Nephrology CBP Prese..

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  • 1.

2. Case Presentation

  • 43 year old gentleman with Crytogenic Cirrhosis is admitted to the ICU after massive GI bleed secondary to bleeding esophageal varices.His varices have been successfully banded and he is admitted post-procedure.He received multiple units of blood, as well as platelets to correct his thrombocytopenia and FFP to correct his coaglulopathy (INR 4.3).He also received 6 L of crystalloid.He is now hemodynamically stable, however, his respiratory requirements have increased, in keeping with his CXR findings of acute pulmonary edema.

3.

  • PSV, 12/5, FiO2 .45
  • He is kept intubated over night and given multiple boluses of Lasix (total of 200mg) to help encourage diuresis.
  • When assessed in the morning, it is noted that he has been anuric over night.His admission BUN/Cr were 11/87, and are now 23/192.He is now on PSV 16/8 and FiO2 is .65.
  • His electrolytes reveal: Na 128, K 5.3, Cl- 97, tCO2 18.
  • ABG: 7.31/39/84/19/-2

4. Question 1

  • Briefly describe Hepatorenal syndrome and its pathophysiology.What are some predisposing factors? (Federico)

5. 6. DEFINITION Hepatorenal syndrome is a clinical condition that usually occurs in patients with advanced liver disease and portal hypertension that is characterized by : -Renal failure, with creatinine level more than 1.5mg/dl -Marked decrease in GFR and renal plasma flow (RPF) in the absence of other identifiable cause of renal failure. -Marked abnormality in systemic hemodynamics -Activation of endogenous vasoactive systems. HRS occurs predominantly in the setting of cirrhosis, but it may also develop in other types of severe chronic liver diseases, such as alcoholic hepatitis, or in acute liver failure . 7. The theory that best fits with the observed alterations in the renal and circulatory function in HRS is the vasodilation theory, which proposes that HRS is the result of the effect of vasoconstrictor systems acting on the renal circulation and activated as a homeostatic mechanisms to improve the extreme underfilling of the arterial circulation .That leads to decreased renal perfusion and glomerular filtration rate( GFR )but tubular function is preserved . 8.

  • There are two well - differentiated clinical patterns of HRS
  • Type 1 HRS
  • Characterized by rapid and progressive impairment of renal function defined as a doubling of the initial serum creatinine to a level greater than 2.5 mg / dl or a 50% reduction of the initial 24-hour creatinine clearance to a level lower than 20 ml / min in less than 2 weeks .
  • Usually occur in severe liver failure (Jaundice, encephalopathy, and coagulopathy)
  • Occur frequently after precipitating factor (e.g. GI bleeding)
  • Median survival time is only 2 weeks

9.

  • Type 2 HRS
  • Characterized by a less severe and non - progressive reduction of GFR .
  • Associated with relatively preserved liver function.
  • The main clinical consequence of this type of HRS is refractory ascites, due to a lack of response to diuretics .
  • Median survival time is about 6 months.

10.

  • TheInternational Ascites Clubhas defined criteria for the
  • diagnosis of HRS. Major criteria, necessary only for the
  • diagnosis, are as follows:
    • Low GFR, defined by a serum creatinine greater than 1.5 mg/dL or 24-hour clearance lower than 40 mL/min
    • Absence of shock, ongoing bacterial infection, fluid losses and current treatment with nephrotoxic drugs
    • No sustained improvement in renal function (decrease in serum creatinine to< 1.5 mg/dL or increase in clearance to> 40 mL/min) following diuretic withdrawal and plasma volume expansion with albumin (or 1.5 L of isotonic saline).
    • Proteinuria less than 500 mg/d
    • Absence of any evidence of obstructive uropathy or parenchymal disease as shown by ultrasonography

11.

  • Precipitating factors
    • Bacterial infections
    • Bleeding
    • Large volume paracentesis without plasma expansion

12.

  • Patient remains anuric and is given a further bolus of 100mg of Lasix.
  • Patient remains anuric despite most recent dose of Lasix.

13. Question 2

  • Any role for increasing doses of Lasix in an anuric patient?Any harm?Any benefit? (Federico)

14. 15. 16. Diuretics in AKI

  • Regarding
  • an increased appreciation for the potential
  • detrimental downstream effects of
  • volume overload, it may be reasonable to
  • try diuretics for control of volume overload.
  • The clinician should, however, be
  • careful not to delay initiation of RRT for
  • volume overload in the critically ill patient
  • with AKI
  • (Crit.Care 2010, vol 38, n1)

17. Question 3

  • Define Acute Kidney Injury (Federico)

18. RIFLE Criteria

  • The Acute Dialysis Quality Initiative Group
  • proposed the RIFLE system classifying ARF into 3 severity groups and 2 clinical outcome categories

19. 20. 21. 22. Incidence of AKI in the ICU

  • AKI occurs in ~ 7% of all hospitalized patients, whereas it occurs in 36% 67% of critically ill patients.
  • On average, 5 % of ICU patients with AKI require renal replacement therapy.

Dennen P, Douglas IS, Anderson R. Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Crit Care Med. 2010 Jan;38(1):261-75 23. AKI and mortality

  • In most studies, mortality rates rise proportionally with severity of AKI.
  • Even small increases in serum creatinine have been associated with increasing mortality in various ICU populations despite adjusting for severity of illness and comorbidities.
  • In patients with AKI requiring RRT, mortality rates reach 50% to 70%.

Dennen P, Douglas IS, Anderson R. Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Crit Care Med. 2010 Jan;38(1):261-75 24. AKI and other outcomes

  • AKI is also associated with:
    • Increased length of stay
    • Increased incidence of CKD and end-stage kidney disease
    • Increased cost
  • For example, an increase in SCr of 0.5 mg/dl (38 mmol/L)was associated with a:
    • 6.5-fold increase in the odds of death
    • 3.5 day increase in LOS
    • nearly $7500 in excess hospital costs

Dennen P, Douglas IS, Anderson R. Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Crit Care Med. 2010 Jan;38(1):261-75 Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005 Nov;16(11):3365-70 25. Traditional methods for detecting AKI

  • Currently available measures do not detect actual kidney injury the way troponin detects myocardial injury:
    • Creatinine
    • Urea
    • Urine output
  • Rather they are markers of abnormal renal function, that can be used to presume kidney inury has occurred.

Bagshaw SM, Bellomo R. Early diagnosis of acute kidney injury. Curr Opin Crit Care. 2007 Dec;13(6):638-44. 26. Serum creatinine

  • Used to estimate GFR
  • Pros
    • Produced at a relatively constant rate
    • Freely filtered by glomerulus
    • Not reabsorbed or metabolized by the kidney.

Bagshaw SM, Bellomo R. Early diagnosis of acute kidney injury. Curr Opin Crit Care. 2007 Dec;13(6):638-44. 27. Serum creatinine

  • Used to estimate GFR
  • Cons
    • 10-40% is secreted by the tubules
    • Relatively insensitive (may need a 50% reduction in function before a detectable rise in SCr is seen)
    • Creatinine production varies based on age/sex/muscle mass/diet
    • Certain disease states can increase production (rhabdo)
    • Certain drugs can decrease secretion (cimetidine, trimethoprim)
    • Certain factorsmay affect assay (ketoacidosis, cefoxitin, flucytosine)
    • Does not reflect real-time changes in GFR

Bagshaw SM, Bellomo R. Early diagnosis of acute kidney injury. Curr Opin Crit Care. 2007 Dec;13(6):638-44. 28. Delay in SCr rise Waikar SS, Bonventre JV. Creatinine kinetics and the definition of acute kidney injury. J Am Soc Nephrol. 2009 Mar;20(3):672-9 29. Urea

  • Rate of production is not constant
    • Increases with protein intake
    • Increases in critical il