A fatal case of Epstein-Barr virus infection with jaundice and renal failure. (65/78)

A fatal case of Epstein-Barr virus infection in a 17-year-old male is described. The patient presented with an illness clinically typical of infectious mononucleosis but death followed development of renal failure, jaundice and pulmonary failure. There was no absolute lymphocytosis nor a significant number of atypical mononuclear cells in his peripheral blood. However, heterophile antibody and Epstein-Barr virus-specific IgM were present.  (+info)

Fractional excretion of trace lithium and uric acid in acute renal failure. (66/78)

The early distinction between prerenal azotemia, characterized by an avid proximal tubular sodium reabsorption, and ATN, in which proximal tubule function is depressed, remains an important but difficult clinical task. Indices of acute renal failure based on urinary sodium excretion may be helpful but have several limitations, among which is the use of diuretics. The effectiveness of the fractional excretion of uric acid (FEUA) and that of endogenous lithium (FELi) in the diagnosis of acute renal failure has been evaluated in an unselected group of 46 patients, 28 with prerenal azotemia and 18 with ATN. In the entire group, FELi concurred with the clinical diagnosis in 78% of the patients, whereas the fractional excretion of sodium (FENa) and FEUA were in agreement in only 63 and 50%, respectively. FELi was more sensitive to identify hemodynamic renal failure, because 93% of prerenal failure patients had a low FELi, contrasting with a low FEUA in only 68% and a low FENa in 75%. The major reason for the discrepancy between FENa and FELi was the administration of diuretics. In both acute renal failure groups, FENa was higher in the subgroups receiving diuretics. In contrast, diuretic therapy had no effect on FELi in either group. These results suggest that FELi is more accurate than either FENa or FEUA for distinguishing prerenal azotemia from ATN. The superiority of FELi appears especially relevant in patients treated with the usual diuretics.  (+info)

Effects of thromboxane A2 receptor blockade on oliguric ischemic acute renal failure in conscious rats. (67/78)

To investigate the potential pathogenetic and therapeutic roles of thromboxane A2 (TXA2) and its receptor blockade, respectively, in the early phase of ischemic acute renal failure (ARF), renal function, TXB2 excretion, and the effects of the specific TXA2 receptor antagonist sulotroban (SU) in a model of unilateral renal artery occlusion in conscious female Sprague-Dawley rats were studied. Occlusion of the left renal artery for 1 h in untreated (i.e., vehicle-treated) rats (N = 8) resulted in oliguric ARF. In SU-treated rats (N = 8), the drug was given as an i.v. bolus of 5 mg/kg body wt, followed by a continuous infusion of 0.5 mg/min.kg body wt from 1 h before and during ischemia and for 6 h after reflow. After 1 h of ischemia, urine volume of left ischemic kidneys from untreated rats had decreased from 13.2 +/- 2.8 to 1.0 +/- 0.3 and 0.5 +/- 0.2 microL/min.100 g at 2 and 6 h of reflow, respectively, and GFR had decreased from 0.32 +/- 0.04 mL/min.100 g body wt to undetectable values. At 6 h of reflow, medullary Na-K-ATPase was slightly (P < 0.05) reduced in left ischemic kidneys, whereas medullary and papillary enzyme activities were compensatorily increased (P < 0.01) in right intact kidneys. The ADP/O ratio of cortical mitochondria was 41% (P < 0.05) and ATP synthesis was 77% (P < 0.01) lower than in right intact kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)  (+info)

Morphologic demonstration of tubular obstruction in acute renal failure. (68/78)

We used the qualitative Hanssen technique in albino rats to seek morphologic demonstration of tubular obstruction in two types of acute renal failure: one induced by folic acid and another by methemoglobin. Immediately after the intravenous injection of folic acid, 250 mg/kg body weight, the animals became almost anuric. Two to three hours after the injection, sodium ferrocyanide remained within the proximal convoluted tubules. After the intravenous injection of methemoglobin, 0.5 to 1.0 g/kg body weight, the animals became oliguric but not anuric. Sodium ferrocyanide injected with methemoglobin was seen mainly in distal tubules and collecting ducts 2 to 3 hours after the injection. The degree of tubular dilatation was more marked in the former model than in the latter, in agreement with the degree of oliguria. These morphologic findings were taken to indicate that the above two types of acute renal failure were caused by tubular obstruction rather than by intrarenal vasoconstriction and subsequent cessation of glomerular filtration. (Am J Pathol 87:323-330, 1977).  (+info)

A study on oliguric standard in the elderly. (69/78)

Water deprivation test was done in 44 healthy elderly persons, 26 were male, and 18 were female. They were deprived of the intake of water for 25 hours. The results showed that the maximal renal concentration function both in the elderly males and females was 887 +/- 91 mmol/L and 888 +/- 127 mmol/L respectively. The renal excretion of waste products in 24 hours both in the elderly males and females was 815 + 170 mmol/d and 620 + 132 mmol/d respectively. On the basis of point estimation, the minimal essential urine volume per day in the elderly males and females was 926 ml/d and 708 ml/d respectively, if the daily urine volume of the elderly is less than this level, then, the metabolic products generated per day can not be excreted by the kidney, and it would result in disorders of internal environment. Therefore, the oliguric standard in elderly males and females must be less than 926 ml/d and 708 ml per day respectively.  (+info)

Electrolyte disturbances in elderly patients with severe diarrhea due to cholera. (70/78)

The purpose of this clinical study was to evaluate prospectively electrolyte disturbances in elderly patients with severe diarrhea due to cholera. A total of 20 adult (Group I; < 60 yr) and 22 elderly (Group II; > or = 60 yr) patients were studied. In all patients, extracellular fluid (ECF) volume reexpansion was achieved with normal saline at 50 mL/kg per hour. Once a diuresis of 40 mL/h was achieved, intravenous therapy was discontinued and patients' ECF volumes were reexpanded orally with a polyelectrolyte solution. Blood and urine samples were obtained on admission, at the time when adequate diuresis ensued, and after 12 h of oral ECF volume reexpansion. On admission, both groups had severe ECF volume contraction but only mild increases in osmolality (308 +/- 12 and 310 +/- 13 mosmol/kg for Groups I and II respectively; P = NS). Acidemia (pH) was equally severe in both (Group I: 7.13 +/- 0.11; Group II: 7.11 +/- 0.09; P = NS), and the anion gap was comparably increased in both groups (30 +/- 8 and 26 +/- 7 mmol/L for Groups I and II, respectively; P = NS). None of the patients was hypokalemic at the time of admission (Group I: 4.3 +/- 0.5 mmol/L; Group II: 4.5 +/- 0.5 mmol/L; P = NS). Adequate diuresis was achieved at 2.0 +/- 0.7 h in both groups. At the end of the rapid ECF volume reexpansion phase, the anion gap normalized in both groups (Group I: 15.6 +/- 3.7 mmol/L; Group II: 14.4 +/- 2.8 mmol/L; P = NS), and serum potassium concentrations remained normal (Group I: 4.4 +/- 0.4 mmol/L; Group II: 4.1 +/- 0.4 mmol/L; P = NS). We conclude that use of aggressive intravenous hydration with normal saline followed by oral ECF volume reexpansion allows prompt correction of electrolyte abnormalities in adult and elderly patients with severe diarrhea as a result of cholera.  (+info)

The reduced urinary output after spinal cord injury: a review. (71/78)

Oliguria in patients following spinal cord injury was first mentioned in 1649, but has since been referred to only occasionally. The work detailed here was completed 30 years ago but is reported because of the lack of any comparable study and because suitable patients are not now readily available. A total of 27 water load tests were carried out on 20 patients. The test included measurement of serum osmolality to confirm absorption of ingested water. Impaired response to the water load was obtained in 17 tests: 12/13 between 1 and 5 days after onset of the cord lesion and 5/14 more than 2 weeks after injury. The possibilities that oliguria was due to dehydration, failure to absorb ingested water, hypotension or renal failure are discounted. In the first few days after injury, oliguria may be due to release of antidiuretic hormone as part of the metabolic response to trauma. The impaired response seen later is discussed in relation to possible neural and hormonal mechanisms. There is a need for further study of factors influencing water excretion in tetraplegic and paraplegic patients.  (+info)

Anaritide in acute tubular necrosis. Auriculin Anaritide Acute Renal Failure Study Group. (72/78)

BACKGROUND: Atrial natriuretic peptide, a hormone synthesized by the cardiac atria, increases the glomerular filtration rate by dilating afferent arterioles while constricting efferent arterioles. It has been shown to improve glomerular filtration, urinary output, and renal histopathology in laboratory animals with acute renal dysfunction. Anaritide is a 25-amino-acid synthetic form of atrial natriuretic peptide. METHODS: We conducted a multicenter, randomized, double-blind, placebo-controlled clinical trial of anaritide in 504 critically ill patients with acute tubular necrosis. The patients received a 24-hour intravenous infusion of either anaritide (0.2 microgram per kilogram of body weight per minute) or placebo. The primary end point was dialysis-free survival for 21 days after treatment. Other end points included the need for dialysis, changes in the serum creatinine concentration, and mortality. RESULTS: The rate of dialysis-free survival was 47 percent in the placebo group and 43 percent in the anaritide group (P = 0.35). In the prospectively defined subgroup of 120 patients with oliguria (urinary output, < 400 ml per day), dialysis-free survival was 8 percent in the placebo group (5 of 60 patients) and 27 percent in the anaritide group (16 of 60 patients, P = 0.008). Anaritide-treated patients with oliguria who no longer had oliguria after treatment benefited the most. Conversely, among the 378 patients without oliguria, dialysis-free survival was 59 percent in the placebo group (116 of 195 patients) and 48 percent in the anaritide group (88 of 183 patients, P = 0.03). CONCLUSIONS: The administration of anaritide did not improve the overall rate of dialysis-free survival in critically ill patients with acute tubular necrosis. However, anaritide may improve dialysis-free survival in patients with oliguria and may worsen it in patients without oliguria who have acute tubular necrosis.  (+info)