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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2008  |  Volume : 19  |  Issue : 2  |  Page : 291-296
Normal Non-Functioning Kidney Transplant


Department of Internal Medicine, Security Forces Hospital Program, Riyadh, Saudi Arabia

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   Abstract 

Severe form of HCV infection complicated by early liver failure was reported after solid organ transplantation and described as fibrosing cholestatic hepatitis (FCH). We highlight the need for early detection and possible treatment in this rare but often fatal complication of HCV infection.

How to cite this article:
Al-Marwani A, Al-Harbi A, Kechrid M, Azhari O. Normal Non-Functioning Kidney Transplant. Saudi J Kidney Dis Transpl 2008;19:291-6

How to cite this URL:
Al-Marwani A, Al-Harbi A, Kechrid M, Azhari O. Normal Non-Functioning Kidney Transplant. Saudi J Kidney Dis Transpl [serial online] 2008 [cited 2019 Nov 14];19:291-6. Available from: http://www.sjkdt.org/text.asp?2008/19/2/291/39048

   Introduction Top


The hepatorenal syndrome refers to the development of acute renal failure in a patient who usually has advanced liver disease due to cirrhosis, severe alcoholic, hepatitis or less often metastasis tumour, but can occur in a substantial proportion of patient with fulminant hepatic failure from any cause.

The hepatorenal syndrome usually repre­sents the end-stage of a sequence of reduction in renal perfusion induced by increasingly severe hepatic injury as in case of fibrosing cholestatic hepatitis (FCH). [1],[2],[3],[4],[5]


   Case Report Top


Forty eight years old male admitted on 16/01/2007 with deep jaundice, itching and poor appetite. Known case of Type 2 diabetes mellitus (DM) since 1984, compli­cated by retinopathy, neuropathy and nephro­pathy. He reached end stage renal disease, needing maintenance hemodialysis on 18/02/2003. He was also found to have diffuse coronary artery disease and left ventricular dysfunction, peripheral vascular disease and ended by right below knee ampu­tation. Nevertheless, he underwent kidney transplant from a living unrelated donor on 4/11/2003 and was maintained on triple Immunosuppression: cyclosporine (CSA) 3-4 mg/kg/day, mycophenolate mofetil (MMF) 1 to 2 grams/day, Prednisolone 5 mg/day. The average serum creatinine (S. Cr.) level was 160 µm/L, ranging from 140 to 200 pm/L. On the 1st August 2006, he presented with deteriorated kidney function and received pulse steroids, S. Cr. came back to baseline, CSA was shifted to Tacrolimus (Tac): 0.03 mg/kg/day. During follow up, blood sugar was poorly controlled and liver function tests mildly deranged inspite of negative viral markers (Hepatitis A, B and C).

On the day of admission (16/01/2007), the patient was in his usual general condition, wheel chair bound, but able to ambulate with an artificial right lower limb. He was jaun­diced but not in pain. Vital signs and body weight were stable, he was afebrile. His chest was clear and he was not in heart failure. The abdomen was soft and lax; the liver was palpable and indolent. The kidney transplant was in the right iliac fossa, firm but not tender, no bruit was detected on local auscultation. Urine output was around 1,200 ml/24 hours. Laboratory investigations showed an increase in the liver enzymes ALT = 154 u/L, AST = 234 u/L, GGT = 3.298 u/L; total bilirubin was high at 125 µm/L and Alkaline Phosphatase 754 u/L. Total protein was low at 58 g/L as well as serum albumin 27 g/L, iNR = 1.0 and Platelet count = 228.10 9 /L, S. Cr. = 187 µm/L, and S. urea = 25.3 mm/L. Serology markers for Hepatitis and C Virus were negative, HBV-DNA probe was nega­tive, but HCV-RNA turned to be highly positive = 18 million copies/mL. Abdominal ultrasound showed fatty liver with a single mobile gallstone but no sign of obstruction in the biliary tree [Figure - 1]A and [Figure - 1]B.

The kidney transplant was echogenic. Mag­netic resonance imaging of the abdomen con­firmed the above findings.

The patient was admitted with the impre­ssion of cholestatic hepatitis secondary to HCV infection. Patient condition was deterio­rated with acute renal failure and anuria. The cause of deterioration was most likely because of sepsis. Ultrasound guided liver biopsy performed to confirm the diagnosis of FCH, which showed diffuse lymphocyte and histiocyte infiltration, scattered lobular inflammation, ballooning degeneration of the hepatocytes with portal and periportal fibrosis. Picture of fibrosing Cholestatic hepatitis (FCH) [Figure - 2]A and B).

Kidney transplant biopsy (27/01/2007) was performed to rule out rejection, shows: tubular atrophy, interstitial fibrosis. No inflammatory infiltrate. Normal vessels. No tubular toxicity. (No evidence rejection or acute tubular necrosis) [Figure - 3]A and B).

Patient continued to be anuric and went to fulminant liver failure. He was shifted to medical intensive care unit (MICU), where he was started on continuous renal replacement therapy (CRRT).

Our final diagnosis was set as hepatorenal syndrome type I, and the patient expired on 14/02/2007.


   Discussion Top


Liver disease is an important cause of mortality and morbidity among recipient of transplant organs biochemical abnormality in liver failure are seen in 7-24% of trans­plant recipients and liver failure is the cause of death in 8-28%of long-term survivors after transplantation. [6],[7] Previously, approxi­mately one-half of the case of liver disease among transplant patients was attributed to variety of etiologies, including viral infection such as hepatitis B viruses (HBV), Epstein­bar virus or cytomegalovirus, drug such as azathioprine or cyclosporine, Hemosiderosis or alcohol.

The remaining one-half of case were attri­buted to none A-non B hepatitis (NANBH). [8],[9] Hepatorenal syndrome is not uncommon complication of HCV related FCH, Acute tubular necrosis secondary to amino­glycoside therapy, radiocontrast agent or an episode of sepsis or bleeding and prerenal failure are an important differential diag­nosis to be ruled out because they are generally reversible. On the other hand, the prognosis is poor in the hepatorenal syn­drome with most patients dying within weeks of the onset of renal failure unless liver transplantation is performed or effective treatment is given. The best hope for reversal of the renal failure is an improvement in hepatic function due to partial resolution of the primary disease or to successful liver transplantation.[10],[11],[12],[13] FCH is a rare but fatal complication of HCV infection among kid­ney transplant recipient; HCV RNA testing has been extremely useful in seronegative patient with chronic hepatitis, particularly immunocompromised individuals, who may lack serologic evidence of HCV infection despite clinical and molecular evidence of hepatitis. [14] Liver biopsy maybe needed to confirm the diagnosis and then starting the management in form of reducing the immu­nosuppressant drugs, INF Alfa-2b in acute hepatitis and liver or liver and kidney transplant.


   Questions and Answers Top


Dr. Akram Askar (Chairman of the Club): Now the presentation is open for discussion.

Audience: Is there any role for antiviral agent for cholestasis in hepatitis C infection?

Dr. Al-Marwni: The α-interferon can be used, but the main issue in such situation is to stop the immunosuppressive drugs.

Dr. Akram Askar: My comment in treating hepatitis C post renal transplantation, it is a controversial issue now a days, and this require a liver biopsy in order to quantify the degree of fibrosis and the inflammation.

Dr. Akram Askar: Can you highlight more about major and minor criteria you mentioned in describing the hepatorenal syndrome.

Dr. Al-Marwni: The main issue here is the presence of reduce GFR and rise in serum creatinine, with advance liver disease, and this is considered as major criterion.

Dr. Ali Al-Harbi: The message we try to highlight in this case is that according to the literature, the fibrosing cholestatic hepatitis is well known and reported in hepatitis B infection, but recently there are more reports published in similar situation with hepatitis C. So it is mandatory to perform PCR (HCV) in any unexplained liver deterioration post renal transplantation because the patient is immunosupressed and we may not detect a sufficient number of antibodies. Second, is that hepatorenal syndrome can occur in transplanted kidney. Third, the management in hepatorenal syndrome post renal trans­plantation in patient with hepatitis C or B is based on stopping the immunosuppressive drugs and liver transplantation.

Dr. Akram Askar: There is MARS proce­dure, can be used in severe liver decom­pensation as liver dialysis modality in acute cases. In order to improve the general condi­tion in hepatorenal syndrome patients and prepare the patient to benefit from liver transplantation within days.

Dr. Akram Askar: The histopathology of renal biopsy was compatible with tubular necrosis or tubular atrophy?

Dr. Kechrid: The findings of renal biopsy showed an area with normal glomerulus/ tubules, and other area with shrinked tubules with fibrosis, which can be seen in hepato­renal syndrome, and it is known that ATN could be seen in hepatorenal syndrome because of severe hyporenal perfusion.

Audience: Can you highlight more about the role of Tacrolimus in this case?

Dr. Al-Marwni: This patient was first treated empirically by anti-rejection pulse therapy with steroids in august and was improved without establishing the cause of rise in serum creatinine either by rejection or cyclosporine toxicity, so the patient was switched to Tacrolimus (Prograf) with good clinical response, but the liver function started to deteriorate with significant eleva­tion in γ-GT and bilirubin. So we are not sure if the change of immunosuppressive regiment in our patient (from cyclosporine to tacrolimus) has any role in this liver decompensation.

Dr. Sadek (Prince Salman Kidney Diseases Center): In case of hepatitis C management post renal transplantation, is there an indi­cation to start Ribavirin to decrease viral activity?

Dr. Ali Al-Harbi: The ribavirin is not effec­tive in reducing the viral replication post renal transplantation and the use of interferon in transplant patients is still controversial issue, our experience with five patients treated by interferon and the results were not so effective, with relapse after termination of drug course. So, in this case the only management plan is to reduce the immuno-suppressive drugs, dialysis and the possi-bility of liver transplantation.

(Question) Audience: Should we screen all dialysis patients with hepatitis C for PCR?

Dr. Ali Al-Harbi: The current available test for antibodies (riba 3) is sensitive test as the PCR-HCV, so if antibody test is negative with unexplained deterioration of liver function. The HCV PCR is indicated to clarify the false negative antibody in such immunosupressed patients.

Dr. Shaheen: I would like to mention that in Saudi Arabia, we have a very good experience and satisfied results of renal transplantation in HCV positive patients and our results are comparable to inter­national data, and the graft survival for HCV positive is comparable to HCV negative patients. The important factor in getting good result is to have a full liver work up before renal transplant in HCV positive patients and to treat those patients for at least six months and repeat the liver biopsy post treatment course before renal transplant. Concerning MARS procedure, I have a limited experience with three cases with fulminant hepatitis and we did not succeed to save them, although it is very expensive procedure and requires high quantity of human albumin.

 
   References Top

1.Arroyo V, Guevara M, Gines P. Hepatorenal syndrome in cirrhosis: Pathogenesis and treatment. Gastroenterology 2002;122(6): 1658-76.  Back to cited text no. 1    
2.Ginez P, Arroyo V. Hepatorenal syndrome. J Am Soc Nephrol 1999;10(8):1833-9.  Back to cited text no. 2    
3.Wong F, Blendis L. New challenge of hepatorenal syndrome: Prevention and treatment. Hepatology 2001;34(6):1242­-51.  Back to cited text no. 3    
4.Gines P, Guevara M, Arroy V, Rodes J. Hepatorenal syndrome. Lancet 2003;362 (9398):1819-27.  Back to cited text no. 4    
5.Wadei HM, Mai ML, Ahsan N, Gonwa TA. Hepatorenal syndrome: Pathophysiology and management. Clin J Am Soc Nephrol 2006; 1(5):1066-79.  Back to cited text no. 5    
6.Pereira BJ. Hepatitis C Infection and post­transplantation Liver disease. Nephrol Dial Transplant 1995;10(Suppl 1):58-67.  Back to cited text no. 6  [PUBMED]  
7.Pereira BJ, Levey AS. Hepatitis C Virus infection in dialysis and renal transplantation. Kidney Int 1997;51(4):981-99.  Back to cited text no. 7    
8.LaQuaglia MP, Tolkoff-Rubin NE, Dienstag JL, et al. Impact of hepatitis on renal transplantation. Transplantation 1981;32 (6):504-7.  Back to cited text no. 8    
9.Rao KU, Erson RW, Kasiske BL, Dahl DC. Value of liver biopsy in the evaluation and management of Chronic liver disease in Renal transplant recipients. Am J Med 1993;94(3):241-50.  Back to cited text no. 9    
10.Epstein M, Berk DP, Hollenberg NK, et al. Renal failure in patients with cirrhosis: The role of active vasoconstriction. Am J Med 1970;49(2):175-85.  Back to cited text no. 10    
11.Caregaro L, Menon F, Angeli P, et al. Limitations of serum creatinine level and creatinine clearance as filtration markers in cirrhosis. Arch Intern Med 1994;154 (2):201-5.  Back to cited text no. 11    
12.Papadakis MA, Arieff AI. Unpredictability of clinical evaluation of renal function in cirrhosis: Prospective study. Am J Med 1987;82(5):945-52.  Back to cited text no. 12    
13.Arroyo V, Gines P, Gerbes AL, et al. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis: International Ascites Club. Hepatology 1996;23(1):164-76.  Back to cited text no. 13    
14.Lok AS, Chien D, Choo QL, et al. Antibody response to core, envelope and non­structural hepatitis C virus antigens: Comparison of immunocompetent and immunosuppressed patients. Hepatology 1993;18(3):497-502.  Back to cited text no. 14    

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Correspondence Address:
Abdulhakeem Al-Marwani
Department of Internal Medicine, Security Forces Hospital Program, Riyadh
Saudi Arabia
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PMID: 18310886

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    Abstract
    Introduction
    Case Report
    Discussion
    Questions and An...
    References
    Article Figures
 

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