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At least 19 recordsLinked to original sources
PubMed2004

Clinicopathologic findings relevant to disappearance or relapse of proteinuria following corticosteroid treatment in IgA nephropathy patients with proteinuria of 0.5 to 2.0 g/day.

BACKGROUND: We investigated the clinical and pathological findings relevant to the efficacy of corticosteroid treatment in IgA nephropathy patients with 0.5 to 2.0 g/day of proteinuria at the initiation of corticosteroid treatment. METHODS: In 27 IgA nephropathy patients who received 2-year prednisolone treatment, we analyzed the differences in clinical and pathological parameters (1) between patients with and without disappearance of proteinuria (less than 0.15 g/day), and (2) between patients with and without relapse of proteinuria (more than 0.5 g/day) at the end of follow-up. RESULTS: The levels of proteinuria and mesangial proliferation at the initiation of prednisolone treatment were significantly lower in patients with disappearance of proteinuria at the end of follow-up than in those without. The levels of active extraglomerular lesions and tubulointerstitial mononuclear cell infiltration and/or fibrosis, and the activity index, were significantly higher in patients with relapse of proteinuria than in those without. CONCLUSIONS: In IgA nephropathy patients with 0.5 to 2.0 g/day of proteinuria, disappearance of proteinuria following 2-year prednisolone treatment can be expected in patients with less proteinuria and less mesangial proliferation at the initiation of the prednisolone treatment. Furthermore, active extraglomerular lesions, the activity index, and tubulointerstitial cell infiltration and/or fibrosis appear to be more suitable risk markers for relapse of proteinuria than the initial levels of proteinuria.

Adrenal Cortex Hormones↗
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↗
PubMed2006

Interpreting post-transplant proteinuria in patients with proteinuria pre-transplant.

Increasing numbers of patients receive kidney transplants before initiation of dialysis or shortly thereafter. Some of these patients have significant proteinuria pre-transplant making the interpretation of post-transplant proteinuria problematic. In this study, we evaluated post-transplant proteinuria in 115 patients who had urine protein measured within 3 months of transplant and assessed the association of proteinuria with allograft pathology. Proteinuria declined rapidly from 3650 +/- 3702 mg/day pre-transplant to 550 + 918 at 3 weeks (p < 0.0001) and continued to decline until 1 year post-transplant (472 +/- 1116, p < 0.0001 vs. 3 weeks). Proteinuria greater than 3000 mg/day was present in 48 patients (42%) pre-transplant, in 1 patient (1%) at 3 weeks and in 4 patients (4%) at 1 year. Surveillance graft biopsies were done at 1 year in 93% of patients. Proteinuria > or = 1500 mg/day and/or an absolute increase in proteinuria > 500 mg/day after 3 weeks post-transplant was associated with allograft glomerular pathology. In conclusion, pre-transplant proteinuria, even when high grade, declines rapidly after transplantation. Failure to decline or persistence of proteinuria greater than 1500 mg/day is indicative of allograft pathology.

Adolescent↗
PubMed2005

Analysis of allograft biopsy specimens in renal transplants with proteinuria: is proteinuria a culprit of graft loss?

It has been proposed that proteinuria occurring after renal transplantation may be not only a marker but also a culprit of allograft dysfunction. We retrospectively analyzed the data from 55 patients who underwent transplant renal biopsy for proteinuria and/or azotemia occurring beyond 1 year after transplantation. Proteinuria was considered as significant when > or = 30 mg/dL, and the results of transplant biopsy were categorized according to the Banff 97 classification. Logistic regression was used to estimate odds ratios (OR) for graft loss associated with proteinuria and transplant pathology. The patients were followed for 86.0 +/- 32.8 months after transplantation, and transplant biopsy was performed at 54.1 +/- 31.0 months. Proteinuria at 1 year after transplantation noted in 29.1% of patients was not significantly associated with graft loss (OR = 1.94, 95% CI from 0.59 to 6.41). In addition, proteinuria at the time of transplant biopsy was not significantly associated with graft loss. Chronic allograft nephropathy was the most frequent transplant pathology. Only glomerulonephritis was significantly associated with proteinuria at the time of the transplant biopsy. On the other hand, graft loss was significantly associated with the presence of proteinuria both at 1 year after transplant biopsy and at the final follow-up. These results suggest that posttransplantation proteinuria is an important marker of graft dysfunction, but is not predictive of graft loss in biopsy-proven cases. Appropriate management guided by the results of a transplant biopsy may improve the outcome.

Biopsy↗
PubMed2000

Glomerulonephritis is the major cause of proteinuria in renal transplant recipients: histopathologic findings of renal allografts with proteinuria.

The proteinuria in renal allograft recipients has been regarded as a sign of poor prognosis. The causes of post-transplant proteinuria include chronic rejection, chronic transplant glomerulopathy, glomerulonephritis (GN), acute rejection, and cyclosporine nephrotoxicity. Among them, chronic rejection is known to be most frequent. We analyzed the histopathologic findings of renal allograft biopsies in 197 Korean recipients with proteinuria. Among them, 26 patients developed proteinuria over 500 mg/d. All patients received baseline immunosuppression with cyclosporine. From 26 patients with post-transplant proteinuria, 29 biopsies were performed and their histologic diagnoses were immunoglobulin A nephropathy (IgAN) in 17, IgAN combined with chronic allograft nephropathy in 1, focal segmental glomerulosclerosis in 2, crescentic GN in 1, membranous GN in 1, diabetic nephropathy in 1, acute tubulointerstitial nephritis in 1, and chronic rejection in 3 biopsies. The remaining two biopsies showed nonspecific findings. The most common cause of post-transplant proteinuria was IgAN (62% of biopsies). The incidence of chronic rejection was relatively low and predominant cyclosporine-associated changes were not observed. In conclusion, our data suggest that the main causes of post-transplant proteinuria in Korea are primary glomerulonephritides rather than chronic rejection or cyclosporine nephrotoxicity, and the kidney allograft biopsies from patients with proteinuria should be handled as native kidney.

Adult↗
PubMed2005

Proteinuria as a determinant of renal expression of heme oxygenase-1: studies in models of glomerular and tubular proteinuria in the rat.

Heme oxygenase-1 (HO-1), a cytoprotective gene, is commonly induced in renal tubules in the diseased kidney. Because proteinuria is a hallmark for kidney disease, we examined the relationship between proteinuria and tubular induction of HO-1, specifically questioning whether increased trafficking of protein across the renal tubular epithelium, as a consequence of proteinuria, induces tubular expression of HO-1. We examined a model of glomerular proteinuria induced by daily injections of BSA, which is associated with increased tubular uptake of filtered protein, and a model of tubular proteinuria induced by maleate, the latter exhibiting decreased tubular uptake and trafficking of protein. The BSA model of glomerular proteinuria failed to exhibit induction of HO-1; HO-1 was not induced in proximal tubular epithelial cells exposed to BSA. In contrast, in maleate nephropathy wherein tubular uptake of protein is decreased because of generalized proximal tubular injury induced by maleate, HO-1 was strongly induced in proximal tubules; inhibition of HO activity in maleate nephropathy worsened proteinuria, renal histological injury, and apoptosis. In renal proximal tubular epithelial cells, maleate induced HO-1 and caused apoptosis, the latter increased when HO activity was inhibited. From these studies, we conclude that expression of HO-1 in the diseased kidney cannot be ascribed to the tubular uptake and metabolism of protein such as albumin, and that the expression of HO-1 in a model of tubular proteinuria reflects a functionally significant stress response to toxin-induced proximal tubular injury.

Animals↗
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↗
PubMed2006

Comparison between 24-h proteinuria, urinary protein/creatinine ratio and dipstick test in patients with nephropathy: patterns of proteinuria in dipstick-negative patients.

OBJECTIVE: Three main tests are commonly employed for the measurement of proteinuria: the dipstick test, the urinary protein/creatinine ratio (P/C) and the 24-h urine collection. The aim of this study was to evaluate the correlation between these methods, comparing linear regression and ROC curve data. MATERIAL AND METHODS: A total of 297 consecutive outpatients with different renal diseases were included in the study. Twenty-four-hour proteinuria was considered the reference test. RESULTS: A high degree of correlation was observed between all the tests (p<0.0001), the highest regression coefficient being between 24-h proteinuria and P/C (R=0.82), and the lowest between P/C and the dipstick test (R=0.72). The dipstick test failed to detect pathological proteinuria in 94 patients (31.6%). Therefore, in these subjects, the patterns of proteinuria were assessed by immunofixation and sodium dodecyl sulphate (SDS) electrophoresis. CONCLUSIONS: Our data strongly support the use of urinary P/C for the detection of proteinuria, at least in nephrology units, where the prevalence of proteinuria is likely to be high.

Adolescent↗
PubMed2002

Randomized controlled crossover study of the effect on proteinuria and blood pressure of adding an angiotensin II receptor antagonist to an angiotensin converting enzyme inhibitor in normotensive patients with chronic renal disease and proteinuria.

BACKGROUND: Proteinuria and hypertension have independent deleterious effects on the progression of chronic renal disease. The objectives of this study were to determine whether the addition of Candesartan, an angiotensin II receptor antagonist, would reduce proteinuria and blood pressure in normotensive patients with chronic renal disease already receiving an angiotensin converting enzyme inhibitor (ACEI). METHODS: This was an open randomized controlled crossover study conducted in a private consultant practice in Melbourne. Sixty patients, aged 23-75, who had chronic renal disease and stable proteinuria over 0.5 g in 24 h and were receiving an ACEI, were enrolled in the study. The patients were randomized to have 8 mg of Candesartan added in the first or second of two 12-week study periods. The primary end point was urine protein excretion, which was measured every 2 weeks for the 24-week period. Secondary end points included systolic and diastolic blood pressure, serum creatinine, urea and potassium levels. Candesartan was added against a background of standard care, which included other blood pressure lowering therapy. RESULTS: Lower urine protein excretion 2.4 vs 2.0 g in 24 h (P<0.04, difference 0.45, CI 0.01, 0.9) and lower levels of systolic blood pressure 134 vs 128 mmHg (P<0.001, difference 6.4, CI 3.2, 9.6) and diastolic blood pressure 82 vs 80 mmHg (P<0.008, difference 2.7, CI 0.7, 4.6) were observed when Candesartan, 8 mg, was added to a regimen, which included an ACEI. No rise in serum creatinine occurred but there was a significant rise in urea, during the Candesartan arm of the study, from 12.3 to 13.8 mmol/l (P<0.001). The addition of 8 mg of Candesartan in normotensive patients with chronic renal disease receiving ACEI appeared safe and was not accompanied by adverse effects apart from postural hypotension in three patients and a serum potassium level of 6.3 mmol/l in one. CONCLUSIONS: In a private consulting practice setting, the addition of 8 mg of Candesartan in normotensive patients with chronic renal disease and proteinuria receiving an ACEI reduced proteinuria and blood pressure. The combination of Candesartan and ACEI appeared safe in this setting and may offer additional protection in preventing progression in chronic renal disease. Although the reduction of proteinuria was small (0.45 g/24 h) this reflected in part a lack of response in diabetic nephropathy and in part a marked rise in proteinuria after ceasing Candesartan in patients who did not complete the Candesartan arm of the study.

Adult↗
PubMed1982

Reversible nephrotic range proteinuria with renal artery stenosis: a clinical example of renin-associated proteinuria.

Nephrotic range proteinuria occurred in a 60-year-old woman with renal artery stenosis and marked hyperreninemia. Treatment by nephrectomy produced resolution of both proteinuria and hypertension. The gradual resolution of the proteinuria postoperatively suggested the proteinuria, at least in part, came from the contralateral kidney. Foot process fusion in the nephrectomy specimen suggested it too was a source of proteinuria. A marked degree of hyperreninemia, as was present in this case, may be necessary before massive proteinuria occurs in renal artery stenosis.

Female↗
PubMed1986

Proteinuria induced by transplantable rat pituitary tumor MtT SA5. Model for homologous protein-overload proteinuria.

Intensive proteinuria accompanied by marked renal enlargement occurs in rats bearing functioning pituitary tumor MtT SA5. Urinalysis showed that protein excretion was up to 700 mg/day, and that the excreted protein consisted mostly of albumin. However, serum total protein and albumin levels remained almost unchanged. Histological examination revealed glomerular lesions, hyaline casts in the tubules, and proliferation of the tubular epithelium. The glomerular lesions consisted of accumulation of proteinaceous material in the subcapsular space; its organization and formation of fibrous crescents was with or without epithelial crescents. Electron microscopy revealed loss of foot processes and accumulation of absorption droplets in glomerular epithelial cells. Removal of the tumor resulted in a rapid reduction in urinary protein excretion. However, proteinuria persisted for at least 4 weeks after tumor removal with levels of approximately one-fourth of those before tumor removal. Histological changes of the kidneys resolved to some extent but damage still remained in the glomerular epithelial cells 4 weeks after tumor removal. Although proteinuria in animals bearing functioning pituitary tumors has long been implicated in hyperprolactinemia, the present study suggests that proteinuria in tumor-bearing rats is a control mechanism for overproduction of albumin in the liver stimulated by elevated serum growth hormone since hyperalbuminemia and possibly the hyperfibrinogenemia would cause the elevation of blood viscosity, resulting in thrombosis, unless control mechanisms were present. This proteinuria may serve for studies of glomerular permeability disorders as a model for homologous protein-overload proteinuria.

Animals↗
PubMed2001

Effect of losartan treatment on the proteinuria in normotensive patients having proteinuria due to secondary amyloidosis.

Secondary amyloidosis (AA amyloidosis) is a well known cause of nephrotic syndrome and renal failure. Several studies in patients with nephrotic syndrome have suggested a beneficial effect of angiotensin-converting enzyme inhibitors (ACEI). Angiotensin II (ATII) receptor antagonists effect on the long term is not known. In this study, we intended to study the effect of losartan, as an ATII receptor antagonist, on proteinuria and renal functions in patients with normotensive secondary amyloidosis. In total 44 patients with biopsy proven AA amyloidosis associated with nephrotic proteinuria were included. The first group of patients (n=22) was treated with losartan 50 mg/day. The second group of patients (n=22) did not receive any specific antiproteinuric treatment. Urinary protein loss was effectively lowered by losartan from 4.38 +/- 1.0 to 2.8 +/- 0.61 g/day (p<0.0001), whereas the control group showed a slight fall in proteinuria as 4.21 +/- 1.06 to 4.12 +/- 1.07 g/day (p = 0.176). Hypoalbuminemia improved significantly from 2.52 +/- 0.69 to 2.78 +/- 0.46 g/dl (p = 0.004), in the losartan group, whereas serum albumin had fallen in the control group from 2.44 +/- 0.57 to 2.27 +/- 0.41 (p = 0.041). Serum creatinine increased in the control group from 1.52 +/- 0.42 to 2.39 +/- 0.51 mg/dl (p<0.0001), and in the losartan group from 1.59 +/- 0.50 to 1.84 +/- 0.6 mg/dl (p<0.001), after 24 months of treatment. The ATII receptor blocker losartan is effective in protecting against the progression of nephropathy due to AA amyloidosis. Symptomatic treatment of proteinuria with losartan is therefore to be considered, especially with severe proteinuria even in normotensive patients.

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↗
PubMed1988

The significance of proteinuria in pre-eclampsia; proteinuria associated with low birth weight only in pre-eclampsia.

To examine the significance of proteinuria in pre-eclampsia, we studied 87 nulliparous patients in whom pre-eclampsia was diagnosed clinically and whose blood pressure and urine findings returned to normal after delivery. There was no difference in the gestation at diagnosis, highest systolic and diastolic blood pressures before treatment/delivery, or the number given antenatal hypotensive therapy between patients with proteinuria (group A, n = 46) and without proteinuria (group B, n = 41). Group A patients had higher plasma urea concentration (p less than 0.02), but similar creatinine and urate concentrations to group B patients. Group A patients had a higher rate of induction of labour (p less than 0.04) and Caesarean section before labour (p less than 0.04), and the mean gestation at delivery as well as the birth weight were less (p less than 0.03 and p less than 0.004, respectively). The results suggest that proteinuria in pre-eclampsia is associated with more severe fetal involvement and growth retardation only, but not with an increased severity of the maternal condition such as hypertension and a higher plasma urate concentration.

Blood Pressure↗
PubMed2002

The product of duration and amount of proteinuria (proteinuria index) is a possible marker for glomerular and tubulointerstitial damage in IgA nephropathy.

BACKGROUND/AIMS: IgA nephropathy (IgAN) is one of the major causes for chronic renal failure (CRF). Presence of massive proteinuria, hypertension, increased serum creatinine level and sclerotic histopathological changes of the glomerulus are known to be determinants for the progression of CRF. However, the relationships between duration of proteinuria/hematuria and histopathological changes, which may be correlated with the renal prognosis, have not been clarified. METHODS: A cross-sectional, univariate analysis of clinical parameters on the four glomerular and three tubulointerstitial histopathological grades in 57 untreated biopsy-proven IgAN patients (M/F = 32/25) was performed. RESULTS: The age at the time of renal biopsy (35.2 +/- 13.0 years; mean +/- SD), average duration of proteinuria (5.3 +/- 5.8 years), mean urinary protein excretion (0.99 +/- 1.22 g/day), serum creatinine (Cr 0.97 +/- 0.28 mg/dl), Cr clearance (Ccr 75.5 +/- 29.4 ml/min), and blood urea nitrogen (BUN 15.4 +/- 3.9 mg/dl) were well correlated with both histopathological grades. The product of duration (years) and urinary protein excretion (g/day) at the time of renal biopsy was more significantly correlated with glomerular and tubulointerstitial histopathological grades and serum Cr. CONCLUSION: The natural course of IgAN is steadily progressive depending on the duration and amount of proteinuria. The product of these two factors (proteinuria index) may be a useful predictor for glomerular and interstitial histopathological changes and the fate of renal function in IgAN.

Adult↗
PubMed2004

[Responsible genes for proteinuria and concept of the treatment for proteinuria].

Proteinuria has been demonstrated to be not only a representative sign of renal lesion but also a risk factor for the progression to renal failure through its injurious effects on tubulointerstitium. The responsible gene for Finnish type congenital nephrotic syndrome was identified and its product was named 'nephrin' which is located on slit membrane between foot processes of glomerular epithelial cells and is considered to be concerned also in the induction of acquired renal lesions with proteinuria. The monoclonal antibody against rat nephrin can induce proteinuria. These facts suggest that the important role for final barrier against macromolecules is played by the slit membrane. Understanding the proteinuria mechanism at molecular level is expected to lead to the establishment of appropriate treatments. Nephrin is regarded as the most promising and attractive molecule for the development of new therapeutic strategy. Many nephrologists are now much interested in the intimate relationship between nephrin and angiotensin II.

Angiotensin II↗
PubMed1983

Echinocytes in the blood of hyperproteinaemic mice with proteinuria. Is the effect of such cells on blood viscosity the cause of the proteinuria?

Early studies in this series failed to obtain evidence for the cause of hyperproteinaemic proteinuria although it was speculated that blood viscosity, increased because of high plasma protein levels, might play a significant role. As we had no means of measuring blood viscosity it was decided to investigate the effects of reducing blood viscosity in a small number of mice made anaemic before subjecting them to albumin overload. All but one of the mice given injections i.p. of 250 mg HSA on 2 successive days developed proteinuria within 24 h of the first injection. This result seemed to show that altered blood viscosity was not a factor in the mechanism of the hyperproteinaemic proteinuria. However, it has been shown that changes in the red cell environment can lead to red cell deformation resulting in an increase in blood viscosity. To check on this possibility another small group of mice were injected with HSA as previously. On the morning after their second injection the mice were bled by percutaneous heart puncture and the blood was examined by scanning electron microscopy. This showed that a vast preponderance of red cells, probably more than 95%, were echinocytes. Although no measurements of blood viscosity were made, it can be speculated that hyperproteinaemic proteinuria is caused by the intraglomerular effects of blood with increased viscosity (because of the red cell transformation) being made more viscous by glomerular filtration. Enhanced protein filtration would occur because of the increase in glomerular pressure needed to restore flow of viscous blood at the efferent arteriole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗