This study shows that sources for systemic inflammation, such as periodontal disease, could affect the pathogenesis of idiopathic edema. Successful elimination of such covert sources of inflammation leads to a clinical benefit in patients who are distressed by this condition.
BACKGROUNDThe aim of the study is to study the outcome of deceased donor kidney transplantation at the end of one year, the effect of cold ischaemia on the outcome of graft survival and the role of various induction agents in the prevention of acute rejection.
MATERIALS AND METHODSA retrospective observational study of 30 deceased donor kidney transplant recipients was conducted. All patients received triple drug immunosuppressive treatment, i.e. tacrolimus, steroids and mycophenolate. Induction with either ATG or basiliximab was given to all recipients. The graft function was monitored serially with serum creatinine and routine urine examination. Graft biopsy was done in the event of graft dysfunction. Development of infection was confirmed by serological examination and cultures of various body fluids.
RESULTSOne year graft survival was 80% and patient survival was 83%. Delayed graft function was seen in 30% and acute rejection in 33%. Cold ischaemia was more than 6 hours in 23%. Induction was given to all patients and graft function was similar in both groups. 40% patients developed infection during the first year.
CONCLUSIONOne year graft survival is 80% and patient survival is 83%. 40% patients developed infection.
Primary IgA nephropathy is characterised by recurrent episodes of gross haematuria concomitant with upper respiratory tract infections or other mucosal inflammatory processes. AIMS Assess the histopathological changes in the kidneys after giving MM with low-dose steroids. SETTINGS AND DESIGN Mesangial hypercellularity-in < or > 50% glomeruli (M0 or M1); Endocapillary hypercellularity-present (E0)/absent (E1); Segmental sclerosis present (S0)/(S1) absent; Tubular atrophy/interstitial fibrosis-0-25% (T0), 26-50% (T1), > 50% (T2). METHODS AND MATERIALS IgA Nephropathy patients receiving MM with low-dose steroids (Group M) and conventional therapy (Group C), biopsied and scored as per Oxford MEST classification were included. The treatment response was assessed for Mesangial hypercellularity, Endocapillary hypercellularity, Segmental sclerosis/adhesions and Tubular atrophy/interstitial fibrosis. STATISTICAL ANALYSIS USED SPSS version 16, Independent sample T test, paired sample T test, one-way ANOVA and McNemar Chi-square tests. RESULTS Of the total enrolled 46 subjects, 32 were included in Group M and 14 were included in Group C. In the Group M, mean proteinuria significantly decreased from 1650 mg to 900 mg, mean eGFR increased from 66 mL/min. to 72 mL/min. (p=.001). In the Group C, mean proteinuria decreased significantly from 1300 mg to 1050 mg (p=0.1), mean eGFR decreased from 72 mL/min. to 69 mL/min. (p=0.25). CONCLUSIONS Mesangial hypercellularity and endocapillary hypercellularity have direct correlation with proteinuria. Therapy with MM and steroids is effective in retarding the proteinuria, microhaematuria and progression of the disease in IgAN; reversing the mesangial hypercellularity and endocapillary hypercellularity and preventing the progression of segmental sclerosis and tubular atrophy. KEY MESSAGES Mesangial hypercellularity and endocapillary hypercellularity have direct correlation with proteinuria. Therapy with MM and steroids is effective in retarding the proteinuria, microhaematuria, progression of the disease in IgAN, reversing the mesangial hypercellularity and endocapillary hypercellularity and preventing the progression of segmental sclerosis and tubular atrophy.
To study the changes in phosphate metabolism in kidney donors, to study the correlation of albuminuria, fractional excretion of phosphorus [FE Pi] and estimated glomerular filtration rate [eGFR] with fibroblast growth factor 23 [FGF 23] in kidney donors, to study the early tubule interstitial injury in the remnant kidney of donors by measuring urine transforming growth factor beta [TGF beta] levels. MATERIALS AND METHODS A cross-sectional study in which kidney donors with 1 year or more after donation were included. 69 kidney donors with a mean duration of 5.86 years after kidney donation were studied. Serum phosphate level, fractional excretion of phosphorus [FE Pi] and serum levels of parathyroid hormone were measured. Plasma levels of FGF 23 were measured by a second generation enzyme linked immune sorbent assay [ELISA]. Renal function was assessed by estimated glomerular filtration rate [eGFR] and degree of albuminuria. Urine levels of transforming growth factor beta [TGF beta] were measured by ELISA. A hypothesis that in kidney donors with reduced nephron number, the single nephron excretion of phosphorus will be increased to maintain normal phosphorus homeostasis and that this increase in single nephron phosphorus excretion may be mediated by FGF 23 was proposed. Testing of this hypothesis was done by studying the correlation between parameters of phosphorus metabolism, FGF 23 and the renal function of the donors.
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