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"Journal of Clinical and Diagnostic Research is at present a well-known Indian originated scientific journal which started with a humble beginning. I have been associated with this journal since many years. I appreciate the Editor, Dr. Hemant Jain, for his constant effort in bringing up this journal to the present status right from the scratch. The journal is multidisciplinary. It encourages in publishing the scientific articles from postgraduates and also the beginners who start their career. At the same time the journal also caters for the high quality articles from specialty and super-specialty researchers. Hence it provides a platform for the scientist and researchers to publish. The other aspect of it is, the readers get the information regarding the most recent developments in science which can be used for teaching, research, treating patients and to some extent take preventive measures against certain diseases. The journal is contributing immensely to the society at national and international level."

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Aug 2018

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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.
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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)
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.
On April 2011

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
On Jan 2020

Important Notice

Year : 2012 | Month : February | Volume : 6 | Issue : 1 | Page : 136 - 138 Full Version

Proteinuria in Primary and Secondary Renal Diseases

Published: February 1, 2012 | DOI:
Anuradha B. Patil, C.V. B. Prasad, Shivap rasad S.

1. Associate Professor, 2. Assistant Professor, 3. Assistant Professor, Department of Biochemistry, Jawaharlal Nehru Medical College Nehru nagar, Belgaum- 590 010, Karnataka, India.

Correspondence Address :
Dr. Anuradha B. Patil
Associate Professor
Department of Biochemistry
Jawaharlal Nehru Medical College
Nehru nagar, Belgaum- 590 010
Karnataka, India.
Email :


Proteinuria is a strong indicator of kidney disease. Various pathological conditions such as diabetes mellitus, cardiovascular disease and hypertension have been shown to provoke secondary kidney problems and significant proteinuria. Studies have demonstrated that the normal glomerulus filters substantial amounts of albumin and, This filtered albumin is then processed by proximal tubular cells by two distinct pathways; a retrieval pathway and degradation pathway. Dysfunction in either one of these pathways gives rise to discrete forms of albuminuria. Different proteinuric factors (PF) and glomerular permeability factors appears to be involved in the abnormal glomerular permeability and are responsible for the development of proteinuria in primary nephritic syndrome. Transforming Growth Factor-β1 (TGF-β1) has prosclerotic property, can induce nephrosclerosis and is implicated in proteinuria of hypertension. Proteinuria is an important marker in renal disease, and an useful prognostic marker for cardiovascular disease. Microalbuminuria is the earliest clue of renal complications of metabolic syndrome. Renal insufficiency was an independent risk factor for death in elderly patients after myocardial infarction.


Albuminuria, Nephrotic syndrome, Hypertensive nephropathies, Diabetic Nephropathies, Nephrin

In this review we have discussed, first, the patho-physiology of albuminuria in three different conditions. Second, we describe the progress of albuminuria. Thirdly albuminuria predict the extent of renal damage and outcome. Proteins filtration, re-absorbtion and excretion by the nephrons is a complex mechanism in renal physiology. The entire glomerular tuft is supported by mesangial cells lying between the capillaries. Basement membrane-like mesangial matrix forms a meshwork through which the mesangial cells are centered (1). Studies have demonstrated that the normal glomerulus filters substantial amounts of albumin and, This filtered albumin is then processed by proximal tubular cells by two distinct pathways; a retrieval pathway and degradation pathway. Dysfunction in either one of these pathways gives rise to discrete forms of albuminuria. Albuminuria in the nephrotic range would arise from retrieval pathway dysfunction. Dysfunction in the degradation pathway leads to albuminuria below the nephrotic range.Tubular reabsorption plays a central role in mediating the effects of albumin on renal function (6). Receptor-mediated endocytosis plays a role in urinary albumin degradation (2). The kidney degrades large amounts of albumin and that the degradation fragments appear in the urine which are not reabsorbed into the blood stream (3).
Albuminuria in the diabetes mellitus
Glucose and Methylglyoxal (MGO) derived modifications of Extracellular membrane (ECM) proteins make distinct contributions to development of characteristic diabetic nephropathy glomerular lesions via perturbation of glomerular cell-matrix interactions. It has been suggested that hyperglycaemia causes early but transient mesangial cell proliferation followed by a decrease in proliferation and development of cell hypertrophy (4). In early diabetes during the stages of glomerular hyperfunction, hypertrophy develops acutely Biochemistry Section at the onset of diabetes, leading to an increase in capillary surface corresponding to the increase in filtration rate. In the advanced stages when glomerular closure involves a proportion of the nephrons compensatory hypertrophy develops, thereby probably helping to preserve capillary surface for a period of time. The endstage is glomerular closure, with elimination of glomerular function (5). The reductions in podocyte numbers in both younger and older diabetic patients indicate a significant risk for functional abnormalities as diabetic nephropathy progresses (6). The glomerulus, particularly the mesangium, has been studied in diabetes, tubulointerstitial injury is also a major feature of diabetic nephropathy and an important predictor of renal dysfunction. In the diabetic state, this includes large quantities of advanced glycation end products and glucose and, at later stages in the evolution of diabetic nephropathy, protein, all of which are factors that may induce TGF-b expression and fibrosis. Diabetic nephropathy should therefore be viewed as a disease affecting the entire nephron (7). Non-enzymatic glycation of albumin increases its renal clearance (8). The glycation of albumin, and not of GBM, leads to enhanced permeability in an in-vitro GBM filtration system. Increased permeability of glycated albumin may contribute to albuminuria and/or renal injury in states of increased circulating glycated albumin such as diabetes (9).
Albuminuria in Hypertension
Albuminuria in hypertension is linked to an inhibition of lysosomal processing as determined by size exclusion chromatography analysis of urine which was correlated with increased renal transforming growth factor-beta (10). Increase in pressure in the glomerular capillaries which resulted in stretch/relaxation resulted in increase in the relative amounts of types I and III collagens produced/cell. Additionally, stretch/relaxation selectively increased the relative amount of type I-homotrimers produced. Thus, when mesangial cells are exposed to cyclic stretch/relaxation, they exhibit significant alterations in morphology, growth, prostaglandin and collagen production (11). High-pressure cyclic stretch leads to MC proliferation, preceded by marked activation of p44/42 and p38/HOG MAPKs. Cell proliferation is not seen with low-pressure stretch, and there is only modest p44/42 MAPK activation, suggesting that glomerular capillary hypertension may lead to cell proliferation and injury partly through differential activation of kinase cascades (12). Stretch-induced activation of SAPK and p42/44 MAPK in MCs can be inhibited by NO. The effect of NO is mediated by the generation of cGMP. These mechanisms may be responsible, at least in part, for the protective effect of NO in animal models of glomerular injury characterized by glomerular capillary hypertension (13).
Nephrotic syndrome
Circulating permeability factor in serum from patients with focal segmental glomerulosclerosis can cause immediate and marked changes in glomerular permeability to albumin. The serum factor is strongly associated with the recurrence of focal segmental glomerulosclerosis after renal transplantation and may be responsible for proteinuria in patients with this disorder (14).Properties and mechanism of action of permeability factor was mentioned by M. Sharma et al (15). Components of normal serum block the focal segmental glomerulosclerosis factor activity in-vitro (16). Protein leakage in nephrotic syndromes also occurs through defective podocyte with disruption of glomerular slit diaphragms (17). Nephrin is a protein, which is synthesized in the podocytes and localized in the slit diaphragm area. Nephrin is a cell adhesion molecule of the immune-globulin super family, and presumably is a part of the zipper-like structure of the slit membrane. Mutation of the gene coding nephrin induces congenital nephrotic syndrome of Finnish type, which is a prototype of nephrotic syndrome, it has been suggested that nephrin also plays a role in acquired proteinuric kidney disease (18). Podocin interacts with nephrin and CD2AP. This forms a complex functional unit that anchors the slit diaphragm to the actin cytoskeleton and establishes its location in the lateral plasma membrane of the podocyte foot processes (19). Applied aspect proteinuria is an important marker in renal disease, and an useful prognostic marker for cardiovascular disease. Microalbuminuria is the earliest clue of renal complications of metabolic syndrome (20). Renal insufficiency was an independent risk factor for death in elderly patients after myocardial infarction (21) is a marker of different pathologic processes. Micro-albuminuria the spectrum of renal vascular manifestations range from systemic endothelial dysfunction (microvascular disease) to systemic atherosclerosis (macrovascular disease) (22).


Whatever be the aetiology the progress of proteinuria varies, especially in secondary proteinuria. Progress of proteinuria of low range of micro-albuminuria to overt proteinuria as it depends on many factors. Studies showing in some patient where it progesses; in some patients micro-albuminuria remained stable. The angiotensin-II-receptor blocker irbesartan is effective in protecting against the progression of nephropathy due to type 2 diabetes. This protection is independent of the reduction in blood pressure it causes (23),(24),(25) whereas in others micro-albuminuria reverted back to normal transiently or even permanently (26)(27)


Kanwar YS, Venkatachalam MA. Morphology of the glomerulus and juxtaglomerular apparatus. In Handbook of Physiology, Section of Renal Physiology, 2nd ed. Washington, DC, American Physiological Society,
Birn H, Christensen EI. Renal albumin absorption in physiology and pathology. Kidney Int. 2006 Feb;69(3):440-9.
Hilliard LM, Osicka TM, Clavant SP, Robinson PJ. Characterization of the urinary albumin degradation pathway in the isolated perfused rat kidney. J Lab Clin Med. 2006 Jan;147(1):36-44.
Wolf G, Ziyadeh FN. Molecular mechanisms of diabetic renal hypertrophy. Kidney Int. 1999 Aug;56(2):393-405.
Osterby R. Structural changes in the diabetic kidney. Clin Endocrinol Metab. 1986 Nov;15(4):733-51
Steffes MW, Schmidt D, McCrery R, Basgen JM. Glomerular cell number in normal subjects and in type 1 diabetic patients. Kidney Int. 2001 Jun;59(6):2104-13.
Gilbert RE, Cooper ME The tubulointerstitium in progressive diabetic kidney disease: more than an aftermath of glomerular injury? Kidney Int. 1999 Nov;56(5):1627-37.
Layton GJ, Jerums G. Effect of glycation of albumin on its renal clearance in normal and diabeticrats. Kidney Int. 1988 Mar;33(3):673-6.
Daniels BS, Hauser EB. Glycation of albumin, not glomerular basement membrane, alters permeability in an in vitro model. Diabetes. 1992 Nov;41(11):1415-21.
Russo LM, Osicka TM, Bonnet F, Jerums G, Comper WD. Albuminuria in hypertension is linked to altered lysosomal activity and TGF-beta1 expression. Hypertension. 2002 Feb;39(2):281-6.
Harris RC, Haralson MA, Badr KF.Continuous stretch-relaxation in culture alters rat mesangial cell morphology,growth characteristics, and metabolic activity. Lab Invest. 1992 May;66(5):548-54.
Ingram AJ, Ly H, Thai K, Kang M, Scholey JW.Activation of mesangial cell signaling cascades in response to mechanical strain. Kidney Int. 1999 Feb;55(2):476-85.
Ingram AJ, James L, Ly H, Thai K, Cai L, Scholey JW.Nitric oxide modulates stretch activation of mitogen-activated protein kinases in mesangial cells. Kidney Int. 2000 Sep;58(3):1067-77
Savin VJ, Sharma R, Sharma M, McCarthy ET, Swan SK Circulating factor associated with increased glomerular permeability to albumin in recurrent focal segmental glomerulosclerosis. N Engl J Med. 1996 Apr 4;334(14):878-83.
Sharma M, Sharma R, McCarthy ET, Savin VJ.The focal segmental glomerulosclerosis permeability factor: biochemical characteristics and biological effects. Exp Biol Med. 2004 Jan;229(1):85-98.
Sharma R, Sharma M, McCarthy ET, Ge XL, Savin VJ.Components of normal serum block the focal segmental glomerulosclerosis factor activity in vitro. Kidney Int. 2000 Nov;58(5):1973-9.
Lahdenkari AT, Lounatmaa K, Patrakka J, Podocytes are firmly attached to glomerular basement membrane in kidneys with heavy proteinuria. J Am Soc Nephrol. 2004 Oct;15(10):2611-8.
Machuca E, Benoit G, Nevo F, Tête MJ Genotype-phenotype correlations in non-Finnish congenital nephrotic syndrome. J Am Soc Nephrol. 2010 Jul;21(7):1209-17.
Horinouchi I, Nakazato H, Kawano T, Iyama K. In situ evaluation of podocin in normal and glomerular diseases. Kidney Int. 2003 Dec;64(6):2092-4.
Schmieder RE, Schrader J, Zidek W, Tebbe U, Paar WD, Bramlage P, et al. Low-grade albuminuria and cardiovascular risk: what is the evidence? Clin Res Cardiol. 2007 May;96(5):247-57
McAlister FA, Ezekowitz J, Tonelli M, Armstrong PW. Renal insufficiency and heart failure: prognostic and therapeutic implications from a prospective cohort study. Circulation. 2004 Mar 2;109(8):1004-9.
Abdelhafiz AH, Ahmed S, El Nahas M. Micro-albuminuria: marker or maker of cardiovascular disease. Nephron Exp Nephrol. 2011;119 Suppl 1:e6-e10
Horinouchi I, Nakazato H, Kawano T, Iyama K. In situ evaluation of podocin in normal and glomerular diseases. Kidney Int. 2003 Dec; 64(6):2095-9.
Lewis EJ, Hunsicker LG, Clarke WR, Berl T, Pohl MA, Lewis JB, et al. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl J Med 2001, 345 :851 –60.
Wiseman MJ, Mangili R, Alberetto M, Keen H, Viberti G. Glomerular response mechanisms to glycemic changes in insulin-dependent diabetes. Kidney Int 1987 ,31:1012 –18 .
Chiarelli F, Verrotti A, Morgese G. Glomerular hyperfiltration increases the risk of developing microalbuminuria in diabetic children. Pa and, ediatr Nephrol,1995, 9 :154 –58.
Viberti GC, Hill RD, Jarrett RJ, Argyropoulos A, Mahmud U, Keen H. and, Microalbuminuria as a predictor of clinical nephropathy in insulindependent diabetes mellitus. Lancet 1982 1:1430 –32.

DOI and Others

ID: JCDR/2012/2506.3237:1874


Date of Submission: May 18, 2011
Date of Peer Review: Aug 01, 2011
Date of Acceptance: Dec 28, 2011
Date of Publishing: Feb 15, 2012

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