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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute renal failure complicating bacterial septicemia has multiple potential causes, prominent among which are endotoxemic and antibiotic nephrotoxic injury. Because the toxic interactions of endotoxin and antibiotics cannot be manipulated for study in human disease, we have developed a model of this interaction in the rabbit. Toxicity was assessed by quantification of tubular necrosis and serum creatinine concentrations 48 hr after single-dose i.v. endotoxin and/or antibiotic administration. A minimally nephrotoxic quantity of endotoxin (Escherichia coli lipopolysaccharide 0111:B4, 0.5 mg/kg b.w.) significantly increased the nephrotoxicity of the cephalosporins cephaloglycin (60 mg/kg) and cephaloridine (90 mg/kg) and the aminoglycoside neomycin (60 mg/kg), each of which was mildly-to-minimally damaging by itself. In studies of the acute functional effects of endotoxemia, the lipopolysaccharide had different effects on the renal handling of the two cephalosporins. Endotoxin increased the uptake of cephaloglycin, but decreased uptake of cephaloridine, in renal cortex in the first 0.5 hr after antibiotic administration. However, a prolonged elevation of serum levels of cephaloridine allowed later uptake of toxic amounts of this cephalosporin. Although these findings suggest a role of altered transport in the endotoxin-cephalosporin toxic synergy, the synergy was not reduced when cephaloglycin was given 1.5 hr before the endotoxin, a time which allows substantial elimination of antibiotic before the endotoxemic insult. Studies in another laboratory have demonstrated an endotoxin-induced increase of cortical concentrations of aminoglycosides, which could be a mechanism of the augmented toxicity seen in the present study. It is concluded that endotoxemia causes significant augmentation of the nephrotoxicity of cephalosporin and aminoglycoside antibiotics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmentation of antibiotic nephrotoxicity by endotoxemia in the rabbit. 402 Jun 78

The results are reported of the incidence, severity, and description of infectious complications in 646 cases of acute renal failure (ARF). Infection was felt to represent an important cause of ARF in 34% of the cases. However, the frequency and extent of the infection varied according to the biologic classification. It was present constantly in postabortion ARF, was frequent in medical and in postoperative ARF, and was rare in traumatic and postpartum ARF. The renal lesions vary according to the cause of the infections. Staphylococcus septicemia, leptospiral infections, and rickettsial infections are the causes of interstitial nephritis; whereas gram-negative septicemia, probably via infectious shock, leads more readily to tubular lesions. Hemolytic septicemias most often cause tubular necrosis, although this is usually reversible. When the initial clinical picture is complicated by disseminated intravascular coagulopathy, bilateral cortical necrosis is a distinct possibility. During the established phase of ARF, infections are equally frequent, whether primary or secondary. The most frequent complications are septicemia and bacteremia--or local complications, most often pulmonary or urinary tract infections. The organisms are mainly Staphylococcus (often mephicillin-resistant) and gram-negative, usually E. coli. The most effective treatment is a combination of cephalothin and gentamicin. Pseudomonas infections are the most difficult to treat. The frequency of these serious infections and the difficulty with antibiotic therapy, often dangerous in renal insufficiency, stress the importance of preventive treatment of prophylactic measures. Infection was primarily responsible for 19% of the deaths in our series and may be also largely responsible for some of the persistent residual renal functional impairments.
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PMID:Infection in acute renal failure. 500 58

25 Patients with metastatic non-seminomatous testicular neoplasms were treated by surgery and cytostatic therapy using a combination consisting of Velban, Bleomycin, Cis-Platinum and/or Ifosfamid. In 22 patients this procedure induced a persistant complete remission with a mean observation time of 23 months. 2 patients died because of post-surgical complications after a second-look-lymphadenectomy. They suffered from rapidly progressive tumor disease. One patient died in a septicemia during chemotherapy. Our experience is that morbidity of an effective chemotherapy should not be underestimated. Transient bone marrow suppression, anorexia, alopecia and hyperpigmentation are unavoidable. However, severe vomiting, disturbed electrolyte metabolism, hemorrhagic cystitis, anemia and septicemia can well be managed by respective supportive care. Septicemia, for instance, may be treated with appropriate antibiotics without inducing tubular necrosis. Supportive measures also will avoid severe chronic defects of ear and kidney function.
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PMID:[Side-effects of polychemotherapy in metastatic testicular neoplasms (author's transl)]. 617 53

Prophylactic hemodialysis has been employed in the treatment of 15 patients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical necrosis (two), and poststreptococcal glomerulonephritis (one). Dialyses, usually lasting six hours each, were begun before clinical evidence of uremia developed in each patient and/or before the nonprotein nitrogen reached 200 mg.%, and were repeated daily or often enough to maintain the nonprotein nitrogen below 150 mg.%. The hypothesis underlying this technic postulates (1) that wasting, sepsis and impaired wound healing in these patients may reflect tissue injury by the same dialyzable toxic agents which produce the uremic symptoms that are readily reversible by dialysis, and (2) that repeated dialyses should therefore prevent both clinical uremia and the later, often lethal sequelae. The results contrast dramatically with our own past experience in treating patients with acute renal failure with a carefully executed medical regimen together with hemodialysis on conventional indications. Except in one instance of crush injury with progressive intracerebral damage, and one brief occasion in another individual, these patients experienced a stable, convalescent clinical course, remained free of uremic symptoms or chemical imbalances, ate at least three meals daily which were unrestricted in amount and composition, and were ambulatory between dialyses unless confined to bed by associated disease. Wounds healed well. Infection either did not occur, or subsided after appropriate therapy. Fluid restriction was liberalized by means of ultrafiltration with dialysis. Regional heparinization of only the extracorporeal circuit eliminated actual or impending bleeding as a contraindication to dialysis. Chronic vessel cannulation made the frequent dialyses possible, but may have provided the route for repeated, transient bacterial contamination of the blood stream in the first hour of many dialyses. Marked anemia, despite reticulocytosis, moderate to mild weight loss and some mental deficit persisted in spite of the general clinical improvement and well-being. Three patients with tubular necrosis died after seven, 11 and 26 days of oliguria; both patients with bilateral renal cortical necrosis also succumbed, on the seventy-third and ninety-second days of renal failure, and after 29 and 40 dialyses, respectively. At autopsy, evidence of sepsis was conspicuously absent. The remaining 10 patients survived. Thus some, but not all, clinical manifestations of acute renal failure appear to be favorably influenced by prophylactic dialysis treatment. Our initial experience in this group of 15 patients does not of course prove that freedom from complications and a significantly better outlook for survival can be assured to patients with acute renal failure by these methods. However, it seems to offer a reasonable hope of this possibility which we cannot attach to management by medical measures alone, or by dialysis on conventional indications. If this hope is realized in greatly extended, subsequent series, then it seems inevitable that some form of prophylactic dialysis, or some equally effective alternative, should be adopted in treating the majority of patients with acute renal failure.
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PMID:Prophylactic hemodialysis in the treatment of acute renal failure. Annals of Internal Medicine, 53:992-1016, 1960. 984 96

Analysis of early and late post-surgical complications in 44 cases of Studer's type bladder replacement due to carcinoma of the bladder performed over a 6-year period. Follow-up ranges between 6 months and 6 years. 4 patients died during the post-operative (9.09%): 1 myocardial infarction, 1 pulmonary embolism and 2 intestinal fistula. 28 patients (63.64%) had post-operative complications: 4 GI fistula (9.09%) 5 ileus (11.36%), 2 GI bleeding (4.54%), 1 ureteral fistula (2.27%), 1 ureteral stenosis, 6 urethro-intestinal fistula (13.36%), 1 tubular necrosis, 1 ruptured ureteral catheter, 5 wound infections (11.36%), 12 urine infections (27.27%), 6 sepsis (13.63%), 1 lymphocele, 1 evisceration and 2 eventrations. Repeat surgery was required in 6 cases. Within 6 months from discharge, 7 of 40 patients (17.5%) had some complication: 3 acute pyelonephritis, 4 episodes of acidosis-dehydration and 1 ureter stenosis. After 6 months, 7 of 38 patients (18.4%) had complications: 1 acidosis, 3 vesical lithiasis, 2 ureteral stenosis and 1 urethro-intestinal, plus 2 cases of chronic urinary retention. Daytime continence was 97.2% and nighttime continence 30%; after 6 months evolution, no further changes were seen.
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PMID:[Studer's type ileal neobladder. Study of complications and continence]. 994 71

Vibrio vulnificus infection with septicemia is a life threatening disease in the immunocompromised hosts. Renal involvement has not been documented. We reported herein 8 patients with V. vulnificus septicemia. All were immunocompromised hosts. Four patients had cirrhosis of the liver, 3 were heavy alcohol drinkers and one had systemic lupus erythematosis. Presenting symptomatology included fever, chills, leg pain and skin rash. Renal failure was observed in 6 patients. Four patients died shortly after admission. Two survived with clinical course of tubular necrosis. Renal failure is therefore common in V. vulnificus infection. This should be brought to attention, and vigorous antibiotic treatment is required. The disease may be confused with leptospirosis, scrub typhus, malaria and other forms of sepsis which also present with renal failure.
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PMID:Renal failure in vibrio vulnificus infection. 1084 44

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

Hepatorenal syndrome (HRS) is a severe complication of cirrhosis that develops in the final phase of the disease. Two types of HRS exist. Type 1 is defined by a rapid reduction of renal function and in type 2 HRS the reduction of renal function is slowly progressive. Type 1 HRS is diagnosed when the serum creatinine level increases by more than 50% of the baseline value to above 133 micromol/L. According to the International Ascites Club, HRS is defined by the presence of five criteria: (1) severe cirrhosis; (2) glomerular hypofiltration; (3) no other functional or organic causes; (4) failure of plasma volume expansion; (5) no proteinuria. Additional diagnostic criteria may be present. The diagnosis of HRS may be difficult in patients with severe cirrhosis. Other types of acute renal failure may occur. For example, ischaemic or toxic tubular necrosis or sepsis may cause renal failure in these patients. Furthermore, uncontrolled HRS may lead to ischaemic tubular necrosis; thus, these patients must be managed as soon as possible in an intensive care unit.
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PMID:Review article: hepatorenal syndrome--definitions and diagnosis. 1533 96

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat '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 (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) 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. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.
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PMID:Diagnosis and treatment of acute renal failure in patients with cirrhosis. 1722

To the best of our knowledge, this is the first biopsy-proven case of streptococcal infection-associated acute interstitial nephritis (AIN) with existence of streptococcal pyrogenic exotoxin B (SPE B) by a controlled immunohistochemical method. Both the intact tubular epithelial cells and oedematous interstitium had strong positive signals, whereas only interstitial inflammation was dominant without tubular necrosis. Reflective of the nature of AIN is that the injury from the hypersensitivity reaction was specific for renal interstitium instead of tubules. SPE B is potentially allergenic and may confuse the clinicians due to its clinical mimicry of drug-induced AIN. Although very rare, AIN might be included into the differential diagnosis of patients with streptococcal sepsis and acute renal failure.
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PMID:A possible rare cause of renal failure in streptococcal infection. 2084 92


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