Background:Local drug delivery agents can effectively deliver the antimicrobial drugs in bactericidal concentration, and have shown improved clinical outcomes when used as an adjunct to mechanical therapy. The aim of this study was to evaluate the efficacy of a xanthan-based chlorhexidine gel versus herbal extracts’ gel as an adjunct to periodontal therapy in the treatment of chronic periodontitis.Materials and Methods:A total of 150 sites, age group of 30-50 years, periodontal pockets measuring 5-8 mm and diagnosed with chronic periodontitis were selected for the study. The selected sites were randomized in five groups: Scaling and root planing (SRP) alone (Group A), SRP + Chlosite gel (Group B), SRP + Herbal gel (Group C), Chlosite gel alone (Group D) and Herbal gel alone (Group E). Clinical parameters such as Plaque Index, Gingival Index, probing pocket depth and clinical attachment level were recorded at baseline and 1- and 3-month intervals.Results:After 3 months, there were statistically significant reductions in all the clinical parameters for Groups B and C compared with Group A. There was no significant reduction in all clinical parameters between Group D and E where no mechanical therapy was performed.Conclusion:The results indicate that the local application of herbal gel can be comparably used as chlorhexidine gel in the treatment of chronic periodontitis as an adjunct to mechanical periodontal therapy.

Background: Non-steroid anti-inflammatory drug (NSAID) usage is associated with kidney injury. Rise in serum creatinine (sCr) often represents irreversible process. Thus to assess the early effects of regular NSAID use, we studied sensitive serum and urine biomarkers of kidney injury. Methods: In a protocol-based intervention study, 103 subjects were enrolled in 3 mutually exclusive groups. Group 1 included 37 healthy controls having minimal baseline NSAID exposure as per a definition, and group 2 had 41 spondyloarthritis (SpA) patients on regular NSAID therapy for >3 months. Group 3 included 25 SpA patients having minimal NSAID exposure at baseline. Blood and urine samples were collected from all the 3 groups at baseline. Furthermore, group 3 was started on 6-week regular NSAID therapy, and blood and urine samples were re-collected at 1, 6, and 12 weeks. Baseline normal kidney function as per the definition was ensured in all the subjects. Creatinine, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), cystatin-C, and microalbumin were measured in urine and serum samples to assess kidney injury. Results: Kidney injury biomarkers were 2-3-fold higher in SpA patients using regular NSAID therapy compared to healthy controls and SpA patients having minimal NSAID exposure (uKIM-1 and uNGAL p < 0.0001, sKIM-1 and sNGAL p = 0.001). There was no difference in sCr and estimated glomerular filtration rate using Cockcroft-Gault equation between the groups. In SpA patients started on 6 weeks of regular NSAID (group 3), biomarker levels started rising at week 1 and showed a significant rise at week 6. The levels in the patients that stopped NSAID use at 6 weeks showed reversibility at 12 weeks. Conclusions: Regular NSAID use in SpA patients induces subclinical kidney injury represented by rise in biomarkers. These levels start rising as early as 7 days of regular NSAID use and are reversible on stopping the drug.

Micro-RNAs (miRs) encapsulated inside urinary exosomes (uEs) have the potential as early biomarkers. Previously, we reported that a rise in uE miR-451 predicted albuminuria in diabetic rats; however, whether the rise was protective or detrimental, and occurred in response to injury or general hyperglycemia, was unknown. To address this, we studied both human and rat models of renal disease. In humans, uE miR-451 was approximately twofold higher in subjects with early-stage chronic kidney disease (CKD; serum creatinine < 2.0 mg/dl; n = 28), as compared to age-matched healthy controls (n = 23), and had a significant negative correlation with estimated glomerular filtration rate (eGFR) (r 2 = −0.10, p = 0.01). Subgroup analysis of CKD subjects showed that those without diabetes had slightly (∼30%) but significantly higher uE miR-451 as compared to those with diabetes, with no differences in albumin excretion, eGFR, serum sodium, and potassium. Using human proximal tubule (hPT) cells, we found that locked nucleic acid (LNA) inhibition of miR-451 resulted in a significant increase in the messenger RNA (mRNA) expression of kidney-injury-associated miR-451 targets, e.g., CAB39, TBX1, and YWHAZ, as compared to treatment with a control LNA. Moreover, hPT cells and their secreted exosomes showed an increase in miR-451 in response to mechanical injury but not high glucose (20 versus 5 mM). For further proof of concept, in diabetic rats, we showed that atorvastatin (AT), a treatment proven to attenuate renal injury without affecting systemic glucose levels, reduced uE miR-451 with the concomitant restoration of renal miR-451. These data elucidate the stimuli for renal miR-451 expression and exosomal release and support its role as a therapeutic target and early biomarker for renal injury in humans.

Background: Vascular endothelial growth factor (VEGF) is a cytokine which plays an important role in the division, proliferation and migration of endothelial cells. In the kidney, VEGF expression is found in glomerular podocytes and in tubular epithelial cells, which may result in acute inflammatory reactions. Methods: The role of VEGF gene polymorphisms (-2578 C/A, -2549 18 bp Ins/Del, -1154 G/A and +936 C/T) was investigated in 272 patients who underwent renal transplantation. ARMS-PCR and PCR-RFLP were used. Patients were categorized into acute allograft rejection (n = 76) and nonrejection (n = 196). Results: The VEGF -1154 GG genotype and the +936 T allele were found to be susceptible to acute rejection (AR). T-A-A-I, T-A-A-D, T-G-C-I and C-A-A-I haplotypes revealed a predisposition among AR cases. In silico analysis revealed +936 T as a significant allele involved in the transcription regulation. Conclusion: These results highlight the role of VEGF polymorphisms in acute allograft rejection.

Introduction: Vitamin D deficiency can impact post-transplant outcomes due to its effect on graft function and rejection. The effect of pre-and post-transplant serum vitamin D levels was evaluated on graft function. Objectives: This study aims to determine the incidence of vitamin D deficiency and its effect on post kidney transplant allograft function in a North Indian cohort. Patients and Methods: We evaluated 57 patients on dialysis, going for transplantation. Estimated glomerular filtration rate (eGFR) was measured using modification of diet in renal disease (MDRD) formula at 2 weeks and 3, 6, 12 months interval after kidney transplantation. Results: Pre-and post-transplant (3 months) vitamin D levels were evaluated for vitamin D deficiency and graft function. Before transplant vitamin D levels were 25.77 ± 13.68 ng/mL, 40.4% of these recipients had vitamin D deficiency (levels <20 ng/mL). After transplant, vitamin D levels at 3 months were 22.08 ± 11.15 ng/mL and 54.4% of recipients had vitamin D deficiency. No patient was on vitamin D supplementation after transplantation. At 3 months post-transplant, recipients with vitamin D levels <20 ng/mL, had significantly lower eGFR and higher serum creatinine value as compared to the group with vitamin D levels >20ng/mL. Recipients were divided into 3 groups based on pre-and post-transplant vitamin D levels (<20, 20-30 and >30ng/mL). Pre-transplant vitamin D levels correlated with graft function at 14 days. On multiple regression analysis, 3-month post-transplant vitamin D levels correlated with 12 months eGFR. There was increased incidence of acute rejection episodes in vitamin D deficiency group. Conclusion: There is a high incidence of vitamin D deficiency and insufficiency in kidney transplant recipients. Low levels of post-transplant vitamin D levels at 3 months were associated with inferior allograft function (eGFR) at 1 year.

Objectives: Cystatin C is emerging as an endogenous marker of glomerular filtration rate. This study sought to assess the usefulness of serum cystatin C as a marker of glomerular filtration rate in comparison with serum creatinine and serum creatinine-based glomerular filtration rate estimations in voluntary kidney donors. 99m Tc-DTPA double plasma sampling method. Glomerular filtration rate-double plasma sampling method was used as a reference value. Results were expressed as means ± SD. Results: The mean age of the participants was 44.23 ± 8.61 years old (19 women, 16 men). The mean serum creatinine was 0.83 ± 0.14 mg/dL, and the mean serum cystatin C was 0.71 ± 0.12 mg/L. Serum cystatin C showed significant correlation with serum creatinine (r = 0.864; P < .001). Glomerular filtration rate-MDRD showed the strongest correlation with glomerular filtration ratedouble plasma sampling method (r = 0.93; P < .001), followed by glomerular filtration rate-CockcroftGault (r = 0.76; P < .001 ), serum creatinine (r = -0.68; P < .001), and serum cystatin C (r = -0.59; P < .001). The mean serum cystatin C values were 22.6% higher in men than in women. There was a significant correlation of serum cystatin C with glomerular filtration rate-Cockcroft-Gault (r = -0.50; P = .002 ), glomerular filtration rate-MDRD (r = -0.59; P < .001 ), and glomerular filtration rate-double plasma sampling method (r = -0.59; P < .001 ). Conclusions: Serum cystatin C is an optimal marker of glomerular filtration rate in voluntary kidney donors.

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Objective: Thrombotic microangiopathy (TMA) is often first detected on a renal biopsy performed for renal manifestations. Apart from hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura, there are various secondary conditions associated with TMA. This study analyzes the clinico-pathological spectrum, etiological factors and renal outcome of TMA diagnosed on renal biopsy. Material and Method:A retrospective evaluation of renal biopsies for TMA over 5.5 years was performed. Clinical and laboratory data was collected from patient records.Results: A total of 40 biopsies from 39 patients showed TMA comprising 33 native and 7 transplant biopsies. Malignant hypertension (n=13) was the most common etiology in native biopsies followed by postpartum TMA (n=7), atypical HUS (aHUS) (n=7), and lupus nephritis (n=6). TMA in transplant biopsies was due to acute rejection (n=4) and CNI toxicity (n=3). Serum creatinine was high in most patients (mean 5.6 + 2.5 mg/ dl). aHUS showed the highest mean LDH levels and the lowest average platelet counts. Renal biopsies in malignant hypertension and postpartum TMA showed isolated arterial changes while aHUS and lupus nephritis showed both glomerular and arterial involvement. Postpartum TMA and aHUS had poor renal outcome requiring renal replacement therapy. Conclusion:Most postpartum TMA and aHUS had systemic features of TMA while malignant hypertension and lupus nephritis showed 'isolated renal TMA' . This emphasizes the importance of careful evaluation of renal biopsies even in the absence of systemic features of TMA.