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Authors are the souls of any journal, and deserve much respect. To publish a journal manuscripts are needed from authors. Authors have a great responsibility for producing facts of their work in terms of number and results truthfully and an individual honesty is expected from authors in this regards. Both ways its true "No authors-No manuscripts-No journals" and "No journals–No manuscripts–No authors". Reviewing a manuscript is also a very responsible and important task of any peer-reviewed journal and to be taken seriously. It needs knowledge on the subject, sincerity, honesty and determination. Although the process of reviewing a manuscript is a time consuming task butit is expected to give one's best remarks within the time frame of the journal.
Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
Timely publication of journal: Publication of manuscripts and bringing out the issue in time is one of the positive aspects of JCDR and is possible with strong support team in terms of peer reviewers, proof reading, language check, computer operators, etc. This is one of the great reasons for authors to submit their work with JCDR. Another best part of JCDR is "Online first Publications" facilities available for the authors. This facility not only provides the prompt publications of the manuscripts but at the same time also early availability of the manuscripts for the readers.
Indexation and online availability: Indexation transforms the journal in some sense from its local ownership to the worldwide professional community and to the public.JCDR is indexed with Embase & EMbiology, Google Scholar, Index Copernicus, Chemical Abstracts Service, Journal seek Database, Indian Science Abstracts, to name few of them. Manuscriptspublished in JCDR are available on major search engines ie; google, yahoo, msn.
In the era of fast growing newer technologies, and in computer and internet friendly environment the manuscripts preparation, submission, review, revision, etc and all can be done and checked with a click from all corer of the world, at any time. Of course there is always a scope for improvement in every field and none is perfect. To progress, one needs to identify the areas of one's weakness and to strengthen them.
It is well said that "happy beginning is half done" and it fits perfectly with JCDR. It has grown considerably and I feel it has already grown up from its infancy to adolescence, achieving the status of standard online e-journal form Indian continent since its inception in Feb 2007. This had been made possible due to the efforts and the hard work put in it. The way the JCDR is improving with every new volume, with good quality original manuscripts, makes it a quality journal for readers. I must thank and congratulate Dr Hemant Jain, Editor-in-Chief JCDR and his team for their sincere efforts, dedication, and determination for making JCDR a fast growing journal.
Every one of us: authors, reviewers, editors, and publisher are responsible for enhancing the stature of the journal. I wish for a great success for JCDR."
Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
E-mail: drrajendrak1@rediffmail.com
On May 11,2011
Dr. Shankar P.R.
"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."
Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
E-mail: ravi.dr.shankar@gmail.com
On April 2011 Anuradha
Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.
Dr. Anuradha
E-mail: anuradha2nittur@gmail.com
On Jan 2020
Case report
Full Version
Mixed Cryoglobulinaemic Glomerulonephritis Type II in the Setting of Rheumatoid Arthritis and Chronic Hepatitis B: A Case Report
Correspondence Address :
Dr. Vijay Jeyachandran,
Senior Resident, Department of Nephrology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Sawangi, Wardha-442107, Maharashtra, India.
E-mail: vijayjeyachandran2010@gmail.com
Mixed (Type II) cryoglobulinaemia is a systemic immune-complex vasculitis often linked to chronic infections especially Hepatitis C Virus (HCV) or autoimmune disease. Chronic Hepatitis B Virus (HBV) associated cryoglobulinaemic is rare, and its coexistence with Rheumatoid Arthritis (RA) is especially unusual. The authors report a 45-year-old female with long-standing seropositive RA on methotrexate and chronic HBV presented with fatigue, arthralgias, palpable purpura on her legs, and new-onset oedema. Laboratory workup showed elevated serum creatinine, nephrotic-range proteinuria, hypoalbuminaemia, haematuria, and a positive Rheumatoid Factor (RF). Antinuclear Antibody (ANA) and Anti-double-stranded deoxyribonucleic acid (anti-dsDNA) were negative. Complement levels i.e., Component 3 (C3) moderately reduced, Component 4 (C4) severely low, and positive mixed cryoglobulins with a high Immunoglobulin M (IgM) cryocrit. HCV and Human Immunodeficiency Virus (HIV) serologies were negative. Renal biopsy showed a diffuse endocapillary proliferative, Membranoproliferative Glomerulonephritis (MPGN) with hyaline “pseudothrombi.” Immunofluorescence disclosed granular capillary wall deposits of IgM, Immunoglobulin G (IgG) (both kappa and lambda), C3, and C1q, consistent with Type II cryoglobulinaemic GN. Treatment included high-dose corticosteroids and HBV antiviral drugs. Despite antiviral therapy and plasmapheresis, renal failure progressed requiring haemodialysis, and the patient died within three weeks due to disease-related complications and nosocomial infection. The present case highlights that RA and HBV can together underlie cryoglobulinaemic GN. Early recognition using RF, complement, and cryocrit testing and biopsy-guided therapy are critical. Purpura, positive RF, and low C4/C3 should prompt consideration of mixed cryoglobulinaemic vasculitis.
Autoimmune disease, Immune complex diseases, Membranoproliferative glomerulonephritis, Vasculitis
A 45-year-old female presented with complaints of gradually worsening fatigue, arthralgia, and new-onset lower extremity oedema for the past few weeks. The patient also noted the appearance of multiple non blanching purpuric lesions over both legs during this period. There was no history of fever, weight loss, or haematuria. She had a past medical history of seropositive RA for 10 years, for which she had been receiving low-dose methotrexate (15 mg/week orally for the past 8 years), with moderately active disease (RF positive and Anti-Cyclic Citrullinated Peptide (anti-CCP) negative). She was also a known case of chronic hepatitis B infection, which had remained untreated with normal Alanine Aminotransferase (ALT) levels and low-level HBV Deoxyribonucleic Acid (DNA). On admission due to superadded immunosuppression related sepsis, her viral loads (HBV DNA copy no. 21,000 IU/mL) became so high suggestive of active infection. The constellation of purpura, arthralgia, and RF positivity raised suspicion for mixed, cryoglobulinaemic vasculitis. Neurological examination was normal, with intact higher mental functions, cranial nerves, motor and sensory systems, and no focal neurological deficits.
Investigations
Laboratory investigations (Table/Fig 1) revealed elevated serum creatinine (2.3 mg/dL from a baseline of ~0.9 mg/dL) with reduced estimated Glomerular Filtration Rate (eGFR) (30 mL/min) and nephrotic-range proteinuria (UPCR 3.5 g/g), along with hypoalbuminaemia (2.5 g/dL). Complement levels were decreased (C3-60 mg/dL, C4-4 mg/dL). Autoimmune evaluation showed markedly positive RF with negative ANA, anti-dsDNA, and Antineutrophil Cytoplasmic Antibodies (ANCA). Cryoglobulin testing was positive, demonstrating mixed cryoglobulins (monoclonal IgMκ with polyclonal IgG; cryocrit-4%). Viral serology confirmed Hepatitis B Surface Antigen (HBsAg) positivity with Antibody to the Hepatitis B core antigen (Anti-HBc) IgG and detectable HBV DNA, while hepatitis-C and HIV were negative. Serum protein electrophoresis showed polyclonal gammopathy, and Urine Protein Electrophoresis (UPEP) revealed no monoclonal protein. These findings were consistent with immune complex-mediated GN, specifically Type II cryoglobulinaemic GN.
Biopsy
A percutaneous renal biopsy was performed. Light microscopy revealed diffuse endocapillary proliferative GN with lobular accentuation (MPGN pattern). Glomeruli were hypercellular with prominent neutrophilic infiltration and mesangial expansion. Notably, numerous Periodic Acid-Schiff (PAS)-positive eosinophilic “hyaline thrombi” (immune complex aggregates) occluded capillary lumina. Basement membranes showed irregular duplication (double contours) and focal intracapillary pseudothrombi. There was no significant necrosis or crescent formation. Vessels and tubule interstitium showed mild inflammatory infiltrates without crescents or fibrinoid necrosis (Table/Fig 2).
Immunofluorescence microscopy showed a diffuse and granular staining along capillary walls: IgM and IgG (with kappa and lambda light chain staining) were present in the immune complexes, along with complement C3 and C1q. IgA was negative. Focally small vessels show deposits of IgG, IgM, C3, C1q, kappa and lambda in the lumen of vessel wall. The dominant pattern (monoclonal IgMκ combined with IgG) matched Type II cryoglobulin deposition. Electron microscopy would reveal mesangial and subendothelial electron-dense deposits, often with rhomboid structures (typical cryoglobulin microtubules). These findings confirmed cryoglobulinaemic GN (a membranoproliferative, immune-complex GN) with associated immune complex mediated extra glomerular small vessel vasculitis.
Radiology
No specific renal imaging (e.g., computed Tomography/Magnetic Resonance Imaging (CT/MRI) of kidneys) was obtained, as the clinical and laboratory picture already indicated glomerular disease. Renal ultrasound showed normal-sized kidneys with mild increased cortical echogenicity. No vasculitic organ involvement required imaging at presentation.
Management
Severe cryoglobulinaemic GN requires combined antiviral and supportive therapy when hepatitis B is present. Given the biopsy-proven cryoglobulinaemic GN, management was directed at both the underlying etiologic triggers and the immune-mediated renal injury. High-dose corticosteroid therapy was initiated with prednisone 1 mg/kg/day to achieve rapid control of active vasculitis and glomerular inflammation. Because chronic hepatitis B infection can act as a persistent driver of immune-complex formation, antiviral therapy with entecavir (0.25 mg once daily, dose adjusted for renal impairment) was commenced to suppress viral replication and prevent reactivation during immunosuppression.
Plasmapheresis was reserved as a contingency strategy for life-threatening complications such as hyperviscosity syndrome, rapidly progressive renal failure, or refractory proteinuria. Supportive management included diuretics for volume control and oedema, and initiation of an angiotensin-converting enzyme inhibitor to reduce intraglomerular pressure and proteinuria. Potent immunosuppressive therapies, including cyclophosphamide, mycophenolate mofetil, cyclosporine, and anti-Cluster of Differentiation 20 (CD20) monoclonal antibodies such as rituximab, were deferred due to the substantial risk of hepatitis B reactivation and hepatic flare despite antiviral prophylaxis. Despite HBV suppressive treatment and plasmapheresis, she developed progressive renal failure necessitating haemodialysis. She worsened due to disease related complications in addition to nosocomial infections and expired within three weeks of treatment.
Cryoglobulinaemia refers to circulating immunoglobulins that precipitate at low temperature and dissolve on rewarming. HCV infection is the dominant cause (~80-90% of mixed cryo) (1),(2),(3). In non-HCV cases, cryoglobulinaemia is associated with other chronic infections (HBV, HIV) or autoimmune diseases (Systemic Lupus Erythematosus (SLE), Sjögren’s, and RA) (2),(4). Mixed cryoglobulinaemia (types II and III) is an immune complex mediated vasculitis of IgM with RF activity bound to IgG characterised by circulating immunoglobulin that precipitate at low temperatures (1). Type II (monoclonal IgMκ+polyclonal IgG) accounts for ~50-65% of cryo cases and account for the most common subtype (2). Typically presents with Meltzer’s triad and variable renal involvement, as described by Ferri C et al., (2004) (3). Hepatitis B–associated cryoglobulinaemic is rare but reported. Li C et al., (2020) and Han HX et al., (2023) described cases with purpura, arthralgia, and renal involvement showing an MPGN pattern, similar to the present case. Autoimmune diseases such as RA also contribute to cryoglobulin formation (2),(4). Dammacco F et al., (2023) reported systemic vasculitis with renal involvement, supporting a dual pathogenic mechanism (5). Histologically, an MPGN pattern with immune deposits is characteristic, as noted in recent studies including Duggal S et al., (2025) (6). Despite therapy, outcomes remain variable. The present case showed rapid progression, highlighting the severity of overlapping aetiologies. The patient’s long-standing RA and chronic hepatitis B likely both contributed to immune complex generation. RA itself can trigger cryoglobulin production, as RF forms part of the cryoglobulin complex, and hepatitis B virus, although rare, is a recognised aetiological factor (3),(4). Clinically, mixed cryoglobulinaemic often presents with Meltzer’s triad (purpura, arthralgias, weakness) plus renal and nerve involvement. Hypocomplementemia (especially low C4) and positive RF are hallmark laboratory clues (5),(6). In fact, severe C4 consumption is highly suggestive of cryoglobulinaemic-related vasculitis (6). Our patient’s purpura, low C4, and high RF prompted testing for cryoglobulins, confirming the diagnosis. Biopsy patterns in cryoGN are typically membranoproliferative (lobular capillary hypercellularity with double-contour basement membranes) (7). Prominent PAS-positive thrombi (“pseudothrombi”) of immune complexes are characteristic (7). Immunofluorescence classically shows both IgM and IgG with complement (C3, often C1q) deposition along capillaries (8). These findings differentiate cryoGN from, say, idiopathic MPGN or lupus nephritis; in our case the dual Ig deposition and clinical context clinched the diagnosis (7),(8). Differential diagnoses included other causes of MPGN (e.g., HBV immune complex GN without cryoglobulins, C3 glomerulopathy, SLE), but the serology and biopsy were most consistent with cryoglobulin. Notably, HBV can cause membranous or proliferative GN by subepithelial immune deposits, but those usually show granular IgG/HBsAg deposits without hyaline thrombi. RA-related renal disease (e.g., amyloid or Nonsteroidal Anti-Inflammatory Drug (NSAID) toxicity) was unlikely. Given the confirmatory biopsy, treatment was aligned with cryoglobulinaemic vasculitis management principles (5),(9). Therapeutically, mixed cryoglobulinaemic demands both aetiological and immunosuppressive approaches. Eradicating or suppressing the source of immune complexes is key: for HCV, Direct-Acting Antiviral agents (DAAs) revolutionised outcomes, and analogously we treat HBV aggressively in HBV-associated cases (10). Immunosuppression (corticosteroids, cyclophosphamide, and rituximab) is reserved for severe or refractory vasculitis. Rituximab (anti-CD20) is particularly effective in cryoGN (6), often resulting in improved renal function. However, in HBV carriers, B-cell–depleting therapy poses reactivation risk; prophylactic antivirals are mandatory (11). The patient of the present case, suffering from Type II cryoglobulinaemia GN with HBV-positive status, warranted anti-HBV treatment (renal dose-adjusted) and plasmapheresis, another adjunct for very high cryocrit or hyperviscosity, though used infrequently (12). Unfortunately, in our patient, these combined measures did not lead to the remission of vasculitis and had progressive renal failure. The patient expired due to disease related complications. Cryoglobulinaemic GN often portends a guarded renal prognosis: up to 30-35% of mixed cryo patients develop proteinuria or renal impairment (13). Early diagnosis by recognising cryoglobulinaemic’s clinical clues (purpura, low C4, RF, and HBV) and confirming with biopsy is therefore critical to improve outcomes. This case underscores that clinicians should consider cryoglobulinaemic in RA patients who develop GN, especially if any infection (e.g., HBV) is present. Comparison of previously reported cases of cryoglobulinaemic GN with the present case, highlighting aetiology, clinical features, renal involvement, histopathological patterns, treatment strategies, and outcomes in (Table/Fig 3) (2),(3),(4),(5),(6),(12).
Type II cryoglobulinaemic GN is a rare but serious immune-complex nephritis that can complicate chronic HBV infection and autoimmune disease. The classic triad of purpura, positive RF, and low complement levels should alert clinicians to order cryoglobulin testing. Kidney biopsy (showing an MPGN pattern with IgM/IgG deposits) confirms the diagnosis. Dual etiologies may be associated with a more aggressive clinical course and poorer outcomes. Management combines treatment of the underlying trigger (e.g., antiviral therapy for HBV) with immunosuppression (steroids, rituximab). The present case illustrates the necessity of a multidisciplinary approach coordinating rheumatology, nephrology, and hepatology to recognise and treat mixed cryoglobulinaemic. Early intervention can stabilise renal function and prevent life-threatening complications. Vigilance for cryoglobulinaemia in atypical GN presentations remains a key learning point.
DOI: 10.7860/JCDR/2026/87352.24395
Date of Submission: Jan 10, 2026
Date of Peer Review: Mar 27, 2026
Date of Acceptance: Jun 17, 2026
Date of Publishing: Sep 01, 2026
Author declaration:
• Financial or Other Competing Interests: None
• Was informed consent obtained from the subjects involved in the study? Yes
• For any images presented appropriate consent has been obtained from the subjects. Yes
PLAGIARISM CHECKING METHODS:
• Plagiarism X-checker: Jan 17, 2026
• Manual Googling: Jun 13, 2026
• iThenticate Software: Jun 15, 2026 (1%)
ETYMOLOGY: Author Origin
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