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Background Kidney transplantation has gained widespread popularity by improving the outcome of end-stage renal disease (ESRD) patients. However, this is a highly complicated and expensive procedure that puts much pressure on the health system in developing countries. We report the costs in Iran model of kidney transplantation. Materials and Methods We reviewed the regulations for kidney transplantation using Dialysis and Transplant Patients Association (DATPA) information, 2005. All data regarding the cost of transplantation procedure, immunosuppression, and the money given to donors were included. The cost of transplantation procedure was categorized into personnel, drugs, paraclinics, hospital bed, and other expenses. To achieve more comprehensive results, all costs were converted into US dollars (1 USD = 9000 Rials). Results The total cost of kidney transplantation procedure was $9224. Of this, 65.8% ($6076) was related to the immunosuppression therapy in the first year, 22.2% ($2048) to the transplantation procedure, and 12% ($1100) to organ procurement. The details of donor nephrectomy were as follows: personnel, $183; accommodations, $107; drugs, $39; paraclinics, $23; and other, $22. These values for kidney recipient were personnel, $331; drugs, $367; paraclinics, $278; accommodations, $475; and other, $222. Conclusion Compared with other countries, the kidney transplantation cost is low in Iran. The health system also pays for all the expenses. These, along with full medical insurance coverage of kidney recipients, make kidney transplantation available for every patient, regardless of the socioeconomic status due to its low cost. It is expected that a higher number of transplantation candidates with a low socioeconomic status will select transplantation.

Objective. Posttransplant diabetes mellitus (PTDM) is a common and serious complication of renal transplantation. Estimates of the incidence of PTDM after renal transplantation vary between 2% and 54%. The aim of the present study was to evaluate the incidence and risk factors for PTDM among our renal transplant patients. Patients and Methods. In this study we evaluated 121 nondiabetic patients with end-stage renal disease (ESRD) who underwent kidney transplantation for the first time at our centers since 2005. All patients received the same protocol of immunosuppressive therapy. PTDM was defined according to the clinical practice recommendations of the American Diabetes Association. Results. At 12 months following renal transplantation, 9.9% of patients developed PTDM. Patients with PTDM were significantly older (P .013) and had higher body mass index (P .001). There were significant differences (P .05) between PTDM and non-PTDM patients with respect to systolic blood pressure, serum triglycerides (TG), peritoneal dialysis as renal replacement therapy before transplantation, and duration of pretransplant dialysis therapy. Upon multivariate analysis, serum TG, systolic blood pressure, and body mass index were associated with PTDM (P .05). Conclusions. The incidence at 12 months of PTDM among our renal transplant recipients was 9.9%. The most important factors associated with PTDM were serum TG, systolic blood pressure, and body mass index.

Background Ischemia-reperfusion (IR)-induced nephrotoxicity is associated with proteinuria. There are reports on the involvement of inducible nitric oxide synthase (iNOS) in proteinuria in conjunction with renal disease. This study was designed to investigate the effect of N6-(1-iminoethyl)-L-lysine hydrochloride (L-Nil), a selective inhibitor of iNOS, to prevent proteinuria in IR injury. Methods Ischemia was induced by 40-minute clamping of the renal arteries followed by 6-hour reperfusion. Rats were administered either L-Nil (3 mg/kg intravenous bolus followed by infusion of 1 mg/kg/h) or saline. To monitor glomerular and tubular functional changes before and after treatment, we measured blood urea nitrogen, plasma creatinine, and urinary N-acetyl-β-D-glucosaminidase activity. Total protein (TP), albumin, and low- (LMW) and high-molecular-weight (HMW) protein excretion rates were determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis of urine samples. Kidney ultrastructure was examined through a transmission electron microscope (TEM). Results IR resulted in significant LMW and HMW proteinuria. L-Nil significantly prevented the IR-induced increases in TP, albumin, and α1-microglobulin excretion. TEM showed loss of microvilli of the proximal tubule cells, injured mitochondria, and foamy changes in the structure of nuclear and cytoplasm in IR group. L-Nil reduced IR-mediated renal ultrastructural changes and tubular proteinuria. Discussion This study suggested possible differences in the mechanism(s) of nephrotoxicity induced by iNOS in the glomeruli and tubular cells. The types of proteins excreted in the urine should be considered in the treatment strategy. In conclusion, this study suggested the involvement of iNOS in IR-induced tubular proteinuria.

National registries provide valuable bases for comparisons and aid innovative policies. Iran, with 70 million inhabitants, has a governmentally supported system of organ and tissue procurement and transplantation. By two acts of legislation, first in 1997 regarding governmental rewarding living kidney donation and second in 2000 regarding cadaveric transplantation, this field has had remarkable growth in the last decade, under the supervision of the Ministry of Health. Since the beginning of each organ or tissue transplantation activity up to 2006, 21,359 kidneys, 338 livers, 122 hearts, 20 lungs, 7 pancreas, 1898 bone marrows, 28,838 corneas, 1380 heart valves, and 1366 bones were transplanted in our country. Increases in the number of live kidney transplantations are taking place, but cannot keep pace with the increasing number of patients. It is highly recommended that we try to increase cadaveric transplantation in coming years.

Objective Cyclosporine (CsA) has been shown to improve long-term survival after organ transplantation. However, CsA therapy is associated with a variety of side effects, among which nephropathy is the major one. Recent studies have suggested increased oxidative stress as a cause of drug nephrotoxicity. Therefore, this study was designed to evaluate the effects of CsA administration on the antioxidant capacity of kidney tissue. Methods Adult male Sprague-Dawley rats were randomly assigned into 2 groups: one group received CsA (25 mg/kg/d, IP for 2 weeks) and a control group (no CsA administration). After 2 weeks, the kidneys of the rats from both groups were removed under anesthesia. A 50 mg fresh kidney tissue sample was homogenized in ice-cold phosphate buffer. Total antioxidant capacity (Ferric Reducing Ability of Plasma [FRAP]) in the homogenates was assayed based on the Benzie spectrophotometric method. Results FRAP in the kidney tissues had been significantly decreased by 2 weeks of CsA administration when compared with control rats (P Conclusions These data suggested that CsA administration may decrease the antioxidant capacity of renal tissues. More studies on the evaluation of the protective effects of antioxidant therapy against CsA nephrotoxicity are underway.

Objective. The clinical use of gentamicin (G) is limited due to its known nephrotoxic actions. Generation of reactive oxygen species has been proposed as a causative factor of cell death in G-induced acute renal failure (ARF). Previous studies using superoxide dismutase (SOD) mimetics have indirectly suggested a role for the superoxide ion in G-induced ARF. In this study, we directly measured the enzyme activities using in situ isolated kidneys seeking to investigate the effects of antioxidant therapy on preservation of endogenous antioxidant levels in ARF. Methods. Thirty-five male Sprague-Dawley rats were randomly assigned to 5 groups: control, Tyrode-perfused; G, gentamicin (200 mg/L) added to the perfusate; G + vitamin E (Vit E; 100 mg/100 g BW, IM); G + vitamin C (Vit C) added to the drinking water for 3 days (200 mg/L) and to the perfusate (100 mg/L); G + Vit E + Vit C. SOD activities were determined in renal tissues based on NAPDH oxidation at 340 nm by spectrophotometry. Results. SOD activity was significantly reduced in the G group compared with the controls (P

According to the WHO criteria many renal transplant patients display osteopenia or osteoporosis. Dual-energy X-ray absorptiometry (DXA), the standard method to assess bone mineral density (BMD), is not always available. Quantitative ultrasound (QUS) of the phalanx is an inexpensive, mobile, and radiation-free diagnostic alternative. Few data address the correlation of this method with DXA in renal transplant patients. This study assessed the value of QUS compared with DXA to detect changes in bone structure among renal transplant recipients. This cross-sectional study of 42 patients (22 women), of mean age 40.2 +/- 11.9 years, mean time since transplantation of 2.8 +/- 2.9 years, and mean dialysis time of 8.55 +/- 10.26 months, included. DXA for bone mineral densitometry of the hip (neck and total femur) and spine as well as QUS to measure the amplitude-dependent speed of sound (Ad-SOS) in the phalanx. Using DXA, osteoporosis was observed in 19% of all patients: 9.5% in femoral neck, 9.5% in total region of the femur, and 9.5% in the spinal region. The sensitivity of Ad-SOS for osteoporosis diagnosis in the above regions were 100%, 75%, and 25%, respectively; its specificity was 45%, 43%, and 37%, respectively. There was no significant relation between the two methods for diagnosis of osteoporosis in any region. QUS of phalanx can be recommended for osteoporosis screening in renal transplant patients. Those suspected of osteoporosis should be examined by additional DXA measurements in order to establish the diagnosis.

Objective Cyclosporine (CsA) causes tubular dysfunction characterized by polyuria, calcium wasting, distal tubular acidosis, and hyperkalemia. The hypercalciuria induced by CsA administration is associated with an inhibition of calbindin D 28k expression. It has also been shown that chronic metabolic alkalosis increased the expression of Ca 2+ transport proteins accompanied by diminished urine Ca 2+ excretion. The aim of this study, therefore, was to determine the effect of acid-base status on CsA-induced hypercalciuria. Methods Experiments were performed on male Sprague-Dawley rats. Metabolic alkalosis and acidosis were induced respectively by adding 0.28 mol/L NaHCO 3 and 0.28 mol/L NH 4 Cl in the drinking water for 7 days; control rats received regular tap water. Seven days after NaHCO 3 or NH 4 Cl administration, rats were treated with CsA (25 mg/kg, IP) daily for 14 days. To estimate glomerular filtration rate (GFR) over time, animals were placed in metabolic cages. Fractional urinary calcium excretion was determined by standard formula. Results The CsA group showed decreased serum calcium and increased fractional urinary calcium excretion compared with the control group. Creatinine clearance was also significantly reduced. Metabolic alkalosis alone did not affect GFR, but significantly prevented an increase in fractional urinary calcium excretion induced by CsA, whereas chronic metabolic acidosis resulted in the exact opposite effect. Conclusions It is essential for nephrologists to fully understand the mechanisms of CsA-induced renal injury. In this study, metabolic alkalosis reduced CsA-induced hypercalciuria. Further studies are needed to elucidate whether this effect may be achieved pharmacologically by the expression of Ca 2+ transport proteins.