, mostly, a difference in RI between the 2 kidneys >0.06-0.1.
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PMID:The US color Doppler in acute renal failure. 1578 27

Renal failure in patients with liver disease is mostly none-organic: prerenal failure or hepatorenal syndrome (HRS). In addition there is organic renal failure, mostly acute tubular necrosis (ATN). In order to avoid functional renal failure cautious diuretic treatment as well as intravenous albumin substitution following paracentesis are pivotal. For prophylaxis of HRS patients with spontaneous bacterial peritonitis shall be given albumin infusions in addition to antibiotic treatment. Patients with HRS type I exhibit a very poor prognosis. Liver transplantation is the only established therapy with long-term success. To bridge the time to transplantation TIPS or terlipressin and albumin can be used.
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PMID:[Renal impairment in liver diseases]. 1704 10


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