Tahir Aziz

A Renal Transplantation Model for Developing Countries

The estimated incidence of end‐stage renal disease (ESRD) in Pakistan is 100 per million population. Paucity and high costs of renal replacement therapy allows only 10% to get dialysis and 4–5% transplants. Our center, a government organization, started a dialysis and transplant program in 1980s where all services were provided free of charge to all patients. It was based on the concept of community government partnership funded by both partners. The guiding principles were equity, transparency, accountability and development of all facilities under one roof. This partnership has sustained itself for 30 years with an annual budget of

Pediatric Kidney Transplantation in the Developing World: Challenges and Solutions

25 million in 2009. Daily 600 patients are dialyzed and weekly 10–12 receive transplants. One‐ and 5‐year graft survival of 3000 transplants is 92% and 85%, respectively. The institute became a focus of transplantation in Pakistan and played a vital role in the campaign against transplant tourism and in promulgation of transplant law of 2007, and also helped to increase altruistic transplants in the country. This model emphasizes that in developing countries specialized centers in government sector are necessary for transplantation to progress and community support can make it available to the common man.

Prevalence of cryptosporidiosis in renal transplant recipients presenting with acute diarrhea at a single center in Pakistan

The prevalence of pediatric RRT and transplantation are low in developing countries, 6–12 and <1 to 5 per million child population (pmcp), respectively. This is due to low GDP/capita of <

Long-term Safety of Living Kidney Donation in an Emerging Economy.

10 000, government expenditure on health of <2.6–9% of GDP and paucity of facilities. The reported incidence of pediatric CKD and ESRD is <1.0–8 and 3.4–35 pmcp, respectively. RRT and transplantation are offered mostly in private centers in cities where HD costs

Plasma cell‐rich acute rejections in living‐related kidney transplantation: a clinicopathological study of 50 cases

20–100/session and transplants

Experience of Fibrosing Cholestatic Hepatitis With Hepatitis C Virus in Kidney Transplant Recipients

10 000–20 000. High costs and long distance to centers results in treatment refusal in up to 35% of the cases. In this backdrop 75–85% of children with ESRD are disfranchised from RRT and transplantation. Our center initiated an integrated dialysis–transplant program funded by a community‐government partnership where RRT and transplantation was provided “free of cost” with life long follow‐up and medication. Access to free RRT at doorsteps and transplantation lead to societal acceptance of transplantation as the therapy of choice for ESRD. This enabled us to perform 475 pediatric transplants in 25 years with 1‐ and 5‐year graft survival of 96% and 81%, respectively. Our model shows that pediatric transplantation is possible in developing countries when freely available and accessible to all who need it in the public sector.

Outcome of living-related donor renal allografts in hepatitis C antibody-positive recipients.

Background: Cryptosporidium is an intracellular protozoan organism which causes diarrhea, both in immunocompetent and immunocompromised hosts. Renal transplant recipients are prone to develop a variety of infections including protozoal infections. Objectives: The aim of this study was to determine the prevalence of cryptosporidiosis in our renal transplant recipients presenting with acute diarrhea. Patients and Methods: During six months of the study, 644 renal transplant recipients presented with acute diarrhea. Single stool sample was obtained for detailed analysis including gross and microscopic examination for red blood cells, pus cells, ova, cysts, and protozoa. The modified Ziehl-Neelsen (ZN) staining was done to identify the oocysts of cryptosporidia. Results: Out of 644 renal transplant patients, oocysts of cryptosporidia were identified in 343 patients (53%). Detailed stool analysis of these patients showed the presence of numerous pus cells in 27 (7.9%) patients, co-infection with giardia intestinalis cysts in 15 (4.3%), and entamoeba histolytica cysts in 10 (2.9%). In all, out of 343 patients, 43 (12.5%) had dual infection with bacteria and protozoa in addition to cryptosporidiosis. Conclusions: Cryptosporidium is an important pathogen causing acute diarrhea in renal transplant recipients in our set up. Stool examination is usually negative for pus cells. It is recommended that in all transplant recipients presenting with acute diarrhea modified ZN staining should be done to rule out cryptosporidiosis in highly endemic areas like Pakistan.

Prevalence and risk factors for early chronic allograft nephropathy in a live related renal transplant program

Background Long-term follow-up and management of donors was undertaken in a specialist kidney transplant unit in Pakistan to identify risk and prevent adverse outcomes in living related kidney donors. Methods In an observation cohort study between 1985 and 2012, 3748 donors were offered free medical follow-up and treatment 6 to 12 months after donation and annually thereafter. Each visit included history, physical examination, blood tests for renal, lipid, glucose profiles, and 24-hour urine for proteinuria and creatinine clearance. Preventive intervention was undertaken for new onset clinical conditions. Donor outcomes were compared with 90 nondonor healthy siblings matched for age, sex, and body mass index. Results Of the 3748 donors, 2696 (72%) were in regular yearly follow-up for up to 27 years (median, 5.6; interquartile range, 7.9). Eleven (0.4%) died 4 to 22 years after donation with all-cause mortality of 4.0/10 000 person years. Six (0.2%) developed end-stage renal disease 5 to 17 years after donation, (2.7/10 000 person years). Proteinuria greater than 1000 mg/24 hours developed in 28 patients (1%), hypertension in 371 patients (13.7%), and diabetes in 95 patients (3.6%). Therapeutic intervention-controlled protein was less than 1000 mg/24 hours, blood pressure was below 140/90 mm Hg, and glycemic control in 85% up to 15 years after onset. Creatinine clearance fell from 109.8 ± 22.3 mL/min per 1.73 m2 predonation to 78 ± 17 at 1 year, 84 ± 19 at 5 years, and 70 ± 20 at 25 years. Comparison of 90 nondonor sibling and donor pairs showed significantly higher fasting glucose and hypertension in nondonors. Conclusions Long-term follow-up of donors has demonstrated end-stage renal disease in 0.6% at 25 years. Regular follow-up identified new onset of disease and allowed interventions that may have prevented adverse outcomes.

Acute Renal Failure Due to Traumatic Rhabdomyolysis

Acute rejections (ARs) with plasma cell‐rich infiltrates (PCARs) are associated with poor outcomes.

The effect of chemokine receptor gene polymorphisms (CCR2V64I, CCR5-59029G>A and CCR5Δ32) on renal allograft survival in Pakistani transplant patients.

BACKGROUND Fibrosing cholestatic hepatitis C (FCH-C) is a rare entity that occurs among immune-compromised patients resulting from the direct hepatotoxicity of a high intracellular viral load along with an ineffective immune system ultimately leading to a fatal outcome. We have describes herein 4 renal transplant recipients who were diagnosed with FCH-C at our institution in the last 8 months. METHODS Four renal transplant recipients presented with jaundice and deteriorating liver function tests. They were diagnosed to display FCH-C based on the presence of hepatitis C virus (HCV) RNA and characteristic liver biopsy findings; there was no evidence of any other cause of cholestasis or biliary obstruction. RESULTS The patients were men of ages 40, 25, 20, and 27 years. The durations after transplantation were 1.5, 10, 1.5 and 2.0 years, respectively. In all cases pretransplantation screening was negative for HCV antibody, HCV RNA, and hepatitis B surface antigen (HBsAg). All 4 patients were infected with genotype 1, whereas case 2 had coinfection with type 3. Cases 1 and 2 who were treated with interferon and ribavirin, showed improvement in cholestasis but did not achieve a rapid virological response. Case 1 developed graft dysfunction secondary to acute cellular rejection at 4 months after initiation of interferon treatment, which was treated with pulse steroids. Interferon-based therapy was stopped prematurely in both cases due to pancytopenia. Case 3 developed florid pyelonephritis and died without receiving therapy for hepatitis C. Case 4 was managed conservatively by decreasing the immunosuppression with regular monitoring. CONCLUSION FCH-C is difficult to treat and shows high morbidity and mortality rates. Treatment is associated with a risk of graft rejection.