Pattern Of Proteinuria Research Articles

Characterization of proteinuria in asymptomatic family members and household contacts of children with hepatitis B virus-associated membranous nephropathy

The biosocial background in which the hepatitis B virus (HBV) carrier state with membranous nephropathy (MN) develops was studied by evaluating HBV carriage and proteinuria among 195 family members and household contacts of 31 index HBV carrier children with MN. Unrelated individuals from the communities of these index cases who were negative for HBV served as controls (n = 123). HBV was determined by using third-generation enzyme-linked immunosorbent assay, slot-blot hybridization, and nested polymerase chain reaction. Patterns of proteinuria were determined by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis; immunoglobulin G and haptoglobulin were suggestive of MN. Seventy-two members (36.9%) of the study group (n = 195) were HBV carriers; 21 of these carriers (29.2%) had proteinuria. Twenty-eight members (41.2%) of the study group who were HBV negative (n = 68) and 26.8% of the controls showed proteinuria. This lack of association between HBV carriage and proteinuria remained when controlled for sex and family relationship. HBV was not protective against the development of proteinuria. Proteinuria suggestive of MN was strongly associated with an abnormal protein-creatinine ratio (P: = 0.001), but was not significantly different between subjects and controls (8.7% versus 6.5%; P: = 0.5). Genetic influences or environmental exposures in these subjects may be responsible for the proteinuria, suggesting underlying glomerular basement membrane damage. Discordance between the HBV carrier state and patterns of proteinuria in the study group suggest that HBV and MN may not be causally related or may reflect exceptional interaction between specifically vulnerable individuals and HBV.

Characterization of proteinuria in primary glomerulonephritides: Urinary polymers of albumin

In 142 patients with primary glomerulonephritis (GN), there were polymers of albumin (PAs) in the urine samples of 87% of 15 minimal-change disease (MCD) patients, 52% of 27 focal segmental glomerulosclerosis (FSGS) patients, 51% of 47 membranous glomerulonephritis (MGN) patients, 55% of 20 membranoproliferative glomerulonephritis (MPGN) patients, and 9% of 33 immunoglobulin A nephropathy (IgAN) patients (P = 0.000). In IgAN, only three patients with nephrotic syndrome were PA positive. The PAs were significantly correlated with nephrotic syndrome (NS) (P = 0.000) and with the degree of proteinuria, ranging from 8% in patients with proteinuria less than 0.5 g/d to 58% in patients with proteinuria ≥ 15.0 g/d (P = 0.001), but 40% of the nephrotic syndrome patients were PA-negative despite values of proteinuria comparable to those of PA-positive patients, suggesting that the presence of PAs is not simply related to protein loss, but probably to some other unidentified factor or lesion. For 72 patients (43 with NS) (22 FSGS, 36 MGN, and 14 MPGN patients) with normal renal function at entry (serum creatinine, 1.02 ± 0.23 mg/dL) and a mean follow-up duration of 52 ± 27 months, for whom PAs were determined and urinary protein characterized by sodium-dodecyl-sulphate polyacrylamide gel electrophoresis (SDS-PAGE) at the beginning of the follow-up period, the functional outcome was correlated with the patterns of proteinuria. Chronic renal failure (CRF) developed in 24% of all 72 patients, in 36% of the PA-positive patients, in 9% of the PA-negative patients (P = 0.007), in 44% of the SDS-PAGE 10-kd mixed glomerulotubular pattern patients, and in 17% of the SDS-PAGE 23-kd mixed-pattern patients (P = 0.001). The association of PAs with the 10-kd pattern enhanced the predictive value for CRF outcome: CRF developed in 62% of the PA-positive patients with the 10-kd pattern compared with 11% of the PA-negative patients with the 23-kd pattern (P = 0.0001). CRF developed in 32% of 43 patients with the nephrotic syndrome, in 48% of the PA-positive patients, and in 11% of the PA-negative patients (P = 0.037); in 50% of the 10-kd patients and in 24% of the 23-kd patients (P = 0.007); and in 70% of the PA-positive patients with the 10-kd pattern and 14% of the PA-negative patients with the 23-kd pattern (P = 0.001). In a retrospective study of 21 treated patients (11 FSGS, nine MGN, and one MPGN patient), a response to therapy with complete or partial remission was observed in 57% of all 21 patients; in 58% of patients with the nephrotic syndrome; in 88% of the PA-negative patients versus 38% of the PA-positive patients P = 0.027); in 90% of the 23-kd patients versus 27% of the 10-kd patients (P = 0.004); and in 100% of the PA-negative patients with the 23-kd pattern versus 12% of the PA-positive patients with the 10-kd pattern (P = 0.001). In conclusion, urinary PAs are associated with GN characterized by lesions mainly localized in the glomerular capillary wall, with the presence of the nephrotic syndrome, and with the degree of proteinuria. In patients with FSGS, MGN, MPGN, and normal renal function at entry, the presence of polymers has a predictive value for CRF outome; this value is enhanced by the contemporaneous presence of an SDS-PAGE proteinuric pattern with low molecular weight proteins up to 10-kd, which is known to be associated with diffuse tubulointerstitial lesions. Therefore, the best predictive value for either CRF outcome or for response to therapy was provided by a combination between a marker associated with the degree of proteinuria and the types of GN characterized by lesions mainly localized in the glomerular capillary wall and a marker associated with tubulointerstitial damage (SDS-PAGE mixed glomerulotubular pattern with low molecular weight proteins between 20 and 10 kd).

Cellular and molecular predictors of chronic renal dysfunction after initial ischemia/reperfusion injury of a single kidney.

Initial ischemia/reperfusion injury occurring secondary to organ retrieval, storage, and transplantation has been associated with late renal allograft deterioration and failure. In addition, there is an apparent synergy, reported in several clinical series, between the initial injuries of ischemia/reperfusion and acute rejection; the long-term results of graft survival are significantly deceased after both events in combination as compared with either alone or if no such episodes occur. In the present study, we examined patterns of proteinuria, cellular infiltration, cytokine expression, and glomerulosclerosis over time in Lewis and Fischer 344 rats after 45 min of warm ischemia of a single kidney and with or without contralateral nephrectomy. Both early (4 hr to 7 days) and late (2-52 weeks) events were studied serially in the affected kidneys morphologically, by immunohistology and by reverse transcriptase polymerase chain reaction. Intercellular adhesion molecule 1, endothelin, and major histocompatibility complex class II expression were up-regulated within 2 to 5 days after injury; T cells and macrophages increased transiently. Proteinuria developed after approximately 8 weeks only in animals bearing a single injured kidney, and not in those with a retained native organ. Progressive morphological changes occurred after 16 weeks, including glomerulosclerosis, arterial obliteration, and interstitial fibrosis. After a period of relative quiescence, expression of intercellular adhesion molecule 1 again increased in relation to progressive macrophage infiltration and their associated products, particularly, interleukin 1, tumor necrosis factor-alpha, transforming growth factor-beta, and inducible nitric oxide synthase. Monocyte chemotactic protein 1 was intensely up-regulated by 24 weeks, coincident with a dramatic rise in this infiltrating population. These changes remained virtually at baseline in animals with a retained native kidney. These data imply that chronic injury after significant initial ischemia and reperfusion occurs when there is already a 50% renal mass reduction, but not when two kidneys remain in place. Permanent nephron loss resulting from such an insult could account for this phenomenon. Early ischemia and reperfusion, if severe enough in a single kidney, may be an important antigen-independent risk factor for later renal deterioration and failure. In the context of a renal allograft, it may contribute to chronic rejection.

Pattern of proteinuria in IgA nephropathy

Summary: Proteinuria is one of the bad prognostic indices in IgA nephritis (IgAN). This study compares the pattern of protein excretion in 10 patients with IgAN (IA) with that 5 years later (IB), when they developed renal impairment or hypertension. The pattern of proteinuria was analysed by SDS‐PAGE and isoelectric focusing (IEF) and assayed for orosomucoid, α‐1‐microglobulin, retinol‐binding protein, lysozyme, beta‐2‐microglobulin and N‐acetyl‐β‐D‐glucosaminidase activity. The data suggest that the changing pattern of proteinuria from IgA1 to IgA2 may reflect hyperfiltration as well as tubular injury.

Clinical Significance of Sodium Dodecyl Sulfate Polyacrylamide Gel Electrophoresis of Urinary Proteins in Preeclampsia

Objective: To establish the correlation between clinical and biochemical parameters and the urinary patterns of proteinuria detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS PAGE) in preeclampsia.Methods: 34 severe preeclamptics (BP ± 110 mm Hg diastolic and s= + + proteinuria) who were < 34 weeks gestational age were included in the study. Blood and urinary samples were obtained and the following tests performed: full blood count, serum urea, electrolytes and urates, 24-h proteinuria and creatinine clearance, and SDS PAGE.Results: The patients were divided into two groups depending on whether they excreted only albumin or both tubular and glomerular proteins as detected by SDS PAGE. There were no significant differences in maternal age, parity, gravidity, and gestational age between the groups. Systolic and diastolic blood pressures were significantly higher in those who excreted both glomerular and tubular proteins than in those who excreted albumin only: 173/116 versus 156/106 mm Hg; P = 0.0167. There were no statistical differences between the groups in relation to hemoglobin, platelets, urea, creatinine, or 24-h urinary protein and creatinine clearance values.Conclusion: The present study shows that SDS PAGE analysis of urinary proteins reveals two distinct patterns of proteinuria. Patients with mixed pattern (tubular and glomerular proteins) have higher blood pressure values than those who excrete albumin only. SDS PAGE appears to be a good noninvasive method of assessing severity of preeclampsia. It may be of value in identifying those patients who require postpartum renal biopsies.

Studies on Preventive Nephrology: Systemic Hypertension in the Pediatric and Adolescent Population of Gassim, Saudi Arabia

Casual blood pressure was recorded for subjects of Faizia East Primary Health District during a cross-sectional population survey. Valid information was obtained from 5671 subjects, out of which 3299 (1561 males and 1738 females) were between the ages of three and 18, constituting therefore the pediatric/adolescent (P/A) sector of our study population. The prevalence of hypertension (HPN), defined as A(3) 95th percentile for total HPN population (mild and severe) and A(3) 99th percentile for severe, was calculated for the three-year age cohorts suggested by the Task Force on Blood Pressure Control in Children (1987). The three subsets of HPN were derived from the suggested cut-off levels without any modifications. Overall prevalence of HPN was, for the P/A, found to be 10.65% (351/3299). Females in all the age cohorts were significantly more hypertensive than males, overall gender prevalence being 7.94% (124/1561) for males against 13.06% (227/1738) for females: P=0.0000019; CI: 0.45<OR7lt;0.73. One hundred and twenty-eight subjects (3.88%) had severe HPN, again with gender difference in favor of females (2.57 versus 5.06%), P=0.00022; CI: 0.33<OR<0.74). Sixty-seven and a half percent (237/351) of the HPN population were in the six to 12 year age group, with the significant gender difference persisting (P=0.000407; CI: 0.41<OR<0.74). Ninety-four of these (73.44%) had the severe HPN, with similarly significant gender difference (P=0.0018; CI: 0.31<OR<0.79). Significantly, 67% of gross proteinuria for the entire population has been found in the same age cohort with the same significant gender difference. ISHPN was found to constitute 51.57% (181/351) of the HPN population, followed by IDHPN with 32.48% (114/351) and S/DHPN the least with 15.95% (56/351). The significant gender difference in favor of females noted seems to be unique to the Saudi population. Similarly, the preponderance of ISHPN subsets is, to our knowledge, being recorded from the first time in literature. When coupled with the pattern of proteinuria, we believe that, in the context of preventive nephrology, greater attention will need to be devoted to the pediatric population, especially females.

The influence of angiotensin-converting enzyme inhibition on renal tubular function in progressive chronic nephropathy

The influence of angiotensin-converting enzyme (ACE) inhibition on renal tubular function in progressive chronic nephropathy was investigated in 69 patients by the lithium clearance (C Li) method. Studies were done repeatedly for up to 2 years during a controlled trial on the effect of enalapril on progression of renal failure. The pattern of proteinuria was followed over the first 9 months. At baseline, the glomerular filtration rate (GFR) was 5 to 68 mL/min. Absolute proximal tubular reabsorption rate of fluid (APR), estimated as the difference between GFR and C Li, was 1 to 54 mL/min. Calculated fractional proximal reabsorption (FPR) was moderately subnormal. During the study, GFR decreased and sodium clearance was unchanged; fractional excretion of sodium therefore increased. In the group of patients randomized to treatment with enalapril (n = 34), GFR at 1 month was 83% ( P < 0.001) and C Li was 88% ( P < 0.01) of the baseline values, APR and FPR had not changed significantly, and potassium clearance was significantly decreased. Through the rest of the study period, APR remained nearly unchanged and FPR even increased in the enalapril group. In the group of patients randomized to treatment with conventional antihypertensive drugs (n = 35), C Li was unchanged until severe reduction in GFR, APR and FPR decreased gradually, and potassium clearance was almost unchanged. These differences in tubular function between the two treatment regimens were significant ( P < 0.05). An unchanged or increased APR in either treatment regimen was associated with a long-term slower progression of renal failure. Over 9 months, the 24-hour fractional clearance of albumin decreased in the ACE inhibitor group ( P < 0.01), whereas the clearances of immunoglobulin G and retinol-binding protein were unchanged in this group. In the conventional group, the fractional clearances of these three plasma proteins all increased. It is concluded that in progressive chronic nephropathy ACE-inhibitor treatment was associated with different adaptive tubular changes in the handling of sodium, water, and protein compared with conventional antihypertensive therapy. During ACE inhibition, the reabsorptive capacity of the proximal tubule appeared to be better preserved, which might be of importance for the beneficial effect of this treatment in chronic renal disease.

Low molecular weight proteinuria in Chinese herbs nephropathy

Urinary excretion of five low molecular weight proteins (LMWP) [beta 2-microglobulin (beta 2m), cystatin C (cyst C), Clara cell protein (CC16), retinol-binding protein (RBP) and alpha 1-microglobulin (alpha 1m)], albumin and N-acetyl-beta-D-glucosaminidase (NAG) were quantified in 16 patients who followed a weight reduction program which included Chinese herbs, which have been incriminated in the genesis of Chinese herbs nephropathy (CHN). An additional group of four patients transplanted for CHN were investigated. Urinary data were obtained for comparison purpose in five groups of proteinuric patients: two groups with normal serum creatinine (SCr) and glomerular albuminura [12 patients with diabetes mellitus and microalbuminuria (DN), 10 patients with primary nephrotic syndrome (NS)]; two groups with normal SCr and toxic nephropathy [6 patients with analgesic (AN), 9 patients with cadmium nephropathy (CdN)]; and one group of seven patients with glomerular diseases and increased SCr (GN). Patients were classified according to serum level S beta 2m to take into account the possibility of overflow proteinuria at S beta 2m > or = 5 mg/liter. Three patients (CHN0) with a S beta 2m < 5 mg/liter, had a normal urinary protein pattern including NAG and a normal S beta 2m. Eight patients (CHN1) with a S beta 2m < 5 mg/liter had various abnormalities of their urinary protein pattern. In four of them (CHN1a) only beta 2m, RBP and CC16 were increased while total proteinuria and SCr were normal. In the other four (CHN1b and c) albumin, cyst C, alpha 1m and NAG were also elevated, while total proteinuria and SCr were moderately raised. Five patients (CHN2) with a S beta 2m > or = 5 mg/liter had a markedly increased excretion of all LMWP, albumin and NAG (CHN1 vs. CHN2, P < 0.05) as well as a further increase in total proteinuria and SCr. The urinary LMWP/albumin concentration ratio was strikingly higher in CHN patients than in patients with glomerular albuminuria (CHN1 vs. DN and NS, P < 0.01) or moderate renal failure with elevated S beta 2m level (CHN2 vs. GN, P < 0.01), confirming the existence of a tubular proteinuria independent of glomerular albuminuria or overflow proteinuria. A similar proteinuria pattern was present in the two toxic nephropathies (CdN and AN). This pattern was no longer recognizable after transplantation. In conclusion, CHN exhibits various profiles of tubular proteinuria which are the hallmarks of the disease. This pattern is still detectable in patients with renal failure and/or glomerular albuminuria. It is identical to that observed in cadmium and analgesic nephropathies. It does not recur after transplantation. Its most sensitive and reliable marker is a raised urinary level of CC16 or RBP.

Angiotensin I converting enzyme activity in uranyl nitrate induced acute renal failure in rats.

Angiotensin I converting enzyme (ACE) was measured in urine, serum, and tissues from rats with acute renal failure (ARF) induced by a single subcutaneous injection (15 mg/kg BW) of uranyl nitrate (UN). Urine was collected daily until day 5, when rats were sacrificed by decapitation for the obtention of blood serum and tissues. Other groups of rats were sacrificed on days 1 and 2. These rats showed proteinuria and polyuria. The damage to the kidney proximal tubule was shown by (a) histological analysis at light and electron microscopy levels on days 1, 2, and 5, (b) the increase in urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase on days 1-5, and (c) the low molecular weight proteinuria pattern on day 1. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance on days 1 and 2, but structural alterations on day 5. These data suggest that the increased urinary excretion of enzymes and proteins is a consequence of the tubular injury on days 1 and 2, and of tubular and glomerular injury on day 5. ACE activity increased in urine on days 1-5 and in serum on day 5. Tissue ACE activity increased in lung, small intestine, and adrenal glands; and remained unchanged in testis, aorta, brain, kidney, heart, and liver. Our data suggest that: (a) the increase in serum ACE may be secondary to the changes in tissue ACE activity, and (b) the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal tubule.

Angiotensin I converting enzyme in glycerol-induced acute renal failure in rats.

Angiotensin I converting enzyme (ACE) activity was measured in serum, urine, and tissues of rats with acute renal failure (ARF) induced by glycerol. Glycerol-injected rats were subdivided in three groups according to the urinary volume: oliguric, nonoliguric, and polyuric. The damage to the proximal tubule was evident by (a) the histological analysis at light and electron microscopy level, (b) the augmented urinary excretion of the enzymes dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase, and (c) the low molecular weight proteinuria pattern. On the other hand, the appearance of the glomeruli at the ultrastructural level was normal. These data suggest that the increased urinary excretion of enzymes and proteins in these rats is a consequence of the tubular injury. ARF was markedly higher in the oliguric rats. Urine ACE activity increased in the rats of the three groups, but statistical significance was reached only in the oliguric rats. Serum ACE activity increased in the oliguric rats and tissue ACE activity did not change. It is concluded that the high urinary ACE in glycerol-treated rats is associated with the damage to the kidney tubules. These data support the contention that urinary ACE may be another marker of injury to the proximal tubule.

Sodium dodecyl sulphate polyacrylamide gel electrophoresis of urinary proteins in steroid-responsive and steroid-resistant nephrotic syndrome in children.

Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS PAGE) of urinary proteins was performed in 56 children with nephrotic syndrome during relapse, of whom 31 had their urines tested within 2 months of the onset of disease. The urines of all 32 steroid-sensitive [presumed minimal change nephrotic syndrome (MCNS)] patients revealed albumin and transferrin bands only; whereas 19 steroid-resistant children with focal glomerular sclerosis showed additional excretion of IgG and low molecular weight proteins (lysozyme, beta 2-microglobulin). This mixed pattern of proteinuria was also detected in 5 other steroid-resistant patients, 3 of whom were Africans with MCNS on biopsy and 2 who were Indians and not biopsied. Findings in patients studied within 2 months of presentation were identical to those investigated later in the course of the disease. SDS PAGE analysis of urine, which appears to distinguish steroid-responsive from steroid-resistant patients may provide a valuable adjunct to the management of childhood nephrotic syndrome.

Sodium dodecyl sulphate polyacrylamide gel electrophoresis patterns of proteinuria in various renal diseases of childhood

This study examined the potential of an automated electrophoretic system (PHASTSYSTEM, Pharmacia. Uppsala, Sweden) to distinguish patterns of proteinuria in children with various renal diseases. It proved possible to produce ready-to-read sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS PAGE) separation of 1 microliter of unconcentrated urine in 2 h. Glomerular, tubular and mixed patterns of proteinuria were identified. Steroid-responsive nephrotic syndrome (SRNS) was readily identified by strong bands of albumin and transferrin during relapses. In contrast, steroid-resistant nephrotic syndrome was associated with two additional bands of haptoglobin and IgG. Albumin dimers (Mr 120 kDa) were found in the active phase of the disease in the urine of 90% of children with SRNS. Patterns of tubular proteinuria were found in children with proximal renal tubular abnormalities. The presence of mixed patterns of glomerular and tubular proteinuria strongly suggest renal insufficiency. SDS PAGE electrophoresis can readily be applied in clinical practice. It may prove helpful in the diagnosis and management of children with renal diseases enabling correlation to be made between proteinuria, renal pathology and prognosis.

Mechanism of cadmium-metallothionein-induced nephrotoxicity: relationship to altered renal calcium metabolism.

Prolonged cadmium exposure has been associated with proteinuria, calcuria and loss of calcium from bones in humans. Previous studies have shown that kidney uptake of cadmium in vivo results from proximal tubule absorption of the circulating cadmium metallothionein complex (CdMT), and intracellular release of the Cd2+ ion prior to induction of renal metallothionein. Parenteral administration of CdMT has been found to selectively damage the proximal tubule cell lysosome system with development of a tubular proteinuria pattern similar to that observed under chronic exposure conditions. The present studies also demonstrate a concomitant calcuria but no changes in the excretion of other electrolytes or glucose using this model. These marked changes in renal calcium metabolism occurred in the absence of mitochondrial damage, changes in total, Na/K or Mg-stimulated ATPase activities, renal ATP levels, membrane 45Ca2+ transport or overt tubule cell necrosis during an 8 hour period following CdMT injection. Proteinuria and calcuria were prevented by prior zinc induction of the renal MT pool. Data from these studies indicate that renal proximal tubule cell uptake and degradation of the circulating CdMT complex produces both a marked proteinuria and calcuria. The calcuria does not appear to stem from changes in renal energy metabolism or membrane transport of this element but is probably a secondary result of calcium binding to excreted proteins which are increased in urine to a similar extent. The studies also suggest that zinc status and maintenance of the renal ZnMT pool may play an important role in regulating cadmium-induced renal proteinuria and calcuria by preventing Cd2+ perturbation of the proximal tubule cell lysosome system.

Prednisone-induced fluctuations of proteinuria in patients with a nephrotic syndrome.

We studied the effect of prednisone on urinary protein excretion in 19 patients with a nephrotic syndrome, who were treated with prednisone (125-150 mg) on alternate days. We found a typical, fluctuating pattern of proteinuria resulting from an increased protein excretion rate on prednisone days and a decreased protein excretion rate on nonprednisone days. The urinary protein excretion on prednisone days was 9.9 +/- 3.3 g/24 h, as compared to 5.7 +/- 3.8 g/24 h on nonprednisone days (mean +/- SD). In the whole group of patients the percentual change in proteinuria was significantly correlated with the endogenous creatinine clearance. However, systematic differences between creatinine excretion rates on prednisone and nonprednisone days were not found in individual patients. In 6 patients, renal hemodynamics were studied more precisely, using a single injection technique. Only a slight and nonsignificant decrease in glomerular filtration rate was found on nonprednisone days (delta = -9.6 +/- 16.3%; mean +/- SD). Filtration fraction remained unchanged. It is therefore suggested that the effects of prednisone on proteinuria are not simply mediated by overall changes in renal hemodynamics.

Proteinuria, hematuria, and leukocyturia in children with mixed urinary and intestinal schistosomiasis

Quantitative parasitological assessment and quantitative analysis of proteinuria, hematuria, and leukocyturia were carried out in 182 Sudanese schoolboys with mixed urinary and intestinal schistosomiasis. Pathological proteinuria was found in 73% of patients (median = 380, 95% confidence limits = 200 to 500 mg/liter). The median protein/creatinine ratio was 0.54. SDS polyacrylamide gel electrophoresis showed an excretion of albumin, transferrin, and IgG consistent with a postrenal pattern of proteinuria. Pathological erythrocyturia occurred in 84% of patients (median = 255, 95% CL = 95 to 629 cells/microliter) and leukocyturia in 77% of patients (median = 148, 95% CL = 93 to 246 cells/microliter). Phase contrast microscopy revealed intact erythrocytes, suggestive of postrenal hemorrhage. Proteinuria, erythrocyturia, and leukocyturia correlated significantly with the ova excretion in the urine, but not with egg excretion in the stool. Oxamniquine reduced ova excretion in the stool but did not influence pathological urine findings. In patients treated effectively with Praziquantel or Metrifonate, pathological PU, EU, and LU decreased markedly 1 month post treatment. PU in severely proteinuric patients reached physiological values 5 months post therapy. We suggest that the proteinuria, erythrocyturia, and leukocyturia in mixed schistosomiasis were of postrenal origin.

1229 GEL ELECTROPHORETIC(GE) ANALYSIS OF PROTEINURIA IN PATIENTS WITH INSULIN DEPENDENT DIABETES MELLITUS (IDDM)

Clinically significant proteinuria indicates a poor renal prognosis in IDDM patients. Microalbuminuria presages worsening proteinuria. Other techniques to evaluate proteinuria may allow an earlier prediction of nephropathy in time to use aggressive therapy to alter morbidity. We analyzed the patterns of proteinuria in 14 IDDM patients (compared with 8 controls) by a novel protocol utilizing spot (random, resting, single void) urines. All patients had < 1 gm/day proteinuria. Diabetic patient characteristics(diab indices): ages 3-24, duration diabetes 1.5-16 yrsf mean HgbA1c(mHA) 4.6-8.6%(nl<4.8%), current HgbA1c 3.4-10.9%. Spot urines were: obtained sterilely, mlcropore filtered, dialyzed, lyophylized, subjected to sodium dodecyl sulphate polyacrylamide GE, stained with Coomassie Blue and then analyzed by an automatic gel scanner/integrator. Peaks were grouped into the following fractions: %albumin(alb), %high molecular weight(haw,>alb>, %low molecular weight(1mw, <alb). The protein to creatinine ratio (p/c) was also determined for each specimen. Fractional ratios were obtained by aultiplying each fraction(%) by p/c yielding: hmw/c, alb/c, 1mw/c.Total p/c and 1mw/c are significantly increased in diabetics with normal creatinine clearances. Multiple regression analysis was performed on the diabetic data; fractional ratios were regressed against all the diab indices. Although none of the correlations reached statistical significance, there was a trend toward higher fractional ratios with increasing age and mHA. The ease of acquisition of spot urine samples, the significant elevation of p/c in diabetics and the trends relating to glucose control makes further exploration with a larger, more heterogeneous sample appear promising.

Evaluation of Proteinuria by Two-Dimensional Polyacrylamide Gel Electrophoresis after Kidney Transplantation

Urinary proteins were studied in patients after kidney transplantation during various functional states (normal function, acute rejection, chronic rejection) by two-dimensional polyacrylamide gel electrophoresis. In the first dimension, the proteins were separated according to their electric charge by isoelectric focusing, and in the second dimension according to their molecular weight by sodium dodecyl sulfate polyacrylamide gel electrophoresis. After electrophoresis the proteins were visualized using a highly sensitive silver stain technique. The combination of these methods allowed the discrimination of up to 250 protein spots in human urine, most of them unidentified up to now. Functional changes of the kidney transplants were accompanied by complex changes of the protein pattern in urine. These changes cannot be simply compared to the tubular and glomerular pattern of proteinuria which can be identified by one-dimensional sodium dodecyl sulfate electrophoresis. The 2D electrophoresis of urinary proteins may develop into a useful tool in localizing of kidney damage and in the evaluation of renal disease.

The patterns of proteinuria in diabetes mellitus. Relevance to pathogenesis and prevention of diabetic nephropathy.

The patterns of proteinuria in diabetes mellitus. Relevance to pathogenesis and prevention of diabetic nephropathy.

Comparison of tubular proteinuria, using sodium dodecyl sulphate polyacrylamide gel electrophoresis, in patients during methotrexate or aminoglycoside treatment or with cadmium or Balkan nephropathy

The pattern of proteinuria found in patients during the administration of methotrexate (MTX) or aminoglycosides (AG) and in cadmium or Balkan nephropathy was investigated using the technique of sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). As renal tubular dysfunction increased, measured by the urinary concentration of 4 low molecular mass (L M r) proteins, SDS-PAGE bands appeared in the following order of molecular mass ( M r): 59, 44, 31, then below 31 000. The presence of bands < 31 000 was not an early indicator of drug-induced renal damage. Tubular proteinuria could be monitored more easily by the serum and urinary measurement of any one of the L M r proteins: α-1-microglobulin (α1m), retinol-binding protein (RBP), β-2-microglobulin (β2m), except α-1-acid glycoprotein (AGP), than by SDS-PAGE.

An evaluation of renal function in workers occupationally exposed to mercury vapour.

The renal function of a population of workers occupationally exposed to mercury in the chlor-alkali industry has been examined and compared to that of a population of workers with no occupational exposure to mercury. Measurement of specific urinary proteins and enzymes have been carried out on each individual on three separate occasions and have been complemented by blood plasma measurements at the final visit. Under the conditions of exposure to mercury sustained in this study, there is no evidence of an increased prevalence of renal dysfunction as indicated by enzyme and protein measurements. The urinary concentration of the low molecular weight protein, beta 2-microglobulin, is significantly lower in the mercury-exposed group than in the control group. In contrast to recently published literature, no relationship is seen between urinary mercury concentration and the appearance of high molecular weight protein in urine. A small increase in the prevalence of higher activities of the urinary enzyme N-acetyl-beta-glucosaminidase and gamma glutamyl transferase is observed when the urinary mercury concentration exceeds 100 micrograms/g creatinine. A small increase in the prevalence of raised urinary N-acetyl-beta-glucosaminidase activity is observed when the duration of exposure to mercury exceeds ten years. The pattern of proteinuria has been characterised in a total of sixteen individuals from both populations; a low molecular weight proteinuria is seen in three individuals from the control group whilst a high molecular weight proteinuria is seen in the remainder (seven in the control and six in the mercury group).