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Update Nephrology 2012

Update Nephrology 2012. Charles J. Foulks, M.D., FACP Professor of Medicine C.S. Lewis, Jr., M.D. Chairman School of Community Medicine University of Oklahoma. Nephrology Update. Timing of dialysis Early start does not improve survival Randomized to eGFR 10-14 mL/min vs. 5-7 mL/min

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Update Nephrology 2012

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  1. Update Nephrology 2012 Charles J. Foulks, M.D., FACP Professor of Medicine C.S. Lewis, Jr., M.D. Chairman School of Community Medicine University of Oklahoma

  2. Nephrology Update • Timing of dialysis • Early start does not improve survival • Randomized to eGFR 10-14 mL/min vs. 5-7 mL/min • Late start group could be overridden by nephrologist • 1.8 months vs. 7.4 months • eGFR 12 mL/min vs. 9.8 mL/min • No difference in survival

  3. Nephrology Update • Problems • No data on patients with Stage 5 CKD who do NOT start dialysis • Influenced by indication bias • Later start leaves more time for access placement and maturation • Started with early dialysis for diabetics and the definition of Stage 5 CKD?

  4. Nephrology Update • Intensive BP control in Type 2 DM and HTN patients: NO effect on cardiovascular events • Practice: control BP to 130/80 (no evidence) • 4733 patients un-blinded randomized to intensive therapy <120 vs. standard <140 • Also randomized to intensive or standard glycemic control and statins used if indicated • End points: nonfatal MI, nonfatal stroke or death from cardiovascular causes

  5. Nephrology Update • 4.7 years of f/u • No difference in the primary composite end point • Intensive control group significantly more hypotension, syncope, and increased creatinine • Problems • Dyslipidemic patients went into the lipid trial putting a lower risk cohort into the HTN trial • Standard therapy group endpoints <50% expected • Creatinine>1.5 mg/dL excluded • Insufficient evidence to support intensive BP control

  6. Nephrology Update • Renal artery stents do not preserve GFR • 10 center European study • 140 patients • Ostial RAS>50% • eGFR<80 mL/min • Stable BP • Randomized to • Medical therapy: BP meds, anti-lipid agents, ASA • End point: Reduction of GFR >20% • Mortality not different • 2 procedure related deaths

  7. Nephrology Update • Problems • Underpowered study • Death, dialysis, transplantation or doubling of serum creatinine should have been used • Almost 40% randomized to stent did not get is secondary to RAS<50% or technical issues. • Recommendations • Maximal medical therapy with BP meds, ASA, lipid-lowering agents

  8. Nephrology Update • Paired donor exchange for transplants • I don’t match my person of interest but between the 4, 6, or 8+ of us, everyone can get transplanted. • It works • No contracts, you could back out • 14 hour cold ischemic time had no effect on graft outcome

  9. Nephrology Update • Aggressive use of ESA (darbopoietin) for anemia in Type 2 DM and CKD: no effect on CV events AND increases risk for stroke. • 4047 patients, eGFR 20-60 mL/min with Type 2 DM randomized to D or placebo if Hgb<9g/dL • Target 13 g/dL • Outcomes: death or non-fatal CV event (stroke, MI, unstable angina, or CHF)

  10. Nephrology Update • Increased strokes and thrombo-embolic events in D patients • No difference in death, other CV events of loss of GFR • More cancer patients in D group died • Cannot extrapolate to dialysis • Goal of 13 g/dL too high

  11. Nephrology Update • Rosuvastatin does not reduce risk for CV events in HD patients • Randomized, double blinded, placebo controlled, n=2776 • Rosuvastatin 10 mg/d • End points: Cardiovascular death, stroke, non-fatal MI • No difference in outcomes • Groups well matched.

  12. Nephrology Update • Frequent daily in-center HD improves physical health and reduces LV mass • 245 HD patients randomized to 6 HD sessions/wk vs. 3 week (conventional) • End points: death, LV mass, cognitive function, change in self-appointed health status • 5.3 sessions/wk vs. 3/wk • Significant decrease in LV mass, better health, better HTN and phos control and more vascular access procedures

  13. Nephrology Update • 6 session/wk patients younger, deaths infrequent in both groups, and more transplants in the frequent group. • Some patients may benefit from more than 3 sessions/wk.

  14. Nephrology Update • High dose CRRT does not enhance survival in critically ill patients with AKI • Aus/NZ, 35 ICUs • 40 mL/kg/h vs. 25 mL/kg/h • Outcome: mortality 90 d after randomization • Problems • AUS/NZ not US. CVVHDF unusually used in US • Focus on preventing AKI

  15. Nephrology Update • Kidney stones less in low fat, low protein high fruit/vegetable diet • 3 large cohorts, Health Professions F/U study, Nurses’ Health Study I and II • 45% reduction in men, 42% in older women, 40% in younger women. • Adjusted for age, BMI, fluid/energy intake, caffeine and alcohol intake, HTN/DM history and use of thiazides • DASH diet will work

  16. Nephrology Update • ESA dosing to maintain Hgb>13.5 or 11.3 • N=1400, 16 months • High Hgb group: significant increase in serum creatinine, dialysis/transplantation, death • Worse renal outcomes with ESA • Hard to keep <13 g/dL

  17. Nephrology Update • The future: • AKI is a very real risk factor for developing CKD • All AKI patients should be followed by a nephrologist • Problems with sodium retention and HTN • eGFR formulas may not be accurate 2d to dec. muscle mass • Role of diet therapy • May take 12 months to regain GFR after AKI • Watch your drugs • Up to 1/3 will have residual CKD even if previously normal • CKD is a risk factor for developing AKI • Clearly age and co-morbid diseases don’t help

  18. Nephrology Update • Of 1610 AKI patients who had GFR return to within 90% of normal at 90 days compared to non-AKI sex, disease, age-matched controls: • 50% increase in mortality at 3 years • Two fold increase in development of CKD • When factored for the AKI event, CKD has independent effect on increasing mortality • Mortality rate of patients with/without AKI who did not develop CKD were equal • Creatinine increase of 0.3 mg/dL SIGNIFICANT

  19. Nephrology Update • 5/6 nephrectomy model: • Increased Qb, glomerular hyperfiltration, hypertrophy • Arteriosclerosis • Glomerulosclerosis • Tubulo-interstitial fibrosis • Impaired myogenic regulation of blood flow • Barotrauma from increased perfusion pressure • But other factors might be operative

  20. Nephrology Update • Tubulo-interstitial fibrosis • Out of proportion to glomerulosclerosis • Major pathology that worsens GFR • May occur in absence of glomerulosclerosis • GFR loss is not linear • Mini-episodes of AKI • AKI in CKD is worse and proportional to stage • 1988-2002: epidemic of AKI in US • Decreased mortality rate acutely • Increased ESRD incidence • AKI promotes worsening of GFR

  21. Nephrology Update • Stressed nephrons with increased SNGFR • More susceptible to AKI injury • AKI injury worsens compensatory response • Here’s that vicious cycle again • Hyperfiltration • Increased hypoxic cell signaling in tubules • Hypertrophy vs. regeneration • Renal work-related stress: • Risk for AKI • Poor regeneration from AKI

  22. Nephrology Update • Caloric restriction retards loss of GFR • Decreased body mass and work load • Iso-caloric protein restriction does not retard loss of GFR • Animal proteins vasodilate the kidneys, increase blood flow, pressure, stretch • Plant proteins do not particularly soy-based • Loss of GFR with casein not with vegetable protein

  23. Nephrology Update • CKD with HTN: tubulo-interstitial fibrosis • CKD without HTN: glomerular and tubular hypertrophy with NO TIF • TIF requires loss of renal mass AND HTN • If auto-regulation fails then kidney may experience multiple “mini-episodes” of AKI • With HTN or • Normotension (?): level of normal BP harmful?

  24. Nephrology Update • Inflammatory reaction in AKI • Early PMN response • Mononuclear cells: best correlate with severity • Repair, regeneration, remodeling • Promote fibroblast proliferation and fibrosis • Damaged tubular cells seem to promote the inflammatory response (uranyl nitrate model) • Tubular damage: • Hypoxic signaling • Decreased VEGF • Capillary rarefaction: progression of disease

  25. Nephrology Update • Failed regeneration of tubular cells • Hyperactive cell signaling • Reduced renal mass (SNGFR) • Response to caloric load (work load) • Mini-episodes of AKI • Transmission of systemic HTN • Abnormal inflammatory response

  26. Riskfactors Risk factors Riskfactors AKI AKI AKI CKD CKD Mortality Recovery Mortality

  27. Nephrology Update • Suggested reading: • Venkatachalam MK et al, Acute Kidney Injury: A Springboard for progression in chronic kidney disease. Am J Physiol Renal Physiol, 298(5), F 1078-F 1094, 2010. • Palevsky PM. Chronic-on-acute kidney injury. Kidney International, 81, 430-431, 2011. • Bibliography of both papers

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