Glomerular filtration rate renal blood flow effects

Renal papillary necrosis and other renal injury with long-term use. Most of the unwanted renal side effects of the class of NSAIDs are related to the inhibi-ton of prostanoid synthesis. The COX-2 enzyme has been implicated as a mediator of renal blood flow, renin release and sodium excretion. As a result, COX-2 inhibitors may lead to an alteration of renal homeostasis resulting in decreases in glomerular filtration rate, renal blood flow, sodium and water retention, and hyperkalemia [1]. 

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. 

West JR, Smith HW, Chasis H. 1948. Glomerular filtration rate, effective renal blood flow, and maximal tubular excretory capacity in infancy. J Pediatr 32a 10-18. 

The major cause of the diuretic effect is an increase in renal blood flow and glomerular filtration rate. 

The rate of total body clearance accounted for by the kidney. Its magnitude is determined by the net effects of glomerular filtration, tubular secretion and reabsorption, renal blood flow, and protein binding. 

An important aspect of a-methyldopa s hemodynamic effects is that renal blood flow and glomerular filtration rate are not reduced. As occurs with most sympathetic depressant drugs and vasodilators, long-term therapy with a-methyldopa leads to fluid retention, edema formation, and plasma volume expansion. While data conflict somewhat, it is generally thought that a-methyldopa suppresses plasma renin activity. 

Isoflurane, like other volatile agents, causes a transient reduction in renal blood flow, glomerular filtration rate and urinary output, but there is no evidence that these changes are harmful to the healthy kidney. Similarly, there is no evidence that isoflurane has any undesirable effects on the transplanted kidney. In... 

Barbiturates reduce hepatic blood flow and glomerular filtration rate, but these drugs produce no adverse effects on hepatic or renal function. Barbiturates can exacerbate acute intermittent porphyria by inducing the production of hepatic ct -aminolevulinic acid (ALA) synthase (see Chapter 22). On rare occasions, thiopental has precipitated porphyric crisis when used as an induction agent in susceptible patients. 

Gastrointestinal ulceration may occur less frequently than with some other NSAIDs. A preparation combining diclofenac and misoprostol decreases upper gastrointestinal ulceration but may result in diarrhea. Another combination of diclofenac and omeprazole was also effective with respect to the prevention of recurrent bleeding, but renal adverse effects were common in high-risk patients. Diclofenac, 150 mg/d, appears to impair renal blood flow and glomerular filtration rate. Elevation of serum aminotransferases occurs more commonly with this drug than with other NSAIDs. 

To varying degrees, all inhaled anesthetics decrease glomerular filtration rate and effective renal plasma flow and increase filtration fraction. All the anesthetics tend to increase renal vascular resistance. Since renal blood flow decreases during general anesthesia in spite of well-maintained or even increased perfusion pressures, autoregulation of renal flow is probably impaired. 

Renal function is depressed by opioids. It is believed that in humans this is chiefly due to decreased renal plasma flow. Opioids can decrease systemic blood pressure and glomerular filtration rate. In addition, opioids have been found to have an antidiuretic effect in humans. Mechanisms may involve both the CNS and peripheral sites, but the relative contributions of each are unknown. Opioids also enhance renal tubular sodium reabsorption. The role of opioid-induced changes in antidiuretic hormone (ADH) release is controversial. Ureteral and bladder tone are increased by therapeutic doses of the opioid analgesics. Increased sphincter tone may precipitate urinary retention, especially in postoperative patients. Occasionally, ureteral colic caused by a renal calculus is made worse by opioid-induced increase in ureteral tone. 

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