Nephrotic Syndrome In Adults Research Articles

Rituximab as a front-line therapy for adult-onset minimal change disease with nephrotic syndrome.

Minimal change disease (MCD) accounts for 15% of adult nephrotic syndrome (NS) cases. Adult-MCD patients may have more severe clinical features than pediatric patients. In children, Rituximab (RTX) has been used since 2006 to treat frequently relapsing NS. In adults, data about the efficacy of RTX for MCD are limited. We report our experience on the use of RTX in adult biopsy-proven MCD. Our series includes 6 adult patients (2 males and 4 females), age 45–73 years, treated with RTX (4 weekly doses of 375 mg/m2). Proteinuria decreased from 11,2 (23–4.8) g/24 hours to 0.6 (0–2) g/24 hours after 6 months, and to 0.4 (0–1, 4) g/24 h in the 4 pts with the longer follow-up. Creatinine decreased from 1.95 (0.5–5) mg/dl to 0.88 (0.6–1.3) mg/l. Five patients achieved a complete renal remission, while in 1 pt proteinuria decreased by 75%. RTX successfully depleted CD19 lymphocytes in 100% of pts for at least 6 months. No clinically relevant adverse events have been observed. This case series shows a remarkable efficacy of RTX in treatment of MCD. RTX can be an attractive alternative both in recurrent forms and in induction-therapy of MCD. RTX may be preferentially used in patients at a high risk of development of the adverse effects of corticosteroids and should be considered as an alternative option in patients with recurrent NS. Additional data are needed to inform clinical practice on how best to use RTX in this patient population, so that definitive randomized trials can be planned.

Genetic determinants of the development and course of membranous nephropathy.

Membranous nephropathy (MN) is one of the most common causes of nephrotic syndrome in adults and is classified as either primary (idiopatic) or secondary MN according to underlying etiology (the later result from some known disease such as systemic autoimmune diseases, infections, malignancies, drugs, etc). In recent years, phospholipase A2 receptor 1 (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A) were identified as two major podocytic antigens involved in the pathogenesis of idiopatic MN (IMN). And the discovery of circulating antibodies specific for these target antigens has transformed the diagnostic workup and significally improved management of IMN. However why do such antibodies develop is not conclusively established. The role of underlying genetic factors is discussed. The review presents the results of recent studies, that have shown significant associations of specific genetic factors (particularly human leucocyte antigen class II and PLA2R1 genes) with IMN.

Role of melatonin receptor 1A and pituitary homeobox-1 coexpression in protecting tubular epithelial cells in membranous nephropathy.

Membranous nephropathy (MN), a type of glomerular nephritis, is one of the most common causes of nephrotic syndrome in adults. Although it is known that melatonin plays a protective role in MN, the role of melatonin receptors in the pathophysiology of MN is unclear. Using an experimental MN model and clinical MN specimens, we studied melatonin receptor expression and found that melatonin receptor 1A (MTNR1A) expression was significantly downregulated in renal tubular epithelial cells. Molecular studies showed that the transcription factor pituitary homeobox-1 (PITX1) promoted MTNR1A expression via direct binding to its promoter. Treatment of a human tubular cell line with albumin to induce injury resulted in the stable reduction in MTNR1A and PITX1 expression. PITX1 levels were significantly downregulated in tubular epithelial cells from mice MN kidneys and MN renal specimens. Knockdown of MTNR1A, PITX1, or cyclic adenosine monophosphate-responsive element-binding protein (CREB) decreased E-cadherin (CDH1) expression, but upregulated Per2 and α-smooth muscle actin (αSMA) expression. Blockade of the MTNR1A receptor with luzindole in MN mice further impaired renal function; this was accompanied by CDH1 downregulation and Per2 and αSMA upregulation. Together, our results suggest that in injured tissue, decreased PITX1 expression at the MTNR1A promoter regions leads to decreased levels of MTNR1A in renal tubular epithelial cells, which increases the future risk of MN.

The expressional disorder of the renal RAS mediates nephrotic syndrome of male rat offspring induced by prenatal ethanol exposure

This study aimed to prove that prenatal ethanol exposure (PEE) can induce nephrotic syndrome in male rat offspring and to explore the underlying intrauterine programming mechanisms. Pregnant Wistar rats were intragastrically administered ethanol (4 g/kg d) from gestational day (GD) 9 to GD 20, and the male fetuses were delivered by cesarean section at GD20 and the male adult offspring were euthanized at postnatal week (PW) 24. In vitro, the primary metanephric mesenchyme cells were treated with ethanol at concentrations of 15–60 mM. The results indicated that the kidneys of adult offspring in the PEE group exhibited glomerulosclerosis as well as interstitial fibrosis. The levels of serum creatinine and urine protein were elevated; the serum total cholesterol level was increased and the serum albumin concentration was reduced. In the fetal kidney, developmental retardation was presented in the PEE group via pathological examinations, accompanied by the expressional inhibition of the glial-cell-line-derived neurotrophic factor/c-ret tyrosine kinase receptor (GDNF/c-ret) signaling pathway. Although serum angiotensin II (Ang II) level and the gene expression of renal angiotensin-converting enzyme (ACE) were increased in the PEE group, the expression of renal angiotensin II type 2 receptor (AT2R) was significantly inhibited, accompanied by a reduction in the H3K27ac level on the AT2R gene promoter. In the non-classical renin-angiotensin system (RAS), the expression of renal angiotensin converting enzyme 2 (ACE2) and Mas receptor (MasR) were inhibited in the PEE group. The above changes of the classical and non-classical RAS all sustained from utero to adulthood. In vitro, ethanol elevated the gene expression of ACE and angiotensin II type 1a receptor (AT1aR) whereas it reduced the expression of AT2R, ACE2, and MasR, accompanied by a reduction in the H3K27ac level on AT2R gene promoter. Taken together, these results suggested that PEE can induce fetal kidney developmental retardation and adult nephrotic syndrome, and direct regulation of ethanol to the renal RAS was involved in the mechanism of nephrotic syndrome induced by PEE.

Membranous nephropathy succeeding autologous hematopoietic stem cell transplant: a case report

BackgroundMembranous nephropathy (MN), the leading cause of nephrotic syndrome in adults, is characterized by the deposition of subepithelial immune deposits. Most of the cases are primary, while only approximately 25% of the cases are secondary to some known diseases. Recently, MN has been considered to be a possible presentation of chronic graft-versus-host disease (GVHD) of the kidney in allogeneic hematopoietic stem cell transplantation (HSCT) patients. In autologous HSCT populations, there have been scarce reports of associated MN, as a result of immune dysregulation leading to systemic autoimmunity and miming chronic GVHD.Case presentationWe report an exceptional case of MN associated to an acute renal failure occurring within days following an autologous HSCT indicated by multiple myeloma. There was no evidence of GVHD or myeloma relapse. A complete remission of nephrotic syndrome with normalization of renal function were rapidly obtained by corticosteroid therapy.ConclusionThis is the first published case of acute renal failure due to MN occurring in the acute phase of an autologous HSCT. These findings support the antibodymediated autoimmune glomerular disease.

Urine proteomics of primary membranous nephropathy using nanoscale liquid chromatography tandem mass spectrometry analysis

BackgroundPrimary membranous nephropathy (PMN) is an important cause of nephrotic syndrome in adults. Urine proteome may provide important clues of pathophysiological mechanisms in PMN. In the current study, we analyzed and compared the proteome of urine from patients with PMN and normal controls.MethodsWe performed two technical replicates (TMT1 and TMT2) to analyze and compare the urine proteome from patients with PMN and normal controls by tandem mass tag (TMT) technology coupled with nanoscale liquid chromatography tandem mass spectrometry analysis (LC–MS/MS). Gene ontology (GO) enrichment analysis was performed to analyse general characterization of the proteins. The proteins were also matched against the database of Kyoto Encyclopedia of Genes and Genomes (KEGG). For validation, Western blot was used to analyze the selected proteins.ResultsA total of 509 proteins and 411 proteins were identified in TMT1 and TMT2, respectively. 249 proteins were both identified in two technical replicates. GO analysis and KEGG analysis revealed immunization and coagulation were predominantly involved. Among the differential protein, the overexcretion of alpha-1-antitrypsin (A1AT) and afamin (AFM) were validated by Western blot analysis.ConclusionsOur data showed the important role of immunologic mechanism in the development of PMN, and the value of urinary A1AT and AFM in biomarker discovery of patients with PMN. The discovery of the overexcretion of A1AT and AFM in the urine can help to further elucidate pathogenetic mechanisms involved in PMN.

Flu B or not Flu B: An atypical case of minimal change disease triggered by Influenza B presenting with multi-organ dysfunction

Minimal change disease (MCD) accounts for 10-15% of idiopathic nephrotic syndrome in adults. Patients typically present with nephrotic range proteinuria, hypertension, microscopic hematuria and can even progress to acute renal failure. MCD can be primary (idiopathic) or secondary from etiologies such as cancer, medications, autoimmune conditions and infections. The link between infectious etiologies for MCD is important to recognize, since MCD tends to show a good response to treatment of the underlying cause. Influenza A has been reported as a secondary cause of MCD and rarely, influenza A, not B, can also present with liver failure. We present an atypical case of a 60-year-old female with no past medical history who presented with liver failure along with acute kidney injury and nephrotic range proteinuria. She was diagnosed with liver failure and secondary MCD from influenza B, the first reported case, and made a full recovery with treatment of Influenza B.

Histopathological study of nephrotic syndrome in adults: A Moroccan report.

The reported causes of nephrotic syndrome (NS) varies between different countries. In this retrospective study, we aimed to evaluate the underlying causes of NS in adult patients who underwent renal biopsy in a region of Morocco and we also determined the distribution of histopathological diagnoses with regard to the age subgroups and genders from January 2007 to December 2016. Patients were divided into four groups according to age at the time of renal biopsy. A total of the 257 patients with NS were included in this study. The mean age of the patients was 40.9 ± 16.7 years; male gender was preponderant (61.9%). One hundred and sixty-six (64.6 %) and 81 (35.4%) patients were diagnosed as primary and secondary glomerulonephritis, respectively. The most common diagnosis in NS was membranous nephropathy (MN) (22.2%), followed by minimal change disease (MCD) (20.6%), and lupus nephritis (LN) (13.6%). Among the patients aged 15-30, 31-45, 46-60, and >61 years, the most common cause of NS was MCD (32.1%), MN (29.6 %), MN (26.1%), and amyloidosis (AM) (28.2%), respectively. The proportion of patients with MCD and LN decreased in parallel with patient age and the proportion of patients with renal AM increased in parallel with patient age. Among the female patients aged 15-30 and 31-45 years, LN was the leading cause of NS (41.5 and 36.7%, respectively). Among the male patients aged 15-30 years, MCD was the leading cause of NS (43.2%). Our study over 10 years represents an important data of regional variations of glomerular diseases presenting with adult-onset NS.

The Genetic and Environmental Factors of Primary Membranous Nephropathy: An Overview from China

Background: Primary membranous nephropathy (pMN) is the most common cause of nephrotic syndrome in adults. The discovery of the 2 autoantigens, M-type phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A), has defined pMN as an autoimmune disease. A remarkable increase in the frequency of pMN in primary glomerular disease was witnessed in China. The genetic and environmental contributors to disease susceptibility have been investigated in these patients. Summary: We reviewed recent publications in genetic and environmental studies of pMN, focusing mainly on those undertaken in China. Following a genome-wide association study, the gene-gene interaction between the 2 most significant risk factors, PLA2R1 and DQA1, was validated in Chinese patients with MN. Fine mapping on human leukocyte antigen (HLA) locus found that DRB1*1501 and DRB1*0301 were risk alleles. Three amino acid residues on positions 13 and 71 of HLA-DRβ1 chain may confer the susceptibility to pMN by presenting T-cell epitopes on PLA2R. Another study found that DRB3*0202 was the most likely culprit allele for the signal at DRB1*0301. One environmental risk factor for pMN has been identified as the long-term exposure to high levels of PM_2.5 in Chinese patients with MN. Each 10 μg/m³ increase in PM_2.5 concentration was associated with 14% higher odds for pMN in the regions with PM_2.5 above 70 μg/m³. Key Message: A gene-environment interaction is suspected as an underlying mechanism for the increasing trend of pMN in China.

Analysis of native kidney biopsy: Data from a single center from Bihar, India.

This is a retrospective study of all native kidney biopsies performed at our center between October 1, 2012 and March 31, 2015. Relevant clinical and laboratory variables were recorded. Biopsy samples were processed for light microscopy and immunofluorescence in all cases. Histological classification was adapted from the World Health Organization recommendations. The indications for kidney biopsy were nephrotic syndrome in adults in 190 cases, rapidly progressive renal failure in 43, unexplained renal failure in 25, and steroid-resistant nephrotic syndrome in children in 12. The mean age of the patients was 31.48 ± 13.46 years. Male-to-female ratio was 1.87:1. Mean serum creatinine (SCr) of the patients was 2.36 ± 2.07 mg/dL. Primary glomerulonephritis accounted for 88.89% of cases (240) while secondary glomerulonephritis accounted for 7.40% of total cases (20). Interstitial disease accounted for 1.5% and vascular disease for 2.2%. The most common lesion among primary glomerulonephritis was focal segmental glomerulosclerosis (FSGS) (31.11%) followed by diffuse proliferative glomerulonephritis (DPGN) (13.33%) and membranous glomerulonephritis (MGN) (12.59%). Among secondary glomerulonephritis, lupus nephritis was the most common (5.56%). In patients with SCr 1.4 mg/dL or less (n = 131), FSGS was the most common histology (17.26%) followed by MGN (23.66%) and minimal change disease (7.63%). Whereas, in patients with SCr more than 1.4 mg/dL (n = 139), DPGN was the most common diagnosis (23.74%) followed by FSGS (17.26%) and IgAN (12.23%). Fourteen patients (5.2%) had one or more episode of gross hematuria, three of whom required blood transfusion. The overall FSGS was the most common lesion seen. When we consider only patients with deranged renal function, DPGN was the most common histopathological lesion. The reason for disproportionate high incidence for DPGN is not clear and requires further research.

Rituximab as a Therapeutic Option for Steroid-Sensitive Minimal Change Nephrotic Syndrome in Adults.

Minimal change nephrotic syndrome (MCNS) usually responds to steroids but frequently relapses, requiring additional treatment with immunosuppressive agents. Rituximab is a chimeric murine/human monoclonal immunoglobulin G1 antibody that targets CD20, a B-cell differentiation marker. B-cell recovery begins at approximately 6 months following the completion of treatment. Rituximab has a beneficial effect, with the sustained remission or reduction of proteinuria in patients with steroid-dependent MCNS. Relapses are thought to be associated with an increase in CD19 cells. The mean serum half-life of rituximab was reported to be 10-15 days in patients with steroid-dependent MCNS. Only infusion reactions, such as rash and chills, occurred after single-dose rituximab infusion and can be managed by pre-medication or infusion rate adjustments. Even though severe adverse effects of rituximab are not expected, we must be aware of potentially life-threatening adverse effects. Controlled randomized trials that include adult patients with steroid-dependent MCNS are required to prove the efficacy and safety of rituximab and to evaluate the cost-effectiveness of rituximab treatment. In this review, we highlight recent studies and discuss the effects of these studies on the management of patients with MCNS in adults.

Histopathological spectrum of Adult Nephrotic Syndrome over 16 years at a Tertiary care center in Mumbai with Clinicopathological ,Electron microscopy and Immunoflurescence Correlation of Renal biopsies

Background: The pattern of diseases causing adult nephrotic syndrome varies globally as well as in India. The aim of our study was to analyze the spectrum of patients with biopsy proven nephrotic syndrome in adults over 15 years, in respect with incidence , age distribution and correlate the clinicopathological features, electron microscopy and immunofluorescence. Methods: We have evaluated and analyzed retrospectively 263 renal biopsies of adult nephrotic syndrome over a consecutive period of 16 years (January 2000 to December 2015) in our tertiary care Hospital. Result: In our study of 235 (89.35%) adequate renal biopsy cases overall male predominance was seen (M: F ratio 1.7:1) with maximum males noted in diabetic nephropathy (M: F ratio 4:1) while SLE was seen exclusively in female (M: F ratio 0:6). Minimal change disease (26.38%), followed by MPGN (16.17%) and FSGS (15.74%) were the common histopathological lesions. In 15-45 years age majority of 78.72% cases were observed with prominently histomorphological pattern as MCD( 25.10%),followed by FSGS ( 13.61%) & MPGN (13.19%). In 45-85 years age , 21.28% cases majority were of membranous glomerulonephritis (5.10%) and diabetic nephropathy (4.25%). Primary glomerular diseases accounted for 78.3% cases commonest was MCD (26.38%) and secondary glomerular diseases in 21.7% of cases, most common being amyloidosis (7.23%) Light microscopy, immunopathology findings correlated with electron microscopy findings in 79 cases (91.86%) out of 86 cases. Sample error was main reason of non correlation of EM & LM diagnosis ,especially in FSGS. Conclusion: This data analysis is essential to study the prevalence of biopsy proven renal diseases and its variation and distribution as per age .Which can improve the understanding of utility of renal biopsy for future research of renal parenchymal diseases in adults.

Phospholipase A2 receptor (PLA2R) related membranous nephropathy - not specific for idiopathic cases any more

Context: Membranous nephropathy is among the most common causes of nephrotic syndrome in adults. Evidence Acquisitions: PubMed, EBSCO, Web of Science, directory of open access journals (DOAJ), EMBASE, and Google Scholar with keywords of phospholipase A2 receptor, PLA2R, membranous nephropathy, nephrotic syndrome, idiopathic nephrotic syndrome and glomerulonephritis have been searched. Results: The recent finding that around 70%-80% of the idiopathic cases of membranous nephropathy express Phospholipase A2 receptor (PLA2R) in their kidney biopsies and antiPLA2R antibody in their serum was initially considered specific to the idiopathic cases. However, more recent studies have shown that while PLA2R glycoprotein expression, and anti-PLA2R antibodies, are specific to membranous nephropathy and are not seen in other glomerulonephritides, they can be as frequently expressed in certain secondary forms of membranous nephropathy. Conclusions: In this communication we intend to briefly review the new data regarding tissue and sero-positivity for PLA2R in different types of secondary membranous nephropathy, as well as pathologic and immunofluorescence features of them as compared to the idiopathic cases.

P256 Hypogammaglobulinemia as presenting sign of nephrotic syndrome

Secondary hypogammaglobulinemia has been described. We report a case of severe rapid-onset hypogammaglobulinemia presenting as adult onset nephrotic syndrome.

Structure of Human M-type Phospholipase A2 Receptor Revealed by Cryo-Electron Microscopy

M-type phospholipase A2 receptor (M-PLA2R) is a member of the mannose receptor family and known as the receptor of secretory phospholipase A2s. It has also been identified as the major autoantigen of idiopathic membranous nephropathy, one of the most common causes for nephrotic syndrome in adults. Here we determine the structure of human M-PLA2R ectodomain by cryo-electron microscopy. The results show that the ectodomain has high internal flexibility and forms a compact dual-ring-shaped conformation at acidic pH and adopts extended conformations at basic pH. The inter-domain interactions of human M-PLA2R are explored by the binding studies with individual domains, showing the mechanism of the conformational change. In addition, the biochemical data suggest that mouse M-PLA2R recognizes mouse secretory phospholipase A2-G1B only at physiological or basic pH, rather than at acidic pH. These results suggest that the pH-dependent conformational change might play important roles in the functional activities of M-PLA2R such as ligand binding and release, and may also be relevant to the immunogenicity in membranous nephropathy.

Immunohistochemical and serological characterization of membranous nephropathy in children and adolescents.

Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults, but is less frequent in children. Antibodies against four antigens leading to MN have been described in children: phospholipase A2 receptor 1 (PLA2R1), thrombospondin type-1 domain-containing 7A (THSD7A), neutral endopeptidase (NEP), and cationic bovine serum albumin (BSA). Twelve children with MN were included in this study. Sera of all patients were analyzed for antibodies against PLA2R1, THSD7A, NEP, and BSA. All sera were also analyzed using Western blot with human glomerular extracts (HGE) under non reducing conditions. In 5 cases renal biopsies were analyzed for PLA2R1, THSD7A, NEP, BSA, and all IgG subclasses. Six patients were PLA2R1-antibody-positive, whereas THSD7A, NEP, and BSA antibodies were not found in any of our 12 patients. All sera were analyzed by Western blot using human glomerular extracts; however, no further potential antigens were found. Five kidney biopsies from 2 PLA2R1-antibody-positive and 3 PLA2R1-antibody-negative patients were available for additional analyses, confirming the diagnosis of PLA2R1-associated MN in 2 cases, whereas none of the biopsies revealed enhanced staining for THSD7A, NEP or BSA. IgG2 and IgG4 stainings were positive in both patients with PLA2R1-associated MN and negative in the other biopsies. During follow-up (median 24 months), 4 children with PLA2R1-associated MN went into remission, preceded by decline of PLA2R1 antibodies. Five of the 6 PLA2R1-antibody-negative children went into remission. In children with MN, PLA2R1-associated MN appears to be common, whereas MN associated with THSD7A, NEP or BSA was not encountered. PLA2R1 antibody levels are closely associated with disease activity, whereas PLA2R1-antibody-negative patients often have a good prognosis. However, the pathophysiology of MN in a considerable number of children remains unclear.

A Comprehensive Narrative Review of Diagnostic Biomarkers in Human Primary Membranous Nephropathy

Membranous nephropathy (MN) is relatively major cause of nephrotic syndrome in adults which is recognized as an organ-specific autoimmune disease. The etiology of most cases is idiopathic, whereas the secondary MN is caused by systemic autoimmune diseases, infections, medications and malignancies. The idiopathic disease is developed by the formation of sub-epithelial immune complex deposits most likely due to binding the circulating auto-antibodies to intrinsic antigen on podocytes. The major auto antibody is the anti-phospholipase A2 receptor(anti-PLA2R), however, it is not enough sensitive. Several attempts for diagnostic biomarker identification by modern analytical technologies have been devoted recently. This article reviews the biomarker candidates for primary type of MN that are detected by different approaches on human subjects.

A case of membranous glomerulopathy associated with lung cancer and review of the literature.

Membraneous nephropathy (MN) is the most commonly occurring nephrotic syndrome in adults as well as the most common paraneoplastic nephropathy associated with solid tumors, and it is mostly associated with gastrointestinal system and lung carcinomas. Accurate diagnosis is important as the treatment of paraneoplastic glomerulonephritis is very varied from that of idiopathic ones. In the current report, a case of a patient that was referred with proteinuria and edema and was diagnosed with lung cancer, and responded markedly to treatment of malignancy, with improvement of MN, is presented. Active cancer is present in all patients with paraneoplastic MN. In numerous patients, the paraneoplastic MN and cancer diagnoses are made within one year of each other. The treatment of paraneoplastic syndromes is usually associated with the treatment of primary malignancy. There are conflicting data on which treatment modality is more suitable. In conclusion, further studies are required in order to determine the actual incidence of cancer in patients with nephropathy, explain the physiopathological association between cancer and nephropathy and to determine the most suitable treatment approaches.

Membranous nephropathy: a retrospective observational study of membranous nephropathy in north east and central London

BackgroundMembranous nephropathy (MN) is the leading cause of nephrotic syndrome in adults. MN is a clinically heterogeneous disease and it is difficult to accurately predict outcomes (including end stage renal failure) at presentation and whom to treat with potentially toxic therapies. We aimed to identify factors predicting outcome in MN in our cohort from two large tertiary London units by undertaking a retrospective data analysis of 148 biopsy-proven MN patients from North East and Central London between 1995 and 2015.MethodsReview of clinical and biochemistry databases.ResultsSurprisingly, patients that reached end stage renal failure (ESRF) had a less severe nephrosis compared to those that did not develop ESRF; serum albumin 33 g/L (3.3 g/dL) versus 24 g/L (2.4 g/dL), p = 0.002 and urinary protein creatinine ratio (uPCR) 550 mg/mmol (5500 mg/g) versus 902 mg/mmol (9020 mg/g), p = 0.0124. The correlation with ESRF was strongest with the presenting creatinine; 215 μmol/L (2.43 mg/dL) compared to 81 μmol/L (0.92 mg/dL), p < 0.0001. Patients presenting with creatinine of >120 μmol/L (1.36 mg/dL; corresponding to an eGFR of ≤60 ml/min in non-Black males) had an increased rate of ESRF and a faster decline. Other traditional risk factors for progression were not significantly associated with ESRF.Black patients presented with higher serum creatinine but no statistically significant difference in the estimated glomerular filtration rate, a higher rate of progression to ESRF and had a poorer response to treatment.ConclusionsThis ethnically diverse cohort does not demonstrate the traditional risk profile associated with development of ESRF. Thus, careful consideration of therapeutic options is crucial, as current risk modelling cannot accurately predict the risk of ESRF. Further studies are required to elucidate the role of antibodies and risk genes.

Spectrum of Nephrotic Syndrome in Adults: Experience in Single Tertiary Care Centre

Spectrum of Nephrotic Syndrome in Adults: Experience in Single Tertiary Care Centre