Urea, blood concentration reduction

Cephalosporins are broad-spectrum antibiotics similar in structure to penicillin. For several cephalosporins, therapy is limited by the development of nephrotoxicity. Cephaloridine-induced nephrotoxicity has been examined extensively in laboratory animals and is characterized by an increase in blood urea nitrogen concentration within 24-48 hr, reductions in PAFI and TEA transport, and inhibition of glucose production following treatment. 

A 3.5 h treatment of a 70 kg patient (V = 40.6 liters) with a urea clearance of 200 ml,/min should result in a 64% reduction in urea concentration or a value of 0.36 for the ratio d (f this parameter almost always falls between 0.30 and 0.45. The increase in urea concentration between hemodialysis treatments is obtained from equation 13, again assuming a constant V, where (f is the urea concentration in the patient s blood at the end of the hemodialysis, and d the concentration at time t during the intradialytic interval. 

Kidney Failure, Acute A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH]... 

Brydon and Roberts- added hemolyzed blood to unhemolyzed plasma, analyzed the specimens for a variety of constituents and then compared the values with those in the unhemolyzed plasma (B28). The following procedures were considered unaffected by hemolysis (up to 1 g/100 ml hemoglobin) urea (diacetyl monoxime) carbon dioxide content (phe-nolphthalein complex) iron binding capacity cholesterol (ferric chloride) creatinine (alkaline picrate) uric acid (phosphotungstate reduction) alkaline phosphatase (4-nitrophenyl phosphate) 5 -nucleotidase (adenosine monophosphate-nickel) and tartrate-labile acid phosphatase (phenyl phosphate). In Table 2 are shown those assays where increases were observed. The hemolysis used in these studies was equivalent to that produced by the breakdown of about 15 X 10 erythrocytes. In the bromocresol green albumin method it has been reported that for every 100 mg of hemoglobin/100 ml serum, the apparent albumin concentration is increased by 100 mg/100 ml (D12). Hemolysis releases some amino acids, such as histidine, into the plasma (Alb). 

As renal function improves, the excretion of urea increases and the concentration of urea in blood declines. So a reduction in blood urea nitrogen (BUN) is also a useful sign of returning kidney function. More complex tests, such as creatinine clearance, would be needed to check whether the glomerular filtration rate (GFR) has returned to normal. 

Functional renal insufficiency is manifested as increases in serum creatinine and blood urea nitrogen. As cardiac output and renal blood flow decline, renal perfusion is maintained by the vasoconstrictor effect of angiotensin II on the efferent arteriole. Patients most dependent on this system for maintenance of renal perfusion (and therefore most likely to develop functional renal insufficiency with ACE inhibitors) are those with severe heart failure, hypotension, hyponatremia, volume depletion, and concomitant use of NSAIDs. - Sodium depletion (usually secondary to diuretic therapy) is the most important factor in the development of functional renal insufficiency with ACE inhibitor therapy. Renal insufficiency therefore can be minimized in many cases by reduction in diuretic dosage or liberalization of sodium intake. In some patients, the serum creatinine concentration will return to baseline levels without a reduction in ACE inhibitor dose. Since renal dysfunction with ACE inhibitors is secondary to alterations in renal hemodynamics, it is almost always reversible on discontinuation of the drug. ... 

Because of increases in plasma volume and cardiac output, renal blood flow increases. The GFR ri.ses early in pregnancy, and creatinine clearance may be 150 ml/min or more by. 10 weeks. Serum urea and creatinine concentrations fall. Tubular function alters and. in particular, there is a reduction in the renal threshold for glucose. Glycosuria may be present in up to 70% of pregnancies. Tubular reabsorption of uric acid and amino acids alters, and their excretion in urine increases. 

By extracting water from intracellular compartments, osmotic diuretics expand the extracellular fluid volume, decrease blood viscosity, and inhibit renin release. These effects increase RBF, and the increase in renal medullary blood flow removes NaCl and urea from the renal medulla, thus reducing medullary tonicity. Under some circumstances, prostaglandins may contribute to the renal vasodilation and medullary washout induced by osmotic diuretics. A reduction in medullary tonicity causes a decrease in the extraction of water from the DTL, which limits the concentration of NaCl in the tubular fluid entering the ATL. This latter effect diminishes the passive reabsorption of NaCl in the ATL. In addition, osmotic diuretics may also interfere with transport processes in the TAL. 

Renal failure with glomerular fibrin deposition and necrotic and degenerative tubular lesions was described in a SS-year-old woman who died following a severe reaction to ibuprofen (100 ). Dysuria, frequency, nocturia and abnormal elevation of the blood urea nitrogen have been noted (63, 99, 105, 106, 111 ). Marked reduction in creatinine clearance and urinary concentration was observed in a number of patients who had taken total doses of 0.43—1.98 kg of ibuprofen over periods of up to 44 months (99 ). Contrary to the reassurances given by the authors, these findings indicate significant impairment of renal function. 

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