Renal physiology glomerular filtration rate

Renal clearance of cotinine is much less than the glomerular filtration rate (Benowitz et al. 2008b). Since cotinine is not appreciably protein bound, this indicates extensive tnbnlar reabsorption. Renal clearance of cotinine can be enhanced by np to 50% with extreme urinary acidification. Cotinine excretion is less influenced by urinary pH than nicotine becanse it is less basic and, therefore, is primarily in the unionized form within the physiological pH range. As is the case for nicotine, the rate of excretion of cotinine is influenced by urinary flow rate. Renal excretion of cotinine is a minor route of elimination, averaging about 12% of total clearance. In contrast, 100% of nicotine Ai -oxide and 63% of 3 -hydroxycotinine are excreted unchanged in the urine (Benowitz and Jacob 2001 Park et al. 1993). 

Pregnancy is associated with enormous changes in physiological functions which start early in the first trimester with vasodilatation and an increase in cardiac output, possibly secondary to the vasodilatation. Fluid retention follows, and intravascular volume may expand by up to 25-30% by the end of the second trimester. Renal blood flow increases, and glomerular filtration rate may be 50% higher than in the non-pregnant state. Miraculously, almost all of these changes return to normal within a week of delivery. 

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 most common cause of hyperphosphatemia is a decrease in urinary phosphorus excretion secondary to decreased glomerular filtration rate. ° Retention of phosphorus decreases vitamin D synthesis and induces hypocalcemia, which leads to an increase in PTH. This physiologic response inhibits further tubular reabsorption of phosphorus to correct hyperphosphatemia and normalize serum calcium concentrations. Patients with excessive exogenous phosphorus administration or endogenous intracellular phosphorus release in the setting of acute renal failure may develop profound hyperphosphatemia. Severe hyperphosphatemia is commonly encountered in patients with chronic kidney disease, especially those with GFRs less than 15 mL/ min per 1.73 m (see Chap. 44). 

The serum concentration of Pi increases with a physiological dechne in renal function associated with aging (but not renal disease per se). Healthy individuals excrete approximately 67% of their absorbed phosphate via the urine and the remainder via the gut as endogenous secretions. As the glomerular filtration capacity of the kidneys declines, the serum Pi concentration increases and more Pi is retained by the body. PTH secretions increase but the typical serum PTH concentrations, although elevated, remain within the upper limits of the normal range, at least for a decade or so. Thereafter, however, serum Pi and PTH both continue to climb as renal function declines and increased rates of bone turnover lead to measurable bone loss. This situation probably affects millions in the United States each year as they enter the 50s and proceed into the 60s many of these individuals are overweight or obese and have the metabolic syndrome, which... 

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