Prediction renal blood flow

An antihypertensive substance is one which does not affect blood volume, blood viscosity, or the function of the heart it lowers blood pressure to normal levels in hypertensive states by generalized arteriolar dilatation, including those of the kidneys. Vasodilators (such as histamine), which lower arterial pressure at the expense of renal blood flow, are not antihypertensive. Furthermore, an ideal substance should affect the blood pressure in normal states to little or no extent. It can be predicted, however, that when true antihypertensive substances are found, they will not increase or maintain renal blood flow in the face of lowered arterial pressure when renal arterioles have lost the ability to dilate because of pathological changes (see Figure 3). 

Braun JP, Perxachs A, Pechereau D, de la Farge F (2002) Plasma cystatin C in the dog reference values and variations with renal failure. Comp Clin Pathol 11 44 19 Cockcroft DW, Gault MH (1976) Prediction of creatinine clearance from serum creatinine. Nephron 16 31-41 Corman B, Michel JB(1987) Glomerular filtration, renal blood flow, and solute excretion in conscious aging rats. Am J Physiol 22 R555-R560... 

The result of the combination of myogenic mechanisms and tubuloglomerular feedback is that the net filtration pressure or Pccap is kept reasonably constant over a very wide range of systemic arterial pressures. It should be noted that renal blood flow and GFR change across this range of systemic pressures but to a significantly smaller extent than would be predicted if these autoregulatory mechanisms were not in place. 

Luciano R, Gallini F, Romagnoli C et al (1998) Doppler evaluation of renal blood flow velocity as a predictive index of acute renal failure in perinatal asphyxia. Eur J Pediatr... 

In patients with heart failure, lidocaine s volume of distribution and total body clearance may both be decreased. Thus, both loading and maintenance doses should be decreased. Since these effects counterbalance each other, the half-life may not be increased as much as predicted from clearance changes alone. In patients with liver disease, plasma clearance is markedly reduced and the volume of distribution is often increased the elimination half-life in such cases may be increased threefold or more. In liver disease, the maintenance dose should be decreased, but usual loading doses can be given. Elimination half-life determines the time to steady state. Thus, although steady-state concentrations may be achieved in 8-10 hours in normal patients and patients with heart failure, 24-36 hours may be required in those with liver disease. Drugs that decrease liver blood flow (eg, propranolol, cimetidine) reduce lidocaine clearance and so increase the risk of toxicity unless infusion rates are decreased. With infusions lasting more than 24 hours, clearance falls and plasma concentrations rise. Renal disease has no major effect on lidocaine disposition. 

All components of the RAS can be found in the brain, heart, vasculature, adipose tissue, gonads, pancreas, placenta, and kidney, among others. Biochemical measurements of ACE activity show that the enzyme is tissue-based. Indeed, <10% of ACE is found circulating in the plasma [4]. The potential importance of the tissue RAS is supported by observations that the beneficial effects of RAS blockers cannot reliably be predicted by measurements of the activity of the circulating RAS. The antihypertensive actions of ACE-inhibitors are better correlated with inhibition of tissue ACE rather than plasma ACE, and hypertensive patients with normal or even low levels of systemic RAS activity can be effectively treated with inhibitors of the RAS. The intrarenal RAS is hypothesized to regulate systemic blood pressure and aspects of renal function such as blood flow and sodium reabsorption. In the brain, the RAS may facilitate neurotransmission and stimu-... 

Answer The fraction of drug A excreted by the kidney (fe) = renal clearance/total clearance. Since 10% of the drug is excreted unchanged (fe = 0.1), it can be assumed that renal clearance = 0.1 x 80L/hour = 8 L/ hour. Assuming that Cltotal = Clrenal + Clhepatic, the hepatic clearance is 80 L/hour - 8 L/hour = 72 L/hour. The hepatic extraction ratio is given by the hepatic clearance divided by the hepatic blood flow, which, in this case, is EH = 72 L/hour/90 L/hour = 0.8. The maximal predicted oral bioavailability (F) is given by the product of the fractional hepatic clearance (fH), which is 1 minus the hepatic extraction ratio EH (1 — 0.8 = 0.2) and the fractional oral absorption (fD), assumed in this case to be unity (maximal case). Therefore, F = 0.2 x 1 = 0.2. 

Power Doppler US using high-frequency transducers to delineate cortical blood flow visualizes the dense cortical interlobular pedicles all the way to the cortex cortices (Martinoli et al. 1996). In renal grafts with impaired function, focal or diffuse absence of interlobular signals can be observed (Fig. 3.32). These changes can be reversed with treatment and are associated with a prediction of poor functional recovery at 12 months (Trillaud et al. 1998). 

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