Risk Of Progressive Renal Damage Research Articles

Determination of Microalbuminuraia and Its Relation to HTN in Type 2 Diabetic Patients and General People

Background: Microalbuminuria is a clinical marker of glomerular injury and identified as a risk of progressive renal damage, cardiovascular disease and morbidity. Hypertension (HTN) is a worldwide public health problem andcommonly coexists with Diabetes Mellitus (DM). Objective: The aim of the study was todetermine the prevalence of microalbuminuriain type 2diabetic patients and general people and the relationship between microalbuminuria withHTN and other clinical parametersin these twogroups of people. Methodology: A cross-sectional study was carried out using a pretested structured questionnaire amongrandomly selected107 participants aged from 35-70 years. Out of 107 participants 64 persons were type 2 diabetic patients and 43 were healthy individuals. Biochemical analysis of blood and urine samples was performed. Result: The prevalence of microalbuminuria was 17.2% in diabetic patients and 25.6% ingeneral people whereas the prevalence of HTN was 48.4% among diabetic patients and 51.6% in normal healthy persons. Regardless of the group considered, when microalbuminuria was analyzed according to the different clinical parameters, microalbuminuricpatients had significantly highersystolic (p=0.03) diastolic (p=0.02) blood pressure, urine creatinine (p=0.000), serum creatinine (p=0.012), urine albumin (p=0.019) and GFR (p=0.000). Microalbuminuria was found to be associated with HTN (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.2-9.7). Conclusion: The study concluded thatmicroalbuminuria prevalence is high among general people and HTN has a significant relationship with microalbuminuria. These findings suggest early screening of microalbuminuria and the proper management of other clinical parameters to halt and prevent end stage renal disease and cardiovascular risk in future.

ACEIs with or without corticosteroids in IgA nephropathy?

A recent study demonstrated the superiority of prednisone plus ramipril in preventing progression of IgA nephropathy compared with ramipril alone in a group of patients at high risk of progressive renal damage. However, future clinical trials need to clarify whether more aggressive supportive therapy may match the benefits of immunosuppression.

Plasminogen activator inhibitor-1 polymorphism is associated with progressive renal dysfunction after acute rejection in renal transplant recipients.

Plasma level of plasminogen activator inhibitor (PAI)-1 is genetically determined by a polymorphism in the promoter region, involving two alleles, 4G and 5G. Plasma PAI-1 concentrations are higher in subjects homozygous for the 4G allele than other genotypes (5G/5G and 4G/5G). Such genetic variation in fibrinolytic system may affect the long-term renal transplant outcome. We determined PAI-1 4G/5G-promoter genotype polymorphism among our renal transplant recipients between 1985 and 2001. Primary event was defined as doubling of baseline serum-creatinine level. Over a median period of 79 months, 130 patients with 132 kidney grafts were assessed. Baseline clinical variables were comparable among three genotype groups. There was no association between primary event and PAI-1 genotype among the entire cohort. However, among subjects with prior acute rejection episodes, those homozygous for 4G had significantly higher risk of serum creatinine doubling than the other two genotypes (relative risk 2.45, 95% confidence interval 1.19-5.04). PAI-1 genotype does not predict primary events in patients without rejection (relative risk 0.57, 95% confidence interval 0.07-4.17). PAI-1 4G/5G-promoter polymorphism modulates the risk of renal transplant outcomes after acute rejection(s). Recipients homozygous for PAI-1 4G allele have a higher risk of progressive renal damage after acute rejection episode(s). PAI-1 promoter polymorphisms are potentially important determinants of renal response to rejection.

Polymorphism of the ACE gene in Henoch-Schönlein purpura nephritis

Individuals with IgA nephropathy (IgAN) who are homozygous for the deletion (D) polymorphism of the gene for angiotensin converting enzyme (ACE) are reported to be at increased risk of progressive renal damage. Since IgAN and Henoch-Schönlein purpura with associated nephritis (HSPN) share a common aetiology, we have investigated this influence in 31 children with HSPN. The distribution of genotypes was as follows: II: 4, ID: 17 and DD: 10 patients. Median length of follow-up was 4.5 years (range 0.5-15.75 years). Severe onset with nephrotic oedema and crescent formation on renal biopsy was seen in 10 of 17 patients with ID genotype and 5 of 10 patients with DD genotype. In the ID group, 2 patients have undergone renal transplantation and 4 have persistent proteinuria 4, 7, 9 and 10 years after presentation. One patient in the DD group has been transplanted and 1 patient has proteinuria and a reduced glomerular filtration rate 5 years after initial presentation. All other patients have either made a complete recovery or have microscopic haematuria alone. These results do not support an association between disease severity and DD genotype in children with HSPN; however larger studies are required to confirm this.

Familial clustering of end-stage renal disease in blacks with lupus nephritis

The factors that determine a patient's susceptibility to specific target organ involvement in systemic lupus erythematosus (SLE) remain unknown. Lupus nephritis can be a particularly devastating complication, with an increased mortality and the risk of progressive renal damage resulting in end-stage renal disease (ESRD). This analysis was performed to determine whether renal disease aggregated in select families or was a sporadic complication in patients with SLE. We compared the family history of ESRD in 50 patients with SLE complicated by lupus nephritis with 37 controls who had SLE but lacked nephritis after a mean follow-up duration of more than 11 years. The frequency of relatives with ESRD in the lupus nephritis cases was compared with that in controls using Fisher's exact test (significance at P ≤ 0.05). Fifty percent (25) of the 50 lupus nephritis patients were black and 50% (25) white, in contrast to 35% (13) and 65% (24) of the 37 lupus nonnephropathy controls, respectively. A first-, second-, or third-degree relative with ESRD was present in 16% (eight) of the 50 lupus nephritis cases and in 0% of the 37 SLE nonnephropathy controls (P = 0.019, Fisher's exact test, two-tail). Twenty-eight percent (seven) of the 25 black patients with lupus nephritis had relatives with ESRD compared with 0% of the 13 black lupus nonnephritis controls (P = 0.07). Only one of the eight relatives with ESRD had SLE or a collagen vascular disease. Lupus nephritis patients and the nonnephritis controls had similar ages (mean ± SD: 38.5 ± 10.0 years v 46.6 ± 11.8 years; P = 0.28), family sizes (6.27 ± 2.61 first-degree relatives v 6.35 ± 3.25 first-degree relatives; P = 0.16), and duration of SLE (9.26 ± 5.94 years v 11.35 ± 6.43 years; P = 0.60). Familial clustering of ESRD was observed in black patients with SLE who had nephritis. This was unlikely to be related to differences in patient age, family size, or duration of SLE. This data, coupled with the known familial aggregation of ESRD in blacks with hypertensive and diabetic ESRD, supports the contention that genetic factors contribute to the familial clustering. The presence of relatives with etiologies of ESRD other than SLE suggests that there is an inherited susceptibility to progressive renal failure, independent of the etiology of ESRD.

Long-term follow up to determine the prognostic value of imaging after urinary tract infections. Part 2: Scarring.

Long term follow up of children with urinary tract infections, in whom imaging investigations were performed at presentation, has been used to identify features that distinguish those at greatest risk of progressive renal damage. No single investigation at presentation was able to predict subsequent deterioration but, by employing a combination of imaging investigations, it was possible to separate groups with high or low probability of progressive damage. In the low risk group the incidence of progressive damage was 0.2% (95% confidence interval (CI) 0 to 1.3%). The combination of both scarring and reflux at presentation, or one only of these but accompanied by subsequent documented urinary tract infection, was associated with a 17-fold (95% CI 2.5 to 118) increase in the relative risk of progressive renal damage compared with children without these features. The recommended combination of investigations at presentation for girls of any age and boys over 1 year is ultrasound and dimercaptosuccinic acid (DMSA) scintigraphy in all, to detect both scarring and significant structural abnormalities, renography in children with dilatation of any part of the urinary tract on ultrasound, to distinguish dilatation from obstruction, and an isotope voiding study in all who have acquired bladder control. This gives the best separation between those at high and those at low risk of progressive damage with least radiation dose and lowest rate of instrumentation. Micturating cystourethrography (MCU) should be restricted to girls who have not acquired bladder control, unless there is reason to suspect a significant structural abnormality such as urethral valves. A single non-febrile urinary tract infection that responds promptly to treatment is not a justification for performing MCU in boys under 1 year or in children of any age with bladder control. No case can be made for any abbreviated schedule of investigation. These risk factors should be taken into account when designing follow up protocols.

Long-term follow up to determine the prognostic value of imaging after urinary tract infections. Part 1: Reflux.

In 3646 children with at least one confirmed urinary tract infection the prevalence of vesicoureteric reflux at presentation was correlated with progressive renal damage during follow up of not less than two and up to 16 years. Reflux was not demonstrated either at presentation or at any subsequent time in almost one half of the children who suffered progressive renal damage and was not a risk factor for progressive renal damage in boys under 1 year. It was an important risk factor in boys over 1 year and in girls of any age. The risk of progressive renal damage in children in whom micturating cystourethrography (MCU) did not reveal vesicoureteric reflux was substantially greater than in those who indirect isotope voiding study (IVS) did not show reflux. The risk of deterioration for those in whom reflux was demonstrated was similar for both techniques. This discrepancy indicates an appreciably higher false negative rate for the MCU than the IVS. Dilatation of the renal pelvis detected by ultrasound was associated with a significantly increased risk of progressive damage only when associated with reflux, but most children with progressive damage did not have a dilated collecting system at presentation.

The antiproteinuric effect of ACE inhibition in renal disease

Proteinuria due to non-steroid-responsive renal disease may be harmful. Firstly, because it may cause a nephrotic syndrome, and, secondly, because it is, like hypertension, associated with an increased risk of progressive renal damage and loss of renal function over the years. Until recently, only non-steroidal antiinflammatory drugs (NSAIDs) were available to reduce proteinuria in such patients. Due to their potential side-effects, however, NSAIDs have never been widely used as antiproteinuric agents. In 1985 some studies were published showing that inhibition of angiotensin-converting enzyme (ACE) not only reduced the elevated blood pressure in rats with chronic renal failure (experimentally induced by renal ablation or by induced diabetic nephropathy), but also prevented the development of glomerular damage with proteinuria and loss of renal function in these animals. This beneficial effect of ACE inhibition was attributed to the prevention of glomerular hypertension. At the same time it was reported that ACE inhibition could reduce proteinuria in patients with advanced diabetic nephropathy. ACE inhibitors might thus be an attractive alternative for NSAIDs as antiproteinuric treatment, possibly being renoprotective, and being generally well-tolerated.

Complications of Hemophilic Disorders Affecting the Renal Tract

Patients with bleeding disorders may bleed into tissues or from damaged skin and mucosal surfaces. Repeated hemorrhage into joints leads to arthropathy. Bleeding from the renal tract may not be recognized as a sign of a severe bleeding disorder in patients who have not undergone excretory urography. Awareness of other possible causes of hematuria, the possible consequences of retained blood clots, and the risk of progressive renal damage should prompt more frequent investigation of the urinary tract in such patients.