ACE I/D gene polymorphism predicts renal damage in congenital uropathies

We investigated angiotensin converting enzyme gene (ACE I/D) polymorphism as a risk for progressive renal damage in congenital uropathies. The ACE I/D genotype was determined in 196 Caucasian patients with congenital uropathies and 163 individuals with no clinical or sonographic evidence of any urological malformations. The study group included patients with ureteropelvic junction obstruction (n=49), primary obstructive megaureter (n=19), primary vesicoureteral reflux (VUR) (n=67), and posterior urethral valves (n=27). Thirty-four patients were excluded because of additional diseases or insufficient follow-up. There was no difference in the ACE I/D distribution between children with uropathies and normal controls (II 16%, ID 56%, DD 28% vs. II 26%, ID 50%, DD 24%). Renal lesions were found in 99 of 162 children by ultrasonography, intravenous pyelography, and nuclear scans. In these children there was significant over-representation of the DD genotype (II 11%, ID 53%, DD 36%) compared with normals (P<0.005, X²=14.9) or with patients with uropathies but no renal lesions (II 23%, ID 62%, DD 15%, P<0.005, X²=14.9). Because ACE I/D has been linked with progressive deterioration of renal function, we evaluated a subset of patients with initially normal kidneys who developed radiographic renal lesions (n=28). Among these patients there was an even greater over-representation of the DD genotype (II 0%, ID 43%, DD 57%, P<0.001, X²=22.6) compared with patients with uropathies but no radiographic lesions. Multivariate analysis revealed that the DD genotype is a risk factor for parenchymal destruction, which was independent of time of diagnosis, surgical intervention, or urinary tract infection. This finding was particularly relevant in patients with VUR who constituted the majority with initially normal kidneys who developed radiographic damage (22/28). Indeed, the odds ratio of developing parenchymal damage with VUR was significantly increased if the individual had the DD genotype (4.2, 95% confidence interval 1.4–13.0). In conclusion the ACE I/D gene polymorphism is a risk factor for renal parenchymal damage in patients with congenital urological abnormalities and appears particularly relevant in children with VUR, where it is an independent predisposing factor. Received: 3 November 1998 / Revised: 3 March 1999 / Accepted: 3 March 1999     

The D-allele of the ACE gene polymorphism predicts a stronger antiproteinuric response to ACE inhibitors

SUMMARY: Angiotensin converting enzyme (ACE) inhibitors have additional renoprotective effects over other antihypertensive drugs in retarding the development and progression of diabetic and non-diabetic nephropathies. This additional beneficial effect has been attributed to their antiproteinuric action. However, individual antiproteinuric responses to ACE inhibitors vary considerably. the mechanism underlying the variable response is unresolved. the role of the insertion/deletion (I/D) polymorphism of the ACE gene in this response was examined. the case series consisted of 96 patients (69 males, median age 46.5 years) on ACE inhibitors with an initial proteinuria in excess of 1.0 g/24h. A control series consisted of 103 patients (43 males, median age 40 years) with autosomal polycystic kidney disease. A second control series consisted of 82 patients (52 males, median age 39 years) with a diagnosis of insulin-dependent diabetes mellitus (IDDM) without microalbuminuria after more than 15 years of IDDM. Angiotensin converting enzyme genotyping was performed by polymerase chain reaction (PCR) analysis of chromosomal DNA. the ACE genotype distribution (DD 44%, ID 28%, II 28%) in the case series was not in accordance with the Hardy-Weinberg equilibrium (χ²= 17.2, P<0.001), whereas it was in both control series. the difference in ACE genotype distribution between the case series and both control series combined was significant as a result of an overrepresentation of patients with the DD genotype (χ²=9.2, P=0.01). the allele frequencies were compared in patients with a reduction of proteinuria above and below the median value of 45%. the antiproteinuric effectiveness of ACEI therapy in the whole group was greater in the presence of the D-allele (OR 1.6, 95% CI 0.9-2.9). the effect of the D-allele was more pronounced in the subgroup of patients with an initial proteinuria in the non-nephrotic range (relative risk 2.8, 95%CI 1.0-8.0) and in patients not receiving diuretics (relative risk 2.3, 95% CI 1.1–4.5). In conclusion, the DD genotype seems to predispose the development of proteinuria in the presence of a kidney disorder. the presence of the D-allele predicts a stronger antiproteinuric efficacy of ACE inhibitor therapy in patients with an initial proteinuria in the non-nephrotic range and in the patients not requiring comedication with diuretics.     

Influence of ACE I/D gene polymorphism in the progression of renal failure in autosomal dominant polycystic kidney disease: a meta-analysis.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is a renal disease characterized by an important variability in clinical course, which cannot be fully explained by the genetic heterogeneity of the disease. Although the role for the angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) polymorphism as a modifier factor in ADPKD renal deterioration has been suggested, direct evidence from genetic association studies remain inconclusive. To provide a more robust estimate of the putative effect of the ACE I/D polymorphism on the renal progression in ADPKD, we performed a meta-analysis pooling data from all relevant studies in which the role of the ACE I/D variant in ADPKD clinical features was evaluated. METHODS: We applied a random-effects model to combine odds ratio and 95% confidence intervals. Q-statistic was used to evaluate the homogeneity, and both Egger's and Begg-Mazumdar tests were used to assess publication bias. RESULTS: Altogether, three distinct meta-analyses were generated using data from 13 studies. Despite the absence of publication bias and the presence of homogeneity among study results, the DD genotype failed to show an influence on risk of end-stage renal disease (ESRD), mean age at ESRD or risk of hypertension in ADPKD patients when compared with I-allele carriers (DD vs ID+II). Likewise, meta-analyses carried out separately for Caucasian and Asian studies showed no indication of an association between the DD genotype and a faster renal deterioration in ADPKD. CONCLUSION: These findings do not support the hypothesis that the enhanced ACE activity associated with the D allele might promote a significantly worse prognosis in patients with ADPKD.     

ACE I/D gene polymorphism in primary FSGS and steroid-sensitive nephrotic syndrome

The role of angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism in various renal disorders has been investigated. We evaluated the association between the clinical characteristics and ACE genotypes of Turkish children with primary focal segmental glomerulosclerosis (FSGS) and steroid-sensitive nephrotic syndrome (SSNS). Patients with FSGS (n=30) were classified into two groups: one with remission together with stable renal function (n=22) and the other without remission and with impaired renal function (n=8). We classified children with SSNS (n=43) that were followed for at least 4 years into two subgroups as having more frequent (n=19) and less frequent relapses (n=11). The DD genotype was more frequent in the SSNS group than that in controls (37% vs. 17%, ²=4.98, P=0.025). However, among SSNS subgroups, the frequency of the DD genotype was not different. The distribution of ACE genotype was similar among patients with FSGS and SSNS. There was no difference in the ACE I/D distribution between children with FSGS and normal controls (II 10%, ID 60%, DD 30% vs. II 13%, ID 70%, DD 17%). The frequency of the DD genotype was higher in FSGS patients with declining renal function (63%) than in those with stable renal function (18%) (P=0.031). Progressive renal impairment was significantly more frequent in patients with FSGS with the homozygous D allele compared with FSGS patients with ID and II genotypes. Our results indicate that the DD genotype may be a risk factor for the development of progressive renal impairment in children with FSGS; however, larger studies are required to confirm this.The abstract of this study was accepted as a poster for the 36th meeting of the European Society of Paediatric Nephrology, Bilbao, September 2002. This study was supported in part by a grant from the Istanbul University Research Fund (no T-849/17072000)     

Meta-analysis of the relationship between ACE I/D gene polymorphism and end-stage renal disease in patients with diabetic nephropathy

Aims: Diabetic nephropathy (DN) is the major cause for end‐stage renal disease (ESRD) and the pathogenesis for DN developing into ESRD is not clear at present. Results from published studies on the relationship between angiotensin‐converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and ESRD risk in DN patients are still conflicting. This meta‐analysis was performed to evaluate the association between ACE I/D gene polymorphism and ESRD risk in DN patients. Methods: Association studies were identified from the databases of PubMed, Embase and Cochrane Library on 1 October 2011, and eligible investigations were identified and synthesized using the meta‐analysis method. Results were expressed using odds ratios (OR) for dichotomous data and 95% confidence intervals (CI) were also calculated. Results: Twelve studies reporting the relation between ACE I/D gene polymorphism and ESRD risk in DN patients were identified. In overall populations, there was a notable association between D allele or DD genotype and ESRD susceptibility (D: OR = 1.32, 95% CI: 1.11–1.56, P = 0.002; DD: OR = 1.67, 95% CI: 1.25–2.21, P = 0.0004). In the sub‐group analysis according to ethnicity, D allele or DD genotype was associated with ESRD risk in Asians. In Caucasians, the association of DD genotype with ESRD risk was observed, but the D allele was not. Furthermore, ACE I/D gene polymorphism was associated with ESRD risk in patients with DN due to diabetes mellitus type 2, but the association was not found for patients with DN due to diabetes mellitus type‐1. Conclusions: Our results indicate that D allele or DD homozygous is associated with the ESRD susceptibility in DN patients. However, more investigations are required to further this association.     

The effect of angiotensin converting enzyme gene polymorphism on chronic allograft dysfunction in living donor renal transplant recipients

BACKGROUND: Chronic allograft dysfunction (CAD), the major cause of the failure of kidney allografts, may be caused by immunological and non-immunological haemodynamic factors. Renin-angiotensin system has been implicated in the development of intraglomerular hypertension and has a central role on progression in chronic renal disease. Polymorphism in 16th intron of the ACE gene has been reported to predict the circulating angiotensin II levels. The aim of this study was to investigate the effect of the both recipient and donor angiotensin converting enzyme (ACE) genotype on the development of CAD in renal allograft recipients. PATIENTS AND METHODS: A total of 143 renal transplant recipients (95 male, 48 female, mean age 32 +/- 10 yr) were included. In order to exclude the effect of cold ischaemia, only patients transplanted from living donors were selected. Factors analysed in the development of CAD were donor and recipient age, past history of acute rejection, presence of hypertension and hypercholesterolaemia, serum uric acid level and ACE gene polymorphism. RESULTS: Forty of the patients (28%) had CAD. Homozygous deletion type ACE gene polymorphism was detected in 59 renal transplant recipients (42%) and in 31 donors of the patients (37%). On comparing patients with and without CAD, donor age, rate of acute rejection and hypertension and serum uric acid levels were significantly higher in CAD (+) groups. Neither recipient nor donor ACE genotype was associated with time to CAD. Cox regression analysis revealed donor age (p < 0.001), presence of hypertension (p=0.002) and serum uric acid levels (p=0.009), but neither donor nor recipient ACE genotype as independent factors for predicting development of CAD. CONCLUSION: Donor age, presence of hypertension and serum uric acid levels was independent factors. Donor and recipient ACE genotype seemed to have no influence on the development of CAD in living donor transplanted patients.     

Human SA gene Pst1 polymorphism and chronic renal failure: results of the family-based study.

BACKGROUND: Because of the heterogeneous aetiology of kidney diseases, interactions between multiple genetic and environmental factors are thought to be involved in the process of progression to end-stage renal disease (ESRD). Raised blood pressure remains a well-established, independent risk factor for a more rapid decline of renal function in various kidney diseases. The aim of the study was to investigate the role of the human SA gene Pst1 polymorphism in the development and/or progression of chronic renal failure (CRF). METHODS: This polymorphism was genotyped in a group of 247 family trios (offspring affected with end-stage renal disease, and both parents): 120 with primary chronic glomerulonephritis, 80 with interstitial nephritis, and 47 with diabetic nephropathy. Transmission/disequilibrium test (TDT) was used to evaluate allele transmission from heterozygous parents to affected offspring. RESULTS: SA gene Pst1 allele transmission did not differ from random proportion of 50:50, with no significant variation in the slope of reciprocal serum creatinine over time between patients with SA Pst1 A1A1, A1A2, and A2A2 genotypes. In addition, no impact of this marker on the rate of progression of CRF in the course of diabetes mellitus, interstitial nephritis, and chronic glomerular nephritis was shown. CONCLUSION: Results of the study suggest no major role of SA gene polymorphism in promoting renal damage. However, the limited numbers of patients having both parents alive included in the analysis might have resulted in insufficient power to detect a minor impact of this polymorphism, especially if such effect is confined to a certain aetiology of CRF.     

The deletion polymorphism of the ACE gene is not an independent risk factor for renal scarring in children with vesico-ureteric reflux.

BACKGROUND: The deletion (D) polymorphism of the gene encoding angiotensin-I converting enzyme has been implicated as a risk factor for progressive renal disease in several conditions. This study was designed to evaluate the association between homozygosity for the D allele and susceptibility to renal scarring in children with vesico-ureteric reflux (VUR). METHODS: Two-hundred-and-six children with VUR (all grades) were recruited into the study. Patients were stratified into two groups according to the presence or absence of renal scarring. One-hundred-and-twelve patients (group 1) had evidence of renal scarring. Ninety-four children had no evidence of renal scarring (group 2). ACE genotypes were determined by polymerase chain reaction (PCR) amplification of genomic DNA samples. RESULTS: There was no association between the DD polymorphism and the presence of renal scarring. Genotype frequencies in group 1 were: II, 29; ID, 56; and DD, 27; and in group 2 were: II, 12; ID, 52; DD, 30 (P=0.21). Neither was there evidence supporting a 'dominant' D allele. There was no association between the DD genotype and the presence of proteinuria or reduced renal function (P>0.05). Hypertension was seen more frequently in those individuals with the DD genotype, compared with the other two genotypes (P=0.012). CONCLUSION: We cannot confirm previous reports that children with vesico-ureteric reflux who are homozygous for the deletion polymorphism of the ACE gene are more susceptible to renal scarring than heterozygotes and II homozygotes.     

Mutation analyses of Uroplakin II in children with renal tract malformations.

BACKGROUND: Uroplakin (UP) proteins cover urothelial apical surfaces. Mice lacking UPIIIa have elevated urothelial permeability and congenital renal tract anomalies, and UPIIIa mutations have been reported in children with kidney and ureter malformations. Mice with null mutation of another UP family member, UPII, are often born with congenital hydronephrosis. We hypothesized that UPII mutations may be present in humans with renal tract malformations. METHODS: Mutations were sought, using direct sequencing of the five UPII exons, in 42 children with diverse renal tract anomalies. RESULTS: No UPII abnormalities were detected in 41 patients, whereas one index case had a heterozygous frameshift change which, if expressed, would generate a truncated protein. This Caucasian child presented with vesicoureteric reflux (VUR), bilateral nephropathy and renal failure. The genetic change was also found in the index case's mother who had normal renal ultrasonography, but it was absent in 150 healthy Caucasian control individuals (96 assessed by direct sequencing and another 54 assessed by restriction digests). UPII was immunolocalized in urothelium of the normal human embryonic renal pelvis in a pattern similar to UPIIIa. CONCLUSION: This study offers no definitive support for UPII mutations causing human renal tract malformations. In rare patients, UPII variants might be implicated in pathogenesis when acting in conjunction with other yet-to-be-defined, genetic or environmental modifying factors.     

Cardiac malformations associated with the congenital nephrotic syndrome

The association of cardiac malformation with the congenital nephrotic syndrome (CNS) has been previously reported in only one family. We report four patients with CNS: three with pulmonary valve stenosis (one requiring valvuloplasty) and one with discrete sub-aortic stenosis requiring surgical resection. We conclude that the cardiac status of all patients with CNS should be reviewed regularly by a paediatrician, with a low threshold for referral to a cardiologist, as flow murmurs due to chronic anaemia may obscure cardiac pathology. It is important to diagnose any associated cardiac lesions as these may require intervention, and may also predispose to the development of bacterial endocarditis if surgical or dental procedures are undertaken without appropriate antibiotic prophylaxis. Received: 3 May 1999 / Revised: 8 March 2000 / Accepted: 9 March 2000     

The 'breakpoint' test, a new statistical method for studying progression of chronic renal failure

The application of a new statistical method ('breakpoint' test) to the study of the progression of chronic renal failure is described. This test establishes whether the best fit of a series of GFR measurements is linear or broken. Such an approach avoids the analytical constraint of the time of intervention assumed by other methods. Re-analysis by this test of previous studies of low-protein diet suggests that in some cases the effect of the dietary regimen has been overemphasized.     

Frequency of renal malformations in Turner syndrome: analysis of 82 Turkish children

We evaluated the frequency of renal malformations in relation to nonmosaic 45,X (group A, 45 patients, 54.9%) and mosaic/structural abnormalities of X (group B, 37 patients, 45.1%) in 82 Turkish patients with Turner syndrome (TS). Ultrasonography of the kidneys and collecting system was performed in all patients. Of the 82 patients, 31 had different renal malformations (37.8%). Horse-shoe kidney was observed in 9 (29.0%) of the 31 patients, and 17 patients (54.8%) had various collecting system malformations, while 5 (16.2%) had malrotation and other positional abnormalities. The prevalence of renal malformations was significantly higher in group A (51.1%) than group B (21.6%) (2:7.94, P<0.05). Although 8 of the 9 patients with horse-shoe kidney had the 45,X karyotype, collecting system malformations were observed more frequently in group B. Recurrent urinary tract infections (UTIs) were detected during follow-up in 7 patients, and hypertension developed in 3 patients. In patients who had a normal baseline nephrological evaluation, no problem suggesting renal disease developed during follow-up. We conclude that all forms of TS should have routine nephrological screening on diagnosis, since structural malformations of the kidney occur more frequently in nonmosaic 45,X TS, while collecting system malformations are mostly seen in mosaic/structural X forms. Those included in the group for nephrological follow-up had an increased risk for hypertension and/or UTI. Received: 15 February 1999 / Revised: 20 January 2000 / Accepted: 25 January 2000     

Association of endothelial nitric oxide synthase gene intron 4 polymorphism with end-stage renal disease

BACKGROUND: Nitric oxide (NO) released from endothelial cells is related to the maintenance of physiological vascular tone. The impairment of endothelial NO generation brought about by gene polymorphism is considered one of the deterioration factors in progressive renal disease. In the endothelial nitric oxide synthase (eNOS) intron 4 polymorphism, the presence of the aa genotype has been associated with cardiovascular and renal disease. The aim of this study was to investigate the presence of eNOS gene intron 4 polymorphism in patients with end-stage renal disease (ESRD). METHODS: A total of 114 patients and 94 controls were studied. DNA specimens were extracted from blood and amplified by polymerase chain reaction. The alleles were separated by agarose gel electrophoresis. Genotype distribution and allele frequencies were compared between groups using the chi-squared test. RESULTS: Statistical analysis revealed that the frequency of the eNOS4 genotype aa was significantly different in ESRD patients and in controls (P=0.016, OR=2.07, CI 95%: 1.14-3.74). There was also a statistically significant difference between ESRD patients and controls regarding allele carriers (P=0.004; OR=2.26; CI 95%: 1.29-3.96). When the frequencies of allele carriers in the diabetic nephropathy group and in the control group were compared, a significant difference was found (P=0.034, OR=2.28; CI 95%: 1.04-5.00). CONCLUSION: This study showed a strong correlation between eNOS4a polymorphism and end-stage renal disease.     

Patchy renal vasoconstriction after exercise in a child without renal hypouricemia

Here, I present a case of patchy renal vasoconstriction and renal injury in a girl without renal hypouricemia, following exercise and ingestion of an analgesic. For the previous 2 years, she had suffered from re-current abdominal pain following exercise. Postcontrast renal computed tomographic scan showed low-density patchy areas immediately after contrast medium injection, and then patchy wedge-shaped contrast enhancement 22 h later. These symptoms and signs are typical findings of patchy renal vasoconstriction. Although precise mechanisms for the development of patchy renal vasoconstriction after exercise in patients without renal hypouricemia remain obscure, both exercise and ingestion of an analgesic were active in the development of patchy renal vasoconstriction and renal injury in our patient. Received: 9 August 2001 / Revised: 10 December 2001 / Accepted: 11 December 2001     

The 1998 report of the Japanese National Registry data on pediatric end-stage renal disease patients

We carried out a nationwide survey on patients less than 20 years of age with pediatric chronic end-stage renal disease (ESRD) in Japan for the year 1998. There were 582 patients who had started on renal replacement therapy before 1998, and 105 patients who had been newly introduced to renal replacement therapy in that year. The prevalence rate of the ESRD patients already on treatment was 22 per million population (aged 0–19 years) in 1998. Older patients had a higher prevalence rate than younger ones. There were 345 patients on dialysis as of 1 January 1998, and 237 patients with transplants. The major diseases causing ESRD were renal hypoplasia/dysplasia and focal segmental glomerulosclerosis. Of the 237 patients (46.9%) who had received renal transplants before 1 January 1998, 262 patients (96%) received their transplants from living kidney donors. The incidence rate for the new ESRD patients was 4 per million population (aged 0–19 years) in 1998. Older patients had a slightly higher incidence rate than younger ones. Peritoneal dialysis was used more frequently than hemodialysis under 15 years (85%–95% and 39% respec-tively), especially in very young patients. The major diseases causing ESRD were the same as in the patients already on treatment. The transplant rate for the year 1998 was 10 per 100 dialysis patient-years (patients aged 0–19 years) with 9 living kidney donors. The death rate was 15.6 per 1,000 dialysis patient-years (patients aged 0–19 years); the major causes of death being cardiovascular diseases and infections. Received: 30 January 2001 / Revised: 3 January 2002 / Accepted: 4 January 2002     

Endothelial nitric oxide synthase gene polymorphism in intron 4 affects the progression of renal failure in non-diabetic renal diseases.

BACKGROUND: Nitric oxide is a very potent regulator of intrarenal haemodynamics and is thought to be an important factor in the deterioration of renal function. Our study sought to verify the hypothesis that endothelial nitric oxide synthase (ecNOS) gene polymorphism in intron 4 might have some relevance to progression in chronic renal failure. METHODS: We studied the frequencies of gene polymorphism of ecNOS intron 4 in patients with end-stage renal disease (302 cases) and compared it with that of healthy subjects (248 cases). ecNOS genotypes were determined by the polymerase chain reaction, followed by agarose gel electrophoresis. RESULTS: Two alleles of ecNOS intron 4, labelled a and b could be detected; a has four and b has five tandem 27-bp repeats. The frequencies of ecNOS4b/b, ecNOS4b/a, ecNOS4a/a genotypes were 81.0% (201/248), 19. 0% (47/248), 0.0% (0/248) in the control group, and 74.8% (226/302), 23.5% (71/302), l.7% (5/302) in all the patients, 72.7% (168/231), 25.1% (58/231), 2.2% (5/231) in the group with end-stage renal diseases, excluding diabetic nephropathy (non-DM group), and 81.7% (58/71), 18.3% (13/71), 0.0% (0/71) in diabetic nephropathy (DM group) respectively. The frequency of the ecNOS4a (ecNOSb/a, and ecNOSa/a) in all the patients and in the non-DM group were significantly higher than that in the control group (P=0.021; P=0. 0096 respectively). In contrast, there was no significant difference in the frequencies of ecNOS genotypes between the DM group and the control group (P=0.81). CONCLUSION: Among the frequencies of ecNOS intron 4 gene polymorphism, a allele displayed a significantly higher frequency in cases with end-stage renal failure (ESRF) not caused by diabetic nephropathy. ecNOS gene polymorphism in intron 4 appears, therefore, to affect the progression of renal failure in non- diabetic renal diseases, but the same conclusion could not be drawn in diabetic nephropathy.     

Transient acute renal failure due to nitrofurantoin poisoning

A 3-year-old girl developed acute oliguric renal failure after accidental ingestion of nitrofurantoin (190 mg/kg body weight). The time interval between poisoning and the onset of renal failure was 9 days. She later recovered with symptomatic management. Received: 4 September 1998 / Revised: 11 February 1999 / Accepted: 15 February 1999     

The influence of hemodialysis on serum sialic acid levels in chronic renal failure

Background. It has been observed that there is an increase in serum sialic acid level in chronic renal diseases and endstage renal failure requiring hemodialysis, and the hemodialysis procedure causes increased cytokine production. Thus, it is expected that hemodialysis causes increases in the serum levels of acute phase reactants and sialic acid. Nevertheless, the changes in serum sialic acid level in hemodialysis have not been examined sufficiently. In our study, we examined the effect of hemodialysis on serum sialic acid level. Methods. A total of 54 patients on hemodialysis therapy for chronic renal failure (32 men; 22 women) were examined. The patients were evaluated in four groups according to their age, sex, duration of hemodialysis, and whether they were diabetic. Serum sialic acid levels before and after hemodialysis, done with a hemophane membrane, were measured by the thiobarbituric acid method described by Warren. Results. The serum sialic acid levels of chronic renal failure patients requiring hemodialysis were increased with respect to the healthy control group, independent of age, duration of therapy, and whether there was accompanying diabetes. Hemodialysis did not provide clearance of sialic acid; to the contrary, it caused an insignificant increase in serum sialic acid levels. Conclusions. In chronic renal failure, the improved serum sialic acid level probably reaches a definite value, and this value is not affected by factors such as diabetes, age, or sex. Serum sialic acid level is minimally influenced by hemodialysis performed with a hemophane membrane. Received: August 20, 2001 / Accepted: May 10, 2002