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Ascites in the chronic renal failure patient with cirrhosis

Ascites in the chronic renal failure patient with cirrhosis. Dr.Rajeev Jayadevan MD (Vellore), DNB (Medicine), MRCP(UK), American Board Certification in Medicine American Board Certification in Gastroenterology Senior Consultant Gastroenterologist Sunrise Hospital.

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Ascites in the chronic renal failure patient with cirrhosis

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  1. Ascites in the chronic renal failurepatient with cirrhosis Dr.RajeevJayadevan MD (Vellore), DNB (Medicine), MRCP(UK), American Board Certification in Medicine American Board Certification in Gastroenterology Senior Consultant Gastroenterologist Sunrise Hospital

  2. Acknowledgements • Dr. Jayant Thomas Mathew MD, DM Consultant Nephrologist, Amala Medical College • Dr. Sooraj Y.S. MD, DNB (Nephrology) Consultant Nephrologist, Sunrise Hospital • Dr. Abi Abraham MD, DM Consultant Nephrologist, Lakeshore Hospital

  3. Outline • Refresh our basic physiology about ascites and discuss what is pertinent here • Practical aspects of treating a patient with CRF and CLD who has ascites

  4. Ascites in CLD: some basic science A major issue here is that kidneys retain Na and H2O excessively. Why? When kidneys of cirrhotic or heart failure patients were transplanted, they stopped retaining Na and H2O. This meant that the signal for Na/H2O retention came from outside the kidney.

  5. What triggered Na/H2O retention? • Could it be low total blood volume? • No, because when measured, these patients had normal or, even increased blood volume! • Could it be low cardiac output? • No, because, pregnancy has high output, but the kidneys still retain Na and H2O!

  6. Who, then, tells the kidneys to retain Na/H2O?

  7. “Arterial underfilling.” Can be from : • Decreased cardiac output • Arterial vasodilatation

  8. Effective vs. Total blood volume Estimates of blood volume distribution indicate that 85% of blood circulates on the low-pressure, venous side of the circulation, whereas an estimated 15% of blood is circulating in the high-pressure, arterial circulation. Schrier, J Am SocNephrol 18: 2028–2031, 2007

  9. How does cirrhosis lead to arterial underfilling?

  10. Vaso- constrictor systems not turned on

  11. How to treat nephrogenic ascites Patient with ascites, CLD and CRF. Question: Is the ascites from the liver or the kidney?

  12. How to differentiatecirrhotic vs. uremic ascites Cirrhotic Uremic Exudate High protein Low SAAG Creatinine > 5 Rapid reaccumulation • Transudate • Low protein • High SAAG > 1.1 • Creatinine < 5 • Slow reaccumulation

  13. HRS Hypovolemia-induced Parenchymal Drug-induced

  14. Ascites in CKD + CLD.Why is treatment difficult? Management difficult as: • Symptoms overlap • Creatinine value unreliable due to CLD • Diuretics don’t work as easily as in CLD: “Diuretic Resistance”

  15. Diuretics and the nephron

  16. Mechanisms of diuretic resistance in CRF 1. Reduced basal level of fractional Na reabsorption 2. Enhanced NaCl reabsorption in downstream segments: DCT hypertrophy: beyond the reach of Furosemide 3. Reduced delivery of diuretic to the kidney. Diuretics are secreted by the organic anion transporters (OATS), in the PCT, these get inhibited by Acidosis. 4. Hypoalbuminemia decreases delivery of Furosemide and also increases its metabolism to glucuronide

  17. Hypertrophy of distal tubule Exposure to loop diuretic DCT Taller cells Larger rounded nuclei Taller lateral cell processes

  18. Na Due to prolonged action of Loop diuretic in the Loop of Henle, more Na gets absorbed by a hypertrophied DCT

  19. Loop diuretic resistance:Curve shifts to the right EFFECT DOSE

  20. NEPHROTIC SYNDROME = ALBUMIN IN LUMEN Luminal action

  21. Measures to combat diuretic resistance in CRF • Restriction of fluid intake 1.5 L daily • Maintain Sodium intake of 2 g daily • Use of escalating doses of loop diuretics up to established ceiling levels. • Judicious use of a second diuretic acting at a downstream site , but watch for ADR • Reducing renal proteinuria in nephrotic syndrome using ACEI or ARB J Am SocNephrol 13: 798–805, 2002

  22. Diuretic resistance:How to test? If < 50 mmol urine sodium in 8 hours after Lasix 80 mg IV: Resistant. HEPATOLOGY, Vol. 49, No. 6, 2009

  23. Choice of loop diuretic: LASIX vs. TORASEMIDE Preferred Better bioavailability Predictable outcome OD dosing Does better than Lasix in the 6-24 hr interval 20mg as good as 80 mg Lasix

  24. Choice of diuretic- 2 Spironolactone Be cautious Monitor K more closely Patients already on ACEI or ARB, chance of spike in K

  25. What if gynaecomastia? Try Amiloride 10-40 mg/d. Less effective, however.

  26. Second-line agents Triamterene, HCTZ, Metolazone (2.5 - 5 mg OD) are second-line agents used to treat ascites.

  27. Choice of Fluids • Be careful with saline: pulmonary edema • Albumin/ Plasma are OK: they stay in the intravascular space

  28. Protein in diet: how much? • In CKD not on dialysis: very conservative. 0.6-0.8 g/kg/day • If on dialysis: can give more: 1.2 g /kg/day

  29. Dialysis patient: what day to tap? • Tap on non-dialysis days • Heparin can cause bleed otherwise

  30. Dialysis patient with ascites:how to tap: Large-volume paracentesis with IV Albumin replacement at 8 g Albumin per liter of ascitic fluid removed

  31. FFP or Platelets before a tap…..?? No. • Routine tests of coagulation do not reflect actual bleeding risk in patients with cirrhosis. • These patients regularly have normal global coagulation because of a balanced deficiency of procoagulantsand anticoagulants. AASLD guideline HEPATOLOGY, June 2009

  32. Do not send CA-125 in patients with ascites • Patients with ascites should not have serum tested for CA-125. • It will be elevated due to pressure on mesothelial cells

  33. CKD + Cirrhosis :What dialysis: HD or PD?Peritoneal dialysis: • Less hemodynamic instability • Less bleed risk • Less Hepatitis B/C risk • No published increased risk of peritoneal sepsis although theoretical risk from cirrhosis (Same rates of sepsis for CKD patients on PD, regardless of presence of cirrhosis) • 40% more expensive

  34. Reinfusion of ascitic fluid into the dialysis machine: PRECEED 2 HD patients with CLD and refractory ascites: quick improvement, well-tolerated

  35. TIPS: any role? Patients with parenchymal renal disease, especially those on dialysis, may not respond as well to TIPS as those with functional renal insufficiency. Michl P, Gulberg V, Bilzer M, Waggershauser T, Reiser M, Gerbes AL. Transjugularintrahepatic portosystemic shunt for cirrhosis and ascites: effects in patients with organic or functional renal failure. Scand J Gastroenterol 2000;35:654-657.

  36. Main points:Ascites in CKD and CLD. • Rule out other causes of ascites • Diuretic resistance occurs in CKD • Furosemide or Torasemide mainstay • Use Spironolactone with caution • Be liberal with IV albumin • Avoid IV fluids like saline • Work closely with the nephrologist

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