Chapter 25: Renal Disease Flashcards
What are the two most common causes of CKD?
- DM
2. HTN
T/F:
Most drugs can pass through the glomerular capillaries into the filtrate?
True
If the glomerulus is healthy, larger substances, like proteins and protein-bound drugs, are not filtered and stay in the blood
Explain the pathophysiology of renal filtration with regards to what is being reabsorbed where.
After blood arrives at the glomerulus and ions, drugs, etc are filtered, the filtrate moves into the proximal tubule where large amounts of water are reabsorbed along with Na, Cl, and Ca. pH is also regulated in this area by H+ and bicarb exchange.
The filtrate then moves onto the descending limb of the loop of Henle. This portion of the tubule is freely permeable to water (meaning water is reabsorbed), but not to Na and Cl causing these ions to concentrate in the filtrate.
The filtrate then moves up the ascending limb of the loop of Henle. This portion of the tubule is freely permeable to Na and Cl, but NOT to water. However, if ADH is present, water WILL be reabsorbed in a dose dependent manner
Second to last, the filtrate moves into the distal convoluted tubule. This portion of the nephron regulates K, Na, Ca, and pH
And finally, the filtrate passes into the collecting duct which is heavily involved with water and electrolyte balance. This is where ADH and aldosterone work. Aldosterone increases Na and water retention and eliminates K. That’s why a aldosterone ANTAGONIST like Aldactone® blocks the action of aldosterone and increases serum K, thus potassium sparing diuretic.
Why are loop diuretics more potent than thiazide diuretics?
It has to do with their site of action on the nephron. Loop diuretics inhibit the Na-K pump in the ascending limb of the loop of Henle. Roughly 25% of Na is reabsorbed here and by inhibiting this pump, a significant amount of water is eliminated (b/c so much Na is staying in the filtrate and being eliminated via urine). Thiazide diuretics inhibit the Na-Cl pump at the distal convoluted tubule where only about 5% of Na is reabsorbed which means less fluid is eliminated.
Name some common medications associated with drug induced kidney disease (DIKD)
- Vanco
- AGs
- RCM
- cisplatin (Platinol®)
- tacrolimus (Prograf®)
- loop diuretics
- NSAIDs
- amphotericin B
- colistimethate (Colistin®)
- cyclosporine (Neoral®, Sandimmune®)
What is BUN? What is SCr?
Besides kidney impairment, what is the primary factor causing an increase in BUN?
BUN is blood urea nitrogen. It is a measure of nitrogen that comes from the waste product, urea
SCr is a measure of the creatinine in the blood. Muscles produce creatine, a waste product of muscle metabolism. Creatine is converted to creatinine by the liver which is then pumped back to the kidneys for elimination. Creatinine is freely filtered by the kidneys. With decreasing renal function, SCr increases.
Dehydration
What is CrCl?
Creatinine clearance is used as a surrogate to measure GFR (since measuring GFR is cumbersome and difficult) and can be useful in estimating kidney function in certain populations.
Creatinine is actively secreted into the filtrate, which tends to overestimate (by ~10%) the ability of the body to clear creatinine from the body.
Which populations would the Cockcroft-Gault equation not be suitable for?
- Patients with rapidly changing renal function
- ESRD
- Very young children
What impact on CrCl would you expect in a patient with liver dysfunction?
Since creatine (produced by muscles) is converted to creatinine in the liver, hepatic dysfunction would limit the amount of serum creatinine which may make the CrCl look better than it actually is thereby overestimating renal function.
Review the stages of CKD (based on KDOQI 2002)
GFR Stage 1: >90 ml/min + kidney damage Stage 2: 60-89 ml/min Stage 3: 30-59 ml/min Stage 4: 15-29 ml/min Stage 5: less than 15 ml/min
According to KDIGO, what is the goal BP for patients with kidney disease?
According to KDIGO, BP goals for CKD patients depend on presence or absence of proteinuria. Goal BP in CKD is less than 140/90 if no proteinuria is present and less than 130/80 if proteinuria is present.
One of the monitoring parameters of ACEi/ARBs is renal function (Scr/BUN). Why?
ACEi/ARBs can increase SCr by 30% during initiation of treatment. This level of increase is acceptable, but any greater than 30% should warrant discontinuing therapy and evaluating the patient
How soon after starting an ACEi/ARB should SCr and K+ be monitored in a patient with CKD?
1-2 weeks after initiating
Adjusting doses in renal impairment is essential to providing safe and effective doses of medications. How would you renally adjust an antibiotic that exhibits time-dependent killing? How would you adjust it with concentration-dependent killing
Adjust THE DOSE in antibiotics that exhibit time-dependent killing such as beta-lactams. This will decrease the peak (toxicity), but maintain the trough concentrations.
Adjust THE INTERVAL in antibiotics that exhibit concentration-dependent killing, such as AGs or quinolone. This will maintain the peak (efficacy), but decrease the trough
Where is erythropoietin produced?
Kidneys
What does erythropoietin do?
stimulates production of reticulocytes (immature red blood cells) in the bone marrow
Generally, what two agents are used in combination to treat anemia of CKD?
- Erythropoiesis-stimulating agents (ESAs)
2. Iron
When is IV iron preferred over oral iron supplementation in CKD?
Patients on HD
Hemoglobin levels of CKD patients receiving ESAs should not be corrected to “normal” levels. Why?
Increases the risk of CV events, stroke, and death
CKD mineral and bone disorder (CKD-MBD) is common in patients with CKD. What lab abnormalities should be screened for in patients with advanced CKD?
PTH, Ca, VitD, phos
Explain in your own words pathogenesis of secondary hyperparathyroidism?
Secondary hyperparathyroidism:
Phos is eliminated by the kidneys. In renal impairment, phos can accumulate which cause bone abnormalities. To compensate for the increased phos, the body releases PTH which acts at bone to increase the serum Ca concentration for Ca to bind phos and eliminate it. Chronically this leads to elevated PTH levels, thus secondary hyperparathyroidism
What is the initial non-pharmacologic treatment of secondary hyperparathyroidism?
Restricting phosphorous in the diet (limit cola, dairy products, chocolate, and nuts)
