Measurement Of Protein Excretion Research Articles

To evaluate and standardize the method of spot urine protein creatinine ratio for estimation of proteinuria

Background: Proteinuria is an independent risk factor for diabetic nephropathy and a predictor of end-stage renal disease. Measurement of protein excretion in a 24hr urine collection is the gold standard for the quantitative evaluation of proteinuria in diabetes. However, this is cumbersome, subjective to collection errors and required good compliance. Aims: To evaluate and standardize the method of spot urine protein creatinine ratio for estimation of Proteinuria. Materials and methods: We compared 24 hr urine protein estimation with urine spot protein creatinine ratio in type 2 diabetes mellitus patients with proteinuria. Results: In our study of 73 patients with type 2 diabetes mellitus and proteinuria, it was found that A maximum number of patients were noted in the age group 41-50 years. Males were more than females in the ratio of 2.04:1. The majority of patients had a duration of diabetes between 5 -10 yrs (52.05%). The mean duration of diabetes was 9.24+/- 6.1 yrs. Twenty-five patients (34.25%) had nephrotic range proteinuria. There was a good correlation between urine PCR and 24 hr urine protein at different levels of GFR. Maximum correlation between urine PCR and 24 hr urine protein was seen in the GFR >60 group. There was a good correlation between urine PCR and 24 hr urine protein at different ranges of proteinuria. A maximum correlation between urine PCR and 24 hr urine was seen in the proteinuria group

Study of Protein/creatinine Ratio in Preeclampsia as an Alternative to 24 Hours Urine Protein in Manipal Teaching Hospital of Nepal

Introduction: Hypertensive disorder in pregnancy complicates around 5 to 10% of all pregnancies. It is one of the leading causes of maternal and fetal morbidity and mortality. Measurement of protein excretion by 24 -hour urine protein collection is gold standard but as it is time consuming, an alternative method like random urine protein/creatinine ratio is required.Objectives: The aim of this study was to assess the diagnostic accuracy of urine protein/ creatinine ratio compared with 24-hour urine protein as an alternative method for evaluating proteinuria in preeclampsia.Methodology: Patients with preeclampsia after 20 weeks of gestation were included in the study. Random urine protein/ creatinine ratio and 24-hour urine for protein was collected and evaluated for proteinuria. Results were entered and analysis was done.Results: Fisher's exact test depicted a positive association between UPCR with 24-hour urine protein, p value being less than 0.05. The area under curve was calculated as 0.87 95% CI (0.74-1.01), which was statistically significant. At cut off point of 0.3, sensitivity was 100%, specificity 90%, positive and negative predictive value 97.2% and 100% respectively.Conclusion: Random urine protein/ creatinine ratio (>0.3) is a reliable indicator of proteinuria >300mg/day. It can be used as an alternative to 24-hour protein estimation. BJHS 2018;3(1)5 : 350-353

Serum free light chain changes offer a more accurate assessment of response to therapy than urine Bence Jones protein excretion measurements in multiple myeloma

e136 (7%) only once a week, and 33 patients (24%) received bortezomib twice a week followed by weekly administration. 37 patients received other schemes. After a median number of 4 cycles (range: 1-12), the overall response rate was of 61%, including 27% of complete response rate, 13% very good partial response and 21% partial response. The median progression free survival was of 22 months. Median overall survival has not been reached and 75% of the patients remained alive at 3 years. 37 patients required starting a second line of therapy and the median time to next therapy was 31 months (29-37). The median treatment-free interval was 16 months. Median bortezomib cumulative dose in the whole series of patients was 39.7 mg/m2. Patients who received more than 39.7 mg/m2 of bortezomib cumulative dose experienced a significantly longer overall survival than those who did not achieve 39.7 mg/m2. The group of patients who received VMP schemes including bortezomib twice a week followed by weekly administration received the highest bortezomib cumulative dose. As far as safety profile is concerned, regarding VMP given with bortezomib sc, it seemed to offer an improved safety profile. Peripheral neuropathy existed at any grade in 59 patients (44%), of which grade 1 are 34 cases (25%), grade 2 are 22 patients (16%) and grade 3 are 3 cases (2%). Conclusion: SC administration of bortezomib in combination with MP in non-transplant eligible newly diagnosed patients resulted in similar efficacy and outcomes as in the VISTA trial, but with a better safety profile.

Knocking out of CD38 accelerates development of a lupus-like disease in lpr mice

CD38 participates in lymphocyte ontogeny and function and may be involved in autoimmunity. Absence of CD38 accelerates development of non-obese diabetic (NOD) mice diabetes and anti-CD38 antibodies are good markers of human disease. Little is known regarding systemic autoimmunity. Active SLE patients have higher numbers of CD38(+) T and B cells. CD38 is a candidate gene for the murine Lmb2 lupus locus. We aimed to investigate whether CD38 was involved in lupus development. We developed Cd38(-/-)-Fas(lpr)/Fas(lpr) mice and monitored them for development of a lupus-like disease through measurement of protein excretion in urine, histological assessment of the kidneys, quantification of circulating immunoglobulins and autoantibodies. We have also immunophenotyped 2- and 6-month old Cd38(-/-)-Fas(lpr)/Fas(lpr) mice. We found that absence of CD38 accelerated disease development: female Cd38(-/-)-Fas(lpr)/Fas(lpr) mice presented severe proteinuria, GN, deposition of ICs in the renal medulla and increased amounts of circulating immunoglobulin G (IgG), although anti-dsDNA autoantibodies and RF were not significantly increased at disease onset. We have found that Cd38(-/-)-Fas(lpr)/Fas(lpr) male mice, similarly to other murine models of lupus, were able to control disease. Absence of CD38 in lpr mice altered differentiation of T cells and dendritic cells (DC). Although the role of CD38 in tolerance is still to be elucidated, we provide evidence that it may play an active role in the control of a murine lupus-like disease.

Role of dietary potassium in the hyperaldosteronism and hypertension of the remnant kidney model.

The remnant kidney model of progressive renal disease is marked by arterial hypertension, especially when produced by nephrectomy and partial infarction. Hyperaldosteronism sustains much of the hypertension, but the stimuli to the increased aldosterone levels are uncertain. It is hypothesized that the hyperaldosteronism attending this model stems from the combination of fixed dietary potassium load in the face of reduced filtration on the one hand, and persistent renin secretion from the scarred remnant kidney on the other. This hypothesis predicted that dietary potassium restriction would lower aldosterone and BP in this model. To test this prediction, two groups of rats with a remnant kidney were studied. Group 1 consumed 0.4 +/- 0.06 mEq (mean +/- SD) of potassium chloride daily, and group 2 ate 4.8 +/- 1.0 mEq daily. Two sham-operated groups with intact kidneys also were studied. Group 3 consumed 1.7 +/- 0.2 mEq daily and group 4 ate 15.2 +/- 1.4 mEq daily. These levels of intake were designed to provide at least as much potassium per liter of GFR in the sham groups as in the remnant kidney rats. Systolic BP (SBP), 24-h protein excretion, plasma aldosterone levels, 24-h urinary aldosterone excretion, and plasma renin activity (PRA) were determined in all groups at 2 wk. At 4 wk, after SBP and protein excretion measurements, remnant kidneys were perfusion-fixed for morphometric analysis. SBP was normal in both sham-operated groups and was not different between the groups (113 +/- 13 versus 117 +/- 2 mmHg, group 3 versus group 4). In the remnant animals, SBP at 2 wk followed potassium intake: Group 1 had a lower SBP than group 2 (140 +/- 26 versus 170 +/- 34 mmHg, P = 0.005). The same SBP pattern persisted at 4 wk (153 +/- 25 versus 197 +/- 27 mmHg, group 1 versus group 2, P = 0.0006). However, 24-h urinary protein excretion was not different between the two groups with remnant kidneys at either 2 or 4 wk. Both plasma and 24-h urinary aldosterone excretion at 2 wk followed potassium intake (120 +/- 124 versus 580 +/- 442 pg/ml for plasma aldosterone, group 1 versus group 2, P = 0.03, and 2.6 +/- 1.8 versus 23.2 +/-9.8 ng/d for urinary aldosterone, group 1 versus group 2, P = 0.0001). PRA, however, followed a reverse pattern in which dietary potassium restriction resulted in higher levels (16 +/- 6 versus 6 +/- 3 ng angiotensin I/ml per h, group 1 versus group 2, P = 0.01). A similar pattern for PRA and aldosterone excretion was also observed in the sham groups, in which lower potassium intake also resulted in a significantly higher PRA and lower aldosterone excretion. The constancy of BP in the sham groups likely reflects their lack of nephron reduction and greater sodium excretory capacity. Morphometric analysis in remnant animals revealed no significant difference between the two dietary groups in the prevalence of glomerular sclerosis, glomerular volume, or interstitial volume. It is concluded that dietary potassium is a potent determinant of hypertension in the remnant kidney model probably through the actions of aldosterone and that the high aldosterone secretion in this model is a function of the dietary potassium load. In this model, reduction in nephron number is also critical in promoting hypertension in conjunction with hyperaldosteronism.