Urinary Protein Excretion In Patients Research Articles

The Effect of Dietary Phosphorus Restriction on Urine Protein Excretion in Patients With Proteinuria: A Randomized Controlled Trial

The present study was designed to determine the effect of dietary phosphorus restriction, independent of protein intake, on the urinary protein excretion in patients with proteinuria. Seventy-one patients with proteinuria were enrolled in a parallel randomized controlled trial study. The patients were randomly allocated to receive either a recommended phosphorus-restricted diet (n=36) or a recommended control diet (n=35), for 8weeks. A diet was designed and recommended to participants in a way that both trial groups would receive the same amount of energy and protein and the only significant difference between them was the amount of phosphorus intake. The study outcomes included the changes in spot urine protein-to-creatinine ratio, the changes in serum and urine levels of phosphorus, as well as the changes in estimated glomerular filtration rate (eGFR). The mean±standard deviation of age, body mass index, and eGFR of the participants were 59±14years, 29±5.5kg/m2, and 56.1±21.7mL/min/1.73m2, respectively. The amount of phosphorus intake decreased significantly in the phosphorus-restricted group compared to the control one (-709 vs. -369mg/day; P<.001). This decrease is accompanied by a significant reduction in urine protein-to-creatinine ratio in the phosphorus-restricted group; however, this change did not reach a significant level when compared to the control one (the mean change: -75.78 vs. -55.25mg/g; P=.539). Limiting the phosphorus intake did not change its serum and urine values as well as eGFR at the end of the trial. Although adherence to a phosphorus-restricted diet by patients with proteinuria led to a significant decrease in urinary protein excretion, this change was not significantly different from that of the control diet. Further studies with larger sample sizes and different designs will reveal more evidence for a link between phosphorus intake and proteinuria.

Correlation of 24-hour urinary protein excretion and spot urine protein-creatinine ratio in women with preeclampsia: A cross sectional study

Objective: To examine the correlation between spot urine PCR and 24-hour urine protein excretion in patients being evaluated for preeclampsia. Material and Methods: A cross sectional study was conducted on 100 patients at the Department of Obstetrics and Gynecology at Chalmeda Anand Rao Institute of Medical Sciences, Karimnagar, Telangana State for a period from December 2019 to August 2020, with inclusion of singleton viable pregnancy, Gestational age between 24 and 38 weeks, Confirmed by last menstrual period and early ultrasound. Result: Among 100 patient’s patients having mean age of 25 ± 3.266 years, among the patients 19% percent of the patients had past history of preeclampsia. Mean gestational age for the patients was 32.39 ± 3.42 weeks. Study showed 62 % of moderate urinary protein levels. There was significant correlation between spot PCR and 24 hour urine protein collection (spearman’s rho=0.7, P<0.0001). Conclusion: Urine protein: creatine ratio is one of the important investigation in hypertensive disorder of the pregnancy. Spot Urine protein: creatine ratio can reliably be taken as a simple, accurate, and convenient replacement for tedious, time consuming 24 hour urine protein estimation, especially in countries like India where hospitals are flooded with a large number of in-patients. Therefore Urine protein: creatine ratio estimation should be introduced and adopted in practice in testing for proteinuria.

Proteinuria in Severe Hypothyroidism: A Prospective Study.

Hypothyroidism is associated with reversible decline in kidney function as measured by estimated glomerular filtration rate (eGFR). eGFR and proteinuria are the most important markers for clinical assessment of kidney function. Though hypothyroidism is associated with proteinuria in cross-sectional data, the impact of treatment on proteinuria is unknown. This study explores the effect of thyroid hormone replacement therapy on eGFR and 24-hour urine protein excretion in patients with severe primary hypothyroidism. This study was a prospective, observational cohort study in adults with severe primary hypothyroidism (serum thyrotropin [TSH] > 50 µIU/mL). Individuals with preexisting or past kidney disease, kidney or urinary tract abnormalities, calculi or surgery, diabetes mellitus, or hypertension were excluded. The participants received thyroid hormone replacement therapy. Thyroid functions, eGFR, 24-hour urine protein excretion, and biochemical parameters were measured at baseline and 3 months. This study took place at a single center, a tertiary care referral and teaching hospital. Of 44 enrolled participants, 43 completed 3 months of follow-up. At 3 months, serum TSH levels decreased and thyroxine levels increased (P < .001 for both). Significant increases in eGFR (mean difference, 18.25 ± 19.49 mL/min/1.73 m2; 95% CI, 12.25 to 24.25, P < .001) and declines in 24-hour urine protein excretion (mean difference, -68.39 ± 125.89 mg/day; 95% CI, -107.14 to -29.65, P = .001) were observed. Serum cholesterol and low-density lipoprotein levels also significantly decreased (P < .001). Thyroid hormone replacement therapy in patients with severe primary hypothyroidism improves eGFR and decreases 24-hour urine protein excretion, thereby suggesting reversible alterations.

Relationship Between Monocyte/HDL Cholesterol Ratio and Urinary Protein Excretion in Patients with Primary Hypertension with Reverse Dipper Pattern

Relationship Between Monocyte/HDL Cholesterol Ratio and Urinary Protein Excretion in Patients with Primary Hypertension with Reverse Dipper Pattern

Effect of Thiazolidinediones on Renal Outcomes in Diabetic Patients with Microalbuminuria or Macroalbuminuria-A Systematic Review and Meta-analysis

Introduction: Diabetic nephropathy (DN), has recently become the leading cause of end-stage renal disease (ESRD) in most countries, recent studies suggest that thiazolidinediones (TZDs) have renal benefits. The aim of this meta-analysis was to assess the effect of TZDs on renal outcomes in type 2 diabetic patients with microalbuminuria or macroalbuminuria. Methods: Medline, Embase, Web of Science and Cochrane Central Register of Controlled Trials were searched from 1991 to September 2017. Randomized controlled trials (RCTs) were selected to evaluate the impact of TZDs on urinary albumin, protein excretion, eGFR or Scr in diabetic patients. Weighted (WMDs) and standardized mean differences (SMDs) were used for changes in urine albumin or protein excretion, eGFR and Scr between the TZDs and control groups. Results: 26 RCTs (9 with rosiglitazone and 17 with pioglitazone) involving 8129 patients with type 2 diabetes were included in this review. Meta-analysis of RCTs showed that in patients with baseline normo- and/or microalbuminuria, the WMD of proportional changes between the TZDs and control groups in urinary albumin excretion was -64.77% (95% CI, -75.60 to -53.94) and the WMD of changes in albumin-creatinine ratio was -24.94% (95% CI, -38.83 to -11.05). Overall, in participants with normo- and/or microalbuminuria, TZDs treatment was associated with a significant decrease in urinary albumin excretion (SMD, -0.91 units of standard deviation [SD]; 95% CI, -1.19 to -0.64). Similarly, TZDs were associated with a significant decrease in urinary protein excretion in patients with macroalbuminuria (SMD, -1.units of SD; 95% CI, -1.86 to -0.27). However, TZDs treatment couldn’t effectively improve eGFR or the level of Scr in diabetic patients whether with microalbuminuria or macroalbuminuria. Conclusions: Treatment with TZDs can benefit patients with early diabetic nephropathy in absence of renal dysfunction. Disclosure Y. Qin: None. X. Wang: None. M. Zhang: None.

A comparison of spot urine protein-creatinine ratio with 24 hour urine proteinexcretion for prediction of proteinuria in preeclampsia.

Objective: To examine the correlation between spot urine PCR and 24-hour urine protein excretion in patients being evaluated for preeclampsia. Population or sample: 98 pregnant women with suspected preeclampsia and a gestational age more than 20 weeks. Methods: A random urine sample was collected immediately before or after the 24-hour urine collection. The protein creatinine ratio was calculated by dividing the urinary protein concentration by the urinary creatinine concentration, and the correlation with the 24-hour urine protein excretion was assessed. Results: PCR at a cut-off value of 0.02 g/mmol (0.18 g/g) had sensitivity and a specificity of 97.6% and 44% respectively in predicting proteinuria of 300 mg/24 hour. The positive predictive value was 58%, and negative predictive value was 96%. Conclusion: There is strong correlation between spot PCR and 24-hour urine protein collection. PCR could be a reasonable alternative to clinicians in order to reduce their dependence on the 24-hour urine collection.

Pattern and predictors of urine protein excretion among patients with type 2 diabetes attending a single tertiary hospital in Lagos, Nigeria.

Testing for proteinuria is used to screen for diabetic nephropathy. However, significant proportion of diabetics has normal urine protein excretion despite impaired renal function. We aimed to determine the factors predicting increased urine protein excretion in patients with type 2 diabetes. This was a cross-sectional study of 358 type 2 diabetics attending the diabetes clinic of a teaching hospital in Lagos. Data regarding patients' demographic characteristics, and disease history were retrieved. Clinical measurement and samples for determination of plasma creatinine, and urine protein/creatinine ratio were obtained. Comparison of means was by student's t-test, while for percentages, Chi-square test was used. Relationship between glomerular filtration rate (GFR) and urine protein excretion was assessed using linear regression while factors associated with increased urine protein was determined excretion logistic regression analysis. Level of statistical significance was set at P <0.05. Mean age was 57.84 + 11.12 years and mean duration of diabetes was 8.63 + 7.53 years. Urine protein excretion was increased in 191 (53.4%) of the patients. Patients with increased urine protein excretion were more likely to be hypertensive, to be on an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker had a higher mean systolic blood pressure, and a lower mean GFR. Patients with a GFR <60 mL/min/1.73 m2 had a six-fold increased odds of having increased urine protein excretion, while patients on an inhibitor of the renin-angiotensin-aldosterone system had a 50% reduced odds of having increased urine protein excretion. Proteinuria and reduced GFR are common among sub-Saharan African patients with type 2 diabetes. GFR below 60 mL/min/1.73 m2 and not receiving an inhibitor of the renin-angiotensin-aldosterone system predict increased urine protein excretion in them.

The relatively poor correlation between random and 24-hour urine protein excretion in patients with biopsy-proven glomerular diseases

Random urine protein creatinine ratios are used to estimate 24-hour urine protein excretion, which is considered a diagnostic gold standard. However, few studies are available of the sensitivity and specificity of this estimation in patients with glomerular proteinuria. To clarify this, wemeasured the urine protein and creatinine centrally in random and 24-hour urine collections at biopsy and longitudinally every 6 months in individuals participating in the Nephrotic Syndrome Study Network (NEPTUNE) cohort with glomerular disease. In the initial developmental cohort, 302 patients had same day random and 24-hour samples with a total of 827 paired measurements across all visits. The protein excretion (g/day) was higher in adult than pediatric patients. The correlation between the random urine protein creatinine ratio and 24-hour urine protein excretion was moderate in both groups (r of 0.60 and 0.67, respectively). However, the log10 transformation of values strengthened correlations in both groups (r of 0.85 and 0.82, respectively). Associations were moderately stronger among obese patients. Prediction equations were developed and validated in 232 unique cases from NEPTUNE (R2 of 0.65). Thus, in patients with glomerular disease and proteinuria, the urine protein creatinine ratio correlates only moderately with 24-hour urine protein excretion. However an estimating equation was developed to derive 24-hour urine protein excretion from random urine protein creatinine ratio values with improved precision. The long-term prognostic value of log10-transformed random protein creatinine ratios values requires future study.

Hypertension in Chronic Glomerulonephritis.

Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of hypertension. Hypertension in chronic GN is primarily volume dependent, and this increase in blood volume is not related to the deterioration of renal function. Patients with chronic GN become salt sensitive as renal damage including arteriolosclerosis progresses and the consequent renal ischemia causes the stimulation of the intrarenal renin-angiotensin-aldosterone system(RAAS). Overactivity of the sympathetic nervous system also contributes to hypertension in chronic GN. According to the KDIGO guideline, the available evidence indicates that the target BP should be ≤140mmHg systolic and ≤90mmHg diastolic in chronic kidney disease patients without albuminuria. In most patients with an albumin excretion rate of ≥30mg/24 h (i.e., those with both micro-and macroalbuminuria), a lower target of ≤130mmHg systolic and ≤80mmHg diastolic is suggested. The use of agents that block the RAAS system is recommended or suggested in all patients with an albumin excretion rate of ≥30mg/ 24 h. The combination of a RAAS blockade with a calcium channel blocker and a diuretic may be effective in attaining the target BP, and in reducing the amount of urinary protein excretion in patients with chronic GN.

Nonprotein Calorie Supplement Improves Adherence to Low-Protein Diet and Exerts Beneficial Responses on Renal Function in Chronic Kidney Disease

Malnutrition is common in patients with chronic kidney disease (CKD) who are on low-protein diets and is a powerful predictor of morbidity and mortality in CKD. Studies have shown that patients on low-protein diets often have difficulty meeting nutritional energy requirements. Our study evaluated the effects of a nonprotein calorie (NPC) supplement on renal function and nutritional status in patients on a low-protein diet. This was a prospective, randomized, open-label, controlled clinical trial. A total of 109 patients with CKD (men, 67%; mean age, 54.5±13 years) with stage 3 to 4 disease were randomly assigned to the intervention group (n=55) or the control group (n=54). All participants received individualized dietary counseling aimed at achieving a daily protein intake of 0.6 to 0.8 g and a daily energy intake of 30 to 35 kcal/kg. The intervention group consumed a 200-kcal NPC supplement daily. The control group received dietary counseling only. The estimated glomerular filtration rate (eGFR) was calculated using the 4-variable Modification of Diet in Renal Disease (MDRD) Study equation. Urine protein excretion, dietary protein and energy intake, and serum levels of creatinine, urea nitrogen, cholesterol, triglycerides, and albumin were assessed at baseline, at 12 weeks, and at 24 weeks. Dietary protein intake and urine protein excretion levels decreased significantly in the intervention group and were significantly lower than those of the control group. In addition, serum levels of creatinine and urea nitrogen decreased significantly, and eGFR increased significantly in the intervention group compared with baseline assessments. No significant differences were observed in the control group. The NPC supplement improved patient adherence to the low-protein diet and reduced urine protein excretion in patients with CKD.

Urinary Sodium Is a Potent Correlate of Proteinuria: Lessons from the Chronic Renal Insufficiency Cohort Study

Background: While higher blood pressure is known to increase proteinuria, whether increased dietary sodium as estimated from 24-hour urinary excretion correlates with increased proteinuria in patients with chronic kidney disease (CKD) is not well studied. Methods: We measured 24-hour urinary sodium, potassium and protein excretion in 3,680 participants in the Chronic Renal Insufficiency Cohort study, to determine the relationship between urinary sodium and potassium and urinary protein excretion in patients with CKD. We stratified our data based on the presence or absence of diabetes given the absence of any data on this relationship and evidence that diabetics had greater urinary protein excretion at nearly every level of urinary sodium excretion. Multiple linear regressions were used with a stepwise inclusion of covariates such as systolic blood pressure, demographics, hemoglobin A1c and type of antihypertensive medications to evaluate the relationship between urinary electrolyte excretion and proteinuria. Results: Our data demonstrated that urinary sodium (+1 SD above the mean), as a univariate variable, explained 12% of the variation in proteinuria (β = 0.29, p < 0.0001), with rising urinary sodium excretion associated with increasing proteinuria. The significance of that relationship was only partially attenuated with adjustment for demographic and clinical factors and the addition of 24-hour urinary potassium to the model (β = 0.13, R² = 0.35, p < 0.0001). Conclusions: An understanding of the relationship between these clinical factors and dietary sodium may allow a more tailored approach for dietary salt restriction in patients with CKD.

Relationships between Levels of Urinary Podocalyxin, Number of Urinary Podocytes, and Histologic Injury in Adult Patients with IgA Nephropathy

Podocalyxin (PCX) is present on the apical cell membrane of podocytes and is shed in urine from injured podocytes. Urinary podocalyxin (u-PCX) is associated with severity of active glomerular injury in patients with glomerular diseases. This study examined the relationship between number of urinary podocytes, levels of u-PCX, and glomerular injury in adults with IgA nephropathy (IgAN). Urine samples voided in the morning on the day of biopsy were obtained from 51 patients with IgAN (18 men and 33 women; mean age, 31 years). All renal biopsy specimens were analyzed histologically. Pathologic variables of IgAN were analyzed per Shigematsu classification, the Oxford classification of IgAN, and the Clinical Guidelines of IgAN in Japan. Levels of u-PCX were measured by sandwich ELISA. Histologic analysis based on Shigematsu classification revealed a significant correlation between levels of u-PCX and severity of acute extracapillary abnormalities (r=0.72; P<0.001), but levels of urinary protein excretion did not correlate with acute glomerular abnormalities. Levels of urinary protein excretion in patients with segmental sclerosis (n=19) were higher than in patients without (n=22) (0.49 [interquartile range (IQR), 0.20-0.88] g/g creatinine versus 0.20 [IQR, 0.10-0.33] g/g creatinine; P<0.01). The number of urinary podocytes in patients with segmental sclerosis was higher than in patients without (1.05 [IQR, 0.41-1.67] per mg creatinine versus 0.28 [IQR, 0.10-0.66] per mg creatinine; P<0.01). Levels of u-PCX and the number of urinary podocytes are associated with histologic abnormalities in adults with IgAN.

Oral Calcitriol for Reduction of Proteinuria in Patients With IgA Nephropathy: A Randomized Controlled Trial

Vitamin D has shown efficacy in the reduction of proteinuria in patients with chronic kidney disease. This study aimed to determine the effect of calcitriol on urinary protein excretion in patients with immunoglobulin A (IgA) nephropathy. Open-label, non-placebo-controlled, randomized study. 50 patients with IgA nephropathy were enrolled. The main criterion for inclusion was urinary protein excretion >0.8 g/d after renin-angiotensin system-inhibitor treatment for at least 3 months. Patients were randomly assigned (1:1) to receive 2 doses (0.5 μg) of calcitriol per week or no treatment for 48 weeks. The primary end point was to compare change in 24-hour urinary protein excretion from baseline to last measurement during treatment. Every 8 weeks, there was measurement of 24-hour urinary protein excretion, serum calcium, serum phosphorus, serum creatinine, and intact parathyroid hormone. Measurement of the primary end point showed changes in urinary protein excretion of +21% (from 1.29 to 1.58 g/24 h; 95% CI, -9% to +52%) in the control group and -19% (from 1.60 to 1.30 g/24 h; 95% CI, -42% to +4%) in the calcitriol-treated group. There was a significant decrease in proteinuria in the calcitriol-treated group compared with the control group (difference between groups, 41%; 95% CI, 5%-79%; P = 0.03). The secondary end point of achieving at least a 15% decrease in proteinuria was attained by 7 of 24 (29%) controls and 17 of 26 (65%) of those treated with calcitriol (P = 0.02). No significant differences were observed in decrease in estimated glomerular filtration rate and change in blood pressure between the 2 groups. The incidence of recorded adverse events was similar between the 2 groups. Small and non-placebo-controlled study. The addition of calcitriol to a renin-angiotensin system inhibitor resulted in a safe decrease in proteinuria in patients with IgA nephropathy.

Beneficial effect of aliskiren combined with olmesartan in reducing urinary protein excretion in patients with chronic kidney disease

Blockade of the renin-angiotensin-aldosterone system is a therapeutic mainstay in patients with chronic kidney disease (CKD). However, the renoprotective effect of the novel direct renin inhibitor aliskiren is unknown. We performed a prospective study in 10 CKD patients. All 10 patients with persistent proteinuria (urinary protein-to-creatinin ratio 0.3-3.5 g/g), despite good blood pressure control (<130/80 mmHg) with olmesartan, were started on 150 mg/day aliskiren. Clinical parameters were examined before and after 4, 8, 12, and 16 weeks of treatment. Urinary protein-to-creatinine ratio significantly decreased by about 40% at 16 weeks from baseline (P = 0.0002), although estimated glomerular filtration rate and blood pressure did not change throughout the study period. Plasma renin activity also decreased significantly from baseline (P = 0.019), although plasma aldosterone concentration did not change. Aliskiren combined with olmesartan reduces proteinuria in CKD patients.

Is Treatment of Nephropathy in Type 1 Diabetes Efficacious but Ineffective?

Increased urinary protein excretion in patients with diabetes has long been known to predict increased mortality, and its absence is associated with near-normal life expectancy.[1][1],[2][2] Recent studies confirmed and extended these findings by illustrating the progressive increase in mortality by

Anti-Proteinuric Effect of Sulodexide in Immunoglobulin A Nephropathy

PurposeWe conducted a multi-center randomized double-blind study to determine the effects of 6-month therapy with sulodexide on urinary protein excretion in patients with idiopathic Immunoglobulin A (IgA) nephropathy.Materials and MethodsA total of seventy-seven patients participated in the study. They were randomly allocated to one of three groups: sulodexide 75 mg or 150 mg daily or the placebo for 6 months. The primary end point was the achievement, at 6 months, of at least 50% reduction in urine protein/creatinine ratio (UPCR) from the baseline value.ResultsAt 6 months, the primary end point was achieved by 12.5% of the patients assigned to the placebo, 4.0% of the patients assigned to sulodexide 75 mg daily and 21.4% of those assigned to 150 mg (p=0.308). Treatment with sulodexide 150 mg daily for 6 months significantly reduced log UPCR from 6.38±0.77 at baseline to 5.98±0.94 at 6 months (p=0.045), while treatment with sulodexide 75 mg daily and placebo did not.ConclusionA 6-month treatment with sulodexide did not achieve 50% reduction of urinary protein excretion in IgA nephropathy patients, but showed a tendency to increase the time-dependent anti-proteinuric effect. Therefore, long-term clinical trials on a larger scale are warranted to elucidate the hypothesis that sulodexide affords renal protection in IgA nephropathy patients.

Role of mast cells, stem cell factor and protease-activated receptor-2 in tubulointerstitial lesions in IgA nephropathy

To elucidate the role of mast cells (MCs) in the pathogenesis of tubulointerstitial lesions in IgA nephropathy (IgAN), we investigated the number of MCs, serum stem cell factor (SCF), protease-activated receptor-2 (PAR-2) and alpha-smooth-muscle actin (alpha-SMA) in the kidney and the correlation between MC number, SCF, PAR-2, alpha-SMA and tubulointerstitial lesions in biopsy specimens and serum creatinine levels, urinary protein excretion in patients with IgA nephropathy. Thirty-five patients with IgA nephropathy were enrolled in this study. Clinical parameters, such as serum creatinine and urinary protein excretion, were obtained from each patient at the time of biopsy. Paraffin-embedded sections were used for immunohistochemical staining. Monoclonal antibodies to human tryptase, alpha-SMA, and SCF and polyclonal antibody to PAR-2 were used as primary antibodies. Ten cortical interstitial fields were randomly selected and assessed using a computer-assisted color image analyzer. Tubulointerstitial fibrosis was assessed as the percentage of the area stained with Masson trichrome in ten cortical interstitial fields. In all of the control subjects, few tryptase-positive MCs were observed in the glomeruli and interstitium. In contrast, sparse MCs were observed in the interstitium, but not in the glomeruli of diseased kidneys. The number of interstitial MCs in the tubulointerstitial lesions, the expression of SCF, PAR-2 and alpha-SMA were positively correlated with the degree of interstitial fibrosis. A close correlation between MCs, alpha-SMA, PAR-2 and SCF was found (r = 0.887 for alpha-SMA, r = 0.844 for PAR-2, r = 0.853 for SCF, P < 0.01). Also a close correlation between alpha-SMA, PAR-2 and SCF was found (r = 0.874 for PAR-2, r = 0.862 for SCF, P < 0.01). PAR-2 was correlated with SCF (r = 0.893, P < 0.01). Moreover, a significant positive correlation was observed between the number of interstitial MCs, the expression of SCF, PAR-2 and alpha-SMA and the serum creatinine level (r = 0.738 for MCs, r = 0.658 for alpha-SMA, r = 0.692 for PAR-2, r = 0.754 for SCF, P < 0.05). Our findings suggest that MC infiltration possibly induced by SCF in renal interstitial tissues seems to be associated with tubulointerstitial fibrosis through PAR-2 in IgA nephropathy.

Effect of Thiazolidinediones on Albuminuria and Proteinuria in Diabetes: A Meta-analysis

Because of the major clinical and economic burden of diabetic nephropathy, new therapeutic tools to delay its progression are needed. Recent studies suggest that thiazolidinediones have renal benefits. We aimed to evaluate the effect of thiazolidinediones on urinary albumin and protein excretion in patients with diabetes mellitus. Systematic review and meta-analysis by searching MEDLINE/PubMed, EMBASE, and Cochrane CENTRAL databases (1991 to September 2009). Patients with diabetes mellitus. Randomized controlled trials. Thiazolidinediones (rosiglitazone and pioglitazone) compared with placebo or other antidiabetic agents. Weighted (WMDs) and standardized mean differences (SMDs) for changes in urine albumin or protein excretion between the thiazolidinedione and control groups. Of 171 originally identified articles, 15 studies (5 with rosiglitazone and 10 with pioglitazone) involving 2,860 patients were included in the analysis. In participants with baseline normo- or microalbuminuria, the WMD of proportional changes between the thiazolidinedione and control groups in urinary albumin excretion measured using time-specified collections was -64.8% (95% CI, -75.6 to -53.9) and the WMD of changes in albumin-creatinine ratio was -24.8% (95% CI, -39.6 to -10.0). Overall, in participants with normo- and microalbuminuria, thiazolidinedione treatment was associated with a significant decrease in urinary albumin excretion (SMD, -0.6 units of standard deviation [SD]; 95% CI, -0.8 to -0.4). Similarly, thiazolidinediones were associated with a significant decrease in urinary protein excretion in patients with proteinuria (SMD, -1.1 units of SD; 95% CI, -1.8 to -0.4). Significant heterogeneity across included studies in several subgroup analyses; patient-level data not available. Treatment with thiazolidinediones significantly decreases urinary albumin and protein excretion in patients with diabetes. This finding calls for clinical trials with hard renal outcomes to elucidate the potential benefits of thiazolidinediones on diabetic nephropathy.

Effect of pravastatin on kidney function and urinary protein excretion in autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is progressive, resulting in end-stage kidney failure in most patients. Experimental and clinical studies have suggested that statins may slow the progression of chronic kidney disease in general and ADPKD specifically. This randomized open-label clinical trial was conducted to assess the effect of pravastatin 20 mg on kidney function and urinary protein excretion in patients with ADPKD. Sixty patients were initially recruited but 49 of these received either pravastatin 20 mg or no treatment for 2 years. Trial visits were conducted every 3 months, assessing kidney function by estimated glomerular filtration rate and 24 h urine creatinine clearance and urinary protein excretion. There were no significant (p > 0.05) changes in markers of kidney function or urinary protein excretion between groups over the 2 years despite a significant fall in total serum cholesterol in pravastatin-treated patients (p = 0.029). This trial found that taking 20 mg pravastatin for 2 years had no significant effect on kidney function or urinary protein excretion in patients with ADPKD. The lack of statistical power limits the external validity of these findings. A larger, longer duration study using a higher dose of a more potent statin is required.

Effect of Spironolactone on Urinary Protein Excretion in Patients with Chronic Kidney Disease

Aim. To investigate antiproteinuric effect of spironolactone in patients with chronic kidney disease (CKD) treated with angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin II type 1 receptor blockers (ARBs). Methods. This study was performed in 33 CKD patients with proteinuria. 24 h urinary protein excretion and biochemical parameters were obtained before the therapy. Then, spironolactone (25 mg/d) was added to the therapy. The antiproteinuric effect of spironolactone was examined for eight weeks. Results. At eight weeks, there was a significant decrease in proteinuria (p < 0.001, 47.9% decrease). Systolic and diastolic blood pressures were significantly decreased (p < 0.004, p < 0.001, respectively). However, no correlation was detected between the reductions in systolic and diastolic BP and the reduction in proteinuria (p = 0.464, p = 0.239, respectively). Serum potassium level increased significantly (p < 0.001). Conclusions. Our study suggests that spironolactone significantly reduces urinary protein excretion. This strategy may be useful to slow the progression of CKD. However, hyperkalemia is the most important side effect of treatment, and it is necessary to monitor potassium level. Further studies are needed to determine the efficacy of spironolactone on proteinuria.