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PubMed1984

Stainable glomerular basement membrane polyanions and renal hemodynamics during hexadimethrine-induced proteinuria.

To clarify the mechanism of hexadimethrine-induced proteinuria, we studied the changes in stainable glomerular basement membrane anions and renal hemodynamics during hexadimethrine (HDM) infusion. To determine whether glomerular anions were neutralized in vivo, animals infused with HDM received cationized ferritin intravenously, or their kidneys were perfused in situ with lysozyme. During its infusion, HDM bound heavily within the glomerular basement membrane, and binding of the cationic probes was virtually abolished. During recovery after HDM infusion, HDM deposits diminished and the binding of the cationic probes recovered to normal. The inverse correlation between HDM binding and binding of the cationic probes confirms that the glomerular binding of HDM is associated with neutralization or shielding of the glomerular basement membrane anions in vivo. Renal hemodynamic parameters and urinary protein excretion rate were measured before, during, and after infusion of HDM. Heavy proteinuria appeared during HDM infusion and persisted for 1 hour after its discontinuation. Although glomerular filtration rate, renal plasma flow, and urine flow rate decreased transiently at the onset of proteinuria, they returned to baseline levels before resolution of proteinuria. Filtration fraction never changed significantly. Thus, proteinuria cannot be attributed solely to renal hemodynamic factors. These results strengthen our hypothesis that HDM induces proteinuria as a consequence of its binding to and neutralization of glomerular basement membrane fixed anions.

Animals↗
PubMed1983

IgA nephritis with nephrotic range proteinuria.

Nephrotic range proteinuria is uncommon in patients with IgA nephritis. For this reason we compared the clinical and pathologic features in 63 non-nephrotic patients with those in 8 patients who had nephrotic range proteinuria at the time of biopsy. Both the mean age and the mean duration of the disease at the time of diagnosis were not significantly different in the 2 groups of cases. Significant associations were found between nephrotic range proteinuria and the following: the extent of glomerular hyalinization, the severity of interstitial fibrosis and tubular atrophy and the degree of foot process effacement and mesangial matrix increase. A significant association was also noted with nephrotic range proteinuria had elevated levels of serum creatinine on follow-up compared with 20% of non-nephrotic cases. The results of our study suggest that patients with nephrotic range proteinuria have a more severe type of IgA nephritis from the outset and that a marked degree of proteinuria is not merely a consequence of the duration of disease.

Adult↗
PubMed1982

Correlation of proteinuria with histopathology in asymptomatic glomerulonephritis.

The glomerular lesions of 90 patients with asymptomatic glomerulonephritis and proteinuria of more than 1.0 gm per day were compared with 8.3 similar patients with less than 1.0 gm proteinuria. 68% of those patients with more than Igm proteinuria had glomerular sclerosis compared to 19% of those with less than Igm proteinuria (p less than 0.001). Immunofluorescence studies revealed that 77% of patients studied had IgA deposits in the mesangial region. There was no correlation between the degree of microscopic haematuria and the severity of glomerular lesions. Patients with more than 1 gm proteinuria also had significantly higher incidence of granular casts (p less than 0.001) and the presence of casts was also significantly associated with the finding of glomerular sclerosis (p 0.005). The data suggest that 1 gm proteinuria is a useful predictive index of glomerular sclerosis in patients with asymptomatic urinary abnormalities.

Adolescent↗
PubMed1982

Symptomless abnormalities proteinuria.

During the last decade enormous progress has been made in the study of the ultrastructure of the glomerular capillary wall, the mechanism of protein filtration and excretion, and the pathophysiology and biochemistry of proteinuria. However, current knowledge concerning each of these problems is incomplete. Nonetheless the mechanisms of proteinuria can be categorized, using available biochemical measurements of plasma and urinary proteins, into four groups of causes. The mechanism most commonly underlying proteinuria is a defect of glomerular permeability but proteinuria may also result from the presence in the plasma of high concentrations of low molecular weight protein, failure of the proximal tubule to reabsorb protein filtered by the normal glomerulus, and protein derived from the renal parenchyma. Glomerular proteinuria may cause the nephrotic syndrome or may persist without symptoms. Investigation and follow-up of persistent asymptomatic proteinuria is important although the natural history of this condition is still uncertain.

Humans↗
PubMed1978

[Proteinuria in the nephropathy of pregnancy and posttoxicosis renal lesion].

Proteinuria was studied in 110 females - 28 pregnant with nephropathy of pregnancy with primary late toxicosis and 82 with past history of the disease with a residual proteinuria after childbirth. Selective type proteinuria was more often found both in pregnant women and in those with a past history of nephropathy. The relative share of the pregnant with non-selective proteinuria is considerably greater. After childbirth, in parallel with the decrease of proteinuria quantity, the non-selective one turns to selective in the majority of the cases. The quantity of the excreted proteins, in the urine, of patients with confirmed glomerular lesions, shows no tendency to decrease. The absence of dynamics in proteinuria quantity and its non-selectivity provides grounds to suspect a deeper lesion of the renal filter, retaining the involution of the morbid process and a tendency to its chronification.

Female↗
PubMedDate not supplied

[Proteinuria].

The finding of proteinuria in the pediatric age is a frequent phenomenon. Once detected, the immediate goal is to investigate other evidences of renal disease or its participation in systemic diseases. If proteinuria is an isolated finding, its transitoriness, persistence or relation with posture must be determined. Transitory proteinuria is a mild finding with good outlook; however, in patients with orthostatic or persistent asymptomatic proteinuria, the prognosis is uncertain; however, the measures taken must be conservative without restriction of physical activity and only in case of association to other signs, or finding of any change in renal function tests, the possibility of renal biopsy should be evaluated. The presence of proteinuria above 1 g/l. in a patient with acute nephritic syndrome, may be a sign of poor prognosis if it persists over one month and is indicative of renal biopsy. If this same degree of proteinuria is found in a nephrotic syndrome without hematuria or arterial hypertension, the necessity to practice renal biopsy is not indicated, except in the case it does not disappear following adequate treatment with corticosteroids.

Humans↗
PubMed1978

The specific proteinuria of cancer patients.

UNLABELLED: Most patients with disseminated cancer have proteinuria. Twenty-four hour urine protein averaged less than 80 mg in normals; 223 mg in patients with acute myelocytic leukemia; 177 mg in subjects with stage IV Hodgkin's; 215, 229, 233, and 280 mg in patients with metastatic cancer of colon, breast, ovary, and pancreas respectively. We recently purified the novel glycoprotein EDC1 (mol wt 27,000) from the urine of patients with several types of cancer and found it to be a fragment of plasma inter-alpha-trypsin inhibitor (IATI) (mol wt 170,000). Both EDC1 and IATI are antiproteolytic. By radial immunodiffusion and radioimmunoassay of the 41 recognized plasma proteins and of EDC1, we have now analyzed the composition of urine protein in: (i) five nephrotics ("glomerular proteinuria"), (ii) four patients with cystinosis and four with hereditary renal tubular acidosis ("tubular proteinuria"), and (iii) 26 proteinuria (200-800 mg/day) patients with the six types of disseminated cancer listed above. In (i), (ii) and (iii) the 41 plasma proteins accounted for 100%, greater than 95%, and 33-60% of the urine protein, respectively, while EDC1 accounted for less than 1%, less than 1%, and 40-63% respectively. In normals, (i), (ii) and (iii), plasma EDC1 averaged less than 1, less than 1, less than 1 and 65 micrograms/ml respectively. Renal clearance of EDC1 in (iii) averaged 3% of creatinine clearance. In three cancer patients with EDC1-proteinuria, postmortem renal histology was normal. CONCLUSION: most types of cancer cell interact with plasma IATI to generate plasma EDC1 which is rapidly filtered by the glomeruli, with a resultant "overflow" or "prerenal" proteinuria which is unique to disseminated neoplastic disease.

Adolescent↗
PubMed1995

Long-term effects of antihypertensive agents on proteinuria and renal function.

BACKGROUND: Although many studies have examined the effects of antihypertensive agents on proteinuria and glomerular filtration rate in patients with kidney disease, many questions remain unresolved. These questions include whether the effects of agents differ, whether their effects are similar in diabetic and nondiabetic patients with renal disease, and whether the effects of any agents are independent of blood pressure reductions. METHODS: We conducted a meta-analysis of studies obtained with MEDLINE and bibliographies from comprehensive reviews but included only investigations with follow-up times of at least 6 months. We combined data (1) in an analysis of randomized controlled trials, (2) in a separate univariate analysis of controlled and uncontrolled trials, and (3) using weighted multiple linear regression. RESULTS: In 14 randomized controlled trials, angiotensin-converting enzyme inhibitors caused a greater decrease in proteinuria (pooled mean [95% confidence intervals], -0.51[-0.68 to -0.35], ln [treatment/control]), improvement in glomerular filtration rate (0.13 mL/min per month [0.10 to 0.16 mL/min per month]), and decline in mean arterial pressure (-4.0 mm Hg [-4.9 to -3.0 mm Hg]) compared with controls. In a multivariate analysis of controlled and uncontrolled trials, each 10-mm Hg reduction in blood pressure decreased proteinuria (regression coefficient [95% confidence interval] -0.14 [-0.22 to -0.06] ln [after/before]), but angiotensin-converting enzyme inhibitors (-0.45 [-0.58 to -0.32]) and nondihydropyridine calcium antagonists (-0.38 [-0.70 to -0.06]) were associated with additional declines in proteinuria that were independent of blood pressure changes and diabetes. Each 10-mm Hg reduction in blood pressure caused a relative improvement in glomerular filtration rate (0.18 mL/min per month [0.04 to 0.31 mL/min per month]), but among diabetic patients there was a tendency for dihydropyridine calcium antagonists to cause a relative reduction in glomerular filtration rate (-0.68 mL/min per month [-1.31 to -0.04 mL/min per month]). CONCLUSIONS: Long-term beneficial effects of antihypertensive agents on proteinuria and glomerular filtration rate are proportional to blood pressure reductions and are similar in diabetic and nondiabetic patients with renal disease. In addition, angiotensin-converting enzyme inhibitors, and possibly nondihydropyridine calcium antagonists, have additional beneficial effects on proteinuria that are independent of blood pressure reductions.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria.

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Prevalence of arterial hypertension, proteinuria and hematuria in patients with simple renal cyst].

The simple renal cyst (SRC) is a common entity even though its actual incidence is difficult to determine given that it tends to manifest itself in an asymptomatic fashion. Occasionally, cases of SRC with clinical manifestations have been described in the literature, such as arterial hypertension (AHT) and biological alterations such as hematuria or proteinuria. The purpose of this article is to find the prevalence of AHT, proteinuria, and hematuria in patients with SRC detected via echography. 1,197 echographs that explored the renal area--a number equal to that of the number of patients--were reviewed. In 66% of the cases, the echographs were taken for some purpose unrelated to renal pathology. For those who presented SRC, blood pressure, proteinuria per 24 hours, and urine sediment were determined. SRC was detected in 93 patients (7.7%). The prevalence of AHT in patients with SRC was 31%, but 57% of those were older than 85 years. Two patients presented AHT and proteinuria; both fulfilled the criteria for nephrongiosclerosis. Two other patients presented hematuria and proteinuria; one was found to be afflicted with IgA nephropathy and the other with vesical carcinoma. A patient with hematuria was a carrier of renal lithiasis. We conclude that the prevalence of AHT in patients with SRC did not yield a significantly different result from that of the general population. In those patients who presented proteinuria and/or hematuria, one cause was found to be responsible; therefore, the presence of such alterations in patients with SRC should be considered coincidental.

Adolescent↗
PubMed1993

[Proteinuria in patients with congestive heart failure. Role of arterial hypertension].

PURPOSE: To evaluate the role of arterial hypertension (AH) in the development of proteinuria in patients with decompensated congestive heart failure (CHF). METHODS: Twenty-four-hour urinary protein determinations were obtained from 30 patients with decompensated CHF, before and after therapy of CHF. The patients were divided in two groups according with the presence of AH as cause of CHF: group A, 18 patients with CHF due to AH and group B, 12 patients with CHF due to idiopathic dilated or chagasic cardiomyopathy without previous AH. RESULTS: There was no differences between the groups concerning age, sex, renal function and duration of CHF. Before treatment, 88% of group A presented proteinuria exceeding 150 mg/24h compared to 25% of group B (p < 0.01). After treatment of CHF, proteinuria > 150 mg/24 h remained in 38% of group A and in none of group B. Proteinuria did not reverse after 6 months of follow-up in 2 patients, one of them showed benign nephrosclerosis in renal biopsy. CONCLUSION: Patients with decompensated CHF, unrelated to AH, presented mild proteinuria reversible after the treatment, that improved renal function. In patients with CHF due to AH, proteinuria was more frequent, more severe and did not improve after the treatment, suggesting renal lesion.

Creatinine↗
PubMed1977

A scanning and transmission electron microscopic comparison of puromycin aminonucleoside-induced nephrosis to hyperalbuminemia-induced proteinuria with emphasis on kidney podocyte pedicel loss.

Ultrastructural changes in the visceral epithelium and proximal tubules of rats were studied by scanning and transmission electron microscopy during the onset and progression of puromycin aminonucleoside nephrosis (PAN)-induced proteinuria. These changes were compared with those that occur during a similar degree of proteinuria induced by intraperitoneal injections of albumin. With the onset of proteinuria and oliguria, PAN rats exhibit loss of podocyte pedicels and podocyte major processes, an increase in pinocytotic activity, and an accumulation of cytoplasmic vacuoles and granules of variable size, shape, and electron density. Loss of podocyte pedicels involves a gradual decrease in pedicel height beginning at the pedicel tip and progressing down the pedicel arm, formation of nublike protrusions and interpedicel microbridges (35 to 45 nm. in width and 40 to 60 nm. in length) along the pedicel's base, the merging of microbridges to form more extensive regions of interpedicel contact, and a gradual broadening and retraction of pedicels. In response to hyperalbuminemia-induced proteinuria, kidney podocytes exhibit reactions during PAN, however, the podocyte pedicels, slit pores, and major processes of rats with hyperalbuminemia-induced proteinuria remain discrete. The loss of pedicels and major processes during PAN, therefore, apparently results from the effects of puromycin aminonucleoside per se rather than from the proteinuria associated with this disease. The proximal tubules of rats with hyperalbuminemia-induced proteinurea exhibit the same characteristic changes as PAN rat proximal tubules (i.e., loss of brush border, dilated lumina, abnormally thin walls, and accumulation of periodic acid-Schiff positive electron-dense luminal casts and cytoplasmic protein absorption droplets). The significance of these ultrastructural findings during PAN and hyperalbuminemia-induced proteinurea are discussed in terms of the etiology of PAN.

Albumins↗
PubMed1995

High lipid levels in very low density lipoprotein and intermediate density lipoprotein may cause proteinuria and glomerulosclerosis in aging female analbuminemic rats.

BACKGROUND: Male rats are generally more prone to developing renal disease than female rats. However, female Nagase analbuminemic rats (NAR) are profoundly hyperlipidemic and develop proteinuria and glomerulosclerosis after uninephrectomy. Male NAR are less hyperlipidemic and are resistant to developing renal damage after uninephrectomy. Ovariectomy markedly decreases hepatic triglyceride secretion and plasma triglyceride levels in the female NAR. EXPERIMENTAL DESIGN: In this study, we investigated the relationship between plasma lipids and lipoprotein composition as well as the development of proteinuria, glomerular apolipoprotein and lipid deposition, and glomerulosclerosis in aging female and male analbuminemic rats. We also studied whether ovariectomy in female NAR at an early age would protect their renal function in old age. RESULTS: Aging hyperlipidemic female NAR with high triglyceride and cholesterol levels in very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) were found to develop spontaneous proteinuria at 9 months of age. Glomerular lipid deposition and glomerulosclerosis were observed at 18 months of age. In male NAR that had lower lipid levels in VLDL and IDL, only mild proteinuria and no glomerular lipid deposition or glomerulosclerosis were observed up to the age of 22 months. Concurrently ovariectomized NAR demonstrated profound and persistent decreases in triglyceride and cholesterol content of VLDL and IDL as well as total plasma triglycerides, without much change in LDL, high density lipoprotein, total plasma cholesterol, or apolipoprotein B, and they remained completely free of proteinuria and glomerulosclerosis. Apolipoprotein B deposition in glomeruli was not different in the oldest female, male, or ovariectomized NAR. No important differences were observed in glomerular diameter between the three different groups up to the age of 1 year. CONCLUSIONS: These findings point to an important role of elevated lipid content of the triglyceride-rich lipoproteins VLDL and IDL in the pathogenesis of proteinuria and glomerulosclerosis in the female NAR.

Aging↗
PubMed1997

Proteinuria in mild to moderate hypertension: results of the VA cooperative study of six antihypertensive agents and placebo. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents.

The prevalence and natural history of severe proteinuria in mild to moderate hypertension are not completely defined. We screened 1635 men with a history of hypertension and randomized 1292 with untreated diastolic blood pressure (DBP) 95-109 mmHg to single-drug treatment with either hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem-SR, prazosin, or placebo in a double-blind prospective trial. Twenty-seven of 1635 patients (1.7%) satisfying clinical criteria for primary hypertension were found to have developed proteinuria > 1000 mg/24 hours and were removed from the study. Follow-up data were obtained on 19 of these 27 patients. One patient was found to have focal segmental sclerosis and progressed to end-stage renal disease. Three other patients developed severe (serum creatinine > 3.5 mg/dl) chronic renal failure (one with diabetic nephropathy), one progressed from serum creatinine 1.4 to 2.2 mg/dl, but 14 of the 19 remained with stable serum creatinine < 2.0 mg/dl on follow-up for 6-9 years. Data were available for 1076 of 1155 (93%) treated study patients at end titration, 522/600 (87%) at one year and 322/444 (73%) at two years. There were significant associations for proteinuria with obesity and higher systolic blood pressure. There was a trend toward significant difference in mean 24-hour protein excretion rates at baseline between black (127 mg) and white (139 mg) patients (p = 0.07). There were no statistically significant changes in urinary protein excretion/24 hours between or within the different treatment groups (including placebo). Eighteen patients were removed from the study during the active treatment phase for proteinuria > 1000 mg/24 hours: hydrochlorothiazide 4, placebo 3, diltiazem 3, prazosin 3, atenolol 2, clonidine 2, and captopril 1. We conclude: (1) the prevalence of severe (> 1 g/24 hours) proteinuria in the hypertensive population is significant but does not necessarily imply a poor prognosis; (2) mean 24-hour urinary protein excretion rates did not vary in response to the different classes of antihypertensive drugs; and (3) there was no drug-specific increase in proteinuria detected in this study.

Adult↗
PubMed1997

Reinstitution of gold after gold induced proteinuria.

OBJECTIVE: To assess the benefits and risks to patients who resumed gold after discontinuation of gold because of proteinuria. METHODS: We conducted a review of records of all patients who had resumed gold after discontinuing treatment because of proteinuria. RESULTS: Eight patients developed proteinuria > or = 500 mg/dl while receiving 50 mg weekly doses in the first year of treatment. Proteinuria took a minimum of 4 mo to resolve. No patient had a recurrence of proteinuria when gold was resumed at a lower dosage of 25 mg every 1-2 weeks. This strategy has been successful in 5/8 patients who continue taking gold and are markedly improved compared to pretreatment status after 3-7 years (mean 5 years) of followup. CONCLUSION: The risk of gold induced proteinuria may be dose related and reinstitution of gold at a lower dose is safe in our experience and effective in selected patients.

Aged↗
PubMed1997

Pattern of proteinuria in tubular injury and glomerular hyperfiltration.

Proteinuria is one of the bad prognostic indices in renal disease. This study compares the pattern of protein excretion in 10 patients with IgA nephropathy (IgAN), 10 patients with chronic glomerulonephritis approaching end-stage renal failure (ESRF) who still had proteinuria and 10 other patients with diabetic nephropathy (DN) with proteinuria but normal renal function. The pattern of proteinuria was analysed by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), isoelectric focusing (IEF) and assayed for orosomucoid, alpha-1-microglobulin, retinol-binding protein, lysozyme, beta-2-microglobulin and N-acetyl-beta-D-glucosaminidase activity. Our data showed much similarity in the pattern of proteinuria between the DN and ESRF groups but significant differences with the IgAN group. The pattern of proteinuria in the IgAN group reflects glomerulonephritis whereas the similar pattern between the ESRF and DN groups may reflect hyperfiltration as well as tubular injury.

Adolescent↗
PubMed1997

Proteinuria is a risk factor for mortality over 10 years of follow-up. MRFIT Research Group. Multiple Risk Factor Intervention Trial.

Proteinuria has been shown to be strongly associated with the prevalence and incidence of cardiovascular disease. It has been difficult to determine if the link is causal and independent. The mortality follow-up for the Multiple Risk Factor Intervention Trial (MRFIT) randomized cohort provides an opportunity to examine these relationships. Between 1973 and 1975, 361,662 men, ages 35 to 57, were screened for blood pressure, serum cholesterol, and cigarette smoking. Patients receiving medication for diabetes were excluded. Men in the upper 10 to 15% of coronary heart disease (CHD) risk (12,866) were randomized into the MRFIT trial. Standard casual urine dipstick determinations (Labstix) for protein were done at baseline and annually for six years. Post-trial cause-specific mortality was ascertained using the National Death Index. During the trial, 2326 (18.1%) of participants had + or higher proteinuria, and 593 (4.6%) had +2 or higher proteinuria. The presence of proteinuria during the six years of follow-up was consistently associated with higher all cause, cardiovascular disease (CVD) and CHD mortality, even after adjusting for other risk factors. The higher and more persistent the proteinuria, the greater the risk. In this data set, proteinuria is a strong and independent risk factor for CVD mortality.

Cardiovascular Diseases↗
PubMed1998

Interferon-alpha-associated focal segmental glomerulosclerosis with massive proteinuria in patients with chronic myeloid leukemia following high dose chemotherapy.

BACKGROUND: Acute renal failure, with or without massive proteinuria, is a rare idiosyncratic toxicity of interferon (IFN)-alpha therapy. The authors sought to review their experience with this toxicity as well as the world literature on the subject. METHODS: The authors describe two patients with chronic myeloid leukemia treated with IFN-alpha following high dose chemotherapy who developed renal failure and proteinuria after 3 and 4 weeks of IFN-alpha therapy, respectively. Fifteen previously reported cases of renal failure and proteinuria associated with IFN-alpha therapy are also reviewed. RESULTS: Renal biopsies performed on the authors' two patients revealed focal segmental glomerulosclerosis. However, the other reported patients with IFN-alpha-associated renal failure and massive proteinuria had an assortment of pathologic findings. CONCLUSIONS: The specific renal pathology associated with proteinuria may be a consequence of the condition and not its cause; differences in renal pathology may be caused by other predisposing factors. Patients treated with IFN-alpha following high dose chemotherapy, with or without autologous transplantation, should be followed for the development of proteinuria and renal failure.

Adult↗