Urine Protein Excretion Levels Research Articles

MO311THE ASSOCIATION BETWEEN NEPHROTIC-RANGE PROTEINURIA AND OXALATE METABOLISM VIOLATION IN PATIENTS WITH PRIMARY GLOMERULONEPHRITIS

Abstract Background and Aims There is a general lack of scientific research on oxalate metabolism in primary glomerulonephritis (PGN) patients. The present study aimed to evaluate plasma oxalic acid (POx) concentration and urinary oxalate (UOx) excretion in PGN patients and determine the role of nephrotic syndrome in oxalate metabolism, which has never before been reported. Method A total of 100 participants were enrolled in this cross-sectional single-center study, including 76 PGN patients aged 41 ± 1.83 years and 24 healthy volunteers on a free-choice diet who served as a control reference group to evaluate POx concentration. Among the patients were 53 (69.7 %) patients with nephrotic syndrome (NS) and biopsy-proven PGN and 23 (30.3 %) patients with a clinical diagnosis of PGN. All patients were treated according to KDIGO Clinical Practice Guidelines for Glomerulonephritis. In addition to routine hematological and biochemical tests, POx concentration and UOx excretion were found in all study participants. POx was measured spectrophotometrically using a commercially available kit (MAK315, Sigma, Spain). Daily UOx excretion was determined using an oxalate oxidase/peroxidase reagent (BioSystems, Spain). Urine protein excretion (UPE) was measured in a 24-h urine collection. The glomerular filtration rate (GFR) was calculated using the CKD-EPI formula. The data were presented as the median and the interquartile ranges [Me (Q25-Q75)] and compared using the Mann-Whitney test. The Spearman correlation test and the partial correlation coefficient were used to evaluate the association between the examined markers. Results POx concentration was significantly higher in the patients with PGN compared with the healthy volunteers: 29.9 (14.9-51.7) vs 18.9 (16.2-23.8) µmol/L, p = 0.01. Although the patients with NS demonstrated a statistically higher GFR level compared with the patients with mild proteinuria [70.5 (47-87) vs 50 (22-76.2) mL/min/1.73 m2, p = 0.01], these patients also had the highest POx level (Fig. 1). Moreover, POx concentration was significantly associated with GFR (r = -0.27, p = 0.005), serum phosphate (r = 0.26, p = 0.007) and UPE (Fig. 2) levels. No significant differences were found in UOx excretions between the groups. However, the higher level of UPE was, the higher level of UOx was observed in the PGN patients with NS (Fig. 3). The partial correlation analysis confirmed a strong association between UPE and POx concentration independently of the patients’ age, gender, GFR and serum phosphate levels (r = 0.22, p = 0.04). Conclusion Nephrotic-range proteinuria was significantly associated with the elevation of POx concentration and UOx excretion in the PGN patients. More research with a larger cohort is needed to confirm this preliminary evidence and validate NS as a risk factor for oxalate metabolism violation in PGN patients.

DECREASING OF ERYTHROCYTES MEMBRANES PLASMALOGENS LEVEL AT THE DIABETES MELLITUS

Introduction. Plasmalogens are important part of glycerophospholipids and plays a role in the tissue development and metabolism. Changing their level shown in coronary heart diseases, peroxysomes disorders, Diabetes Mellitus (DM).Aim. Study the role of plasmalogens in the development of diabetes complication, especially in diabetic nephropathy (DN) presented interest in our study.Material and methods. In 12 healthy subjects (HS) and in 49 patients with DM2 in age 39 – 65 with disease duration from 2 month to 25 years the level of fasting blood glucose (FBG) and HbA1c, plasma triglycerides (TG) content, plasmalogens in blood serum (SP) and erythrocytes membrane (EP) were observed. The stage of DN detected by urine protein excretion level, glomerular filtration rate (GFR), blood urine nitrogen (BUN) and creatinine level. Patients according to GFR and BUN level were selected into the main 3 groups: without proteinuria (BPU), with proteinuria and normal BUN (PU), with proteinuria and higher BUN (CKD).Results. FBG and HbA1c level were significantly higher in all DM patients than HS, by 2.1, p<0.01 and in 1.7, p<0.05 respectively and was comparable between DN groups. TG level were significantly higher by 1.7 times in DM group and shown relationship with severity of DN. SP and EP level were significantly lower in DM group and showed strong linkage between GFR and BUN level and suggest about involvement of plasmalogens into development of DN.Conclusion. In patients with DM SP and EP level significantly decreased, had a strong linkage with GFR, BUN and can reflect the severity of DN.

MiR-152 Attenuates the Severity of Lupus Nephritis Through the Downregulation of Macrophage Migration Inhibitory Factor (MIF)-Induced Expression of COL1A1.

Background: The role of miR-152 in lupus nephritis has not been elucidated. The aim of this study was to investigate the role of miR-152 in the pathogenesis of lupus nephritis (LN).Methods: miR-152 expression was detected using RT-PCR in LN tissue and normal controls. The miR-152 expression was compared with clinical parameters such as 24 h urine protein excretion level, serum creatinine, and serum complement level and SLEDAI score. The function of miR-152 was examined using human renal proximal tubular epithelial cells (HRPTE). miR-152 mimics and inhibitors were transfected to HRPTEs to ascertain the effects of miR-152.Results: miR-152 expression was downregulated in LN tissue. There was an inverse correlation between miR-152 expression in LN tissue and clinical parameters like 24 h urine protein excretion levels and serum creatinine, but not serum complement levels or SLEDAI. Further analysis showed that macrophage migration inhibitory factor (MIF) was a direct target of miR-152. Downregulation of MIF through complementary binding of miR-152 inhibited the renal expression of COL1A1.Conclusion: miR-152 expression was tapered in LN tissue and miR-152 expression was inversely correlated with chronicity index (CI), serum creatinine and severity of proteinuria. miR-152 may attenuate the severity of LN through the downregulation of MIF-induced expression of COL1A1. These findings suggest that miR-152 may be a potential target for the treatment of LN.

Association of Baseline Proteinuria and Adverse Outcomes in Pregnant Women With Treated Chronic Hypertension.

To assess the importance of baseline proteinuria in women treated for chronic hypertension during pregnancy. This retrospective cohort study included women with chronic hypertension who received antihypertensive therapy in the first half of pregnancy and completed urine protein quantification before 20 weeks of gestation. Maternal and neonatal outcomes were analyzed according to the presence or absence of baseline proteinuria, defined as 300 mg or greater per 24 hours identified before 20 weeks of gestation. Frequencies of superimposed preeclampsia, preterm birth, and small-for-gestational-age neonates were further evaluated according to stratified urine protein excretion levels from less than 50 mg to greater than 1,000 mg/24 hours. Between January 2002 and December 2014, a total of 447 women met inclusion criteria. Of these, 56 (13%) had baseline proteinuria. Women with baseline proteinuria were statistically significantly more likely to develop superimposed preeclampsia (79% compared with 49%), deliver preterm (18% compared with 6% 30 weeks of gestation or less, 34% compared with 17% 34 weeks of gestation or less, and 48% compared with 26% less than 37 weeks of gestation), and deliver an small-for-gestational-age neonate (41% compared with 22% less than the 10th percentile, 20% compared with 9% less than the third percentile) when compared with women who did not have proteinuria (all P<.05). Furthermore, the rates of superimposed preeclampsia and small for gestational age were significantly increased as 24-hour protein excretion levels increased across stratified levels (P for trend .002 and .015, respectively). When proteinuria levels less than 300 mg/d were analyzed separately, a significant association was observed for rates of superimposed preeclampsia and preterm birth. In pregnant women with treated chronic hypertension, baseline proteinuria was significantly associated with increased rates of preeclampsia, preterm birth, and growth restriction-even at proteinuria values previously considered to be within normal range (less than 300 mg/d).

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.

Adiponectin,leptin: focus on low-protein diet supplemented with keto acids in chronic glomerulonephritis with hbv patients

Leptin and adiponectin come from adipose tissue, which can reflect patients' inflammation and status of lipid metabolism. Our study is aim to evaluate the effects of short-term restriction of dietary protein intake (DPI) supplemented with keto acids on nutrition and lipid metabolic disturbance in chronic glomeruloneph-ritis with HBV patients. 17 patients were randomized to either low DPI with keto acid-supplemented (sLP) or low DPI (LP) group for 12 weeks. Low-protein diet (LPD) wasindividualized with protein intake of 0.6–0.8 g/kg/day and keto acids were supplied in 0.1 g/kg/day. Nutritional index other clinical index were measured to evaluate the effect and safey respectively. Serum levels of adiponectin, leptin were determined by ELISA assay.The urine protein excretion level was significantly decreased after 12 weeks in the sLP group compared to the basal value and the LP group (baseline:4.52±1.74,4 weeks:3.19±1.52 g,8 weeks: 2.19±1.1 g,12 weeks:1.64±0.77 g, P In conclusion: Short-term restriction of DPI 0.6–0.8 g of protein/ kg IBW/day is safe, when combined with keto acids, is associated with decreased of urinary protein and improvement of lipid metabolism

Valsartan attenuated oxidative stress, decreased MCP-1 and TGF-β&lt;sub&gt;1&lt;/sub&gt; expression in glomerular mesangial and epithelial cells induced by high-glucose levels

Our previous studies revealed that valsartan, an angiotensin II type I receptor blocker, exhibited renoprotective effects through decreasing urine protein excretion levels due to improving glomerular permeability in rats with diabetic nephropathy (DN). In this study, we sought to investigate the underlying mechanisms in perspectives of oxidative stress, transforming growth factor beta-1 (TGF-β1) and monocyte chemoattractant protein-1 (MCP-1) expressions in glomerular mesangial cells (GMCs) and glomerular epithelial cells (GECs) since their roles are well-established in the development and progression of DN. High-glucose levels significantly increased oxidative stress in GMCs and GECs, as evidenced by enhanced generation of reactive reactive oxygen species (ROS), reduced levels of glutathione (GSH) and antioxidant enzyme superoxide dismutase (SOD), and increased production of malondialdehyde (MDA). Treatment with valsartan significantly restored the levels of those oxidative stress relevant molecules. Furthermore, valsartan obviously diminished the expression of proinflammatory cytokine MCP-1 in GMCs and GECs induced by high-glucose levels both at mRNA and protein levels, as determined by real-time PCR, immunocytochemistry, western blotting, and ELISA. In addition, the increased expressions of TGF-β1 mRNA and protein induced by high-glucose level were also abrogated by valsartan treatment in GMCs, as evaluated by real-time PCR and ELISA. These results suggest that the renoprotective effects of valsartan may be related to its potential in decreasing oxidative stress and the expressions of MCP-1 and TGF-β1 in GMCs and GECs.

A low-dose combination of valsartan and low molecular weight heparin better improved glomerular permeability than did high-dose monotherapy in rats with diabetic nephropathy

Diabetic nephropathy is the most common and severe renal complication of diabetes mellitus. The present study sought to investigate the renoprotective effects of a combination therapy of valsartan and low molecular weight heparin (LMWH) in rats with diabetic nephropathy induced by uninephrectomy and streptozotocin. The animals were divided into five groups as follows: sham-operated rats, diabetic control rats, diabetic rats treated with 20 mg/kg/day valsartan, diabetic rats treated with 600 IU/kg/day LMWH, diabetic rats treated with a combination of valsartan and LMWH (valsartan 10 mg/kg/day and LMWH 300 IU/kg/day). The treatment regimen was maintained for 8 weeks. Treatment with valsartan, LMWH, or a combination of the two had no significant effect on blood glucose levels. However, the urine protein excretion levels significantly decreased for the three drug treatment groups; the most dramatic decreases were observed in the combination treatment group. Kidney histology was examined using periodic acid-Schiff staining and immunohistochemical staining of extracellular matrix proteins. Results indicated that histopathology improved markedly in the three drug treatment groups; combination therapy had an equal or better effect than monotherapy in terms of decreasing the abnormal thickness of the glomerular basal membrane, the ratio of the area of the mesangial region with respect to the total area of renal glomeruli, and the accumulation of collagen IV and laminin in kidney tissue. In addition, serum levels of transforming growth factor-β1 (TGF-β1) also markedly decreased in the drug treatment groups according to ELISA. However, there were no significant differences between the combination therapy group and monotherapy group. These results suggest that a combination of valsartan and LMWH at half the dose used in monotherapy is better at improving glomerular permeability in rats with diabetic nephropathy.

ACTN4 Gene Mutations and Single Nucleotide Polymorphisms in Idiopathic Focal Segmental Glomerulosclerosis

Aim: To investigate the association between mutations or single nucleotide polymorphisms (SNPs) of the gene ACTN4 in Chinese patients with idiopathic focal segmental glomerulosclerosis (FSGS). Materials and Methods: Genomic DNA of 82 Chinese idiopathic FSGS patients and 70 healthy people were used to analyze ACTN4 gene mutations by polymerase chain reaction, direct sequencing and GenBank matching. Hair follicle DNA of novel mutated patients’ parents were sequenced and α-actinin-4 expression in patients’ kidney was examined by immunofluorescence. For SNPs, after the Hardy-Weinberg equilibrium test, allele association and the frequencies of genotypes were analyzed, followed by association analysis between genotypes and clinical diagnosis. Results: We found a heterozygous candidate mutation 184T>A (S62T) in 1 patient and a 5′ UTR candidate mutation 1-34C>T in another patient. Both patients had non-nephrotic syndrome FSGS with reduced kidney α-actinin-4 expression. Promoter activity analysis suggests that the 1-34C>T candidate mutation may affect the transcriptional regulation of ACTN4 gene. Additionally, 6 novel silent variants and 2 novel SNPs were also found in this study. Novel SNP 484 + 87C>G had a significant association with the level of urine protein excretion in these idiopathic FSGS patients. Conclusions: Our data suggest that mutations and SNP of ACTN4 gene may contribute to be associated with Chinese idiopathic FSGS.

Therapeutic Effect of Y-27632 on Chronic Allograft Nephropathy in Rats

Chronic allograft nephropathy (CAN) is a major cause of late allograft loss. Recent evidences suggest that Rho and its downstream effector ROCK may be greatly involved in the progression of renal fibrosis. Inhibition of Rho/ROCK pathway might interact with the inflammatory process in the renal interstitium, and antagonize the process of epithelial-to-mesenchymal transition (EMT). We hypothesized that Y-27632 could inhibit the chronic inflammatory process and prevent the progression of CAN. Fisher (F344) kidneys were orthotopically transplanted into Lewis rat recipients. Lewis to Lewis rat kidney transplantation was served as the syngeneic control (Syn group). Allograft recipients were randomized and treated with either cyclosporine A alone (Allo group), or in combination with Y-27632 (30 mg/kg body weight/d intragastric, Y-27632 group). Renal function and urine protein excretion levels of the rats were analyzed. Animals were sacrificed 12 wk post-transplantation for histological and immunohistochemical studies, as well as analysis of the expression levels of chemokines, transforming growth factor (TGF-beta) 1 and alpha smooth muscle actin (alpha-SMA). Renal function deteriorated progressively in the Allo group, and there was typical CAN morphology in the kidneys. However, Y-27632-treatment significantly prevented the deterioration of graft function, lessened the level of urine protein excretion, and preserved the renal structure. Attenuation of ED1 positive mononuclear cell infiltration and amelioration of tubulointerstitial fibrosis were achieved by Y-27632 intervention. This was associated with down-regulation of the expression of tubular monocyte chemoattractant protein-1, RANTES (regulated upon expression normal T cell expressed and secreted), and phosphorylated NF-kappaB (which was a marker for activation). Profibrotic protein (TGF-beta1) and alpha-SMA, a marker of EMT, were significantly down-regulated by Y-27632 treatment as well. The Rho/ROCK pathway plays an important role in the progression of CAN, and specific inhibition of Rho activity by Y-27632 showed favorable effects on blocking renal interstitial inflammation and fibrosis, thus efficiently retarding the development of CAN, which might provide us with a novel strategy to improve long-term renal graft survival.

Proteinuria as a modifiable risk factor for the progression of non-diabetic renal disease

Angiotensin-converting enzyme (ACE) inhibitors reduce urine protein excretion and slow the progression of renal disease. The beneficial effect in slowing the progression of renal disease is greater in patients with higher urine protein excretion at the onset of treatment. We hypothesized that the greater beneficial effect of ACE inhibitors on the progression of renal disease in patients with higher baseline levels of proteinuria is due to their greater antiproteinuric effect in these patients. Data were analyzed from 1860 patients enrolled in 11 randomized controlled trials comparing the effect of antihypertensive regimens, including ACE inhibitors to regimens not including ACE inhibitors on the progression of non-diabetic renal disease. Multivariable linear regression analysis was used to assess the relationship between the level of proteinuria at baseline and changes in urine protein excretion during follow-up. The Cox proportional hazards analysis was used to assess the relationship between changes in urine protein excretion during follow-up and the effect of ACE inhibitors on the time to doubling of baseline serum creatinine values or onset of end-stage renal disease. Mean (median) baseline urine protein excretion was 1.8 (0.94) g/day. Patients with higher baseline urine protein excretion values had a greater reduction in proteinuria during the follow-up in association with treatment with ACE inhibitors and in association with lowering systolic and diastolic blood pressures (interaction P < 0.001 for all). A higher level of urine protein excretion during follow-up (baseline minus change) was associated with a greater risk of progression [relative risk 5.56 (3.87 to 7.98) for each 1.0 g/day higher protein excretion]. After controlling for the current level of urine protein excretion, the beneficial effect of ACE inhibitors remained significant [relative risk for ACE inhibitors vs. control was 0.66 (0.52 to 0.83)], but there was no significant interaction between the beneficial effect of ACE inhibitors and the baseline level of urine protein excretion. The antiproteinuric effects of ACE inhibitors and lowering blood pressure are greater in patients with a higher baseline urine protein excretion. The greater beneficial effect of ACE inhibitors on renal disease progression in patients with higher baseline proteinuria can be explained by their greater antiproteinuric effects in these patients. The current level of urine protein excretion is a modifiable risk factor for the progression of non-diabetic renal disease. ACE inhibitors provide greater beneficial effect at all levels of current urine protein excretion.

Factors predictive of outcome in severe lupus nephritis

In 1992, we published the results of a prospective, controlled trial of aggressive therapy (high-dose prednisone plus oral cyclophosphamide alone or with plasmapheresis) in 86 patients with severe lupus nephritis. During this study, remission (serum creatinine ≤1.4 mg/dL [≤123 μmol/L] and proteinuria ≤330 mg/d of protein) in renal disease occurred in 37 patients (43%). To assess the long-term effect of remission on patient and renal survival, we now report the results of our extended follow-up of these patients. After an average of 10 years of follow-up in the 86 patients, patient survival rates at both 5 and 10 years were 95% in the group that had a remission and 69% at 5 years and 60% at 10 years in the no-remission group (P < 0.001). Renal survival rates were 94% at both 5 and 10 years in the remission group compared with 46% at 5 years and 31% at 10 years in the no-remission group (P < 0.0001). Features predictive of remission included stable renal function after 4 weeks on therapy, category IV lesion, lower chronicity index, white race, lower urine protein excretion level at baseline, and lower baseline serum creatinine level. The features predictive of end-stage renal disease were higher baseline serum creatinine level, presence of anti-Ro antibodies, and failure to attain a remission. Thus, in patients with the most severe forms of lupus nephritis, a remission of clinical renal abnormalities is associated with dramatic improvement in long-term patient and renal survival.

Cigarette smoking is associated with augmented progression of renal insufficiency in severe essential hypertension

Hypertension-associated renal disease is a major cause of end-stage renal disease (ESRD) in the United States, but its risk factors remain incompletely defined. Identification and correction of amendable ESRD risk factors among patients with essential hypertension could reduce ESRD prevalence. Patients referred by their primary care physician for hypertension management to an academic nephrology clinic during calendar year 1995 were followed up prospectively. Studied patients had no evidence of secondary hypertension, diabetes, or primary renal disease. All were treated pharmacologically toward a target mean blood pressure (MBP) of 100 mm Hg or less. The course of renal function during follow-up was assessed as the slope of the reciprocal of plasma creatinine concentration (1/Pcr ) plotted against months of follow-up and as the change in calculated glomerular filtration rate (GFR) in milliliters per minute per month. The following patient characteristics were prospectively examined as possible predictive factors for altered renal function: age, sex, ethnicity, initial MBP, initial Pcr level, initial level of urine protein excretion, and smoking status. Fifty-three patients were enrolled, and follow-up data were available for 51 patients after a mean follow-up of 35.5 months. Despite MBP reduction from 126.8 ± 1.3 to 96.5 ± 1.1 mm Hg (P < 0.0001), Pcr level increased from 1.5 ± 0.1 to 1.9 ± 0.2 mg/dL (P < 0.01). Multivariate regression analysis showed that smoking, greater initial Pcr level, and black ethnicity were the only examined parameters that independently predicted both a decrease in the 1/Pcr slope and calculated GFR with at least 95% confidence. Smoking was by far the most powerful of the examined factors, with initial Pcr and ethnicity being much less predictive. These studies show for the first time that smoking is an independent risk factor for renal function decline in patients with severe essential hypertension.

Microalbuminuria and cardiovascular risk.

The term 'microalbuminuria' has been introduced to describe a measurable increase in urine albumin excretion, which is still within normal total urine protein excretion levels. Many data suggest that microalbuminuria is of value as an index of vascular damage, especially in hypertension and diabetes, and there is increasing information on its associations with traditional cardiovascular risk factors and its prognostic value. The association between microalbuminuria and peripheral markers of endothelial damage or dysfunction, such as von Willebrand factor, suggests the possibility that microalbuminuria may be a simple, cheap and easy index of endothelial abnormalities in cardiovascular disease. Nevertheless, further information on the value of microalbuminuria in other atherosclerotic vascular complications, such as ischaemic heart disease, stroke and peripheral artery disease is still needed.

Enhanced glomerular prostaglandin formation in experimental membranous nephropathy

To determine whether the induction of immune-mediated glomerular injury influences the formation of cyclooxygenase products by glomerular cells, we determined prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) (as the stable metabolite of TXA2) formation in isolated glomeruli of rats with passive Heymann nephritis (PHN). PHN is a model of membranous nephropathy mediated by antibody and complement independent of inflammatory cells. Five days following induction of PHN by injection of heterologous antibody to rat proximal tubular brush border antigen (Fx1A) rats developed proteinuria 36.5 +/- 34 (controls 3.8 +/- 1 mg/day). Treatment with cobra venom factor, which depleted complement C3 levels to less than 10% of baseline, prevented the development of proteinuria (6.9 +/- 2 mg/day). The development of subepithelial, glomerular immune-complex deposits and proteinuria was associated with a significant stimulation of glomerular PGE2 (87%) and TXB2 (183%) formation. This increment in glomerular prostanoid biosynthesis was significantly inhibited (PGE2 increased 22%, TXB2 increased 75%) in animals that were complement depleted with cobra venom factor. Cobra venom factor had no effect on glomerular prostanoid formation in normal rats. In additional experiments we tested the hypothesis that TXA2 may contribute to mediation of proteinuria in PHN. We utilized a thromboxane synthetase inhibitor UK38485. UK38485 reduced glomerular TXB2 formation by 80% without influencing glomerular deposition of 125I-labeled antibody, and did not alter levels of urine protein excretion in rats with PHN (control 42 +/- 21, UK 38485, 39 +/- 24 mg/day, P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Focal glomerular sclerosis: contrasting clinical patterns in children and adults.

In a retrospective clinicopathological study, 48 kidney biopsy specimens from 16 children (mean age, 7 years) and 17 adults (mean age, 33 years) with histological evidence of focal glomerular sclerosis (FGS) were examined using light, immunofluorescence and electron microscopy. The histopathological findings were related to the clinical course of each patient. At the clinical onset of the disease, the nephrotic syndrome was seen more commonly in children (12/16) than adults (7/17), while the incidence of both hypertension (children 1/16 versus adults, 9/17) and renal insufficiency (children, 0/16 versus adults, 7/17) was greater in adults. Despite a shorter average follow-up, (adults 3 10/12 years versus children, 7 years), the incidence of hypertension (adults, 13/17 versus children, 7/16) and renal functional impairment (adults, 13/17 versus children, 3/16) remained greater in the adult patients. One child and three adults died in renal failure while two adults underwent transplantation and on requires regular dialysis therapy. Nine of 15 pediatric patients treated with corticosteroids experienced partial or complete remission in either their nephrotic syndrome or level of urine protein excretion, while just 3 of 6 adult patients treated with corticosteroids experienced a partial remission, but never became protein-free. There was an excellent correlation in all patients between the degree of functional renal impairment and the extent of glomerular and nonglomerular histopathological damage in the kidney. It is concluded that in the adults, FGS represents a more severe and progressive disease process and is less responsive to therapy.