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Quiz
QUIZ
Quiz
Chris Callaghan MRCS MRCS(Ed) is an SpR in General Surgery on the East Anglian Rotation in the UK. J Andrew Bradley MBChB FRCS PhD FMedSci is Professor of Surgery and Director of Transplantation, Addenbrooke’s Hospital, Cambridge, UK.
retroperitoneal dissection, though some surgical units in the UK use a transperitoneal approach. Laparoscopic nephrectomy can be transperitoneal or retroperitoneal. The left kidney is usually taken because of its long renal vein, which makes the recipient operation technically easier. A donor kidney is shown in Figure 2.
Mr TY is 50 years old with end-stage renal failure due to polycystic kidney disease; he requires haemodialysis. His wife, who is ABO blood group compatible, has offered to donate a kidney, and her kidney is transplanted into his right iliac fossa. Both donor and recipient have an uneventful recovery. On discharge from hospital, his serum creatinine concentra tion is 145 μmol/l.
On routine transplant clinic follow-up, his serum creatinine concentration was stable at 145–155 μmol/l. However, today, in clinic 2 months post-transplant, his serum creatinine level is 260 μmol/l. He has been admitted to the transplant ward for investigation. He is feeling generally well, though he has felt ‘a bit hot’ recently and has mild diarrhoea. Current immuno suppressive medication includes tacrolimus, azathioprine and prednisolone.
Q H ow is polycystic kidney disease inherited, and which other diseases are associated with it? A T here are two modes of inheritance: autosomal dominant and autosomal recessive. The dominant form is more common, presents in middle age (Figure 1) and is most often due to a mutation in the PKD1 gene on chromosome 16. It also causes liver cysts and is associated with intracranial aneurysms, aortic root dilation and cardiac murmurs. Autosomal recessive polycystic kidney disease presents in infancy or, if severe, with pulmonary hypoplasia and oligo hydramnios at birth. This recessive form of the disease is also associated with hepatic cysts.
Q G ive a differential diagnosis for his deterioration in renal function 2 months post-transplant.
A D onor nephrectomy can be open or laparoscopic. The open operation is usually undertaken through a flank incision with
A • a cute rejection (which can be associated with systemic symptoms) • opportunistic infection, e.g. infection of the urinary tract, pneumonia, cytomegalovirus gastroenteritis • tacrolimus toxicity • ureteric obstruction and infection of the urinary tract • arterial/venous thrombosis is very unlikely at 2 months post- transplant
Figure 1 Polycystic kidney removed from a patient with the autosomal dominant form of the disease.
Figure 2 The donor kidney is being flushed with cold preservation fluid via a single renal artery. The ureter is draped over the hilum, and the renal vein is obscured.
Q W hat are the surgical techniques for performing living-donor nephrectomy? If both kidneys have single vessels, which is usually taken for transplantation and why?
THE FOUNDATION YEARS 3:2
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© 2007 Published by Elsevier Ltd.
QUIZ
Q Which first-line investigations are required and why? Which invasive investigation(s) should be performed if the first-line tests are non-diagnostic? A T he following first-line investigations should be performed: • Full blood cell count azathioprine can cause lymphopenia neutrophilia is associated with infection lymphocytosis is associated with viral infections • Urea and electrolytes check for any further deterioration in renal function; if very severe, venous access and haemodialysis may be needed • Concentration of tacrolimus in blood • Monitoring of cytomegalovirus by polymerase chain reaction of whole blood • Renal transplant ultrasound scan to assess arterial and venous patency and exclude obstruction in the transplant ureter arising from extrinsic compression (e.g. by a hydrocele around the graft caused by lymphatic disruption during transplant surgery) • Mid-stream urine and dipstick • Blood cultures, faecal cultures • Chest radiograph If no cause for reduced renal transplant function is found using the above investigations, a renal transplant biopsy is required. Consider rigid sigmoidoscopy and bowel biopsy to look for a histological diagnosis of cytomegalovirus.
Figure 3 Courtesy of Dr S Thiru, Consultant Histopathologist, Addenbrooke’s Hospital, Cambridge, UK.
If the episode of acute rejection does not respond to cortico steroids, possible treatments include anti-thymocyte globulin or anti-CD-3 monoclonal antibody. Both are associated with signifi cant risks of anaphylaxis and fatal pulmonary oedema secondary to cytokine release and increased vascular permeability.
Figure 3 is a histopathology slide from a renal transplant biopsy. Q What does the slide show?
Further reading Callaghan CJ, Bradley JA. Current status of renal transplantation. Methods Mol Biol 2006; 33: 1–28. Halloran PF. Immunosuppressive drugs for kidney transplantation. N Eng J Med 2004; 351(26): 2715–29. Harris PC, Rosetti S. Molecular genetics of autosomal recessive polycystic kidney disease. Mol Genet Metab 2004; 81: 75–85. Ko DSC, Cosimi AB. The donor and donor nephrectomy. In: Morris PJ, ed. Kidney transplantation, 5th edn. Philadelphia: WB Saunders; 2001. Morrissey PE, Mohaco AP. Living kidney donation: evolution and technical aspects of donor nephrectomy. Surg Clin North Am 2006; 86: 1219–35. Ong AC, Wheatley DN. Polycystic kidney disease—the ciliary connection. Lancet 2003; 361: 774–76. Racusen LC, Solez K, Colvin RB, et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999; 55: 713–23.
A T he slide shows acute cellular rejection, with a pleomorphic interstitial infiltrate of mononuclear cells (T cells and macrophages) and occasional eosinophils, accompanied by interstitial oedema. Foci of tubulitis (lymphocytes infiltrating tubular epithelial cells) are also present (see asterisk on the slide). Acute cellular rejection is mediated by T cells responding to foreign major histocompatibility complex or minor histocompatibility antigens. Acute cellular rejection is more common than antibody-associated rejection. Q H ow would you treat this case? What treatment would you use if your first-line medications did not lead to an improvement in renal function? A F irst-line treatment for acute rejection is high-dose corticosteroids given intravenously, e.g. 1 gm methylpredniso lone i.v. o.d. for 3 days.
THE FOUNDATION YEARS 3:2
98
© 2007 Published by Elsevier Ltd.
Quiz
Chris Callaghan MRCS MRCS(Ed) is an SpR in General Surgery on the East Anglian Rotation in the UK. J Andrew Bradley MBChB FRCS PhD FMedSci is Professor of Surgery and Director of Transplantation, Addenbrooke’s Hospital, Cambridge, UK.
retroperitoneal dissection, though some surgical units in the UK use a transperitoneal approach. Laparoscopic nephrectomy can be transperitoneal or retroperitoneal. The left kidney is usually taken because of its long renal vein, which makes the recipient operation technically easier. A donor kidney is shown in Figure 2.
Mr TY is 50 years old with end-stage renal failure due to polycystic kidney disease; he requires haemodialysis. His wife, who is ABO blood group compatible, has offered to donate a kidney, and her kidney is transplanted into his right iliac fossa. Both donor and recipient have an uneventful recovery. On discharge from hospital, his serum creatinine concentra tion is 145 μmol/l.
On routine transplant clinic follow-up, his serum creatinine concentration was stable at 145–155 μmol/l. However, today, in clinic 2 months post-transplant, his serum creatinine level is 260 μmol/l. He has been admitted to the transplant ward for investigation. He is feeling generally well, though he has felt ‘a bit hot’ recently and has mild diarrhoea. Current immuno suppressive medication includes tacrolimus, azathioprine and prednisolone.
Q H ow is polycystic kidney disease inherited, and which other diseases are associated with it? A T here are two modes of inheritance: autosomal dominant and autosomal recessive. The dominant form is more common, presents in middle age (Figure 1) and is most often due to a mutation in the PKD1 gene on chromosome 16. It also causes liver cysts and is associated with intracranial aneurysms, aortic root dilation and cardiac murmurs. Autosomal recessive polycystic kidney disease presents in infancy or, if severe, with pulmonary hypoplasia and oligo hydramnios at birth. This recessive form of the disease is also associated with hepatic cysts.
Q G ive a differential diagnosis for his deterioration in renal function 2 months post-transplant.
A D onor nephrectomy can be open or laparoscopic. The open operation is usually undertaken through a flank incision with
A • a cute rejection (which can be associated with systemic symptoms) • opportunistic infection, e.g. infection of the urinary tract, pneumonia, cytomegalovirus gastroenteritis • tacrolimus toxicity • ureteric obstruction and infection of the urinary tract • arterial/venous thrombosis is very unlikely at 2 months post- transplant
Figure 1 Polycystic kidney removed from a patient with the autosomal dominant form of the disease.
Figure 2 The donor kidney is being flushed with cold preservation fluid via a single renal artery. The ureter is draped over the hilum, and the renal vein is obscured.
Q W hat are the surgical techniques for performing living-donor nephrectomy? If both kidneys have single vessels, which is usually taken for transplantation and why?
THE FOUNDATION YEARS 3:2
97
© 2007 Published by Elsevier Ltd.
QUIZ
Q Which first-line investigations are required and why? Which invasive investigation(s) should be performed if the first-line tests are non-diagnostic? A T he following first-line investigations should be performed: • Full blood cell count azathioprine can cause lymphopenia neutrophilia is associated with infection lymphocytosis is associated with viral infections • Urea and electrolytes check for any further deterioration in renal function; if very severe, venous access and haemodialysis may be needed • Concentration of tacrolimus in blood • Monitoring of cytomegalovirus by polymerase chain reaction of whole blood • Renal transplant ultrasound scan to assess arterial and venous patency and exclude obstruction in the transplant ureter arising from extrinsic compression (e.g. by a hydrocele around the graft caused by lymphatic disruption during transplant surgery) • Mid-stream urine and dipstick • Blood cultures, faecal cultures • Chest radiograph If no cause for reduced renal transplant function is found using the above investigations, a renal transplant biopsy is required. Consider rigid sigmoidoscopy and bowel biopsy to look for a histological diagnosis of cytomegalovirus.
Figure 3 Courtesy of Dr S Thiru, Consultant Histopathologist, Addenbrooke’s Hospital, Cambridge, UK.
If the episode of acute rejection does not respond to cortico steroids, possible treatments include anti-thymocyte globulin or anti-CD-3 monoclonal antibody. Both are associated with signifi cant risks of anaphylaxis and fatal pulmonary oedema secondary to cytokine release and increased vascular permeability.
Figure 3 is a histopathology slide from a renal transplant biopsy. Q What does the slide show?
Further reading Callaghan CJ, Bradley JA. Current status of renal transplantation. Methods Mol Biol 2006; 33: 1–28. Halloran PF. Immunosuppressive drugs for kidney transplantation. N Eng J Med 2004; 351(26): 2715–29. Harris PC, Rosetti S. Molecular genetics of autosomal recessive polycystic kidney disease. Mol Genet Metab 2004; 81: 75–85. Ko DSC, Cosimi AB. The donor and donor nephrectomy. In: Morris PJ, ed. Kidney transplantation, 5th edn. Philadelphia: WB Saunders; 2001. Morrissey PE, Mohaco AP. Living kidney donation: evolution and technical aspects of donor nephrectomy. Surg Clin North Am 2006; 86: 1219–35. Ong AC, Wheatley DN. Polycystic kidney disease—the ciliary connection. Lancet 2003; 361: 774–76. Racusen LC, Solez K, Colvin RB, et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999; 55: 713–23.
A T he slide shows acute cellular rejection, with a pleomorphic interstitial infiltrate of mononuclear cells (T cells and macrophages) and occasional eosinophils, accompanied by interstitial oedema. Foci of tubulitis (lymphocytes infiltrating tubular epithelial cells) are also present (see asterisk on the slide). Acute cellular rejection is mediated by T cells responding to foreign major histocompatibility complex or minor histocompatibility antigens. Acute cellular rejection is more common than antibody-associated rejection. Q H ow would you treat this case? What treatment would you use if your first-line medications did not lead to an improvement in renal function? A F irst-line treatment for acute rejection is high-dose corticosteroids given intravenously, e.g. 1 gm methylpredniso lone i.v. o.d. for 3 days.
THE FOUNDATION YEARS 3:2
98
© 2007 Published by Elsevier Ltd.