Renal Pathophysiology Flashcards
What is azotemia?
The accumulation of nitrogenous waste products due to a decrease in the kidney’s ability to excrete them.
How do prerenal, renal, and postrenal azotemia differ?
Prerenal azotemia typically results from an abrupt decrease in renal blood flow. Renal azotemia is due to a disorder in the renal parenchyma from intrinsic disease, ischemia, or nephrotoxins. Postrenal azotemia occurs as a result of obstruction of the urinary outflow tract.
Is an elevated BUN always indicative of renal dysfunction?
No. Increased protein intake can elevate the BUN level leading to an inaccurate diagnosis of renal dysfunction. Other causes of altered BUN levels include altered intravascular fluid volume and co-existing diseases.
How does the urine sodium level change with renal tubular damage?
The urine sodium increases. Urinary sodium > 40 mEq/L is associated with damage to the renal tubules.
Which is associated with the highest incidence of postoperative renal failure in the patient undergoing abdominal aortic aneurysm repair, infrarenal, suprarenal, or supraceliac clamping?
Suprarenal clamping has an incidence of postoperative acute renal failure (8%) and is higher in incidence than supraceliac and infrarenal clamping. The incidence of acute renal failure increases substantially (10-30%) in cases involving complicated aneurysms.
What form of renal failure is most commonly associated with the perioperative period?
Prerenal causes of renal failure are related to decreased blood flow to the kidneys such as blood and volume losses, cardiac pump failure, renal vascular disease, and clamping and comprises about 60% of all causes of renal failure. Acute tubular necrosis from ischemia or toxins such as aminoglycosides or radiocontrast media is the most common renal cause of acute renal failure and comprises 30% of all causes of renal failure. Postrenal causes such as obstructive nephropathy and ureteral obstruction comprise the remaining 10%.
Massive proteinuria (exceeding 750 mg/day) would be consistent with extensive damage to what renal structure?
Proteinuria greater than 750 mg/day is always abnormal and usually indicates severe glomerular damage. It may also be present when the renal tubules fail to reabsorb the small amount of protein that gets filtered.
How does renal tubular damage affect the urine and plasma osmolality?
A normal urine osmolality (around 1400 mOsm/Kg compared to the normal plasma osmolality of about 290 mOsm/Kg) indicates an excellent ability of the tubules to concentrate urine. A situation wherein the plasma and urine osmolality become fixed together indicates serious damage to the renal tubules.
What does the presence of nitrites in the urine indicate?
Nitrites are typically positive if large numbers of bacteria are present in the urine.
How do patients with renal disease respond to different intravenous induction agents?
Although the pharmacokinetic profile of barbiturates and etomidate are largely unchanged in patients with renal failure, the dose must often be decreased due to an enhanced sensitivity to the drugs, possibly due to an increase in free circulating drug related to decreased protein binding. The pharmacokinetic profile of ketamine and propofol are also largely unchanged by renal failure. Repeated doses of ketamine however, can result in accumulation of the drug as some of its active metabolites depend upon renal excretion. Additionally, many patients with renal vascular disease may exhibit hypertension which may be worsened by the administration of ketamine.
s nitrous oxide contraindicated in patients with renal failure?
Although some clinicians avoid nitrous oxide because they wish to administer 100% oxygen in the presence of anemia due to renal failure, this omission appears to only be justified when the serum hemoglobin is
Is succinylcholine contraindicated in patients with renal failure? Why or why not?
Succinylcholine can be used safely in patients with renal failure provided the serum potassium is less than 5 mEq/L. There are some cases describing decreased pseudocholinesterase levels in uremic patients after dialysis. However, the risk of prolonged duration of action appears to be minimal.
How will the pharmacokinetics of anticholinergics be affected by the presence of renal failure?
Atropine and glycopyrrolate can be safely used in patients with renal failure, but because about 50% of the drugs or their metabolites are excreted in the urine, repeat doses can potentially accumulate. Scopolamine is not as dependent upon renal excretion as atropine and glycopyrrolate, but the presence of azotemia can enhance its central nervous system effects.
Which two intravenous opioids would be the most likely to result in prolonged action in patients with renal failure?
Most of the commonly used opioids are inactivated by the liver and some or all of the metabolites are excreted in the urine. With the exception of morphine and meperidine, most do not result in significant prolongation. The metabolites morphine-6- glucuronide and normeperidine however, are capable of exerting clinical effects and may result in respiratory depression in patients with renal failure.
How are the pharmacokinetic profiles of benzodiazepines altered by renal failure?
Most benzodiazepines undergo hepatic metabolism and conjugation and are eliminated by the kidneys. They are highly protein bound, which can result in increased drug sensitivity due to hypoalbuminemia. Diazepam may exhibit prolonged action due to accumulation of active metabolites.
