Proteinuria In People Research Articles

Role of perirenal adiposity in renal dysfunction among CKD individuals with or without diabetes: a Japanese cross-sectional study

IntroductionIt remains unclear whether increased perirenal fat (PRF) accumulation is equally related to renal involvement in patients with and without diabetes mellitus (DM). We evaluated the association between PRF volume...

PS-C17-10: ORAL SEMAGLUTIDE REDUCES ALBUMINURIA IN PATIENTS WITH TYPE 2 DIABETES, OBESITY AND HYPERTENSION, WITH PARTIAL DEPENDENCE ON BLOOD PRESSURE CONTROL

Objective: GLP-1 receptor agonists reduce blood pressure (BP) and proteinuria in people living with type 2 diabetes (T2D) and obesity, but data on patients with uncontrolled hypertension are very scarce. Oral semaglutide showed interesting results in patients with moderate renal impairment in PIONEER 5, but their BP was well controlled, with SBP < 140 mmHg. We sought to assess the antiproteinuric effect of oral semaglutide in a group of patients with T2D, obesity and uncontrolled hypertension, and whether this effect is dependent on BP reduction. Design and Methods: Retrospective analysis of the data on SBP and albuminuria were performed in consecutive patients with T2D, obesity and uncontrolled hypertension (office sitting SBP < 140 mmHg) who started therapy with oral semaglutide. Data were obtained from a baseline visit in which oral semaglutide was initiated, and a second visit after 3–4 months. Mediation analyses with SBP reduction as mediator were performed post-hoc to quantify its relative contribution to albuminuria reduction. Patients who initiated or changed antihypertensive medication simultaneously with oral semaglutide were excluded. Consent was obtained from all included subjects. Results: Data were obtained from 33 patients, 21 (64%) were female, age 54.2 ± 11.9 years, diabetes duration 6.8 ± 2.7 years, baseline BMI 36.7 ± 5.2 kg/m2, baseline SBP 166 ± 12.2 mmHg, baseline eFGR (CKD-EPI) 58 ± 11.6 ml/min/1.73m2 and baseline albuminuria (geometric mean) 134 ± 125 mg/g Cr, with 16 patients (48.5%) having < 30 mg/g, 12 (36.4%) 30–300 mg/g and 5 (15.1%) > 300 mg/g. SBP reduction was 4.8 ± 2.1 mmHg (p = 0.012, paired t-test), albuminuria reduction was 36 ± 27 mg/g (-27%; p = 0.026, paired t-test), and eGFR change + 1.3 ± 1.6 mL/min/1.73m2 (not significant). There was a significant correlation between SBP and albuminuria reductions (Pearson's r: 0.26, p = 0.002). The mediation analyses showed that albuminuria reduction of 11 ± 10 mg/g (8.3%) was mediated by SBP reduction while 25 ± 14 mg/g (18.7%) was SBP-independent. 4 patients (12.1%) reduced their albuminuria to < 30 mg/g (Figure). Conclusions: In patients with T2D, obesity and uncontrolled hypertension, oral semaglutide significantly reduced SBP and albuminuria, without change in eGFR, and a relevant fraction of them (about 1/8) reduced albuminuria below the conventional normality threshold (< 30 mg/g). The decrease in albuminuria was only partially mediated by SBP reduction, suggesting additional mechanisms, possibly direct glomerular and/or tubular effects.

444. Effect of multidisciplinary management of CKD on proteinuria in people with HIV

Abstract Background Optimizing management of chronic kidney disease in people with HIV has become a more pressing priority both to minimize morbidity and preserve HIV antiretroviral options. Part of standard care is employing the beneficial effects of angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARB) in patients with clinically significant proteinuria. Our analysis looks at the proteinuria outcomes of PWH with CKD co-managed by a multidisciplinary team of infectious disease and nephrology physicians nested in a Ryan White-funded clinic in New Orleans. Methods Patients with HIV and at least grade 3 CKD or with significant proteinuria were referred to the multidisciplinary clinic. Patients were evaluated by an HIV specialist and nephrologist at the initial visit for a jointly developed management plan. Renal function and proteinuria were measured at baseline and longitudinally per standard of care. Change in proteinuria and GFR over time were calculated. Patients were also assessed for whether they were prescribed ACE/ARB therapy, if appropriate. Patients included in this analysis were evaluated between January 1, 2021 and March 31, 2022. Results During the analysis period, 46 patients with at least CKD 3 or proteinuria were evaluated. 35 patients were Black non-Hispanic, 9 were White non-Hispanic, and 2 were Hispanic. 39 were male, and 7 were female. 35 had a previous diagnosis of hypertension, and 10 had diabetes mellitus. Of the 42 with a recorded baseline urine protein measurement, 24 were found to have clinically significant proteinuria. Of those with proteinuria, 16 were on an ACE or ARB at their baseline evaluation. 20 were on ACE/ARB’s the end of the analysis period (p=0.058). Average baseline proteinuria was 1,158 mg/g, while average final was 938 mg/g, which was less but not significantly different (p=0.54). Mean baseline GFR was not significantly different from final GFR (50.8 mL/min vs 50.5 mL/min, p=0.67). Conclusion A multidisciplinary model of managing CKD among people with HIV may improve adherence with management guidelines and limit progression of proteinuria and decrease in GFR. In general, the natural history of kidney disease with proteinuria is to worsen over time, so while not significant, proteinuria in this cohort did decrease over time Disclosures All Authors: No reported disclosures.

Accepting Living Kidney Donors with Preexisting Diabetes Mellitus: A Perspective on the Recent OPTN Policy Change-July 2022.

Accepting Living Kidney Donors with Preexisting Diabetes Mellitus: A Perspective on the Recent OPTN Policy Change-July 2022.

Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease.

Sickle cell disease is a group of disorders characterized by deformation of erythrocytes. Renal damage is a frequent complication in sickle cell disease as a result of long-standing anemia and disturbed circulation through the renal medullary capillaries. Due to the improvement in life expectancy of people with sickle cell disease, there has been a corresponding significant increase in the incidence of renal complications. Microalbuminuria and proteinuria are noted to be a strong predictor of subsequent renal failure. There is extensive experience and evidence with angiotensin-converting enzyme (ACE) inhibitors over many years in a variety of clinical situations for patients who do not have sickle cell disease, but their effect in people with this disease is unknown. It is common practice to administer ACE inhibitors for sickle nephropathy due to their renoprotective properties; however, little is known about their effectiveness and safety in this setting. This is an update of a Cochrane Review first published in 2013 and 2015. To determine the effectiveness of ACE inhibitor administration in people with sickle cell disease for decreasing intraglomerular pressure, microalbuminuria and proteinuria and to to assess the safety of ACE inhibitors as pertains to their adverse effects. The authors searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Hameoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings. Date of the most recent search: 18 October 2021. We also searched clinical trial registries. Date of the most recent search: 22 August 2021. Randomized or quasi-randomized controlled trials of ACE inhibitors designed to reduce microalbuminuria and proteinuria in people with sickle cell disease compared to either placebo or standard treatment regimen. Three authors independently applied the inclusion criteria in order to select studies for inclusion in the review. Two authors assessed the risk of bias of studies and extracted data and the third author verified these assessments. Seven studies were identified through the searches. Six studies were excluded. The included study randomized 22 participants (7 males and 15 females) having proteinuria or microalbuminuria with sickle cell disease and treated the participants for six months (median length of follow up of three months) with captopril or placebo. Overall, the certaintyof the evidence provided in this review was very low, since most risk of bias domains were judged to have either an unclear or a high risk of bias. Because of this, we are uncertain whether captopril makes any difference, in total urinary albumin excretion (at six months) as compared to the placebo group, although it yielded a mean difference of -49.00 (95% confidence interval (CI) -124.10 to 26.10) or in the absolute change score, although it yielded a mean difference of -63.00 (95% CI -93.78 to -32.22). At six months albumin excretion in the captopril group was noted to decrease from baseline by a mean (standard deviation) of 45 (23) mg/day and the placebo group was noted to increase by 18 (45) mg/day. Serum creatinine and potassium levels were reported constant throughout the study (very low-certainty evidence). The potential for inducing hypotension should be highlighted; the study reported a decrease of 8 mmHg in systolic pressure and 5 mmHg in diastolic and mean blood pressure (very low-certaintyevidence). Overall, we judged the certaintyof the evidence to be very low. The included study selectively reported its results, was not powered to detect a group difference, should it exist, and otherwise did not offer enough information to allow us to judge the bias inherent in the study. Indirectness (in relation to the limited age and type of population included) and imprecision (wide confidence intervals around the effect estimate) were observed. More long-term studies involving multiple centers and larger cohorts using a randomized-controlled design are warranted, especially among the pediatric age group. Detailed reporting of each outcome measure is necessary to allow a clear cut interpretation in a systematic review. One of the difficulties encountered in this review was the lack of detailed data reported in the included study. Overall, we judged the certaintyof this evidence to be very low.

Reduction in sodium intake is independently associated with improved blood pressure control in people with chronic kidney disease in primary care.

Decreasing sodium intake has been associated with improvements in blood pressure (BP) and proteinuria, two important risk factors for CVD and chronic kidney disease (CKD) progression. We aimed to investigate the role of sodium intake by examining the effect of changes in sodium intake over 1 year on BP and proteinuria in people with early stage CKD. From thirty-two general practices, 1607 patients with previous estimated glomerular filtration rate of 59-30 ml/min per 1.73 m² and mean age of 72.9 (sd 9.0) years were recruited. Clinical assessment, urine and serum biochemistry testing were performed at baseline and after 1 year. Sodium intake was estimated from early morning urine specimens using an equation validated for this study population. We found that compared with people who increased their sodium intake from ≤ 100 to >100 mmol/d over 1 year, people who decreased their intake from >100 to ≤ 100 mmol/d evidenced a greater decrease in all BP variables (Δmean arterial pressure (ΔMAP) = -7.44 (SD 10.1) v. -0.23 (SD 10.4) mmHg; P<0.001) as well as in pulse wave velocity (ΔPWV = -0.47 (SD 1.3) v. 0.08 (SD 1.88) m/s; P<0.05). Albuminuria improved only in albuminuric patients who decreased their sodium intake. BP improved in people who maintained low sodium intake at both times and in those with persistent high intake, but the number of anti-hypertensive increased only in the higher sodium intake group, and PWV improved only in participants with lower sodium intake. Decreasing sodium intake was an independent determinant of ΔMAP. Although more evidence is needed, our results support the benefits of reducing and maintaining sodium intake below 100 mmol/d (2.3-2.4 g/d) in people with early stages of CKD.

Angiotensin-converting enzyme (ACE) inhibitors for proteinuria and microalbuminuria in people with sickle cell disease.

Sickle cell disease is a group of disorders characterized by deformation of erythrocytes. Renal damage is a frequent complication in sickle cell disease as a result of long-standing anemia and disturbed circulation through the renal medullary capillaries. Due to the improvement in life expectancy of people with sickle cell disease, there has been a corresponding significant increase in the incidence of renal complications. Microalbuminuria and proteinuria are noted to be a strong predictor of subsequent renal failure. There is extensive experience and evidence with angiotensin-converting enzyme (ACE) inhibitors over many years in a variety of clinical situations for patients who do not have sickle cell disease, but their effect in people with this disease is unknown. It is common practice to administer ACE inhibitors for sickle nephropathy due to their renoprotective properties; however, little is known about their effectiveness and safety in this setting. This is an update of a Cochrane Review first published in 2013. To determine the effectiveness of ACE inhibitor administration in people with sickle cell disease for decreasing intraglomerular pressure, microalbuminuria and proteinuria and to to assess the safety of ACE inhibitors as pertains to their adverse effects. The authors searched the Cochrane Cystic Fibrosis and Genetic Disorders Group's Hameoglobinopathies Trials Register comprising references identified from comprehensive electronic database searches and handsearches of relevant journals and abstract books of conference proceedings.Date of the most recent search: 03 June 2015. Randomized or quasi-randomized controlled trials of ACE inhibitors designed to reduce microalbuminuria and proteinuria in people with sickle cell disease compared to either placebo or standard treatment regimen. Three authors independently applied the inclusion criteria in order to select studies for inclusion in the review. Two authors assessed the risk of bias of studies and extracted data and the third author verified these assessments. Five studies were identified through the searches, only one met our inclusion criteria. The included study randomized 22 participants (seven males and 15 females) having proteinuria or microalbuminuria with sickle cell disease and treated the participants for six months (median length of follow up of three months) with captopril or placebo. The overall quality of the outcomes reported was high, since most aspects that may contribute to bias were regarded to be of low risk, although allocation concealment was not reported. At six months, the study reported no significant difference in urinary albumin excretion between the captopril group and the placebo group, although the mean urinary albumin excretion in the captopril group was lower by a mean difference of -49.00 (95% confidence interval -124.10 to 26.10) compared to that of placebo. However, our analysis on the absolute change score showed significant changes between the two groups by a mean difference of -63.00 (95% confidence interval -93.78 to -32.22). At six months albumin excretion in the captopril group was noted to decrease from baseline by a mean of 45 ± 23 mg/day and the placebo group was noted to increase by 18 ± 45 mg/day. Serum creatinine and potassium levels were reported constant throughout the study. The potential for inducing hypotension should be highlighted; the study reported a decrease of 8 mmHg in systolic pressure and 5 mmHg in diastolic and mean blood pressure. There is not enough evidence to show that the administration of ACE inhibitors is associated with a reduction of microalbuminuria and proteinuria in people with sickle cell disease, although a potential for this was seen. More long-term studies involving multiple centers and larger cohorts using a randomized-controlled design are warranted, especially among the pediatric age group. Detailed reporting of each outcome measure is necessary to allow a clear cut interpretation in a systematic review. One of the difficulties encountered in this review was the lack of detailed data reported in the included study.

Ten-year incidence of gross proteinuria in people with diabetes

Ten-year incidence of gross proteinuria in people with diabetes

Incidence of Gross Proteinuria in Older-Onset Diabetes: A Population-Based Perspective

A few population-based studies describe the incidence of gross proteinuria in people with diabetes. We performed a population-based study in southern Wisconsin of diabetic individuals diagnosed at > or = 30 yr of age either taking insulin (n = 398) or not taking insulin (n = 441). The presence of gross proteinuria (> or = 0.3 g/L) was determined by means of a reagent strip. The incidence of proteinuria in the 4-yr interval was 17.3% (95% CI 13.6-21.0) in those taking insulin and 10.7% (95% CI 7.8-13.6) in those not taking insulin. The relative risk of developing proteinuria for those in the highest level of total pack-yr smoked compared with those who had never smoked was 2.0 (95% CI 1.2-3.3) for those taking insulin and 2.5 (95% CI 1.3-4.5) for those not taking insulin. After controlling for other risk variables, the incidence of gross proteinuria was also associated with higher GHb. These data suggest that smoking and glycemic control, both potentially modifiable factors, are significant risk factors for the development of gross proteinuria.

The Incidence of Gross Proteinuria in People With Insulin-Dependent Diabetes Mellitus

Epidemiologic data on the incidence of gross proteinuria in people with diabetes are important in medical counseling, in projecting estimates of needs and costs of health care, and for developing approaches to prevent renal complications. We performed a population-based incidence study in southern Wisconsin of insulin-taking diabetic persons diagnosed before 30 years of age. The presence of gross proteinuria (greater than or equal to 0.30 g/L) was determined by means of a reagent strip. The incidence of proteinuria in a 4-year interval was 14.4% (95% confidence interval, 11.7% to 17.0%). The relative risk of developing proteinuria after 4 years for those with glycosylated hemoglobin levels in the highest quartile compared with those in the lowest quartile was 3.0 (95% confidence interval, 1.6 to 5.3). The incidence of proteinuria was also associated with higher diastolic blood pressure, being male, taking more insulin, and having more severe retinopathy at the baseline examination. The relationship between glycosylated hemoglobin level and the incidence of proteinuria was significant even after controlling for these other risk variables. These data suggest that hyperglycemia, as measured by glycosylated hemoglobin level, is a significant risk factor for the development of gross proteinuria.

The incidence of gross proteinuria in people with insulin-dependent diabetes mellitus

The incidence of gross proteinuria in people with insulin-dependent diabetes mellitus

Screening for hematuria, glucosuria and proteinuria in people aged 55-64. Technical, clinical and cost-benefit experience from a pilot study.

A total of 754 persons randomly selected from the age group 55-64 years were invited by letter to take part in a screening for hematuria, proteinuria and glucosuria. Each person was asked to provide one sample of morning urine and immediately mail it to the laboratory. A total of 413 persons (55%) responded. Two dipsticks: BM-Test-5L and a new single strip for hematuria determination preliminary named BM 33075 were used, both manufactured by Boehringer Mannheim GmbH. The test strips gave positive reaction for hematuria in 21 persons (5.1%), for proteinuria in 14 persons (3.4%), and for glucosuria in six persons (1.5%). All persons with positive tests were invited to follow-up investigations. In the hematuria group we found one person with a malignant disease, 13 with benign conditions and in seven persons we found no reason for the hematuria. Among those with proteinuria one person had a nephritis. Four persons with glucosuria knew about their diabetes mellitus. The cost of the screening was NOK 99 per participant.