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Acute kidney insufficiency was simulated in rats by means of intramuscular administration of glycerol. Intensity of protein biosynthesis and content of proteins were increased, while their catabolism was decreased in kidney under these conditions. At the same time, half-life and a period of the proteins turnover were elongated, whereas the rate of their substitution was decreased.
Acute renal failure often has a complex origin, especially in critically ill patient. Moreover, the tools for investigation of renal failure are generally unspecific, so that the work-up must be based on several elements. It is particularly important to differentiate failure of the kidney itself from prerenal or postrenal failure, since the therapeutic implications are very different. We propose to base the investigation of acute renal failure on some elements to be evaluated in a rapid succession. The complete evaluation should also take into account the consequences of renal failure, which also have therapeutic implications.
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Acute renal failure (ARF) is defined as a renal insufficiency of sudden onset (increase of creatinine and urea in the serum) combined with or without oliguria (less than 500 ml of urine per day). Nephrotoxins (drugs, contrast medium) or renal ischemia (hypovolemia, hypotension, shock, septicemia, treatment with CEI) may affect the renal tubulus through several pathways, all of which may result in ARF. Ultrasound allows to distinguish hydronephrosis from ARF which is characterized by increased width of the parenchyma and low echodensity of the medulla. ARF is usually reversible. If conservative therapy fails, dialysis treatment is necessary.
Acute renal failure was treated by intermittent hemofiltration in 19 patients (8 males and 11 females), 13 of which survived and 6 died. All of them underwent examinations for kinetics and clearance of middle-mass oligopeptides (MMOP) performed by gel filtration (sephadex G-15) and densitometry in UV light (280 nm) using C phi-24 device. Plasma levels of oligopeptides in acute renal failure were found increased 20-fold. They consisted mainly of MMOP (1000-3000 D) entering the 13th eluate fraction. There appeared a correlation between oligopeptides and creatinine plasma levels. Under hemofiltration lasting for 6.45 hours and replacing approximately total body fluid, nearly all the baseline extracellular oligopeptide pool was removed. The average rate of the filtration reached 127 ml/min, clearance of oligopeptides being 57.9 ml/min or more than 22 1 of fluid per one procedure. Intermittent hemofiltration went in enhanced (8-fold) MMOP generation responsible for residual high levels of them in plasma after the procedure.
Acute renal failure (ARF) is related to reversible tubular necrosis, usually caused by ischemia or toxic substances. Our knowledge of the pathophysiology of ARF stems from the study of animal models which reproduce either an ischemic or a toxic form of ARF. Classical studies using microdissection and micropuncture have characterized the salient mechanisms of ARF: vascular compromise with hypoperfusion and decrease in glomerular filtration rate, and tubular insult with cell necrosis and high intratubular pressure. More recent studies have emphasized the cellular and molecular events occurring during the course of ARF, including changes in cytoskeleton and matrix proteins, apoptosis and the role of Heat Shock Proteins. Endothelin and growth factors such as epidermal growth factor or hepatocyte growth factor seem to be important mediators in the regeneration phase of ARF. In various animal models, EGF, HGF or antagonists of endothelin receptors have a protective effect on renal function. These findings may be of clinical relevance, and suggest future therapeutic approaches in the treatment of ARF.
UNLABELLED: Acute renal failure is a common and severe complication in ICU. Renal laboratory examinations like creatinine and urea are late signs of renal dysfunction: Most of the functional abilities are reduced and there is no time for therapeutical interventions. The aim of this study was to find some earlier sensitive parameters of renal dysfunction and the order of appearance, the cause of acute renal failure and the value of the measured parameters. METHODS: After agreement of the local ethic committee, 21 patients of the ICU were investigated. They were divided into two groups: 1st (n = 14) with no signs of renal dysfunction and were regarded as control group and 2nd (n = 7) were examined until the beginning of acute renal failure. For five days the glomerular filtration rate, proteinuria (immunoglobulin G, Tamm-Horsfall protein, alpha-1- and beta-2 microglobulin, lysozyme), the brush border enzymes angiotensinase A and the lysosomal enzyme N-acetyl-beta-d-glucosaminidase were daily measured and compared with clinical standards like the excretion of albumin, the clearances of creatinine and urea and the fractional excretion of sodium. RESULTS: Both groups were comparable with respect to drug therapy, APACHE-II-score (with the exception of the last day before ARF), and infusion therapy. There were differences in tubular functions between the 2 groups. Patients developing renal insufficiency showed an increased excretion of alpha-1-microglobulin, and decreased excretions of Tamm-Horsfall-protein, angiotensinase A as well as a low renal blood flow. Significant differences were also detectable in glomerular functions (glomerular filtration rate), albumin, and immunoglobulin G. DISCUSSION: Only a short time interval (1 to 2 days) between tubular and glomerular damage were detectable in patients with renal insufficiency. Renal failure must be due to circulatory problems because of the nearly simultaneous increase of tubular and glomerular parameters after RPF decreased. The parameters alpha 1-microglobulin, angiotensinase A and Tamm-Horsfall-protein gave early indications for the acute renal failure. They showed satisfactory sensitivity and specificity, but the positive predictive value was poor.
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Explore the source record for details and available documents.
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Prerenal acute renal failure is defined as a reduction in the glomerular filtration rate due to a primary disturbance in renal hemodynamics in the absence of any structural kidney damage. In case of moderate hypotension or hypovolemia, a number of adaptative systemic and intrarenal responses preserve renal perfusion and filtration rates, particularly by inducing a marked reduction in preglomerular arteriolar resistance and an increase in postglomerular resistance. However, these mechanisms are inherently limited. In the presence of advanced circulatory failure or iatrogenic pharmacologic interventions compromising these renal defense mechanisms, prerenal failure becomes evident. Therefore, prerenal failure may occur during acute hemodynamic disturbances due to hypovolemia or systemic vasodilatation, in severe cardiac failure, in cirrhosis with ascites, and in certain clinical situations following administration of nonsteroidal antiinflammatory agents or angiotensin converting enzyme inhibitors. The treatment depends on the underlying cause.
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BACKGROUND: Acute kidney failure in children is a catastrophic, life-threatening event. OBJECTIVE: To compare and contrast 2 decades of data, analyzing the underlying causes, associated multiple organ system failures, outcome of dialysis procedures, and other variables of interest. DESIGN: Retrospective examination of clinical data collected between January 1, 1979, and December 31, 1998. SETTING: Regional health care center in the mid-Atlantic area. PARTICIPANTS: Two hundred twenty-eight patients, aged from 1 day to 18 years, had acute kidney failure and were referred to a pediatric nephrology service. MAIN OUTCOME MEASURES: Characteristics, percentage of mortality, intensive care unit admission, procedures, and other variables and causes of acute renal failure. RESULTS: The total number of cases analyzed represented 7% of all patients presented to the pediatric nephrology service. Sex distribution, ethnicity, and survival statistics were unchanged between both decades. The overall survival rate was 73%. One hundred fifty-four patients (68%) were admitted to the pediatric intensive care unit. The following 106 acute extracorporeal procedures were performed on 93 patients (41%): 12 patients received extracorporeal membrane oxygenation, 52 patients underwent peritoneal dialysis, 32 underwent hemodialysis, 3 patients received continuous venovenous hemofiltration, and 7 patients received continuous arteriovenous hemofiltration. Sepsis and burns, other leading causes of acute renal failure in the first decade, are replaced in the second decade by hematologic-oncologic complications and pulmonary failure. CONCLUSIONS: Acute kidney failure following repair of cardiac lesions remains unchanged as a leading risk factor of mortality in both decades. Three organ system failures were associated with more than a 50% mortality rate. Predialysis low serum albumin concentrations emerged as a significant copredictor of mortality.