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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.
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PMID:Effect of potassium depletion on ischemic renal failure. 253 74

Clinical and epidemiological data on 16 patients with HFRS admitted to the University Hospital of Infectious Diseases in Zagreb during the past 10 years (1977-1986) are reported. In 13 of them, the diagnosis was confirmed serologically by indirect fluorescent method. All but two were men between 20 and 45 years of age (80% of patients). The disease appeared sporadically only. According to the domicile, way of living and working all the patients but three mentioned the contact with rodents in the fields or in other places (mill, storehouse). Three patients live in Zagreb and there was no possibility to get infected out of the town. The disease had moderate course, more rarely severe course when shock and acute renal failure developed. General symptoms with fever and algias dominated (febrile stage). Some of the patients had ophthalmic disturbances. Patients with a pronounced gastroenteritis developed shock the most frequently. In some of the patients back and abdominal pains followed by obstipation appeared. HFRS was incriminated disease because of febrile stage followed by the acute renal failure, oliguria, azotemia, polyuria and low urine osmolity. One female patient with active rheumatoid arthritis died after two-week staying in hospital due to irreversible shock followed by cardiopulmonary and renal failure.
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PMID:[Clinical and epidemiologic characteristics of hemorrhagic fever with renal syndrome]. 256 68

In a serological survey among Dutch patients suspected of leptospirosis, using a recently developed enzyme-linked immunosorbent assay, a patient was traced with a high antibody titre to Hantaan virus. No anti-leptospira antibodies were detected in this 27-year-old man. Shortly before he had been admitted to the hospital with progressive dyspnoea and coughing, accompanied with high fever. An interstitial pneumonia was diagnosed. He subsequently developed a progressive renal failure with proteinuria and polyuria. Later a liver failure accompanied with thrombocytopenia, anaemia and coagulation disturbances occurred. Before an aetiological diagnosis was made, the patient was treated with erythromycin. The patient eventually recovered completely. Based on the clinical symptoms and the positive serology, it was concluded that the disease diagnosed had probably been caused by a Hantaan virus infection. The diagnostic value of Hantaan virus serology in patients with similar symptoms is stressed.
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PMID:[Another case of Hantaan virus infection in The Netherlands]. 257 78

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

An acute ethylene glycol intoxication is reported. 100 to 130 ml monoethylene glycol which is used as antifreeze were taken by mistake. On admission to hospital the 41-year-old patient was not remarkable. Despite the lethal dose--according to literature--no renal failure developed by immediate intravenous ethanol therapy. While the patient was given 10 g of ethanol hourly, the serum glycol level decreased steadily (93 mg/dl). After a short oral treatment with 5 to 7 g of ethanol hourly, the serum glycol increased to 350 mg/dl, but could be lowered again--after the reinstitution of the intravenous therapy--to those values recorded before the oral therapy. The level of blood ethanol differed between 2.41 and 0.01 mg/l. The creatinine clearance was normal and the serum electrolytes could be kept in the normal range with adequate compensation despite of the polyuria of 13.81/24 h. It is known that even a low ethanol level inhibits the enzymic metabolism of ethylene glycol by ethanol dehydrogenase and prevents the formation of toxic metabolites. The patient luckily had already consumed about 40 g of alcohol (2 bottles of beer), so that an ethanol level existed already before this intoxication. From this case report one could conclude, that the parenterally given ethanol influences the serum glycol level far better than the orally given especially in case it is not more than 7 g/h. If glycol intoxication is sure, hemodialysis is--despite this especially good course of conservative treatment--the more efficient and quicker method because of its good ability of elimination.
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PMID:[Accidental glycol poisoning]. 258

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

Aminoglycoside antibiotics cause transient, usually nonoliguric, renal failure in up to 10-30% of patients treated with these drugs, and are the cause of the largest proportion of drug-induced acute nephrotoxicities. The toxic mechanism includes (i) uptake of the drug by proximal tubular cells, where it is first sequestered within lysosomes and (ii) development of a lysosomal phospholipidosis, which is rapidly associated with cell necrosis and various alterations to subcellular structure and function. Tubular necrosis is often accompanied by (and probably triggers) tubular regeneration and peritubular proliferation. The means whereby such tubular alterations eventually cause a decline in glomerular filtration and hypo-osmotic polyuria has not been established. Various in-vitro and acellular models have been designed to assess and screen for the nephrotoxic potential of aminoglycosides; of these, methods based on the analysis of aminoglycoside-phospholipid interactions appear to be the most meaningful. A number of patient- and drug-related risk factors have been identified, and their avoidance could significantly reduce the risk of nephrotoxic reactions. Because the uptake of aminoglycosides by the kidney is saturable, administration of daily doses of these drugs as one or two injections, rather than as multiple injections or by continuous infusion, may also decrease the risk for toxicity.
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PMID:Nephrotoxicity of aminoglycoside antibiotics. 265 18

Over a 15-year period we observed seven children (four girls, three boys) who presented within the first months of life with severe renal failure and acidosis, associated with hypertension in five patients and polyuria in four. In addition, one patient had a severe cholestatic liver disease. In two families, a similarly affected sibling had died previously. Four patients were referred with the clinical diagnosis of polycystic kidney disease because of moderate enlargement of kidneys, but renal imaging (intravenous pyelography and ultrasonography) did not confirm this diagnosis. A renal biopsy, performed in all patients, showed similar features characterized by a diffuse chronic tubulo-interstitial nephritis (TIN) and particularly by the presence of microcystic dilatation of proximal tubules and Bowman's space. Liver pathology was normal in two patients, including one with hepatomegaly. However, in the patient with cholestasis there was inflammatory portal fibrosis with mild duct proliferation. Progression of the renal disease was extremely rapid and all patients reached end-stage renal failure (ESRF) before the age of 2 years (11-22 months). Two children had successful renal transplants. Although this chronic TIN shares some features with nephronophthisis, we suggest that it represents a distinct entity both on clinical and morphological grounds. The specific clinical features of this disease are its early onset and rapid progression to ESRF. Pathologically, it differs from nephronophthisis by the absence of medullary cysts and thickened tubular basement membranes and by the presence of cortical microcysts.
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PMID:Infantile chronic tubulo-interstitial nephritis with cortical microcysts: variant of nephronophthisis or new disease entity? 270 88

Four children (aged 2 1/2-14 years) were given infusions of fructose, sorbitol and xylitol after sustaining head trauma (n = 3) or after attempted suicide with carbromal (n = 1). After transitory polyuria renal failure of varying severity set in three to five days after onset of the infusion treatment. Serum osmolality fell to 265-274 mosm/kg, haematocrit to 0.25-0.31, and hyponatraemia developed. Serum creatinine rose to maximally 256-930 mumol/l. Liver damage developed in parallel to the renal failure, two children dying with acute yellow liver atrophy. Two children--given symptomatic treatment with balanced equalization of the hyponatraemia, administration of frusemide and adjusted carbohydrate substitution--were discharged after four to eight weeks with normal renal and hepatic functions. Dialysis was not required. The hepatic and renal abnormalities must have been due to the high amounts of fructose, sorbitol and xylitol, to a total of 7.1-23.0 g/kg on the first day, well above recommended levels.
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PMID:[Primary polyuric kidney failure and acute yellow liver dystrophy following infusion of glucose substitutes in children]. 308 68

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.
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PMID:[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage]. 322 Oct 52


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