We have no data. thank-you.
Various definitions of AKI change the prevalence and prognosis of AKI.
In RIFLE use the worse of cr or u.o to define category
States 200,000 patients have been used to validate RIFLE.
Systemic review of RIFLE in KI in 2008 by Ronco.
AKIN changes R to include increase in Cr of 0.3. Otherwise just sw2ithches I to 2 and F to 3.
Also the two creatines used to determine the 5change must be measured within 48 hours of each other.
Early initiation of RRT has theoretical benefits
Defintion on how to measure/define this are not established
He feels the failure of the ATN is due to Pagamini’s high, medium and low severity argument.
Much better talk
Need to adjust serum Cr for fluid balance. He states that this will allow Cr to determine renal failure 24 hours earlier. He fails to give an equation to do this. Is creatinine distributed in total body water or extracellular water? My guess is total body water.
eGFR would be more helpful in eliminating the curvelinear relationship of GFR and Cr but not validated in ARF.
Jelliffe method takes into account Cr generation and is better in ARF. Fails to provide information on calculating the eGFR by Jelliffe method.
Mentions Thurau’s article on Acute renal success. Am J Med 1976
Shaw in Nephron Physiology article on the time course of AKI as determined by differing etiologies.
Oliguria is bad
diuretic matter, but he wont tell us how.
Mehta is the worst lecturer. He throws a ton of data up and fails to describe any of the implications.
66 yo woman with ESRD due to analgesic nephropathy. Hx of Crohn’s Disease. Extended criteria deceased donor allograft transplant 1.5 yrs ago.
Now SBP of 160.
Next Speaker Ojo. Greatest name in Nephrology.
CVD and CKD in Transplantation
Progressive reduction of acute rejection since 2000 from 17.4 to 10.3% at one year. This should improve outcome of graft and patient; however post-transplant life-span has decreased from 14 in 1995 to 12.7 in ’06.
CVD is the explanation for this conundrum.
After the first year the most common cause of loss of graft is: death with a functioning graft (56%). This is twice as common as number 2, chronic rejection (21%).
43.5% die of CVD.
Hypertension, DM, hypercholesterolemia, obesity, and anemia are all more prevalent in transplant patients than transplant candidates or prevalent dialysis patients.
Focus on immunosupressant drugs
- In HIV patients with lower cd4 have higher higher CVD death rate
- Same relationship of CD4 to CVD is seen in patients with radiation exposure (Hiroshima) causing lower cd4 counts
- also seen in transplant patients.
Rabbit data showing that increased cholesterol plaques with concurrent CSA, without change in lipid profile. Roselaar jci 1995 96 1389.
Steroids are dangerous even at low doses in the normal population.
CSA increase BP.
CSA also causes endothelial dysfunction.
Sirolimus is antiatherogenic, as seen in cardiac stents.
MMF also appears to reduce cholesterol plaque Romero Atherosclerosis 2000: 152:127-133.
Cr alone is a predictor of CVD independent of immunosupression and traditional risk factors.
Case report of a patient with HTN
Ray Townsend is the MC (sweet). He presnts a patient with HTN and modest CKD. Cr 1.4 up from 0.9 in 2001.
Ray passes off to Domenic Sica.
Antihypertensive Drug Therapy in patients with HTN and CKD.
- Patient was on 25 mg of HCTZ. No need to change to loop if the patient is euvolemic. Chlorathalidone vs hctz
- Ernst HTN 2006. chlorathalidone reduced 24hr mean bp more (7 vs 12) non-ckd patients. night time bp drop was even more pronounced 6 vs 13 mmHg.
- Recommends switch within class from hctz to chlorthalidone
- the increase in calcium may help with PTH. interesting.
- elison JCI 83: 113; 1989 images of hypertrophy of DCT with loop diuretics
- He’s pushing torsemide
- Using FeNa to determine if patient is responding to loops (look for fena>3%)
- Why is there variability in bioavailability of furosemide: floculation of pills stops some absorption. Use of liquid furosemide doesn’t help because of only a limited area of absorbtion: early duodenum only.
- He likes the torsemide
At gfr 30-50 need to think about dose adjustment.
Renally cleared: atenolol, nadolol, betaxolol
propanolol, metoprolol, carvedilol
Dose response to beta-blockers is flat in CKD.
Don’t titrate atenolol. It is renally cleared and patients are already retaining the drug before you increase the dose. Though the BP effect is not dose dependent, the adverse effects are.
- 20% of patients with CKD.
- Likely this patient will have aldo level of 14-20 and renin less than 1
- Aldosterone antagonists (AA) reduce proteinuria
- Need diuretic on board to get much BP effect
- Half-life of spironolactone is 24 hours, in liver disease 120 hours, and in CKD multiple days. These figures include active metabolites. He feels eplerenone is safer because you won’t get accumulation.
- Consider qod dosing of spironolactone. Consider 12.5 mg qd
- beware of heparin causing hyperkalemia with AA
- Similar warning for ACEi, ARB, TMP/SMX
- in CKD clonidine is renally cleared. This decreases rebound htn by extending the half life
- initially clonidine has a steep dose responce at low doses but then flattens
- causes dose dependent volume retension. this is worse with TTS
- at higher doses the peripheral alpha stimulation will overcome the central reduction in alpha activity so patients get increase in BP. This is seen in clonidine OD or with autonomic dysfunction.
- Amlodipine has half-life of 40 hours
- nifedipine’s half-life goes from 2 to 4 hours in renal failure
- Edema with CCB is worse in patients with CKD because they already have increased volume
- 10 in the US
- fosinopril and trandolopril have significant hepatic clearance
- ARB are not renally excreted
- dialyzable: captopril, enalepril, lisinopril. Use in overdose.
- AUC of simva increases 4 fold with diltiazem
- Cool case report of a patient on 80 of simva who was admitted for A-fib with RVR and gets started on a diltiazem gtt. He developed rhabdo a few days later.
That’s it. Question time.
New month. Back on the consult service.
Dr. Jabri is the consult fellow and we are going to read the NephSAP on GNs. Should be good.