Plasma N terminal pro-brain natriuretic peptide levels and its determinants in a multi-ethnic population.

This study documents the determinants and plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) among hypertensive and normotensive subjects in a multi-ethnic population in the United Arab Emirates (UAE). We obtained demographic, anthropometric and clinical data, together with fasting NT-proBNP and biochemical indices from 128 hypertensive patients and 138 normotensive subjects matched for age, gender and ethnicity. Plasma NT-proBNP levels were significantly (P<0.001), and several-fold higher among hypertensives (median 5.92, inter quartile range (IQR): 1.79-18.48 pmol/l) than normotensives (median 1.78, IQR: 0.59-4.32 pmol/l) in the total study population, and the same was true for the ethnic groups separately. Similarly, plasma levels of glucose, blood urea nitrogen (BUN) and creatinine, but not insulin, were significantly (P<0.05) higher among hypertensives than normotensives. For all subjects combined, log NT-proBNP correlated positively and significantly with age (P<0.01), log glucose (P<0.05), systolic blood pressure (SBP, P<0.001), log BUN (P<0.001) and log creatinine (P<0.001). Multivariate regression analysis showed that NT-proBNP levels were independently and positively correlated with SBP, age, gender, log BUN, Emirati and South East Asian ethnic groups and inversely associated with current exercise. In conclusion, we found circulating levels of NT-proBNP to be significantly increased in hypertensive versus normotensive subjects in the UAE and independently related to SBP, age, gender, indices of renal function and possibly exercise. Our results further suggest a possible modulating effect of ethnicity on NT-proBNP levels.

Predicting proteinuria in hypertensive pregnancies with urinary protein-creatinine or calcium-creatinine ratio.

OBJECTIVE: Evaluate the value of random urinary protein-creatinine (PrCr) and calcium-creatinine (CaCr) ratios to predict 24-h proteinuria in hypertensive pregnancies. STUDY DESIGN: Spot urine samples were collected before routine 24-h urine collections from consecutive pregnant women with hypertension (n=83). Reliability of spot urinary PrCr and CaCr to detect significant proteinuria (>or=300 mg/day) using 24-h urine protein as 'gold-standard' was assessed by receiver-operating characteristic (ROC) curve. RESULTS: Fifty-one patients (61.4%) had significant proteinuria (45 pre-eclampsia, 5 superimposed pre-eclampsia, 1 renal hypertension). Area under ROC curve to predict proteinuria was 0.82 (95% confidence interval (CI) 0.73 to 0.92, P<0.001) for PrCr and 0.55 (95% CI 0.43 to 0.68, P=0.2) for CaCr. A cutoff value of >0.19 for PrCr best predicted significant proteinuria with sensitivity, specificity, positive and negative predictive values and likelihood ratios (positive and negative), respectively, of 80.4, 68.8, 80.4, 68.8%, 2.57 and 3.51. CONCLUSION: Spot urinary PrCr predicts total urinary protein excretion in hypertensive pregnancies.

Natriuretic peptide and adrenomedullin levels in chronic renal failure and effects of peritoneal dialysis.

Plasma levels of B-type natriuretic peptide (BNP) and its N-terminal propeptide (NT-BNP) are elevated in renal impairment and provide a robust prognostic index. The effect of peritoneal dialysis on plasma NT-BNP, however, is unknown. Furthermore, no information exists regarding levels of the N-terminal propeptide for C-type natriuretic peptide (NT-CNP) in renal failure and the effects of peritoneal dialysis. Accordingly, we documented venous levels of these peptides, and adrenomedullin, across peritoneal dialysis. We measured venous BNP, NT-BNP, NT-CNP, adrenomedullin, blood urea nitrogen (BUN) and creatinine before, during and after completion of overnight peritoneal dialysis in 11 patients, and identical sampling was carried out in eight patients (controls) but between peritoneal dialysis treatments. Peptide levels were measured using well-validated, published methods. Baseline levels of NT-CNP (212, 150-303 pmol/l, median and 25th and 75th percentiles) were much higher than recorded previously in healthy volunteers or in heart failure, and correlated with plasma creatinine (rs=0.53, P<0.05). Peritoneal dialysis had no effect on plasma NT-CNP, nor on NT-BNP, BNP or adrenomedullin (all elevated above normal), whereas both BUN and creatinine levels, as expected, declined (P<0.001). We conclude that plasma levels of NT-CNP are grossly elevated in chronic renal failure and correlated with plasma creatinine, but are not altered by peritoneal dialysis. Likewise, BNP, NT-BNP and adrenomedullin are elevated but are not altered by peritoneal dialysis. This information is needed if levels of these hormones are to be used as prognostic indicators or as a guide to the management of patients with chronic renal failure.

Streptozotocin-induced diabetic nephropathy in rats: the role of inflammatory cytokines.

The role of inflammatory cytokines in the pathogenesis of diabetic nephropathy has been studied in streptozotocin-induced diabetic rats. Rat kidneys were examined by light and electron microscopy and kidney homogenates were also analyzed by Western blot and flow cytometry for the expression of markers of inflammation namely, CD4+ and CD8+ T cells, macrophages, MHC classes I and II, the proinflammatory cytokines tumor necrosis factor-alpha, interferon-gamma and nitric oxide (NO). Light and electron microscope examination revealed infiltration of mononuclear cells throughout the renal parenchyma, with the glomeruli being more severely affected especially at 8 months after disease induction. Western blot and flow cytometric analyses revealed the infiltrating cells to be CD4+ T cells, CD8+ T cells and macrophages. Western blot analyses also revealed increased expression of the proinflammatory and Th1 cytokines tumor necrosis factor-alpha, interferon-gamma as well as nitric oxide. Using flow cytometry, we have shown that the difference in expression of CD4+ T cells in control and diabetic kidneys is more significant at 1 month than at 8 months, while expression of CD8+ T cells is more significant at 8 months. We speculate therefore that diabetic nephropathy is probably initiated and driven by a Th1 process. CD8+ T cells, however, become more significant at later stages of the disease when tissue loss is evident. Since NO induction also occurs only after 8 months, we hypothesize that NO might be significant for the later stages of the disease. Our data implicate inflammation in the pathogenesis of diabetic nephropathy in view of the overexpression of the proinflammatory cytokines TNF-alpha and IFN-gamma and the cells that secrete them in the early and late phases of the disease.

Hypertension--still an important cause of heart failure?

Hypertension has been the single most important risk factor for heart failure until the last few decades. Now, it is frequently claimed that atherosclerotic coronary artery disease dominates as the major underlying cause, and hypertension is of lesser importance. We here review evidence regarding the contribution of hypertension to heart failure in the recent decades. It is not possible, in our view, to be confident of the relative importance of hypertension and coronary artery disease since there are significant limitations in the available data. The often-questionable diagnostic criteria used in defining heart failure is one such limitation. The absence or inadequacy of blood pressure recordings over the years prior to a diagnosis of heart failure seriously hinders the reaching of firm conclusions in many reports. Extrapolations from aetiological observations in one racial group to those in other racial groups, and from highly selected study groups in tertiary referral centres to patients with heart failure in primary and secondary care, may not be justified. Finally, the situation of heart failure primarily due to impaired left ventricular diastolic function, where hypertension is a frequent precursor, is often ignored in discussions of aetiology. Our view is that hypertension remains and probably is the single most, important modifiable risk factor for cardiac failure in some races and countries, where the dominant cardiac abnormality is left ventricular diastolic dysfunction. The situation is less clear for patients with heart failure primarily due to left ventricular systolic dysfunction.

Loss of kidney IGF-1 receptors in experimental long-term diabetic rats.

The present study was undertaken to assess the long-term effects of streptozotocin-induced diabetes mellitus on insulin-like growth factor-1 (IGF-1) receptors in rat kidneys. Morphological changes were also evaluated using light and electron microscopy. Using receptor autoradiography the levels of IGF-1 were investigated in rat kidneys diabetic for eight months and controls. Sections from both diabetic and control rats were stained with haematoxylin and eosin for morphological studies. Ultra-thin kidney sections were examined using a transmission electron microscope. IGF-1 receptors were significantly lower in the cortex and the medulla of the diabetic rats compared with controls. Morphological differences between normal and diabetic kidneys were observed in both the cortex and medulla. Glomerular changes and necrosis of the renal cortical and medullary parenchyma were demonstrated in the diabetic rats. Necrosis of cells of the collecting ducts and loops of Henle could explain the loss of IGF-1 receptor concentration in the medulla. Shrinkage of glomeruli and normal proximal convoluted tubules of diabetic kidneys were also observed. Our results also revealed extensive damage to the distal convoluted tubules that have not been reported to possess any insulin-like growth factor-1 receptors. Our results demonstrate a reduction of kidney IGF-1 receptors after long-term diabetes mellitus possibly because of the extensive morphological loss of renal tissue. It could be speculated that early administration of IGF-1 might be useful in longterm diabetes mellitus to prevent the degeneration and/or help regeneration of damaged renal tissue.

Evaluation of Plasma Beta-2-microglobulin in Patients with the Nephrotic Syndrome.

In patients with the nephrotic syndrome, it is often desirable to assess the disease process, not only by proteinuria but also by indices of glomerular inflammatory process. We investigated the importance of beta-microglobulin (betaM) as a means of assessing renal function in patients with the nephrotic syndrome with normal or abnormal values of creatinine clearance. There were 46 patients (mean age, 42.2 + 10.4 years; male/female (M/F) ratio = 31/15) and 35 healthy controls (mean age 39 + 4.5 years, M/F ratio 25/10). We subdivided the study patients into group A (n = 18, mean age 39.6 + 10.6 years, M/F ratio 8/10) and group B patients (n = 28, mean age 45.6 + 8.9 years, M/F ratio 23/5) who had normal and abnormal values of creatinine clearance respectively. An enzyme-linked-immunosorbent assay (ELISA) was used to quantitate plasma beta2M in the study patients and controls. The median 132M levels of the study patients and controls were 44.0 and 1.7 mg/l respectively (p < 0.0001). Beta-2-M levels correlated significantly with serum creatinine (r = 0.56, p < 0.0001), and creatinine clearance (r = -0.6, p < 0.0001). In group A patients, the median beta2M level was significantly higher than normal (4.1 vs. 1.7 mg/1, p < 0.01). Plasma beta2M levels did not correlate well with any other parameter measured in group A patients. When groups A and B were compared, the median plasma beta2M level in group B was significantly higher than group A (20.3 vs. 4.1 mg/1, p < 0.0001). The urinary beta2M (expressed per mg urine creatinine) was also higher in group B than group A patients (6.8 vs. 0.7 p < 0.05). We conclude that elevation of beta2M-microglobulin in patients with the nephrotic syndrome who have normal creatinine clearance suggests early abnormal renal function in these patients. It may be used to assess the rate of normalisation of renal function or progression to chronic renal failure.

Levels of cholesteryl esters and other lipids in the plasma of patients with end-stage renal failure.

BACKGROUND: The importance of plasma lipid abnormalities in chronic renal failure (CRF) is well recognized, but surprisingly little attention has been given to the study of some plasma lipid fractions, including cholesteryl esters (CE) and phospholipids, which might be expected to be important factors in the pathogenesis of the disease. MATERIALS AND METHODS: Fasting blood samples were taken from 25 control subjects and 53 CRF patients (29 predialysis and 24 on hemodialysis). Samples were analyzed for urea nitrogen, creatinine, triacylglycerols, total and individual phospholipids, total and free cholesterol, as well as cholesterol bound to very low-, low- and highdensity lipoproteins (VLDL, LDL and HDL). Plasma CE was calculated and expressed as a percentage of total cholesterol. RESULTS: Over half of the patients had CE levels more than two standard deviations below the control value. In this subgroup of low CE patients, total, LDL- and HDL-cholesterol levels were also significantly lower than for controls, while levels of phosphatidylcholine and lysophosphatidylcholine were decreased and increased, respectively. In patients with high CE, no significant lipid abnormalities were observed. CONCLUSION: In this study, CE was an excellent marker for lipid disturbances--if CE was high, then the other lipid fractions were normal, but if CE was low, most other lipid fractions were abnormal. The changes noted appear to be consequences of or related to deficiency of the plasma enzyme lecithin-cholesterol acyltransferase.

An association study of five genetic loci and left ventricular hypertrophy amongst Gulf Arabs.

We carried out an association (case-control) study of five candidate genes--G-protein beta3 subunit gene variant; methylene tetrahydrofolate reductase (MTHFR); angiotensin converting enzyme (ACE) gene; and paraoxonase 1 and 2 (PON 1 and 2) genes--in a United Arab Emirati population. The aim was to establish a possible relationship between these five candidate genes and clinical left ventricular hypertrophy (LVH) in a genetically homogenous group. DNA samples were collected from 213 unrelated Nationals who were further segregated into 98 subjects with LVH (78 hypertensives and 20 normotensives) and 115 (23 hypertensives and 92 normotensives) age- and sex-matched controls who did not present with LVH. Of the five candidate gene markers studied, no significant differences in the genotype distribution of the MTHFR, PON 1 and 2 or ACE markers were found between the LVH and non-LVH groups. However, a possible association was found between the beta3 G-protein C825T marker and LVH. In conclusion, our results suggest an association between LVH and the C825T allele of the G-protein beta3 subunit gene.

Lecithin: cholesterol acyltransfer, dyslipoproteinaemia and membrane lipids in uraemia.

BACKGROUND: Dyslipoproteinaemia is the most important complication linked to the increased morbidity and mortality of uraemic patients from cardiovascular disease. Many factors contribute to the dyslipoproteinaemia, including increased production of very low density lipoproteins (VLDL), decreased lipolysis and impaired low density lipoprotein (LDL) receptor activity. In this study, the role of decreased lecithin:cholesterol acyltransferase (LCAT) activity in relation to plasma and membrane lipid changes is examined. METHODS: Fasted blood samples were taken from 65 uraemic patients, including roughly equal numbers of haemodialysis, peritoneal dialysis and undialysed subjects, and from 29 apparently healthy individuals. Plasma total and free cholesterol, cholesteryl esters (CE), total and individual phospholipids, high density lipoprotein (HDL)-, LDL- and VLDL-cholesterol were all measured, as were erythrocyte and lymphocyte free cholesterol and phospholipids. RESULTS: More than half of all patients, including those both on haemodialysis and peritoneal dialysis, as well as untreated individuals, had relative plasma concentrations of CE below the normal mean - 2SD. These patients had significantly decreased LDL- (2.62 +/- 1.04 compared to 3.61 +/- 0.97 mmol/L; p < 0.001) and HDL-cholesterol (0.71 +/- 0.30 compared to 0.94 +/- 0.27 mmol/L; p < 0.01) and increased VLDL-cholesterol (0.60 +/- 0.50 compared to 0.47 +/- 0.26 mmol/L; p < 0.05) as well as significant increases in membrane cholesterol and cholesterol/phospholipid molar ratio in erythrocytes (3.30 +/- 0.49 and 0.87 +/- 0.08 compared to 2.95 +/- 0.18 mmol/g wet weight and 0.76 +/- 0.04 mol/mol respectively, both p < 0.001) and cholesterol/phospholipid molar ratio of lymphocytes (0.58 +/- 0.14 compared to 0.45 +/- 0.04 mol/mol; p < 0.001). They were markedly deficient in LCAT activity (56.1 +/- 20.4 compared to 105.5 +/- 17.5 nmol/ml/h; p < 0.001). The LCAT activity in plasma of patients with high CE was higher than for those with low CE, but it was also significantly less than normal and this group showed smaller changes in other lipid parameters. CONCLUSIONS: LCAT deficiency is common in uraemia and is associated with changes not just in plasma lipids, but also in membrane lipids which may be relevant to the progression of the disease.

Morphological changes in the rat kidney following long-term diabetes.

The morphological basis of diabetic nephropathy has been studied using light and electron microscopy. Kidneys of streptozotocin-induced diabetic rats were examined on the light microscope at 4 weeks and 8 months after induction of diabetes mellitus. In addition, the 8-month diabetic kidneys were examined with the electron microscope. Renal hypertrophy was evidenced by the increase in the weight of kidneys of diabetic rats. Whilst the diabetic kidneys were approximately twice as large after 4 weeks they were only 30% larger compared to age-matched controls after 8 months of induction of diabetes. After 4 weeks, light microscopy revealed dilated tubules within the cortex of the diabetic kidneys. Light microscopy showed a significant amount of destruction of the distal convoluted tubules while electron microscopy revealed a spectrum of damage that included basement membrane thickening, loss of podocytic foot processes, disruption of tubular basal infoldings and their related mitochondria and fibrosis of the tubules 8 months after induction of diabetes. It is concluded that renal hypertrophy persists after a prolonged occurrence of diabetes but the extensive damage and loss of renal tissue including the loss of the foot processes of podocytes might be partly responsible for the clinical presentation of diabetic nephropathy.

Association of an apolipoprotein B gene marker with essential hypertension.

We designed an association (retrospective, case control) study aimed at evaluating associations between genetic variations of the human apolipoprotein B (apoB) gene and clinical diagnosis of essential hypertension. Our approach was to compare the distribution of the alleles of a highly polymorphic variable number of tandem repeats localized 3' to the human apoB gene, the apoB 3' hypervariable region (HVR), in a group of normotensive and a group of hypertensive individuals. We collected DNA samples from 437 unrelated nationals (215 normotensives and 222 hypertensives) from the United Arab Emirates (UAEs), and we determined their apoB 3' HVR allele and genotype status with a polymerase chain reaction-based assay. In the UAE population, we found 18 alleles underlying a total of 51 genotypes. The distribution of these alleles was significantly different between normotensive and hypertensive UAE nationals. The main peak of the distributions occurred at 35 repeats among hypertensives (with a relative frequency of 25.7% versus 19.6% in normotensives) and at 37 repeats among normotensives (28.8% versus 20.3% in hypertensives). Alleles with 21, 23, 25, 49, and 55 repeats were found in hypertensives only (with a combined relative frequency of 7.6%). We conclude that variations of the apoB gene, or of a nearby gene, that may be in linkage disequilibrium with these alleles play a role in the development of essential hypertension in the UAEs.

Associations of angiotensinogen gene mutations with hypertension and myocardial infarction in a gulf population.

To date, the human angiotensinogen (AGT) gene and some of its variants represent the best examples of genetic influences that are involved in the determination of essential hypertension (EH) and associated cardiovascular diseases (CVDs). To assess the value of genotyping AGT in a genetically homogeneous population, we carried out a retrospective, case control study of variants M235T and T174M for putative correlations with CVDs among nationals from the United Arab Emirates (Emirati)--an ethnic group characterized by no alcohol intake and no cigarette smoking. We investigated a sample population of 229 Emirati (119 males and 110 females), comprising groups of controls and patients with clinical diagnoses of EH, left ventricular hypertrophy (LVH), ischaemic heart disease (IHD) and myocardial infarction (MI). M235T and T174M alleles were determined via assays based on the polymerase chain reaction. T174M showed no correlation with any of the four clinical entities included in this study. T235 alleles, however, occurred more frequently in the EH group and less frequently in the group of MI survivors. We also found that T235 allele frequencies decreased with age, indicating that in the Emirati population, T235 alleles are associated with a reduced life span and that this effect could occur through independent mechanisms underlying genetic susceptibilities to both EH and MI.

An MboI two-allele polymorphism may implicate the human renin gene in primary hypertension.

As a key enzyme of the renin-angiotensin-aldosterone system, the renin gene (REN) is a good candidate quantitative trait locus that may be implicated in the molecular etiology of essential hypertension. Among mixed reports on the subject, a REN MboI restriction fragment length polymorphism has been shown to be significantly associated with a family history of hypertension in a Japanese population. We show here that the REN MboI dimorphic site is located in the ninth intron of the gene, and we describe a polymerase chain reaction-based assay for detection of this site. We investigated MboI genotype distributions in 331 hypertensive and 279 normotensive subjects from the United Arab Emirates (UAE), a genetically homogeneous ethnic population with no history of smoking or alcohol consumption. A statistically significant association was found between alleles on which the MboI site is present and clinical diagnosis of essential hypertension, indicating that 1) the presence of the MboI site is a marker for susceptibility to hypertension in the UAE (the associated odds ratio is 3.16); and 2) variations of the REN (or of a nearby) gene that may be in linkage disequilibrium with this marker play a role in the development of essential hypertension in the UAE.

The angiotensin-converting enzyme (ACE) gene insertion/deletion dimorphism tracks with higher serum ace activities in both younger and older subjects.

BACKGROUND: The absence of a 287 base pair alu sequence in the ACE gene (D allele) is associated with higher ACE levels than its presence (I allele) in adults. We carried out a case-control study of the ACE*I/D dimorphism in relation to circulating ACE activities to evaluate associations between the two variables in adults, compared to younger (18 years or less) individuals. MATERIALS AND METHODS: Genotypes of the ACE*I/D dimorphism were determined on DNA samples from a population of 164 random (unrelated) Emirate nationals, composed of two groups: 112 subjects above 18 years of age (range=20-77 years), and 52 subjects of 18 years or less (range=1-18), and analyzed for putative associations with serum ACE activities. ACE*I/D genotypes of the 164 individuals were determined by assays based on polymerase chain reaction. ACE activities were determined on serum samples of these subjects by colorimetric assays. RESULTS: The D allele was associated with increased ACE values in both adult and younger individuals. Mean ACE activity levels associated with II, ID and DD genotypes, however, were 42%-61% higher in the 18 years and under group of subjects. The ACE*I/D marker accounted for 28% of the variance of the phenomenon determining ACE levels in adults, and for 30% among youngsters. CONCLUSION: The ACE*I/D dimorphism correlated strongly with circulating ACE activities in both adult and young Emirati subjects, and the corresponding mean ACE activities were significantly higher among the youngsters.

Association study between the ANF gene and hypertension in a Gulf Arab population.

We have studied an insertion/deletion (I/D) dimorphism located in the second intron of the human atrial natriuretic factor (ANF) gene among 232 United Arab Emirates (UAE) nationals (112 normotensives and 120 hypertensives) from the Abu Dhabi Emirate, with a view to evaluating the value of this marker in relation to hypertension. Our findings show that genotype frequencies of this I/D marker occur in Hardy-Weinberg proportions (respective genotype frequencies in the overall sample population are: II, 51%; ID, 42%; DD, 7%). No association, however, was evidenced between this dimorphic site and clinical diagnosis of essential hypertension. This suggests that: 1) this I/D dimorphism is not a useful marker to study the relationship between the ANF gene and hypertension in the UAE; and 2) variations of the ANF gene that may be in linkage disequilibrium with this marker do not play a major role in the determination of hypertension in this Arab population.

Deletion polymorphism in the angiotensin-converting enzyme gene is not associated with hypertension in a Gulf Arab population.

We have studied an insertion/deletion dimorphism in the human angiotensin-converting enzyme gene amongst UAE nationals from the Abu Dhabi Emirate. Our findings show lack of association between the I/D allele marker system and clinical diagnosis of essential hypertension, suggesting that variations of the angiotensin-converting enzyme gene do not play a major role in the determination of elevated blood pressure in this Arab population. This agrees with results reported on other ethnic groups.

Outcome of bought living non-related donor kidneys followed up at a single centre.

Between October 1985 and November 1991, 16 dialysis patients travelled to Bombay and bought kidneys from living non-related Indian donors for U.S. $7,372. One patient died peri-operatively; one contracted HIV and another hepatitis B virus infections. Six patients are presently positive for hepatitis C virus antibody compared to two cadaver graft recipients (P = 0.03); two of the six patients have chronic active hepatitis. Five-year patient and graft survival rates (75% and 43%, respectively) were similar to those of recipients of 24 cadaver grafts obtained in the United States (67% and 55%, respectively), as was graft function during the first 5 years of follow-up. Graft survival may have improved following commercial kidney transplantation in Bombay, but this practise still poses a risk of dangerous infections and exploitation of donors and recipients. The establishment of a centralized programme of anonymous "rewarded gifting" in countries that cannot eradicate rampant organ commerce may help to expunge exploitation and to ensure uniform, acceptable clinical standards and the safety of patients.

Prevalence of complement-fixing antibodies to Mycoplasma pneumoniae in the savannah and forest belts of Nigeria.

A survey of complement-fixing antibodies to Mycoplasma pneumoniae in 1673 children (aged 5-13 years) was conducted in Nigeria. Although the antibodies were detected in 25.7% of the children from the savannah belt and 20.4% of those from the forest belt, only 8.9% and 7.4%, respectively, had titres considered high enough to protect them from infection. The geometric mean titres (GMT) tended to increase with age up to 8 years and then gradually fall. The age-specific differences in GMT were significant (F = 2.98; analysis of variance with x = 0.05) but those due to the child's sex (F = 2.49) and belt of origin (F = 2.61) were not. The results indicate that Nigeria is a highly endemic area for M. pneumoniae infection, with a large pool of susceptible children in which epidemic outbreaks could occur.

High incidence of post-transplant diabetes mellitus in a single-centre study.

Twelve of 29 Saudi patients (41.4%) developed diabetes mellitus following renal transplantation. Post-transplant diabetes mellitus occurred within the first 2 months in eight patients; two others presented with diabetic ketoacidosis associated with severe infections. The diabetic and non-diabetic patients had received similar doses of prednisolone and cyclosporin (CsA) during the initial 2 months post-transplantation, and their mean CsA blood values at 3 months were not significantly different. Increasing patient age (over 40 years), but not sex, donor source, or body mass index, was associated with an increased risk for developing diabetes mellitus. Post-transplant diabetes mellitus was controlled with oral hypoglycaemic agents in most patients, but one-third required insulin. Patients who developed diabetes had significantly decreased mean creatinine clearance/1.73 m2 at a mean graft age of 3.4 years (P less than 0.001). Diabetes mellitus after transplantation may be more common among Saudi patients than elsewhere, especially those aged over 40 years. It develops rapidly, may present with ketosis, and is associated with graft dysfunction.