losartan-potassium and Nephrotic-Syndrome

Nephrotic syndrome is one of the most common glomerular diseases that affect in children. Complications may occur in nephrotic syndrome as a result of the disease itself as well as its treatment. Most of these complications result from excessive urinary protein losses, and control of proteinuria is the most effective treatment strategy. Anemia is one of the many complications seen in patients with persistent nephrotic syndrome and may occur as a result of excessive urinary losses of iron, transferrin, erythropoietin, transcobalamin and/or metals. This leads to a deficiency of substrates necessary for effective erythropoiesis, requiring supplementation in order to correct the anemia. Supplementation of iron and erythropoietin alone often does not lead to correction of the anemia, suggesting other possible mechanisms which need further investigation. A clear understanding of the pathophysiologic mechanisms of anemia in nephrotic syndrome is necessary to guide appropriate therapy, but only limited evidence is currently available on the precise etiologic mechanisms of anemia in nephrotic syndrome. In this review we focus on the current state of knowledge on the pathogenesis of anemia in nephrotic syndrome.

Topics: Anemia; Child; Epoetin Alfa; Erythropoiesis; Erythropoietin; Gluconates; Hematinics; Humans; Iron; Kidney; Nephrotic Syndrome; Proteinuria; Renal Elimination; Transferrin; Treatment Outcome; Vitamins

Topics: Anemia; Animals; Diabetic Nephropathies; Disease Progression; Epoetin Alfa; Erythropoietin; Female; Humans; Kidney Failure, Chronic; Male; Nephrotic Syndrome; Proteinuria; Quality of Life; Randomized Controlled Trials as Topic; Recombinant Proteins

Cardiovascular disease (CVD) is a major cause of mortality in patients with mild to moderate chronic kidney disease (CKD) and end-stage renal disease (ESRD). Dyslipidemia has been established as a well-known traditional risk factor for CVD in the general population and it is well known that patients with CKD exhibit significant alterations in lipoprotein metabolism. In this review the pathogenesis and treatment of renal dyslipidemia are discussed.. Studies on lipid abnormalities in CKD stages 1-4, in nephrotic syndrome, and in hemodialysis and peritoneal dialysis patients are analyzed, as well as the lipid profile of kidney graft recipients. Also, the results of the effects of epoietin treatment and hypolipidemic drugs in CKD patients are reported.. Disturbances in lipoprotein metabolism are evident even at the early stages of CKD and usually follow a downhill course that parallels the decline of renal function. However, several intrinsic or exogenous factors can influence the phenotypic expression of these alterations. According to the literature, current evidence suggests that unlike dialysis patients, mild to moderate CKD patients could be benefit from the use of statins.. The use of statins is indicated in patients with mild to moderate CKD, while in subjects with ESRD lipid-lowering therapy should be individualized.

Topics: Dyslipidemias; Epoetin Alfa; Erythropoietin; Humans; Hypertriglyceridemia; Kidney Failure, Chronic; Kidney Transplantation; Lipid Metabolism; Lipids; Models, Biological; Nephrotic Syndrome; Peritoneal Dialysis; Recombinant Proteins; Renal Dialysis; Treatment Outcome

Topics: Anemia; Biomarkers; Diagnostic Techniques, Endocrine; Enzyme-Linked Immunosorbent Assay; Erythropoietin; Humans; Myelodysplastic Syndromes; Nephrotic Syndrome; Polycythemia; Radioimmunoassay; Reference Values; Specimen Handling

Topics: Anemia; Child; Erythropoietin; Humans; Kidney; Nephrotic Syndrome

Nephrotic syndrome is characterized by marked urinary excretion of albumin and other intermediate-size plasma proteins. This results in a profound alteration of the metabolism of many plasma proteins and protein-bound substances, as well as certain cellular and tissue proteins. This review summarizes available data on the effect of nephrotic syndrome on the metabolism and regulation of erythropoietin (EPO) and transferrin, which are essential for erythropoiesis. Studies of humans and animals have documented significant urinary losses of both EPO and transferrin in nephrotic syndrome. Urinary losses of EPO have been shown to cause EPO-deficiency anemia and prevent the normal increase in plasma EPO level in response to anemia and hypoxia in nephrotic syndrome. Similarly, transferrinuria and increased transferrin catabolism have been shown to cause hypotransferrinemia and, in some cases, iron-deficiency anemia. In addition, dissociation of iron from filtered transferrin, occasioned by a reduction in tubular fluid pH, can promote tubulointerstitial injury through the iron-catalyzed generation of oxygen free radicals. This can account in part for the role of proteinuria as a risk factor for the progression of renal disease. Subcutaneous administration of recombinant EPO has been successfully used in the management of EPO-deficiency anemia in nephrotic syndrome. Similarly, iron supplementation and nutritional support are indicated in nephrotic patients with severe transferrinuria and iron-deficiency anemia. However, correction or amelioration of the underlying proteinuria, when possible, is the ideal approach to reversal of these complications.

Topics: Animals; Erythropoietin; Humans; Nephrotic Syndrome; Transferrin

Nephrotic syndrome has been recently shown to cause erythropoietin (EPO) deficiency in humans and experimental models. However, efficacy and safety of recombinant EPO (rEPO) in the treatment of the associated anemia has not been previously investigated. We report a patient with nephrotic syndrome and only moderately impaired renal function. This patient showed severe disabling EPO-deficiency anemia that was treated with subcutaneous rEPO. This treatment led to a marked amelioration of the anemia and a dramatic improvement in the patient's sense of well-being and quality of life. The patient's glomerular filtration rate remained stable and the pre-existing hypertension remained under control with appropriate therapy throughout the 30-week course of rEPO therapy. Thus, rEPO therapy appears to be effective in the treatment of EPO-deficiency anemia caused by the nephrotic syndrome. Controlled studies are required to further substantiate the efficacy and safety of rEPO in the nephrotic syndrome.

Topics: Adult; Anemia; Erythropoietin; Humans; Male; Nephrotic Syndrome; Recombinant Proteins; Time Factors

The nephrotic syndrome can profoundly affect metabolism and regulation of protein or protein-bound hormones or prohormones. The present paper provides an overview of the published studies on erythropoietin, vitamin D and thyroid metabolism as well as hypothalamic-pituitary-gonadal axis in nephrotic syndrome. On each occasion the clinical significance and practical implications of the reported abnormalities are emphasized. In addition, attention is drawn to the areas needing further investigations.

Topics: Animals; Erythropoietin; Gonadal Steroid Hormones; Hormones; Humans; Nephrotic Syndrome; Pituitary Hormones; Thyroid Hormones; Vitamin D

Urinary transferrin loss is a typical feature in relapse of the idiopathic nephrotic syndrome, however, the impact on serum iron homeostasis and hematological parameters has not been studied systematically so far.. Therefore, we investigated serum iron (Fe), erythropoietin (EPO), ferritin (FN), transferrin (TF), total iron-binding capacity (TEBK), transferrin saturation and the soluble transferrin receptor (sTFR) combined with hematological parameters (hemoglobin, MCV, MCH) in 42 children with relapsing, steroid-sensitive nephrotic syndrome (NS) in remission (RM, n = 26) and relapse (RL, n = 16), including 13 patients who were studied in both states. Thirty-three age-matched healthy children served as controls.. Fe, TEBK and TF were significantly reduced in RL compared to RM in cross-sectional as well as in paired studies while ferritin, hematological parameters and EPO levels remained unchanged. A significant increase, however, of the soluble transferrin-receptor could be demonstrated in cross-sectional analysis comparing RL to RM and healthy controls (3568+/-713 mg/ml vs 2625+/-576 vs 2646+/-697; p < 0.001 respectively) as well as in paired analysis of 13 patients in RL and RM (p < 0.001).. We conclude that transient transferrin and iron deficiency occurs in RL of INS but this seems to be counterbalanced by upregulation of the sTFR, a mechanism that might be important in preventing the development of iron deficiency anemia during the active nephrotic state.

Topics: Adolescent; Child; Child, Preschool; Cross-Sectional Studies; Erythropoietin; Ferritins; Hemoglobins; Homeostasis; Humans; Iron; Nephrotic Syndrome; Recurrence; Reference Values; Transferrin

Primary nephrotic syndrome can, although infrequently, cause severe anemia. However, the mechanisms of the anemia remain unknown. We investigated the mechanism of anemia in nephrotic syndrome by measuring parameters of nephrotic syndrome and anemia in 44 nephrotic patients (male: female; 21:23, average age; 43.6 +/- 20.3 years). Nephrotic patients had significantly lower hematocrits than did healthy controls (43.3 +/- 3.7 vs. 46.8 +/- 3.4% in males, 37.4 +/- 3.5 vs. 40.8 +/- 2.8% in females). Serum erythropoietin (Epo) concentrations were correlated inversely with hemoglobin (Hb), hematocrit (Hct), and red blood cell corpuscle (RBC) counts. Furthermore, serum Epo correlated with the serum iron concentration, but not with the other parameters, such as reticulocytes, serum protein and proteinuria. However, the maximum Epo concentration was less than 100 mU/ml in spite of severe anemia, and this was thought to be inappropriate. On the contrary, urine Epo was not detected by the same method of serum Epo determination in spite of aggressive dialysis with distilled water. When four patients with severe anemia were subcutaneously administered recombinant Epo 6,000 unit two times a week, they showed marked improvement in Hb/Hct/RBC. The precise mechanism of anemia in NS was not elucidated by this investigation, but further study should clarify the causes of the inappropriately low concentration of serum Epo in patients with primary nephrotic syndrome.

Topics: Adult; Aged; Aged, 80 and over; Anemia; Erythrocyte Count; Erythropoietin; Female; Hematocrit; Hemoglobins; Humans; Male; Middle Aged; Nephrotic Syndrome

The most important contributors to the anemia of patients with chronic kidney disease are insufficient erythropoietin production and erythropoietin hyporesponsiveness, decreased red blood cell half-life, iron deficiency, and inflammation. However, in contrast to the role of kidney failure, that of proteinuria and nephrotic syndrome is less clear. Bissinger et al. now provide evidence in mouse models and patients with chronic kidney disease that heavy proteinuria alters erythrocyte metabolism and increases erythrocyte death.

Topics: Anemia; Animals; Erythropoietin; Humans; Mice; Nephrotic Syndrome; Proteinuria; Renal Insufficiency, Chronic

The increasing technological effectiveness has undoubtedly produced an improvement in clinical parameters of dialysis patients, but this satisfactory therapeutic result did not follow an adequate improvement in mortality or in the perception of quality of life as per patients. Furthermore, dialysis treatment is often associated with "inapparent charges" that reduce the perception of well-being, independently of clinical changes. Thirty years ago, we carried out a national survey on inapparent charges, which represent frustrating aspects that negatively affect patients' perception of their quality of life. Thirty years later, it seemed important for us to repeat the survey to understand if Italian legislative remodeling have introduced changes in procedures and social aspects of dialysis, as preservation of quality of life is an important aspect of the replacement treatment.

Topics: Chelation Therapy; Diagnostic Tests, Routine; Diet Therapy; Erythropoietin; Frustration; Geography, Medical; Humans; Italy; Nephrotic Syndrome; Patient Satisfaction; Patient Transfer; Patients; Procedures and Techniques Utilization; Quality of Life; Renal Dialysis; Surveys and Questionnaires

We report here the interesting case of a 76-year-old man with severe proteinuria who was diagnosed with systemic mastocytosis accompanied by a clonal non-mast-cell lineage haematological disorder (a non-secretory plasma cell dyscrasia). This is a unique report of systemic mastocytosis with a non-secretory plasma cell dyscrasia and nephrotic syndrome. The pathophysiological relevance between these entities along with the probability of occult amyloidosis is discussed.

Topics: Aged; Amyloidosis; Anemia; Biopsy; Bone Marrow; Clone Cells; Coloring Agents; Congo Red; Darbepoetin alfa; Drug Therapy, Combination; Erythropoietin; Factor X Deficiency; Gingiva; Hemorrhagic Disorders; Histamine Antagonists; Humans; Male; Mastocytosis, Systemic; Nephrotic Syndrome; Paraproteinemias; Prednisone; Proteinuria; Splenectomy; Splenomegaly; Subcutaneous Fat

Recent studies have demonstrated that erythropoiesis-stimulating agents (ESAs) induce a tissue-protective effect in the kidney. In this study, we examined whether continuous erythropoietin receptor activator (CERA), a long-acting ESA, could prevent kidney injury, especially podocyte damage, in a rat model of nephrotic syndrome induced by puromycin aminonucleoside (PAN).. Rats were injected with CERA (30 µg/kg) or vehicle 4 h before the injection of PAN (50 mg/kg). Renal function, kidney injury, and podocyte damage were assessed at 7 days.. The levels of proteinuria, BUN, and plasma creatinine significantly increased in rats with PAN-induced nephrosis. Treatment with CERA significantly prevented these deteriorations induced by PAN. Glomerular lesions, especially vacuolation of podocytes, and the increase of desmin expression in PAN-treated rats were significantly ameliorated by treatment with CERA. Treatment with CERA also significantly prevented the decrease in the protein productions of nephrin and podocin in the kidneys of PAN-treated rats. We found persistent activation of the Akt signaling pathway in the kidneys of CERA-treated rats.. CERA could ameliorate renal dysfunction in PAN-induced nephrosis, which might be due to the amelioration of podocyte injury. CERA inhibited the depletion of nephrin and podocin, key components of the glomerular filtration barrier, and alleviated proteinuria. Activation of the Akt signaling pathway might be involved in the renoprotective effect of CERA.

Topics: Animals; Erythropoietin; Male; Nephrotic Syndrome; Polyethylene Glycols; Puromycin Aminonucleoside; Rats; Rats, Wistar

Congenital nephrotic syndrome of the Finnish type (CNF) is due to NPHS1 mutation and is responsible for a variety of urinary protein losses. We report the case of a 4-month-old girl with a particularly severe form (proteinuria approximately 150 g/l) of CNF. She developed severe non-regenerative anaemia requiring bi-monthly blood transfusions despite daily EPO (600 UI/kg) and iron supplementation. Epoetin pharmacokinetics revealed a urinary loss of 27% of the given dose within the first 24 h after IV injection. However, plasma levels remained increased after 24 h (228 UI/l). Plasma transferrin and transcobalamin levels were undetectable. Atransferrinaemia and atranscobalaminaemia seem to be responsible for disturbed erythropoiesis.

Topics: Anemia; Blood Transfusion; Erythropoietin; Female; Hematinics; Humans; Infant, Newborn; Nephrectomy; Nephrotic Syndrome; Transcobalamins; Transferrin

Topics: Anemia; Angiotensin II Type 1 Receptor Blockers; Biphenyl Compounds; Child; Erythropoietin; Hemoglobins; Humans; Irbesartan; Iron; Kidney Transplantation; Male; Nephrotic Syndrome; Tetrazoles; Treatment Outcome

Podocyte injury is a significant contributor to proteinuria and glomerulosclerosis. Recent studies have shown a renoprotective effect of erythropoietin (EPO) during ischemic kidney disease. In this study, we examine mechanisms by which a long acting recombinant EPO analog, darbepoetin, may confer renoprotection in the puromycin aminonucleoside-induced model of nephrotic syndrome. Darbepoetin decreased the proteinuria of rats treated with puromycin. This protective effect was correlated with the immunohistochemical disappearance of the podocyte injury markers desmin and the immune costimulator molecule B7.1 with the reappearance of nephrin expression in the slit diaphragm. Podocyte foot process retraction and effacement along with actin filament rearrangement, determined by electron microscopy, were all reversed by darbepoetin treatment. The protective effects were confirmed in puromycin-induced nephrotic rats that had been hemodiluted to normal hematocrit levels. Furthermore, puromycin treatment of rat podocytes in culture caused actin cytoskeletal reorganization along with deranged nephrin distribution. All these effects in vitro were reversed by darbepoetin. Our study demonstrates that darbepoetin treatment ameliorates podocyte injury and decreases proteinuria by a direct effect on podocytes. This may be accomplished by maintenance of the actin cytoskeleton and nephrin expression.

Topics: Actins; Animals; Apoptosis; B7-1 Antigen; Cells, Cultured; Cytoskeleton; Darbepoetin alfa; Desmin; Disease Models, Animal; Dose-Response Relationship, Drug; Erythropoietin; In Situ Nick-End Labeling; Male; Membrane Proteins; Nephrotic Syndrome; Podocytes; Protective Agents; Proteinuria; Puromycin Aminonucleoside; Rats; Rats, Wistar; Receptor Protein-Tyrosine Kinases; Receptors, Erythropoietin; RNA, Messenger; Time Factors

Nephrotic syndrome (NS) is characterized by an excessive urinary protein excretion.. A woman, followed-up for NS, present progressive anemia, with no simple explanation. Plasma EPO is low with significant urinary EPO excretion. Treatment with EPO corrects hemoglobin level.. EPO deficiency due to excessive urinary excretion is an underestimated cause of anemia during NS.

Topics: Anemia; Erythropoietin; Female; Humans; Middle Aged; Nephrotic Syndrome; Recombinant Proteins; Time Factors; Treatment Outcome

ICR-derived glomerulonephritis (ICGN) mice are a novel inbred strain with hereditary nephrotic syndrome and are thus considered a good animal model of human idiopathic nephrotic syndrome. In the present study, we investigated the effect to erythrocyte production by human erythropoietin (hEPO) treatment in ICGN mice during the early nephrotic stage. Erythrocyte count, hemoglobin concentration and hematocrit value in hEPO-treated (5 U/body/day, for 5 days) ICGN mice were recovered to the levels found in normal ICR mice. In addition, there was no correlation between plasma creatinine level, a marker of renal function, and erythrocyte count after hEPO treatment. Therefore, anemia in ICGN mice may be caused by decreased production of EPO in the kidney following progressive parenchymal damage.

Topics: Anemia; Animals; Blood Chemical Analysis; Disease Models, Animal; Erythropoiesis; Erythropoietin; Female; Hematologic Tests; Humans; Kidney; Male; Mice; Mice, Inbred ICR; Nephrotic Syndrome; Recombinant Proteins

Anemia in persistent nephrotic syndrome (NS) has been described in a few case reports but has not been studied systematically. We present a group of 19 children with NS who developed anemia before the deterioration of kidney function. The aim of our study is to determine whether erythropoietin (EPO) and/or iron deficiency are causative factors and to evaluate the effect of EPO replacement therapy. Serum EPO levels, iron status, and vitamin B(12) concentrations were measured in nephrotic patients with anemia (NS-A) and compared with those of nephrotic children with normal hemoglobin (Hb) levels (NS-NHb; n = 13). Two control groups consisted of age-matched patients without kidney disease or hypoxemia with either iron deficiency anemia (IDA; n = 19) or normal Hb concentrations (NHb; n = 16). Most NS-A patients experienced persistent steroid-resistant NS, whereas most NS-NHb children had steroid-responsive NS. Although serum iron, ferritin, and B(12) levels were significantly lower in NS-A children, appropriate replacement therapy that resulted in normalization of ferritin and/or cobalamin levels did not lead to correction of the anemia. NS-A patients had greater EPO levels than those without anemia (21.6 +/- 3.3 versus 5.5 +/- 0.8 IU/L; P: < 0.001), but their response to anemia was inappropriately low compared with IDA children (EPO, 94.6 +/- 15.1 IU/L) despite similar Hb concentrations. EPO therapy for 4 to 9 months in 6 NS-A children with Hb levels less than 9 g/dL led to resolution of the anemia. In conclusion, anemia is a common feature of persistent NS that develops before the deterioration of kidney function. Depletion of iron stores may contribute to the development of anemia, but iron replacement therapy is ineffective. Nephrotic patients have EPO deficiency with a blunted response to anemia. The EPO deficiency is amenable to EPO therapy, which is recommended for this group of patients.

Topics: Adolescent; Anemia; Anemia, Iron-Deficiency; Child; Child, Preschool; Comorbidity; Erythropoietin; Female; Humans; Male; Nephrotic Syndrome

Topics: Alopecia; Epoetin Alfa; Erythropoietin; Hematinics; Humans; Male; Middle Aged; Nephrotic Syndrome; Recombinant Proteins; Zinc

Hemodialysis (HD) of infants with end-stage renal disease (ESRD) is technically difficult and labor intensive, although there are few data in the literature to document the outcomes of this treatment. We retrospectively reviewed all patients with ESRD who received HD between 1983 and 1997 who weighed <10 kg at the beginning of HD. A total of ten patients aged 2-27 months, weighing 3.5-9.5 kg, were identified. All patients were dialyzed through a central venous line; three had a failed sapheno-femoral loop and one a failed brachial shunt. Line clot was observed in nine and line sepsis in six patients. Subclavian vein stenosis was documented in one patient following removal of a clotted subclavian line. The mean urea reduction ratios calculated during the 1st and 3rd month of HD were only 54% and 49%, respectively. Anemia was a frequent problem, despite the use of erythropoietin in seven of the infants. Outcomes included: successful renal transplant in four, switch back to peritoneal dialysis in two, improved renal function and dialysis discontinuation in one, and death after withdrawal of treatment in three patients. All three patients who died were <5 months of age, weighed <5 kg, and were anuric; two of the three had congenital nephrotic syndrome. In conclusion, successful HD is possible in small children with ESRD, but morbidity is substantial and mortality is high.

Topics: Age Factors; Anemia; Body Weight; Child, Preschool; Erythropoietin; Humans; Infant; Kidney Failure, Chronic; Nephrotic Syndrome; Renal Dialysis; Retrospective Studies; Treatment Outcome

Topics: Aged; Anemia; Erythropoietin; Female; Humans; Nephrotic Syndrome; Recombinant Proteins

Topics: Anemia; Angiotensin-Converting Enzyme Inhibitors; Child; Enalapril; Erythropoietin; Female; Humans; Nephrotic Syndrome

Topics: Aged; Anemia; Erythropoietin; Humans; Male; Nephrotic Syndrome; Recombinant Proteins; Thalassemia

Topics: Adult; Anemia; Angiotensin-Converting Enzyme Inhibitors; Azathioprine; Drug Therapy, Combination; Enalapril; Erythropoietin; Female; Humans; Hypertension; Immunosuppressive Agents; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Nephrotic Syndrome; Recombinant Proteins; Reoperation; Tissue Donors

A 62-year-old woman presented with nephrotic syndrome and severe anemia although the renal function was not impaired. Renal biopsy revealed the histology of membranoproliferative glomerulonephritis, and the proteinuria was resistant to steroid therapy. Iron deficiency, bleeding and other causes of anemia were ruled out, however, her serum erythropoietin level was inappropriately low. The anemia was rapidly corrected by administration of recombinant human erythropoietin. It is suggested that inappropriately low erythropoietin level, in part at least, accounts for the anemia in nephrotic syndrome. It is proposed that erythropoietin therapy should be taken into consideration for severe anemia in nephrotic syndrome even when the renal function is not impaired.

Topics: Anemia; Erythropoietin; Female; Humans; Kidney; Middle Aged; Nephrotic Syndrome

Recent data indicated the importance of urinary losses of erythropoietin (Epo) in the pathogenesis of anaemia in patients with nephrotic syndrome. In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. We found that patients with SNP were characterized by lower plasma levels of Epo than healthy subjects but no differences were found in urinary excretion of Epo, endogenous Epo clearance and its fractional excretion (FEEpo). There were no differences between groups in FE beta 2m and FENa and plasma aldosterone levels but plasma renin activity was higher in patients with SNP than in the controls. No relationships were found between Epo levels and activity of the RAAS and sodium metabolism, respectively. Our data suggest that lower levels of plasma Epo in patients with SNP and normal renal excretory function are not due to urinary losses of Epo but rather to the decreased production/degradation ratio.

Topics: Adult; Albuminuria; beta 2-Microglobulin; Diabetes Mellitus, Type 2; Erythropoietin; Humans; Hypertension; Nephrotic Syndrome; Proteinuria; Renin-Angiotensin System; Sodium

Topics: Animals; Erythropoietin; Humans; Kidney Failure, Chronic; Nephrotic Syndrome; Rats

To prevent anemia in seven small children with congenital nephrotic syndrome of the Finnish type (age range 1 to 4 years), we gave recombinant human erythropoietin in a dose up to 150 IU/kg/per week. We then studied the limiting factors during 14 weeks. On a peritoneal dialysis regimen after nephrectomy, the patients grew considerably (range +0.1 to 2.2 kg/14 wk; mean + 1.3 kg/14 wk). The amount of blood taken for laboratory studies was estimated. Although the estimated erythrocyte volume increased, the improvement was masked in most patients by enhanced growth. In two patients the target hemoglobin value of 10 gm/dl was reached, and in three patients transfusions were avoided. The reticulocyte count rose in dose-dependent fashion. In five patients protein malnutrition was not prevented, although intake of protein was as recommended. The gradual decrease in serum ferritin values indicated that mobilization of iron stores was adequate. Serum iron values decreased, although in general remaining within normal limits. In six patients the serum copper concentration was low and in two the serum aluminum concentration was slightly elevated. Two patients had several episodes of infection. We conclude that in rapidly growing infants and small children receiving peritoneal dialysis after nephrectomy, the maintenance or elevation of the hemoglobin concentration depends on several limiting and coinciding factors. We speculate that, when protein is limited, body growth has priority over erythropoiesis. A higher dose of erythropoietin might have evoked a better response in hemoglobin concentration but might also have resulted in progression of the protein deficit.

Topics: Anemia; Blood Component Transfusion; Child, Preschool; Erythrocyte Count; Erythrocyte Indices; Erythrocytes; Erythropoiesis; Erythropoietin; Ferritins; Growth; Hemoglobins; Humans; Infant; Injections, Subcutaneous; Iron; Nephrectomy; Nephrotic Syndrome; Peritoneal Dialysis; Protein Deficiency; Protoporphyrins; Recombinant Proteins; Serum Albumin

Nephrotic syndrome (NS) is associated with a significant alteration of protein metabolism. While lowering the plasma concentrations of certain proteins, the disease often raises the level of certain other proteins. The current study was undertaken to determine the effect of NS on erythropoietin (EPO) metabolism.. We measured the EPO concentration in plasma and urine of 26 patients with NS by an immunologic assay using a rabbit antiserum against recombinant human EPO. The results were compared with those obtained in a group of 12 normal control subjects.. Despite a significant reduction in the hemoglobin concentration in the NS group compared with the control group (125 +/- 25 g/L versus 148 +/- 11 g/L, p less than 0.05), the plasma EPO concentration in the NS group was not significantly different from that seen in the control group (6.2 +/- 4.5 mU/mL versus 6.7 +/- 2.4 mU/mL, p = NS). No significant correlations were found between plasma EPO and hemoglobin concentration, serum creatinine, serum albumin, or urinary albumin excretion rate. Moreover, comparison of the NS patients with serum creatinine concentrations less than or equal to 1.5 mg/dL (133 mumol/L) with those exhibiting creatinine concentrations exceeding 1.5 mg/dL did not reveal a significant difference in mean plasma EPO concentration. Significant amounts of EPO were found in the urine of the patients with NS, while none was detected in the urine of the control subjects.. We conclude that plasma EPO is inappropriately low in patients with NS. This is due, at least in part, to the urinary/renal losses of this protein and can potentially contribute to anemia in NS patients or compound the problem in those with concurrent renal insufficiency and diminished EPO production.

Topics: Adolescent; Adult; Aged; Erythropoietin; Female; Humans; Male; Middle Aged; Nephrotic Syndrome

Erythrocytosis has been observed in association with a number of renal diseases. We report for the first time the occurrence of true erythrocytosis in a patient with nephrotic syndrome due to idiopathic membranous glomerulopathy. Serum erythropoietin activity was found to be normal. The mechanism responsible for the erythrocytosis of renal parenchymal disease remains to be elucidated.

Topics: Adult; Basement Membrane; Erythropoietin; Humans; Kidney Glomerulus; Male; Microscopy, Electron; Nephrotic Syndrome; Polycythemia; Renin

A 23-year-old-man had true erythrocytosis and the nephrotic syndrome. A renal biopsy specimen showed focal sclerosing glomerulonephritis and nephrosclerosis. Both serum and urinary erythropoietin levels were increased, and plasma renin activity was in the high normal range. The association of erythrocytosis and glomerulonephritis with the nephrotic syndrome is reviewed, and the uniqueness of this association is proposed. Finally, a dissociation between these hormones was demonstrated using water immersion to the peck as a suppressive maneuver.

Topics: Adult; Biopsy; Erythropoietin; Glomerulosclerosis, Focal Segmental; Humans; Immersion; Kidney; Male; Microscopy, Electron; Nephrotic Syndrome; Polycythemia; Renin

Topics: Aged; Anabolic Agents; Anemia, Aplastic; Erythropoietin; Hematopoietic Stem Cells; Humans; Male; Nephrotic Syndrome