656 Hypertension after renal transplantation is associated with a hyperreninemic state. The major causes of hypertension include renin secretion from native diseased kidneys, immunosuppressive drugs, allograft rejections and transplant renal artery stenosis. Renal allograft perfusion could be reduced due to the presence of renal artery thrombosis/stenosis or as a result of allograft rejection. Aorto-renal transit times (ARTT) have been used as a marker of renal perfusion and vascular resistance in native kidneys. The effect of hypertension, if any, on renal allograft perfusion has not been studied. We prospectively evaluated 10 patients with post renal transplant hypertension and 11 normotensive renal transplant recipients with normal allograft functions. Hypertensive patients with renal insufficiency (serum creatinine >1.5 mg%) underwent an allograft biopsy before inclusion in the study. They were excluded if the biopsy showed evidence of acute or chronic rejection. Tc99m DTPA renal transplant scans were done and dynamic studies were acquired on the computer every second for 1 minute and time activity curves generated. The ARTTs were calculated from the graphs obtained as the time to transplant peak minus the time to aortic peak. The mean ARTTs in normotensive controls were 4.3±0.9 seconds as compared to 5.9±1.5 seconds in patients with post-transplant hypertension (p<0.01). There was no significant difference in the ARTTs in patients receiving cyclosporine (4.9±1.0 seconds) as compared to those not receiving the drug (5.2±1.8 seconds, p>0.05). The basal plasma renin activity (normal 0.2-2.8 ng/ml/hr) in hypertensives (25.6±13.9 ng/ml/hr) was significantly higher than normotensive controls (7.4±5.6 ng/ml/hr, p<0.05). There was no significant correlation in the degree of prolongation of ARTTs with elevation of plasma renin activity when hypertensive recipients (r=0.846) were compared against normotensive controls (r=0.967, p>0.05). Transplant renal artery stenosis was excluded on color doppler in 6 and on angiography in 4 hypertensive patients. Three of these 4 patients had reduction in antihypertensive drug requirements after bilateral native kidney nephrectomies. We conclude that aorto-renal transit times are prolonged in severely hypertensive renal transplant recipients with otherwise normal graft functions. This appears to be a result of hyper-reninema due to persistent renin secretion from native diseased kidneys.

Delay in reporting the immunofluorescence findings on renal biopsies, owing to an interruption in supply of reagents, made possible a retrospective analysis of the effect of the lack of this information on patient management. Hospital case records of the 39 patients so affected were reviewed to determine what changes in their management took place after the immunofluorescence findings became available. The clinical, laboratory, and light microscopic findings in all except a case of pauci-immune crescentic glomerulonephritis allowed management decisions to be made that were not influenced by immunofluorescence findings. This was owing to correct prediction of the immunofluorescence findings, as in cases of IgA nephropathy presenting with recurrent haematuria; the adequacy of light microscopy in the interpretation of graft biopsies, in classifying lupus nephritis and in most cases of nephrotic syndrome; and the absence of entities identifiable only by immunofluorescence among these patients.

Summary: Data on zinc status in Indian patients with chronic renal failure is lacking. There are conflicting data in the literature on plasma and erythrocyte zinc levels in renal failure patients and the effect of haemodialysis on zinc status. of the multiple factors believed to be involved in the pathogenesis of uraemic impotence, attention has been focused on the possible role of zinc depletion and hyperprolactinaemia. We report a longitudinal study on 27 patients with end‐stage renal disease (ESRD). Plasma and erythrocyte zinc, serum prolactin and serum total testosterone were studied at diagnosis, 4 weeks after haemodialysis, and 3 and 6 months after successful renal transplantation. Zinc status and hyperprolactinaemia are both normalized within 6 months after renal transplantation. While there was a significant positive correlation between plasma zinc and serum testosterone, there was no correlation between serum prolactin and testosterone. This observation suggests that plasma zinc may be a more important determinant of normal gonadal function than prolactin in renal transplant recipients.

The role of converting enzyme inhibitor enhanced radionuclide investigations in post-transplant hypertension is not clearly defined. Presence of renal failure, chronic rejection and use of cyclosporin A complicates the results. Captopril-induced changes in effective renal plasma flow (ERPF) were studied in 10 patients with severe post-transplant hypertension and no evidence of rejection. Angiographic correlation was available in all. Six patients had a significant increase in ERPF after captopril, and all had a negative angiogram. One patient on CsA with a negative angiogram had no change in ERPF. Three patients had a fall in ERPF, and all 3 had transplant renal artery stenosis. Captopril-induced changes in ERPF can differentiate patients with native-kidney-induced hypertension from those with hypertension secondary to transplant renal artery stenosis in patients without evidence of rejection.

Infections are a major cause for mortality and morbidity in renal transplant recipients all over the world. In the tropics, infections account for the majority of deaths in the transplant population (1). Published accounts on the chronological appearance of various infections have helped physicians target investigative protocols and empirical treatment based on the probability of disease at varying intervals after transplantation. Risk of infection is determined by epidemiologic exposure to the infective agents and the net state of immunosuppression (2, 3). Even though the immunosuppressive protocols at this center are similar to those in the developed western countries, the added immunosuppression caused by concomitant infections, undernutrition, and organ dysfunction are different, as is the environmental exposure to various infective agents. The sequence of infections encountered after transplantation in this center is reported. From 1986 to 1994, 920 patients received living-related renal allografts. Low-dose prednisolone and azathioprine were employed initially, and cyclosporine-based immunosuppression was used since 1989 (4). Prednisolone-azathioprine-cyclosporine schedule consisted of oral prednisolone 20 mg/day from days 0 to 90. Azathioprine 1-1.5 mg/kg from days 0-5 was adjusted as per leukocyte response. Oral cyclosporine was initiated at a dose of 8 mg/kg on day 0 and tapered to 2 mg/kg by the 180th day. For the prednisolone-cyclosporine group 20 mg of prednisolone was given from days 0 to 90. Then it was tapered to a maintenance dose of 10 mg by the 180th day. Oral cyclosporine was initiated at 12 mg/kg on day 0 and reduced to 10 mg/kg by day 15. It was tapered to 3 mg/kg by the 180th day. Cyclosporine doses were modified as per cyclosporine blood levels (whole blood Enzyme Immuno Assay Syva, San Jose, Ca) in association with clinical features. The conventional immunosuppression consisted of azathioprine 2-2.5 mg/kg/day started on days 0-5 and modified by leukocyte response; 100 mg of prednisolone was started on day 0, reduced to 20 mg/day by the 28th day, and tapered to 10 mg by the 180th day. Acute rejections were treated with i.v. methylprednisolone 1 g on 3 consecutive days. Acute vascular rejections in patients receiving conventional therapy were treated with cyclosporine (5). Cyclosporine was added at a dose of 5 mg/kg/day, reduced to 4 mg/kg/day by 4 weeks and 3 mg/kg/day by 8 weeks. All patients were seen frequently for the first 6 months, then at the 9th month and 12th month. Thereafter, yearly followup was advised with earlier visits in case of complications. Our patients originate from all the states of India and neighboring countries like Nepal, Bhutan, Bangladesh, and Srilanka. Because communications were difficult and distances vast, all our transplant recipients stayed at Vellore for 6 months after surgery. Our policy was to discontinue cyclosporine at the end of 1 year. Hence, the followup at 6 months was 100%, 9th month about 80%, and 12th month 95%. Subsequent followup falls to about 40%; however, patients communicate with us or come to the center in case of major medical problems. Patients with fever of unknown origin or features of organ involvement had appropriate tests. The transplant-disease interval in 9 important infective syndromes is presented in Table 1 and charted (Fig. 1). Rubin categorized infections as those occurring within 1 month, 2-6 months, and thereafter. The first group included urinary infections, vascular access, catheter, and surgery related infections. In our patients also, urinary tract infections clustered around the first month, which was free from opportunistic infections. Pneumocystis carinii pneumonia was first seen in 1991 (6). Of the 12 cases a later report indicated that 9 manifested the disease within 6 months of transplantation (7). Cryptococcal infections occurred after 6 months of transplantation in all but one case who had received added immunosuppression (8). All the above findings fit into Rubin's schema. Thirty cases of deep mycoses encountered included candida (13), zygomycetes (11), aspergillus (10), and one each of histoplasma, T. bigelii, C. globosum(9), individually or in various combinations. There were 17 cases of nocardiosis. There was no significant difference in the number or type of risk factors like renal failure, liver disease, hyperglycemia, extra immunosuppression, or leucopenia contributing to the development of these two infections before or after 6 months. The sixth month marks the beginning of maintenance immunosuppression but does not influence the occurrence of these two groups of infections. The environmental exposure factor was highlighted by the large number of patients with posttransplant tuberculosis. This appears to occur earlier in cyclosporine-treated patients as compared with those receiving azathioprine and prednisolone immunosuppression (4)(Table 1). HBsAq positivity in our hemodialysis population is 40-50% (10), and in the absence of cirrhosis or portal hypertension was not considered, as a contraindication for transplantation, hence this was a risk factor even in the early posttransplant period. The overall risk of posttransplant tuberculosis increased 4-fold in patients with chronic liver disease and 2-fold in those with hyperglycemia. Varicella-zoster was seen 24.5±15.7 months after surgery and is an endemic disease in southern India with a bimodal peak incidence annually among staff and students of this hospital (11). Despite these epidemiologic features only one was infected during the first 6 months. Five patients without clinical leprosy at transplantation had the disease from 3.5 years after transplantation. Leprosy can occur 5 years after transplantation as has been reported from Brazil (12). In summary our experience validates Rubin's observations and provides further information on tuberculosis, M. leprae, and varicella-zoster infections prevalent in the tropics. We found that the 6th month milestone did not demarcate the onset and susceptibility in our patients, which appeared as a continuum from the first month. This may reflect an altered balance between the compromised host and the environmental risks.Figure 1: A time table for infections after renal transplantation in the tropics.

Summary: The aim of this study was to compare the alimentary phosphate‐binding capacity of calcium acetate to calcium carbonate in stable chronic renal failure patients who were not on haemodialysis. Intestinal absorption of phosphate and calcium was measured on three occasions in five patients with chronic renal failure who were not on maintenance haemodialysis. During each test period they received either no drug, calcium carbonate or calcium acetate (both containing 1g elemental calcium) in a randomized manner, along with a standardized meal. Intestinal contents were recovered after 10h by whole gut lavage, and phosphorus and calcium measured in meal and intestinal contents. Faecal excretion of ingested phosphorus increased from 13.85% in the absence of drug to 29.91% after calcium carbonate administration. Phosphorus excretion was significantly higher after calcium acetate (43.92%) compared to calcium carbonate ( P <0.05). Less calcium was absorbed from calcium acetate than from equimolar amounts of calcium caronate ( P <0.05). In patients with stable renal failure, calcium acetate is a better alimentary phosphate binder than calcium carbonate and binds more phosphorus for each mol of calcium absorbed.

Of 213 renal allgroft recipients suspected to have had pulmonary tuberculosis, 132 had sputum examinations and 14 showed acid-fast bacilli. Of the remaining 118 patients, 25 had gastric aspirations, 18 had bronchoalveolar lavage, and 75 did not require further investigation because of spontaneous improvement or confirmation of an alternative diagnosis. While 9 of the 25 patients' gastric aspirate examination was positive, all the 18 who had bronchoalveolar lavage were negative for acid-fast bacilli. Eighty-one patients without expectoration had gastric aspiration directly and 14 showed acid-fast bacilli. Of the remaining 67 patients only 17 had bronchoalveolar lavage, of which three were positive for AFB and the rest did not require further testing for tuberculosis.A total of 106 patients had gastric aspiration, Acid-fast bacillus positivity was significantly more (P<.01) in patients with abnormal chest radiographs as compared with patients with normal chest radiograph results. We suggest gastric aspiration for AFB in all renal transplant recipients who have fever, scanty expectoration, and abnormal chest radiograph with clinical suspicion of pulmonary tuberculosis.

Summary: Impaired allograft function is an important cause of hypertension in cadaveric renal transplant recipients. the risk factors for post‐tranplant hypertension in living related transplant recipients with inherent good graft functions are likely to be different and have not been studied. In addition, controversy surrounds any independent effect hypertension might have on renal allograft functions. Four hundred and seventy three living related renal allograft recipients were retrospectively analysed to study the risk factors for development of post‐transplant hypertension and its effect on graft outcome. Prevalence of hypertension was 76.1%. the presence of pre‐transplantation hypertension was the most important independent risk factor for development of hypertension after transplantation. This suggests an important role of retained native diseased kidneys as a cause of hypertension. Other risk factors included: cyclosporin A immunosuppression, patient age less than 40 years and the presence of renal insufficiency at last follow up. Hypertension did not have any effect on patient or graft survival during the mean follow‐up period of 20.1 ± 13.7 months; however, it was associated with an independent risk for the presence of renal insufficiency in the post‐transplant period.

Journal Article The emergence of Pneumocystis carinii pneumonia in renal transplant patients in a south Indian hospital Get access Anand Date, Anand Date 1Department of Pathology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar Hemalatha Krishnaswami, Hemalatha Krishnaswami 1Department of Pathology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar George T. John, George T. John 2Department of Nephrology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar Elizabeth Mathai, Elizabeth Mathai 3Department of Microbiology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar Chakko K. Jacob, Chakko K. Jacob 2Department of Nephrology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar J.C.M. Shastry J.C.M. Shastry 2Department of Nephrology, Christian Medical College and Hospital, Vellore, 632004, Tamil Nadu, India Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 89, Issue 3, May-June 1995, Page 285, https://doi.org/10.1016/0035-9203(95)90542-1 Published: 01 June 1995 Article history Received: 19 December 1994 Revision received: 01 February 1995 Accepted: 03 February 1995 Published: 01 June 1995

John, George T.; Mathew, Mary; Snehalatha, Elizabeth; Anandi, V.; Date, Anand; Jacob, C. K.; Shastry, J. C.M. Author Information

Plasma and renal tissue levels of lipid peroxide and plasma vitamin E were estimated as measures of free radical injury in five renal allograft recipients with untreated and four with unsuccessfully treated acute cellular rejection and compared with 11 control patients with minimal change disease. Plasma lipid peroxide was significantly higher in patients studied before antirejection therapy (13.2 +/- 3.5 nmol/ml; P < 0.01) as well as in those after unsuccessful antirejection treatment (11.7 +/- 0.7 nmol/ml; P < 0.01), compared to controls (5.7 +/- 2.8 nmol/ml). Levels of plasma vitamin E and renal tissue lipid peroxide were similar in both groups, however the latter was significantly raised in patients evaluated prior to antirejection therapy than in those after unsuccessful antirejection therapy (5.1 +/- 1.7 and 3.0 +/- 0.8 nmol/mg protein; P < 0.05). These findings suggest possible free radical mediated injury during renal allograft rejection.

Eighty patients with non-insulin-dependent diabetes mellitus being treated in a south Indian hospital were biopsied to confirm suspected nondiabetic renal disease (NDRD). The positive predictive value of the standard clinical indicators for NDRD in the presence or absence of diabetic retinopathy was 54 and 87%, respectively. These values are higher than those given by comparable studies in Western populations. This is probably due to a higher prevalence of NDRD in the population of south India, and especially of proliferative glomerulonephritis, which was found in 21.5% of the patients studied. Standard clinical predictors of NDRD in diabetics have a high predictive value in the tropics where there is a high prevalence of proliferative glomerulonephritis.

A retrospective study of 1000 live renal transplants was performed in order to assess the factors associated with hypertension in renal transplant recipients. The prevalence of hypertension prior to transplantation was 48%. The need for antihypertensive drugs decreased in 43%, increased in 31% and remained the same in 26%. The presence of hypertension before transplantation, rejection episodes, transplant renal artery stenosis and native kidney disease were the main factors associated with post-transplant hypertension. An algorithm for the management of post-transplant hypertension is suggested.

The prevalence of post-transplant diabetes mellitus in 222 consecutive live related renal allograft recipients over a 3-year period was found to be 11.7%. Most of them (20 of 26) developed diabetes mellitus within the first 4 months of transplantation. Post-transplant diabetic patients were older, and had a significantly greater incidence of avascular necrosis of bone. An assessment of risk factors showed that abnormal postprandial blood sugar pretransplant was a significant predictor for development of post-transplant diabetes, whereas cumulative oral steroid dose, weight gain after transplant, type of immunosuppression employed, and graft function were not important. We conclude that post-transplant diabetes mellitus frequently develops in patients with a predisposition by virtue of older age and pretransplant postprandial hyperglycaemia. While steroids are important in the pathogenesis, there was no demonstrable dose-response relationship; post-transplant diabetic patients may be a group with a greater propensity to steroid-induced complications.

Fifty-five consecutive patients with end-stage renal disease entering haemodialysis programmes over a two-month period and 48 consecutive recipients of renal allografts during a period of 6 months were investigated for hepatitis B virus (HBV) and hepatitis D virus (delta) infection. HBV markers were present in 25 of the former and 40 of the latter. Of the 65 patients with HBV infection, 12 were not available for delta antibody screening. HBV infection was present for a mean of 2.5 months and 45.3% of those infected had clinical hepatitis; none had fulminant hepatitis. All the patients tested were negative for antidelta antibody. An additional patient on dialysis with delta superinfection and hepatic encephalopathy is also reported.

THOMAS, PAULOSE P.; DAKSHINAMURTHY, K. V.; JACOB, CHAKKO K.; KIRUBAKARAN, M. G.; SHASTRY, J. C. M. Author Information