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PubMed1976

Blood pressure, edema and proteinuria in pregnancy. 6. Proteinuria relationships.

1. The blood pressures of pregnant patients with proteinuria seem to be no higher than the levels of blood pressure in patients with no proteinuria. The presence of proteinuria and pregnancy in the absence of blood pressure elevation increases perinatal mortality above the values where blood pressure elevation occurs alone. This relationship is most prominent among nulliparous median-age pregnant patients. Even though the number of patients is small, the highest rates occur in the young white nullipara from the sixteenth to twenty-third week of pregnancy. Attempts to compare black and white median-aged nulliparas are meaningless because of the tremendous variability of data. 2. The findings in all cohorts with proteinuria were essentially the same as those in Cohorts I, II and III. Proteinuria of 2+ or greater occurs more frequently in black than in white gravidas. 3. Our observations indicate that perinatal mortality rates in patients with proteinuria are, for the most part, at least twice the rates of patients without proteinuria. 4. The volume of data available is insufficient to determine whether proteinuria influences prematurity rates or mean birth weights. However, our data suggest that some vascular or renal lesion must be affecting perinatal mortality. 5. The small number of patients in the proteinuria study group does not permit meaningful comparisons with the patient group presenting no edema or proteinuria. 6. Adherence to suitable criteria for discovering and measuring proteinuria is necessary to make the diagnosis of preeclampsia. These criteria include careful collection of urine in the clinic or hospital, utilization of acceptable standard testing methods, and the application of uniform principles of medical practice to the overall care of obstetric patients. 7. The data are presented, not interpreted. However, we cannot discount the value of the present data in suggesting the urgent need to restudy more of the current data available. It also seems desirable to initiate another program to investigate a smaller group of patients made up of the same sequential cohorts where it may be possible and more practical to apply strict supervision of statistical design, patient care, personnel, laboratory testing, data recording, data processing and reporting and statistical analysis.

Adolescent↗
PubMed1978

[Cholinesterase, arylesterase and proteinuria. A clinical trial in glomerular and tubular proteinuria (author's transl)].

A study is presented on the activity of cholinesterase (substrate acetylcholine) and of arylesterase (substrate phenylactate) in proteinuria, classified according to the results of electrophoresis of glomerular and tubular proteinuria. Comparison is made with the corresponding serum. The urine is concentrated by dialysis on polyethylene-glycol to 60 g protein per 1000 before determination of the activities. In the presence of equal quantities of protein, cholinesterase is slightly more active in glomerular than in tubular proteinuria. In selective glomerular proteinuria, cholinesterase and arylesterase are less active than in cases with little or no selectivity. Comparison with serum, in each individual case, indicates that the ratio of activity in concentrated urine to that in serum, is higher for cholinesterase and arylesterase in tubular than in glomerular cases, whereas the reverse is true in urine at its natural concentration, on account of the lower degree of proteinuria in tubular cases. The ratio of cholinesterase to arylesterase activity in concentrated urine and serum is determined. Since cholinesterase activity is greatly increased in glomerular cases (nephrosis) this ratio is on average markedly higher in glomerular proteinuria than in serum, whereas it is similar in urine and serum of tubular cases. These results, seen in the light of the molecular weights of the enzymes, are difficult to interpret with certainty, especially as regards tubular proteinuria.

Adult↗
PubMed1976

Blood pressure, edema and proteinuria in pregnancy. 7. Edema-plus-proteinuria relationships.

1. A total of 488 pregnancies had the combination of two-plus or more proteinuria and edema of the hands and face. Of these, 208 were white and 280 were black gravidas. In the white gravidas, 8 fetal and neonatal deaths occurred with a perinatal mortality of 38.5 per 1,000. There were 13 perinatal deaths in the black subgroup with a perinatal mortality rate of 46.4 per 1,000. The overall perinatal mortality rate was 43.0 per 1,000, which could be compared to the overall perinatal mortality rate of 32.8 per 1,000 for the segment of the study population without edema or proteinuria. This underscored the implication of increased hazard to fetal outcome of these clinical signs in combination. 2. The analysis of the matrix data showed scattered rates throughout gestation in white median-age nulliparas. Their black counterparts had comparable increased mortality rates. In the white multiparas of ages 20 to 34 years, the highest rates were found at relatively low blood pressure levels. The black median-age multiparas had rates associated with higher pressure readings, especially at or above 125/75. In teenage mulliparas with edema and proteinuria, perinatal mortality rates were similar for both subgroups and were found in somewhat lower blood pressures. 3. The incremental analysis was remarkable in that rates were scattered widely in the white subgroups, but tightly clustered in the black subgroups. The black median-age nulliparas had perinatal mortality concentrated about 115 to 134 mm. Hg systolic and 65 to 84 mm. Hg diastolic. The overall mortality rates of this subgroup were the highest of the subgroups studied. The black 20 to 34 year old multiparas had highest coassociated deaths in the 134-154 mm. Hg systolic levels throughout pregnancy. The clustering effect was most pronounced in black teenage nulliparas in both systolic and diastolic blood pressure groups at much lower levels. 4. The use of a critical cut-off blood pressure level of 125 mm. Hg systolic and 75 mm. Hg diastolic emphasized the combination factor effect, especially by the increased perinatal mortality rates in the black median-age subgroups of both nulliparas and multiparas. In the white median-age subgroups the rates were not uniformly affected. The teenage nulliparas as a group showed increased mortality rates with lower pressure levels in general. This was seen when the diastolic level was above 75 mm. Hg. 5. Perinatal mortality rates of nulliparas were increased by proteinuria and edema. This increase was great in the case of the 20 to 34 year old black nulliparas, particularly in association with increased blood pressure. Trends are not so apparent for the white median-age nulliparas. Nulliparas of 19 years of age or less have higher perinatal loss with edema and proteinuria, but this is not necessarily augmented with blood pressure elevation. This is notably so in teenage black nulliparas in the early periods of gestation and at term.

Adolescent↗
PubMed1990

[A study of proteinuria. (12) The incidence of the patients with proteinuria, microscopic hematuria and glycosuria in Fukuoka Dental College students in 1987 and 1988].

An investigation was made on the incidence of patients with proteinuria, microscopic hematuria and glycosuria in 757 (in 1987) and in 681 (in 1988) students of Fukuoka Dental College; and the results were as follows. 1) The incidence of patients with proteinuria was 6.3% (48/757) in 1987, and 6.9% (47/681) in 1988. 2) The incidence of patients with microscopic hematuria was 4.0% (30/757) in 1987, and 5.0% (34/681) in 1988. 3) The incidence of patients with glycosuria was 0.5% (4/757) in 1987, and 0.1% (1/681) in 1988. 4) Further medical examinations were made on 33 students in 1987, and 37 students in 1988. a) 27 students in 1987 and 34 students in 1988 were diagnosed as normal respectively. b) In three cases, clinical diagnoses could not be established without long-term observation and two cases were diagnosed as urinary tract infection and a case was diagnosed as possible chronic glomerulonephritis in 1987. c) In 1988, a case was diagnosed as urinary tract infection, a case was urethritis and a case should be needed a longterm observation.

Adult↗
PubMed1989

[Studies of enzymuria and proteinuria: Report 2; Relationship between glomerular filtration rate and urinary enzymuria and proteinuria].

Urinary splitting enzymes and proteins including N-acetyl-b-D-glucosanimidase (NAG), beta 2 microglobulin (beta 2MG), and alpha 1 microglobulin: (alpha 1MG), which are established to be useful in the evaluation of renal dysfunction, especially renal tubular impairment, were measured to determine the extent of renal tubular impairment in relation to the degree of glomerular dysfunction in patients with renal deterioration. In healthy volunteers, urinary NAG, alpha 1MG and beta 2MG levels were 3.5 +/- 1.4 (mean +/- SD) U/g creatinine, 2.5 +/- 2.0 mg/l and 88 +/- 75 micrograms/l, respectively. While serum beta 2MG level (SBMG; microgram/ml) was between 2.0 and 2.9, among the patients with renal dysfunction, NAG, alpha 1MG and BMG levels showed 8.6 +/- 5.5, 9.8 +/- 5.8 and 785 +/- 1,264, respectively, and further elevated to 10.1 +/- 5.0, 16.5 +/- 0.7 and 525 +/- 440, respectively with a SBMG level over 3.0. Thus glomerular function was deteriorated, urinary alpha 1MG level elevated to significantly higher with a parallel to renal dysfunction. In patients with more severe renal dysfunction, the corresponding urinary NAG and alpha 1MG levels became significantly higher. However, urinary beta 2MG level was significantly higher in patients with moderate renal dysfunction compared to healthy volunteers only when SBMG level was more than 2.0. Therefore, it was more valuable to measure urinary alpha 1MG with NAG or beta 2MG at SBMG level of less than 1.9 and to determine urinary NAG and alpha 1MG at greater than 2.0. These results indicated that the measurement of the levels of urinary splitting enzymes and proteins is valuable in the evaluation of proximal tubular impairment, even when the degree of glomerular impairment is minimal.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1991

Pattern of proteinuria in IgA nephritis by SDS-PAGE: clinical significance.

Of sixty patients with IgA nephritis, none had CRF at first examination, 13 developed CRF with creatinine above 1.6 mg/dl within 6 years. Among these patients who had analysis of proteinuria by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), 31 patients had middle molecular weight (MMW) proteinuria alone (pattern 1), 10 had MMW and Low MW (LMW) or tubular proteinuria (pattern 2), 10 had high MW (HMW) and MMW proteinuria (Pattern 3) and 9 had HMW, MMW and LMW proteinuria (Pattern 4). At the end of a follow up period of 6 years (1983-1989) patients with mixed proteinuria had a higher incidence of chronic renal failure (CRF), 11/29 (38%) compared to those with pattern 1 proteinuria, 2/31 (6%) (chi 2 = 8.7, p less than 0.005). Based on the glomerular selectivity index (GSI), 19 patients had nonselective proteinuria but they did not have a higher incidence of CRF. By the selectivity index (SI), 18 patients had nonselective proteinuria and they showed a significantly higher incidence of CRF. Compared to the 41 patients who did not have LMW proteinuria, 19 patients with LMW proteinuria had more severe proteinuria. After a follow-up period of 6 years, patients with LMW proteinuria had a higher incidence of CRF (10% versus 47%, p less than 0.001). The presence of LMW proteinuria indicates a less favourable outcome and the pattern of proteinuria as assessed by the SDS-PAGE appears to be a better prognostic index in IgA nephritis than the SI and the GSI.

Adult↗
PubMed1975

[Proteinuria in mature diabetic patients. Quantitative and qualitative analysis].

Proteinuria has been analysed in 334 maturity-onset diabetics and 80 matched controls. Proteinuria measured in the recumbent position exceeded 100 mug/min in 53% of the diabetic population. The percentage of excessive proteinuria increased with duration of the disease. Sex and age had no influence. Out of 55 first year diabetics, 49% had abnormal quantitative proteinuria; this is in contrast to 76 longterm diabetics (over 12 years) of whom 38% had proteinuria under 100 mug/min. Electrophoresis and immuno-electrophoresis showed a glomerular pattern in 40%, a tubular pattern in 15% and a mixed pattern in 8% of all the diabetics. 32% of the diabetics with quantitatively normal proteinuria were abnormal qualitatively, and this may be the first manifestation of diabetic nephropathy. Thirty-eight other patients had a normal electrophoretic pattern in spite of increased proteinuria. Proteinuria levels were significantly associated with hematuria, bacteriuria and reduced GFR, but not with leukocyturia, insulin dependence and hypertension. Upright position increased the proteinuria to a greater degree amongst the patients with normal proteinuria. We discuss the role of increased filtration pressure and glomerular permeability in modifying proteinuria in diabetes. Sensitive quantitative and qualitative proteinuria determinations are important tools both in early diagnosis of diabetic nephropathy in clinical practice and in epidemiological studies.

Adult↗
PubMed1991

Proteinuria in essential hypertension.

Proteinuria was estimated using modified biuret method in 100 consecutive essential hypertensives of both sexes with mean age of 40 +/- 0.9 (18-50 yr) attending hypertension clinic. Proteinuria (mg/1.73 M2/24 h) in 60 mild hypertensives ranged from 45.4 to 493.0 with 9 (15%) patients having abnormal proteinuria (greater than 250 mg). In 26 moderate hypertensives proteinuria ranged from 96-1010; 7 (27%) had abnormal proteinuria. The proteinuria in 14 severe accelerated, malignant hypertensives ranged from 146.5-6132.6 with 10 (71%) having abnormal proteinuria. Duration of hypertension had no correlation with the amount of proteinuria. The amount of proteinuria was much higher (P less than 0.001) in patients with renal insufficiency (1322.5 +/- 586.4) and in patients with grades III and IV hypertensive retinopathy. LVH on ECG also correlated positively with proteinuria. The group with abnormal proteinuria had more patients with LVH (42.3% vs 12.2%), severe hypertensive retinopathy (30.8% vs 4.1%) and renal insufficiency (34.6% vs 0%) as compared to patients without elevated proteinuria.

Adolescent↗
PubMed1990

Proteinuria in cyclosporine-treated renal transplant recipients.

Of 704 renal transplant recipients receiving long-term cyclosporine immunosuppression, 71 patients experienced proteinuria greater than 1 g/24 hr beyond the first month posttransplant. Eight patients displayed transient proteinuria, defined as lasting less than 3 months. In most cases this condition was attributed to biopsy-proved acute rejection. The transient proteinuria cohort experienced good graft outcome--namely, 87.5% one-year and 52.5% five-year actuarial graft survivals, which was similar to that observed in patients without proteinuria. In contrast, 52.4% of the 63 patients with nontransient proteinuria experienced graft loss within a median time of 6.1 months. The one- and five-year actuarial graft survivals in patients with nontransient proteinuria were 75.3% and 37.5%, respectively. Among the 63 patients with nontransient proteinuria, histopathologic diagnosis included chronic rejection in 19, transplant glomerulopathy in 14, acute rejection in 9, glomerulonephritis (GN) in 7 including 2 cases of membranous GN, and nonspecific interstitial fibrosis in 10 cases. Despite the overall poor prognosis for graft survival among the entire cohort of patients with nontransient proteinuria, the seven with allograft GN maintained prolonged graft function. They showed an 83.3% five-year actuarial graft survival versus 31.2% in patients with other causes of proteinuria (P = 0.043). These results suggest that posttransplant proteinuria in CsA-treated renal transplant recipients arises primarily as a consequence of allograft rejection and portends a poor graft outcome.

Cyclosporins↗
PubMed1991

Reactive oxygen metabolites cause massive, reversible proteinuria and glomerular sieving defect without apparent ultrastructural abnormality.

To identify the specific in vivo renal effect of reactive oxygen species (ROS), hydrogen peroxide (H2O2) was infused directly into the left renal artery in Munich-Wistar rats. H2O2 (5 to 50 mumol over 1 h) induced a dose-dependent increase in urine protein excretion rate in infused kidneys, reaching a maximum at the dose of 35 mumol (on average, a 60-fold increase from baseline). The H2O2 (35 mumol)-induced proteinuria peaked over 1 h and completely normalized by 24 h after the infusion. Electrophoresis revealed that the urine protein is primarily of glomerular origin. Fractional clearances of graded-size neutral dextran of larger molecular radii, an index of glomerular size selectivity, were significantly and substantially elevated immediately but normalized by 24 h after the infusion. GFR and RPF rate remained unchanged throughout the entire time course examined. The H2O2-induced proteinuria was largely prevented by pretreatment with catalase (20 mg, iv) or deferoxamine (30 mg/100 g body wt, iv). Thus, iron-dependent metabolites of hydrogen peroxide appear to be involved in this proteinuria and glomerular size-selective defect. Light and electron microscopy, including determination of anionic site density at lamina rara externa of glomerular capillary wall by polyethyleneimine staining, did not reveal any appreciable abnormality throughout the study period, including at the peak of proteinuria. Thus, ROS can cause massive, reversible proteinuria by inducing a molecular size-selectivity defect of the glomerular capillary wall without apparent ultrastructural abnormalities. The results raise the possibilities: (1) that persistent proteinuria of a variety of renal diseases may reflect persistence of pathogenic ROS acting on glomeruli because the potent proteinuric effect of ROS can be transient (2) that the light and electron microscopy abnormalities in glomeruli of ROS-induced renal injuries reported thus far may have no direct causal linkage to proteinuria; and, finally, (3) ROS-induced reversible proteinuria may relate to the mechanism of clinical functional proteinuria, which involves increased oxygen and ROS metabolism, e.g., exercise-induced proteinuria.

Animals↗
PubMed1989

Circadian rhythm of proteinuria: consequences of the use of urinary protein:creatinine ratios.

Proteinuria in patients with glomerular disease has a circadian rhythm, but for creatinine such a rhythm is either absent or of low amplitude. We found in 18 of 23 admitted patients (group I) and in seven outpatients (group II) a marked circadian rhythm of the protein: creatinine ratio. Estimates of 24-h proteinuria were obtained by multiplying the protein:creatinine ratio of 3-h urine samples with 24-h creatinine excretion, calculated from age, sex and bodyweight. Estimated proteinuria could be as low as 19% or as high as 349% of actually measured 24-h proteinuria; the mean SD was 23%. The best estimate was obtained with the 06.00-09.00 hours urine samples. The estimates correlated better with actually measured 24-h proteinuria than the protein: creatinine ratio per se correlated with the 24-h proteinuria. Day-to-day variation of proteinuria estimates from samples taken at the same time of the day was of similar magnitude as day-to-day variation of actual 24-h proteinuria. We conclude that the usefulness of the protein: creatinine ratio of a random urine sample for estimation of proteinuria is limited, because of the circadian rhythm of proteinuria. However, samples collected at a fixed time of the day are an acceptable alternative for 24-h urine collections in the clinical follow-up of individual patients.

Adolescent↗
PubMed1989

Current concepts in proteinuria.

Proteinuria, long recognized as a sign of renal disease, is a common laboratory abnormality in children and adults. Proteinuria may be transient or persistent; when persistent, the cause must be determined. Proteinuria may be primarily glomerular or tubular in origin. Glomerular proteinuria is usually an important concern. Tubular proteinuria often indicates the presence of tubulointerstitial or obstructive renal disease. Screening tests are available to detect albumin (the major protein in glomerular proteinuria), but there are no simple tests for immunoglobulin light chains and low-molecular-mass proteins, which predominate in overflow proteinuria and tubular proteinuria. These small proteins can only be detected by more sophisticated assays such as electrophoresis, isoelectric focusing, and chromatography. The association of glomerular and tubular types of proteinuria with specific disorders is reviewed in this paper, and current concepts in laboratory methodology for the study of proteinuria are summarized.

Humans↗
PubMed1977

Glomerular lesions in patients with asymptomatic persistent andorthostatic proteinuria discovered on routine medical examination.

The incidence of asymptomatic proteinuria in young healthy men entering the army service in Singapore was 0.94%; 0.56% had intermittent orthostatic proteinuria and 0.38% with persistent proteinuria. Renal biopsies from 45 cases with persistent proteinuria and 10 cases with orthostatic proteinuria were studied by light microscopy, electron microscopic and immunofluorescent antibody techniques. Three cases with orthostatic proteinuria showed a minimal lesion ('Nil'), and 7 a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity. Focal and segmental capillary loop changes were seen in two cases. No immunoglobulin deposits were found in orthostatic proteinuria. A raised anti-streptolysin O titer was found in 3 cases. 13.3% of cases with persistent proteinuria showed a minimal lesion ('Nil'); 66.6% a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity: Focal global sclerosis, focal segmental sclerosing glomerulonephritis and diffuse proliferative GN (mesangial hypercellularity) were each found in 6.7% of patients in this group. Focal and segmental changes in capillary loops were found in 30% of cases. Changes in visceral epithelium such as the appearance of cytoplasmic swelling, vesicles and dense aggregates, and areas of focal foot process fusion were common findings. Mesangial deposits of IgA were found in 34.3%, with an IgA-IgG-beta1C globulin combination in 28.6% of cases. IgM-beta1C globulin was present in 5.7% of cases with persistent proteinuria. Early complement components, C1q and C4, and IgA secretory piece were absent. A raised antistreptolysin O titer was found in 25% of cases. The changes inthe glomeruli may represent the end or healing stages of an early bout of glomerulonephritis. Changed hemodynamic responses on assuming an upright position may play a role in the loss of protein across the glomerular basement membrane in patients with orthostatic proteinuria.

Adolescent↗
PubMed1979

Diagnostic significance of SDS-PAA-electrophoresis of urinary proteins: different forms of proteinuria and their correlation to renal diseases.

Different types of urinary protein excretion may be recognized by determination of the proteins molecular weight. Beside chromatography different electrophoretic procedures have been applied to urinary proteins to study the underlying renal disease. The various zone electrophoreses separate merely by surface charge, proteins however covered by sodium dodecyl sulfate (SDS) migrate according to their molecular radius. So by SDS-polyacrylamide electrophoresis (SDS-PAe) macromolecular proteinurias (Mr 60,000- greater than 300,000 daltons) due to glomerular damage may be distinguished from micromolecular forms (Mr 10,000-70,000 d) due to tubular dysfunction. By densitometric quantitation of the separated Ig and transferrin an index of the glomerular selectivity is obtained, i.e. the capacity of the glomerular system, to retain serum proteins of a Mr above 150,000 d. By this procedure proliferative and degenerative glomerulopathies may be distinguished from minimal change disease, focal glomerular sclerosis and early membranous nephropathy; serial determinations of this selectivity index in the latter two disease entities show a gradual deterioration of glomerular protein handling with time. A glomerular proteinuria of even "physiological" quantity has been proved as early sign of renal involvment in systemic diseases; it may be detected earlier as for example the retinopathy in juvenile diabetics. Micromolecular proteinurias also occur at least in two forms: the typical tubular proteinuria (MW 10,000-70,000 d) is associated with acute or chronic severe tubular dysfunction as in interstitial nephritis and acute kidney failure; rejection episodes of kidney transplants lead to transient tubular proteinurias, too. The second form of micromolecular proteinuria (Mr 40,000-70,000 d) has been found frequently in association with a glomerular in diabetic and hypertensive glomerulosclerosis. By measuring clearances of the microproteins, the proteinuria with this pattern could be established as form independant from glomerular and tubular proteinurias. The constancy of the two micromolecular proteinurias led to the hypothesis of at least two selective mechanism of tubular protein resorption. SDS-PAe additionally allows the differentiation of extrarenal proteinurias, as caused by overflow, paraproteins, postrenal Ig-secretion or bleeding etc. In comparing clinical and in part histological data of about 2,000 patients suffering from kidney diseases the analysis of urinary proteins by this method has been proved as valuable non-invasive tool for diagnosis and follow-up.

Electrophoresis, Polyacrylamide Gel↗
PubMed1989

Sudden onset of proteinuria in chronic serum sickness in rats.

1. Daily intravenous administration of bovine serum albumin (BSA) to rats produces chronic serum sickness glomerulonephritis, an immune-complex-mediated renal disease that is eventually always fatal. We have performed a detailed study of the onset of proteinuria in chronic serum sickness in order to assess the long-term consequences of discontinuing daily BSA injections precisely at that very early and well-defined stage of disease. 2. Urine and plasma samples from rats receiving daily BSA injections were collected and analysed daily before the onset of proteinuria, at which time the rats were divided into three groups. Group 1 continued to receive daily BSA injections, in group 2 injections were stopped on the first, and in group 3 on the third, day of proteinuria. Proteinuria began suddenly and was not preceded either by microalbuminuria or abnormalities of plasma composition. The sudden expression of proteinuria was accompanied by an equally rapid development of hypoalbuminaemia and hypercholesterolaemia. Development of the characteristic glomerular histopathology of serum sickness coincided with, but did not precede, the onset of proteinuria. Despite the discontinuation of antigen injections at the onset of proteinuria, basement membrane thickening was evident 8 weeks later; proteinuria persisted and hypercholesterolaemia increased. 3. In this model of immune complex glomerulonephritis, changes in kidney function and immunopathology were abrupt and closely linked, precluding the use of those criteria to predict when proteinuria would begin. Furthermore, extremely brief periods of active immunological injury to the peripheral capillary wall were sufficient to produce persistent abnormalities of glomerular structure and function.

Animals↗
PubMed1990

Proteinuria and progression in human glomerular diseases.

Proteinuria is characteristic of many glomerular conditions, and often exceeds 2-3 g/24 h. There are several possible routes by which such profuse proteinuria might contribute to progression of the underlying pathology, whatever its type. First, proteinuria leads to a transit of protein through glomerular structures, including the glomerular capillary basement membrane, the mesangium and the epithelial cells, and to increased traffic of protein through the proximal tubules by pinocytosis of filtered protein. This traffic may be toxic to the cells concerned, and there is some evidence from 'overload' proteinuria induced in animals that this is so. Second, proteinuria leads to secondary hyperlipidemia with raised lipoproteins: mesangial cells have receptors for lipoproteins and in vitro, they are damaged by high concentrations, and there is evidence that hyperlipidemia leads to glomerulosclerosis. Third, proteinuria leads to hyperaggregability of platelets through alterations in plasma proteins, principally a fall in concentration of serum albumin and a rise in that of the von Willebrand factor, and possibly to increases in humoral coagulation cascades as well through losses of regulator proteins such as antithrombin III. There is evidence that anticoagulation and antiplatelet drugs will inhibit glomerulosclerosis in animals. Whether all or any of these mechanisms operate in human disease is not known; however, prognosis correlates well with duration and intensity of proteinuria in almost all proteinuric states and with the appearance and persistence of proteinuria in hematuric conditions. Therapies designed to reduce proteinuria per se may have a role in the treatment of glomerulopathies.

Animals↗