:Lipid abnormalities remain to be a major cause of early mortality in patients with chronic renal failure (CRF). In present study, 114 (one hundred fourteen) CRF patients without any additional cause of dyslipidemia were divided into groups on the basis of etiologies of CRF. Blood samples from each group were analyzed for total cholesterol, triglyceride and HDL cholesterol along with blood urea nitrogen and serum creatinine. 25 healthy individuals without any obvious disease were taken as control. Patients from all the groups showed a marked hypertriglyceridemia of 232 (SD + 77) mg/dl (P < 0.001) as compared to control. Levels of HDL cholesterol were found to be significantly low 20 ( ~ 11) mg/dl (p < 0.001) in all the groups. LDL cholesterol showed an increase 104 ( _+ 30) mg/dl as compared to control group which is not statistically significant. Present study reveals that, CRF patients show an uniform dyslipidemia irrespective of etiologies leading to CRF. This dyslipidemia is also independent of serum creatinine levels. Although, these lipid abnormalities may not solely cause mortality in CRF patients, they may act as modulators in accelerating atherogenesis which in turn cause early mortality in CRF patients.

<p class="abstract"><strong>Background:</strong> Traditional risk factors like elevated homocysteine levels may not completely explain the higher CVD seen in RTRs. Identification and optimisation of modifiable risk factors may help to reduce the occurrence of CVD in such population. To study the role of homocysteine level as risk factor in the occurrence of cardiovascular events in renal transplant patients. Another objective was to evaluate the other risk factors in the occurrence of CVD in such population.</p><p class="abstract"><strong>Methods:</strong> Thirty renal transplant recipients and thirty healthy controls were studied. Inclusion criteria were transplant duration &gt;6 months and patients with chronic stable renal function over the last 3 months. Samples for fasting plasma homocysteine were collected and plasma homocysteine was then estimated. All the patients were followed up every month for 6 months and evaluated for occurrence of any cardiovascular event.</p><p class="abstract"><strong>Results:</strong> The mean hornocysteine levels were found to be 27.4±7.902 µmol/L in cases and 10.86±1.98 µmol/L in controls. There was no statistically significant relationship between homocysteine levels and transplant duration, mean IMT levels, proteinuria, and presence of left ventricular hypertrophy or choice of immunosuppressive regimen. Of the 30 patients, 6 patients (20%) had evidence of cardiovascular event. In the absence of other conventional factors, age of the patient, creatinine clearance (index of graft function) and mean intima-media thickness were more closely related with cardiovascular events.  </p><p><strong>Conclusions:</strong> Plasma homocysteine failed to show as an independent risk factor for cardiovascular events. New, emerging cardiovascular risk factors (e.g. Lipoprotein (a), high sensitivity C-reactive protein, fibrinogen, tissue plasminogen activator and plasminogen activator inhibitor-1) should be studied to design effective therapy to delay the progression of atherosclerosis and prolong the life of renal transplant recipients.</p>

Introduction: Laparoscopic living donor nephrectomy (LLDN) offers many advantages compared to open living donor nephrectomy. However, the perceived difficulty in learning LLDN has slowed its wider implementation. Herein, we describe the evolution of LLDN at a single center, emphasizing the approach and technical modifications and its impact on outcome. Methods: The series included a 2½-year period and three different surgeons. We started with two-stage plan for establishing LLDN at the institute (introduction and consolidation). Data of laparoscopic donor nephrectomy performed at the institution were prospectively evaluated regarding donor and recipient outcome. Results: From December 2016 to April 2019, 221 donors underwent LLDN. Three donors required conversion to open surgery. The mean operation time was 96.4 (62–158) min and the mean warm ischemia time was 186 (149–423) s. The complications were observed in 11.6% of donors from LLDN group and all complications were Class I and Class II only (Clavien–Dindo classification). No Class III and Class IV complications occurred. In the present study, there was some learning curve effect observed only in operative time (OT) with longer OT in initial cases. However, the overall operative complications were minimal, showing that this learning curve had no deleterious effects on donor safety. Conclusion: The present study demonstrates that with proper planning, team approach, and a few technical modifications, the transition from open to LLDN could be safe and effective.

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