Assessment of chronic kidney disease using skin texture as a key parameter: for South Indian population

Periodical monitoring of renal function, specifically for subjects with history of diabetic or hypertension would prevent them from entering into chronic kidney disease (CKD) condition. The recent increase in numbers may be due to food habits or lack of physical exercise, necessitates a rapid kidney function monitoring system. Presently, it is determined by evaluating glomerular filtration rate (GFR) that is mainly dependent on serum creatinine value and demographic parameters and ethnic value. Attempted here is to develop ethnic parameter based on skin texture for every individual. This value when used in GFR computation, the results are much agreeable with GFR obtained through standard modification of diet in renal disease and CKD epidemiology collaboration equations. Once correlation between CKD and skin texture is established, classification tool using artificial neural network is built to categorise CKD level based on demographic values and parameter obtained through skin texture (without using creatinine). This network when tested gives almost at par results with the network that is trained with demographic and creatinine values. The results of this Letter demonstrate the possibility of non-invasively determining kidney function and hence for making a device that would readily assess the kidney function even at home

Epidemic of Chronic Kidney Disease in India -What Can Be Done?

The exact prevalence of chronic kidney disease in India is not clear in the absence of regular national registry data and provided only by small observational series or rely on reports from personal experience, but the quality of data is quiet uneven. There are only three population based studies in India commenting on the magnitude of chronic kidney disease. In a prevention program started at community level in Chennai, the reported prevalence is 0.86% in the project population and 1.39% in the control region. The second study is based on Delhi involving 4972 urban patients. The prevalence of chronic renal failure (defined as serum creatinine more than 1.8 mg/dL) to be 0.79 % or 7852 per million/population. The third study perhaps the only longitudinal study to identify the incidence of end stage renal disease is based on 572,029 subjects residing in city of Bhopal suggests that the average crude and age adjusted incidence rates of end stage renal disease were 151 and 232 per million population respectively. The resources and skill for taking care of this large case load, both in terms of personal and health care infrastructure do not exist currently and would need to be created. To tackle the problem of limited access to renal replacement therapy, an important method would be to try and reduce the incidence of end stage renal disease and the need of renal replacement therapy by preventive measures. It is clear that treatment of chronic kidney disease and its advanced stage end stage renal disease is expensive and beyond the reach of average Indian. Thus it is crucial that prevention of chronic kidney disease has to be the goal of medical fraternity, government of India and the general public. This article suggests a series of primary, secondary and tertiary preventive measures for prevention of chronic kidney disease. Clearly there are already many effective and attractive interventions for the treatment and prevention of chronic kidney disease exist and many more surely be developed

Pathways, perspectives and pursuits in polycystic kidney disease

Polycystic kidney disease (PKD) is characterized by the growth of numerous cysts in the kidneys. When cysts form in the kidneys, they are filled with fluid. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure. Autosomal dominant polycystic kidney disease (ADPKD) is a hereditary disease that occurs in one out of 1000 humans. PKD and its causes are being dissected through studies of human populations and through the use of animal models. Mouse models in particular have made a substantial contribution to our understanding of the gene pathways involved in the pathogenesis and the nature of signaling molecules that act in a tissue-specific manner at critical stages of cyst development. PKD has a number of characteristics that make it uniquely challenging for the development of therapies to slowdown disease progression. This review provides current understanding of the etiopathology, pathways involved and therapeutic targets of PKDs

Curvularia lunata, a rare fungal peritonitis in continuous ambulatory peritoneal dialysis (CAPD); a rare case report

Peritonitis is an inflammation of the peritoneum that occurs in patients with end-stage renal disease (ESRD) treated by peritoneal dialysis. Fungal peritonitis is a dreaded complication of peritoneal dialysis. Curvularia lunata is known to cause extra renal disease like endocarditis, secondary allergic bronchopulmonary aspergillosis and endophthalmitis. This case report presents a case of continuous ambulatory peritoneal dialysis peritonitis with this disease and its management. This case is of a 45-year-old man, presented with ESRD, secondary to diabetic nephropathy. After 3 months of hemodialysis the patient was put on continuous ambulatory peritoneal dialysis (CAPD). Local Examination at catheter site showed skin excoriation and purulent discharge. Further peritoneal dialysis (PD) fluid analysis showed neutrophilic leukocytosis and diagnosis of Curvularia lunata PD peritonitis

Renal tubular dysfunction with nephrocalcinosis in a patient with beta thalassemia minor

Thalassemia is a hereditary anemia resulting from defect in hemoglobin production. Beta thalassemia is due to impaired production of beta globin chains, leading to a relative excess of alpha globin chains. The term beta thalassemia minor is used to describe heterozygotes, who carry one normal beta globin allele and one beta thalassemic allele. The vast majority of these patients are asymptomatic. However, a variety of renal tubular abnormalities including hypercalciuria, hypo-magnesemia with renal magnesium wasting, decreased tubular absorption of phosphorus, hypo-uricemia with renal uric acid wasting, renal glycosuria and tubular proteinuria have been described even in patients with beta thalassemia minor. We here in report a 24-year old female patient who was found to have thalassemia minor and nephrocalcinosis with evidence of renal tubular dysfunction. Investigations revealed normal renal function, hypercalciuria, reduced tubular reabsorption of phos-phorus, hypomagnesemia and renal magnesium wasting. Screening for aminoaciduria was found to be negative. An acid loading test revealed normal urinary acidification. Ultrasonogram of the abdomen revealed nephrocalcinosis and splenomegaly. Detailed work up for anemia showed normal white cell and platelet count while peripheral smear showed microcytic hypochromic anemia with few target cells. Hemoglobin electrophoresis revealed hemoglobin A of 92%, hemoglobin A2 of 6.2% and hemo-globin F of 1.8% consistent with beta thalassemia minor. Her parental screening was normal. A diag-nosis of beta thalassemia minor with renal tubular dysfunction was made and the patient was started on thiazide diuretics to reduce hypercalciuria and advised regular follow-up

CMV genotyping using different samples in post renal transplant recipients with CMV disease

CMV is the most common viral infection which occurs in post renal transplant recipients (PTR). There are four different gB genotypes (gB1 to gB4) which exist in CMV. Studies have reported that mixed infection with different genotypes will cause severe clinical manifestations as well as co-infection with other herpesvirus including Epstein-Barr virus (EBV) [1]. CMV can cause compartmentalized disease involving different organs with different genotypes. There are reports in immuno compromised individuals with different genotypes [2, 3]. Institutional ethics committee approval was obtained prior to conduct of the study (IEC-NI/08/DEC/07/46). Whole blood, saliva and urine were collected from PTR. DNA were extracted (Qiagen DNA mini kit) and CMV quantitative PCR targeting ppUL83 gene was performed with CMV R-gene™ using an ABI 7900 Fast real time PCR (SDS Version: 2.4). PTR who had high viral load (>1000 copies/ml) in any three or two samples were included for CMV genotyping PCR targeting gB region (410-bp) [2]. DNA sequencing was performed in ABI 3730 GA platform by Sanger method and sequences were analyzed by reference strains. A total of 24 samples were collected from 9 PTR. Among these four PTR had high viral load in all three samples (whole blood, urine & saliva) and those with high viral load (n=5) in 2 samples (Whole blood & urine/saliva) were screened for CMV genotyping. Majority of the strains belonged to genotype B1 and only one PTR was infected with genotype B2 in three samples. In PTR with genotype B1, gastro intestinal infection (GI) was predominantly found in 78% (n=7) followed by graft dysfunction (GDF) in 56% (n=5) of the PTR. PTR who detected with genotype B2 was associated with fever, leukopenia (CMV syndrome), GDF and also found with EBV infection. Co-infection with EBV was observed in 44% (n=4); VZV and HSV type 1 was also observed. Genotypes are associated with the severity of the disease and co-infection with other herpes virus infections. In our study subjects, genotype B1 predominantly noted as reported in western countries. Study on distribution of genotypes among PTR may help to determine the specific strains for vaccine development

TRPC6 gene promoter polymorphisms in steroid resistant nephrotic syndrome children

Introduction: Nephrotic syndrome (NS) is the most frequent cause of proteinuria in children and is emerging as a leading cause of uremia. Among idiopathic NS, 10% of children do not respond to steroids or to any other immunosuppressive therapy, and progress to end-stage renal disease (ESRD). Several studies have investigated the mutations in genes encoding podocyte proteins and their possible associations with several forms of hereditary NS. Objectives: The present study aimed to determine the distribution of the TRPC6 gene promoter polymorphisms in subjects with features of steroid resistant nephrotic syndrome (SRNS) and controls. Patients and Methods: About 49 unrelated patients with SRNS and 45 age matched controls no renal or other disorders were included in the study. PCR-RFLP was used for genotyping rs3824934 (-254C>G) and rs56134796 (-218C>T) polymorphisms located in TRPC6 gene promoter region. Results: Both -254C>G and -218C>T are polymorphic in both SRNS patients and controls. No statistically significant differences in genotypes or allele frequencies between SRNS patients and controls were observed. Linkage disequilibrium was not strong and significant and haplotypes were not associated with SRNS. Interaction analysis by multifactor dimensionality reduction (MDR) revealed a significant interaction between -254G>C and -218C>T in <10 years age group. Conclusion: The results demonstrate that the TRPC6 polymorphisms do not affect susceptibility of SRNS in Indian population. Further replications, preferably a systematic search for TRPC6 functional variants that affect gene expression are desirable for validation of our findings

Assessment of abdominal aortic calcification in predialysis chronic kidney disease and maintenance hemodialysis patients

Vascular calcification is associated with increased morbidity and mortality among chronic kidney disease (CKD) patients. The aim of the study was to assess the abdominal aortic calcification (AAC) in predialysis CKD patients and patients on hemodialysis (HD) and to study the risk factors associated with it. In this prospective study, 205 patients were including 104 patients with predialysis CKD and 101 patients were on maintenance hemodialysis. AAC was assessed using lateral lumbar radiography. Blood urea nitrogen, serum creatinine, albumin, calcium, phosphorus, highly sensitive C-reactive protein (hsCRP) and total cholesterol were analyzed. AAC was observed in 26 % of predialysis CKD patients and 34% in HD patients. Using multivariate analysis, the age (P = 0.001) was identified as independent predictor for the presence of AAC in predialysis patients, and for HD, the predictors were age (P = 0.025), time on dialysis (P = 0.001), hsCRP (P = 0.002), and corrected calcium (P = 0.030). In conclusion, the prevalence of AAC varies mainly with age and glomerular filtration rate levels in predialysis CKD patients. Advanced age, time on dialysis, and inflammation may be associated with presence and extent of AAC in HD patients. Further research into the risk factors and outcome for AAC is warranted

Expression of TNF-α and RANTES in drug-induced human gingival overgrowth

Objectives : Regulated on activation, normal T cell expressed and secreted (RANTES) is a chemokine that is produced by fibroblasts, lymphoid and epithelial cells of the mucosa in response to various external stimuli. RANTES expression has been demonstrated in a variety of diseases characterized by inflammation, including asthma, transplantation-associated accelerated atherosclerosis, endometriosis and fibrosis. RANTES mRNA is quickly up-regulated by tumor necrosis factor (TNF)-α stimulation. Cyclosporine A (CsA) is widely used in organ transplant patients, often causing various side-effects including gingival overgrowth, which is fibrotic in nature. This study was carried out to assess the mRNA expression of TNF-α and RANTES in healthy individual, chronic periodontitis and CsA-induced gingival overgrowth tissues. Materials and Methods : Gingival tissue samples were collected from chronic periodontitis, CsA-induced gingival overgrowth patients and healthy individuals. Total RNA was isolated and reverse transcription polymerase chain reaction (RT-PCR) was performed for TNF-α and RANTES expression. Results : The results suggest that CsA-induced gingival overgrowth tissues expressed significantly increased TNF-α and RANTES compared to control and chronic periodontitis. Conclusion : The findings of the present study suggest that CsA can modify the expression of TNF-α and RANTES in drug-induced human gingival overgrowth