Kidneys glomerular filtration rate

Survivors had decreased kidney glomerular filtration rate within 24 h (Lock 1979)... 

Renal function is an indication of the physiological state of the kidney glomerular filtration rate (GFR) describes the flow rate of Altered fluid through the kidney, while creatinine clearance rate (Ccr) is the volume of blood plasma that is cleared of creatinine per unit time, and is a useful measure for approximating the GFR. Most clinical tests use the plasma concentrations of the waste substances of creatinine and urea, as well as electrolytes, to determine renal function. The nephron is the functional unit of the kidney (Figure 10.1) it consists of two parts ... 

The clinical use of cisplatin is limited by nephrotoxicity, characterized by a decline in glomerular filtration rate that is in proportion to the number of cycles of cisplatin chemotherapy. Progressive and persistent reductions in glomerular filtration rale and renal blood flow may follow each successive treatment cycle [17]. Renal plasma flow, whole kidney glomerular filtration rate, single nephron glomerular filtration rate, and stop-flow pressure are reduced compared to controls... 

Hackstein N, Heckrodt J, Rau WS (2003) Measurement of single-kidney glomerular filtration rate using a contrast-enhanced dynamic gradient-echo sequence and the Rutland-Patlak plot technique. JMagn Reson Imaging 18 714-725... 

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

In the kidney, ANG II reduces renal blood flow and constricts preferentially the efferent arteriole of the glomerulus with the result of increased glomerular filtration pressure. ANG II further enhances renal sodium and water reabsorption at the proximal tubulus. ACE inhibitors thus increase renal blood flow and decrease sodium and water retention. Furthermore, ACE inhibitors are nephroprotective, delaying the progression of glomerulosclerosis. This also appears to be a result of reduced ANG II levels and is at least partially independent from pressure reduction. On the other hand, ACE inhibitors decrease glomerular filtration pressure due to the lack of ANG II-mediated constriction of the efferent arterioles. Thus, one important undesired effect of ACE inhibitors is impaired glomerular filtration rate and impaired kidney function. 

In the kidney, bradykinin increases renal blood flow, whereas glomerular filtration rate remains unaffected. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Information is available on the renal toxicity of ingested lead in several species, including rats, dogs, monkeys, and rabbits. The results indicate that histopathological changes in the kidneys of lead-treated animals are similar to those in humans (see Section 2.2.1.2). Reduced glomerular filtration rates and aminoaciduria were reported in some of the animal studies. Key animal studies on lead-induced renal toxicity will be discussed below. 

Kidneys are exquisitely sensitive to changes in perfusion pressures. Moderate alterations can lead to significant changes in glomerular filtration rate. Oliguria, progressing to anuria, occurs because of vasoconstriction of afferent arterioles. 

Furosemide and ethacrynic acid preserve glomerular filtration rate and are, therefore, the diuretic agents of choice in hypertensive patients with impairment of kidney function(17,18,... 

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]... 

The glomerular filtration rate (GFR) defines how much plasma water passes from the blood into the top of the nephron per minute. In health, the true GFR for a 70 kg adult is typically 100-120 ml/minute. Expressed another way, we can say that, in health, every minute each of the approximately 2 million glomeruli present in both adult kidneys filters between 0.05 and 0.06 pi of plasma water. The GFR is a good overall measure of renal function and the clinical laboratory has many ways of estimating its value. 

The glomerular filtration rate (GFR) measures the rate at which blood is filtered by the kidneys. 

In the muscle, phosphocreatine and creatine undergo cyclisation to form creatinine (Figure 8.20(b)). Since creatinine cannot be metabohsed, it is released from muscle and is then excreted in the urine. This biochemical process is useful in clinical practice, since creatinine production is spontaneous and is remarkably constant 1.7% of the phosphocreatine and creatine in muscle cyclises each day, so that its concentration in blood provides an indication of the glomerular filtration rate, and hence provides an indication of the function (i.e. the health) of the kidney. 

In the isolated perfused kidney model, the artery of the kidney is perfused and urinary samples as well as venous blood samples can be collected to determine the drug concentration. A serious drawback of the model is that isolation and artificial perfusion greatly affect the function of the organ as shown by a dramatic drop in the glomerular filtration rate. Another in-vitro model is the isolated tubule in which samples can be taken from both the luminal and basolateral sites of the tubule [140,141]. The disadvantage of this technique as well as of the isolated kidney model, is that they require specific equipment and expertise and therefore can only be performed in rather specialized laboratories. Experiments using freshly isolated or cultured cells are more simple to carry out [142,143]. Tubular cells can be grown in a po-... 

Uric acid is the end product of the purine metabolism. When uric acid excretion via the kidneys is disturbed, gout can develop (see p. 190). Creatinine is derived from the muscle metabolism, where it arises spontaneously and irreversibly by cyclization of creatine and creatine phosphate (see p. 336). Since the amount of creatinine an individual excretes per day is constant (it is directly proportional to muscle mass), creatinine as an endogenous substance can be used to measure the glomerular filtration rate. The amount of amino acids excreted in free form is strongly dependent on the diet and on the ef ciency of liver function. Amino acid derivatives are also found in the urine (e.g., hippu-rate, a detoxification product of benzoic acid). 

Renal function impairment In hypertensive patients with normal kidneys who are treated with hydralazine, there is evidence of increased renal blood flow and a maintenance of glomerular filtration rate. Renal function may improve where control values were below normal prior to administration. Use with caution in patients with advanced renal damage. 

Renal function Impairment- Ceftazidime is excreted by the kidneys, almost exclusively by glomerular filtration. In patients with impaired renal function (glomerular filtration rate (GFR) less than 50 mL/min), reduce dosage to compensate for slower excretion. In patients with suspected renal insufficiency, give an initial loading dose of 1 g. Estimate GFR to determine the appropriate maintenance dose. 

Renal development is also immature in both the premature and the full-term baby. At birth overall renal function is approximately 20% of the adult value, but increases rapidly up to around one year of age when it is usually the same as that of an adult (when adjusted for body size). Glomerular filtration rate in particular may increase four-fold over the first week of life. As renal blood flow, glomerular filtration rate and tubular secretion of drugs are all low in the neonate, drugs cleared by the kidney need to be given in reduced dose - particularly if the drug has a narrow therapeutic window , and the potential to produce toxicity if Cp rises too greatly. 

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