The Patient with Lupus Nephritis: Comprehensive Assessment and Potential Risks

Research Article | DOI: https://doi.org/10.31579/2690-4861/1021

The Patient with Lupus Nephritis: Comprehensive Assessment and Potential Risks

  • N.F. Soroka *
  • K.A. Chyzh
  • A.K. Tushina

Belarusian State Medical University Department of Internal Diseases, Cardiology and Rheumatology with a course of advanced training and retraining Minsk, Belarus.

*Corresponding Author: Nikolay Soroka., Belarusian State Medical University Department of Internal Diseases, Cardiology and Rheumatology with a course of advanced training and retraining Minsk, Belarus.

Citation: N.F. Soroka, K.A. Chyzh, A.K. Tushina, (2026), The Patient with Lupus Nephritis: Comprehensive Assessment and Potential Risks, International Journal of Clinical Case Reports and Reviews, 33(4); DOI:10.31579/2690-4861/1021

Copyright: © 2026, Nikolay Soroka. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: 17 December 2025 | Accepted: 15 January 2026 | Published: 20 January 2026

Keywords: systemic lupus erythematosus; lupus nephritis; risk factors

Abstract

Systemic lupus erythematosus is a potentially fatal, chronic, multisystem autoimmune condition. Kidney damage plays a special role in the course and prognosis of SLE, being associated with the greatest number of complications and high mortality. The main type of renal damage in lupus is the development of secondary glomerulonephritis - lupus nephritis. Therefore, it’s of great importance to establish so-called “risk factors” that would make it possible to predict the development of LN in patients with SLE, its exacerbations, features of the course and possible outcomes. It is noteworthy that at the onset of the disease, kidney damage was noted in almost half of the patients with SLE (48.2%), and in many cases, the first clinical and laboratory manifestations of LN were only changes in urine tests.

Introduction

Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology, based on a genetically determined disorder of immune regulation, which determines the formation of organ-nonspecific antibodies to antigens of cell nuclei and immune complexes with the development of immune inflammation in the tissues of many organs [1]. It is a potentially fatal, chronic, multisystem autoimmune condition that primarily affects women of reproductive age. Its pathogenesis involves multiple components of the immune cascade, resulting in a striking heterogeneity of clinical manifestations. Almost any organ or system of the body can be involved in the pathological process - skin, joints, heart, lungs, serous membranes, nervous system, hematopoietic system, etc. It is obvious that late diagnosis of SLE is associated with an increased risk of damage to vital body systems. The severity and clinical course of SLE are extremely variable - from very mild with arthralgia and skin rashes to life-threatening when there is severe impairment of renal or central nervous system function. Kidney damage plays a special role in the course and prognosis of SLE, being associated with the greatest number of complications and high mortality. The main type of renal damage in lupus is the development of secondary glomerulonephritis - lupus nephritis. Lupus nephritis (LN), one of the most serious manifestations of SLE, occurs in up to two-thirds of patients, depending largely on ethnicity and race. It is much more common in African-American and Hispanic patients, less common in Asians, and even less common in Caucasian patients. The presence of LN predicts worse survival compared to patients without kidney disease, with the cause of death being due to both disease-related and treatment-related factors [2, 3, 4]. The 10- and 20-year survival rates (renal and/or overall) are approximately 70% and 60%, respectively. LN is associated with a twofold increase in complications and mortality compared with individuals without renal pathology and a fourfold increase in individuals receiving renal replacement therapy [5, 6]. More severe course of SLE in the presence of LN also requires more intensive treatment (high doses of glucocorticosteroids, immunosuppressive drugs), which, in turn, leads to a significant increase in the number of complications [4]. Despite significant improvements in survival (both renal and patient) over the past decades associated with the advent of new treatment strategies, a significant proportion of patients (10 to 30%) continue to steadily progress to end-stage chronic kidney disease (CKD) within 10 to 15 years from diagnosis of LN. For example, 44% of people with proliferative forms of LN (morphological classes III and IV) after 15 years are forced to resort to methods of renal replacement therapy (hemodialysis, peritoneal dialysis, kidney transplantation). [5,6] Clinical and laboratory manifestations of LN almost the same as the symptoms of primary chronic glomerulonephritis. Clinical signs of kidney involvement in the pathological process are observed in 40-80% of patients with SLE, most often occurring in childhood [7]. They range from minimal changes in urinary sediment to frank nephritic or nephrotic syndrome, as well as rapidly progressive glomerulonephritis or acute kidney injury (AKI). In the absence of adequate therapy (and in some cases, despite its presence), over time, LN ends with the development of the end stage of CKD. In the early stages of the disease in lupus patients, changes in urine tests or impaired renal function are observed approximately in 25-50% of cases. Kidney damage often manifests as proteinuria, microhematuria, decreased glomerular filtration rate (GFR), increased blood creatinine levels, or the presence of casts in the urine (approximately in 50% of cases). In most cases, kidney damage is accompanied by extrarenal clinical manifestations and changes in laboratory parameters, which ultimately makes it possible to suspect the likelihood of lupus kidney damage. An essential part of renal involvement in lupus is proteinuria, which is detected in 100% of patients with lupus nephritis, and in 45-65% of cases it can reach the nephrotic level.  Hematuria (in the vast majority of cases, microhematuria), as well as the presence of red blood cell casts, are found approximately in 80% of patients during the course of the disease. The presence of LN should be considered in any lupus patient with renal impairment, proteinuria, arterial hypertension or active urinary sediment. Active sediment includes the detection of hematuria, especially acanthocytes, indicating the glomerular origin of erythrocytes in the urine, leukocyturia when excluding its infectious genesis (especially lymphocyturia), as well as erythrocyte, leukocyte and other casts. The great diagnostic importance in verifying the diagnosis of LN has intravital puncture biopsy of the kidney. The histological data obtained through this manipulation serve as the basis for establishing the morphological class of LN, assessing the activity of inflammatory and chronic changes in the renal tissue, recommendations for developing treatment tactics, as well as prognosis of the disease. LN is often asymptomatic and requires active screening to detect it. Clinical and laboratory features reflect the type of renal histological lesions present in a given patient. Proteinuria, microhematuria, casts and hypertension (in some cases severe) are often found in individuals with proliferative LN, and may be accompanied by the development of renal failure. Patients with membranous or proliferative LN often develop nephrotic syndrome with the presence of peripheral edema, serous effusions, cachexia and hypercoagulation. LN can also manifest itself as AKI or have a rapidly progressive nature associated with severe glomerular inflammation (the presence of cellular crescents and fibrinoid necrosis of capillary loops in the glomeruli of the kidneys), which is observed relatively rarely. Most patients with LN have a relapsing course, with treatment-induced remissions and spontaneous relapses of renal tissue inflammation being quite common. At the same time, the course of LN is extremely variable. In some cases, a long-term stable chronic course is observed, accompanied by the presence of minimal or no urinary syndrome, with preserved renal function. In another situation, a rapidly progressive course is observed, accompanied by nephrotic or nephritic syndrome, severe hypertension and a steady decline in the functional state of the kidneys, leading within several years to the end stage of CKD with the necessity of renal replacement therapy. Most patients have a wave-like course, in which exacerbations of nephritis are replaced by more or less long periods of complete or partial remission, with gradual progression of existing CKD to later stages.  The presence of different variants of the course of LN is associated with the complexity of the pathogenesis of both SLE and LN. Many researchers believe that the term “systemic lupus erythematosus” includes various diseases that meet the classification criteria of SLE. This polymorphism of clinical and laboratory manifestations, as well as the rarity of SLE in general, makes difficulties in providing multicenter clinical trials for novel treatment. The most important risk factor for progression of LN is the frequency, nature and degree of its exacerbation. After an exacerbation of LN, irreversible structural changes are formed in the renal tissue, leading to the formation of sclerosis and the progression of CKD. Therefore, it is extremely important to predict such exacerbations, which would allow the use of adequate therapeutic agents to prevent them, stop them and control the course of the disease while minimizing the side effects of the drugs used [8]. Therefore, it’s of great importance to establish so-called “risk factors” that would make it possible to predict the development of LN in patients with SLE, its exacerbations, features of the course and possible outcomes. A variety of genetic, demographic, clinical and laboratory parameters have been attempted. Patient age, gender, ethnicity, disease duration, presence of hypertension, anemia, elevated serum creatinine, rapid decline in GFR, and many others parameters have been studied as possible prognostic factors. Potential risk factors include any parameters (modifiable and non-modifiable) that contribute to the progression of CKD. More specific indicators that influence the nature of the course of LN were also studied, such as SLE activity (determined by the indices SLEDAI, SELENA-SLEDAI, BILAG, etc.), the influence of damage to other organs and systems in lupus (SLICC/ACR Damage Index), immunological indicators (C1q, C3 and C4 complement components in the blood and urine, the level of antinuclear antibodies and antibodies to double-stranded DNA (dsDNA) in the blood). In various studies, many of the mentioned parameters had a certain impact on the activity and progression of LN, but to date, a universal predictor of exacerbation of nephritis in SLE has not been established. The most significant factors were the level of proteinuria (especially daily), the presence of impaired renal function at the onset of LN, high titers of anti-dsDNA antibodies in the blood, and low levels of the complement component C1q. LN has been found to be more aggressive and have a worse prognosis in people of African-American ethnicity, especially males. And, of course, many studies have noted lack of adherence to treatment in patients with LN as a poor prognostic sign. A key role in diagnosis of lupus nephritis plays kidney biopsy. Indications for its implementation are proteinuria (in a general urine test, in the daily amount of urine, when calculating the protein/creatinine ratio in a single portion of urine), especially above 0.5 g/day (g/l), the presence of changes in the urinary sediment (hematuria, casts, leukocyturia, not associated with an infectious process in the urinary tract), an otherwise unexplained impairment of the functional state of the kidneys, manifested by signs azotemia and a decrease in GFR, or one or another combination of these signs. Performing a nephrobiopsy followed by morphological examination using light, immunofluorescence, and in some cases electron microscopy makes it possible to clarify the histological class of LN according to the 2003 ISN/RPS classification (modified 2018), develop a suitable therapeutic regimen and assess the prognosis [9]. Also, this invasive diagnostic procedure helps in differential diagnosis - excluding kidney damage due to secondary or primary antiphospholipid syndrome (APS), hypertension, primary glomerulonephritis, tubulointerstitial nephritis, diabetic nephropathy, renal amyloidosis, etc. To assess morphological changes in LN, the 2003 International Society of Nephrology/Society of Renal Pathologists (ISN/RPS) classification, which includes 6 classes of the disease, is currently used.  This classification subdivides LN according to the location of immune complex deposition in the glomeruli, the presence or absence of mesangial or endocapillary proliferation, the overall degree of glomerular involvement (focal or diffuse) and glomerular damage (global or segmental), as well as active (inflammatory) or chronic (sclerotic) glomerular damage.

  • I class. Minimal mesangial LN. Light microscopy (LM): normal glomeruli. Immunofluorescence (IF): mesangial immune complexes (IC)
  • II class. Mesangial proliferative LN. LM: mesangial hypercellularity and/or expansion of the mesangial matrix. IF: mesangial IR
  • III class. Focal LN. LM: segmental or global endo- or extracapillary GN affecting <50% of the glomeruli. IF: subendothelial ± mesangial IF. There are active (A) - proliferative, chronic (C) - sclerosing, and a combination of active and chronic (A+C) focal LN
  • IV class. Diffuse LN. LM: segmental or global endo- or extracapillary GN affecting 50% of the glomeruli. IF: subendothelial ± mesangial IF. A, C or A+C diffuse LN is distinguished
  • V class. Membranous LN. LM: thickening of the wall of glomerular capillaries. FI: many subepithelial ICs, >50% glomerular capillaries. Membranous changes can be isolated or combined with proliferative ones. Their combination is designated as class V+ III or class V+ IV.
  • VI class. Sclerosing LN. LM: sclerosis >90% of glomeruli.

Although immunocoplex-mediated glomerulonephritis is the most common cause of renal damage in SLE, there are other mechanisms that can only be diagnosed by biopsy and require a different treatment approach than immune-complex LN. For example, thrombotic microangiopathy and podocytopathy, can be observed in 24% and 1.3% of patients with LN, respectively. The finding of isolated tubulointerstitial nephritis is rare.In general, the morphological class of LN according to ISN/RPS determines decisions on further treatment tactics. Patients whose glomerular involvement is limited to the mesangium (Class II) generally do not require specific therapy, but immunosuppression may be required to treat extrarenal manifestations of SLE. With the predominance of chronic damage (any morphological class) or with the total development of glomerulosclerosis (class VI), there is also no need for immunosuppressive treatment of LN, and a positive therapeutic effect can be obtained with the help of antiproteinuric, renoprotective measures. Proliferative classes of LN (III and IV) usually require active immunosuppression, whereas nonproliferative, membranous LN (class V) can be treated conservatively (antiproteinuric therapy) if patients have subnephrotic proteinuria, or with immunosuppression if patients have nephrotic syndrome. The role of repeat renal biopsy in LN remains controversial, but emerging evidence suggests that serial biopsies may influence ongoing treatment decisions and long-term renal prognosis. Repeat nrphrobiopsies showed significant discrepancy between clinical and histological disease activity. 6-8 months after completion of immunosuppressive therapy, 20-50% of patients with complete clinical remission of LN still had histological evidence of active inflammation, and 40-60% of patients without histological evidence of disease activity had persistent proteinuria. Even after several years of immunosuppressive treatment, histological activity occurred in almost 20% of patients with long-term clinical remission. Conversely, 40% of patients with complete histological remission remained persistently clinical after long-term treatment. These results indicate the need for repeated nephrobiopsies when deciding whether to discontinue maintenance immunosuppressive therapy [10]. There are currently no recommendations regarding the duration of maintenance therapy for LN.

Materials and methods

Medical documentation (medical histories, outpatient records, etc.) of 574 patients with SLE treated in the rheumatology department of the 9th city hospital in Minsk (since 2018, Minsk Scientific and Practical Center for Surgery, Transplantology and Hematology) for the period from 1990 to 2024 was studied. In addition, some of the patients were observed on an outpatient basis by staff of the Republic Rheumatology Center. The diagnosis of SLE was established based on the classification criteria of the American College of Rheumatology (ACR, 1997) and the International Society of Systemic Lupus Erythematosus Clinics (SLICC, 2012) [11, 12]. 284 patients were observed prospectively, and in 290 cases a retrospective analysis of the available data was performed. All patients were divided into two groups depending on the presence (397) or absence (177) of LN. Diagnosis of LN was based on the ACR classification criteria (2012), including persistent daily proteinuria of at least 0.5 grams and/or erythrocyturia (5 or more red blood cells in the microscopic field), leukocyturia (5 or more white blood cells in the microscopic field) not associated with a urinary tract infection, and casts. In almost half of the cases (195 patients - 49% of all cases of LN), the diagnosis was confirmed by the results of histomorphological examination of renal biopsies.

Results and discussion

Among the examined patients, female patients predictably predominated - 537 (93.6%), the number of males - 37 (6.4%). The average age of the subjects was 35.3±0.5 years. The age of onset of the disease was 28.6±0.5 years. The average duration of SLE at the time of observation was 6.5±0.3 years. The first group consisted of patients with an established diagnosis of LN- 397 patients (69.2% of all examined), among whom there were 30 men (7.6%). The average age in this group was 34.9±0.6 years. The age of onset of the disease in the presence of LN is 28.0±0.6 years. The average duration of SLE at the time of observation was 6.9±0.3 years. The age of onset of LN was 28.9±0.7 years. The duration of LN at the time the patient was taken under observation was 5.9±0.6 years.  Clinical and laboratory signs of kidney damage at the onset of the disease were noted in 47.2% of all cases of LN. The comparison group consisted of 177 patients with SLE without signs of LN. The groups of patients with or without LN did not differ significantly in gender, age, or age at diagnosis of SLE. However, the duration of the disease at the time of the initial examination of the patient was higher in the group of people with LN. (Tables 1 and 2)

ParameterLN+LN-χ²P 
 
Gender, n (%)М30 (7,6)7 (4,0)-1,624>0,05 
F367 (92,4)170 (96,0) 

Table 1: Proportion of patients by gender in the study groups.

 

Parameter

Number of observations

 

LN+

 

LN-

 

t -criteria

 

P

LN+LN-
Age, years39717734,9±0,636,1±1,0-1,019>0,05
SLE duration, years3911606,9±0,35,4±0,52,344<0,05
Patient’s age on onset of SLE, years39116028,0±0,630,1±0,9-1,928>0,05
Observation duration, monthes2836248,6±3,025,3±4,33,425<0,001

Table 2: Age of patients at the time of inclusion in the study and at the onset of the disease, as well as the duration of SLE in the study groups.

In most cases of LN, a subacute course of the disease was observed (81.7%), while in the absence of kidney damage, the overwhelming majority of patients with SLE had a chronic course (68.9%).  (Table 3)

 

Course

Number of observations

 

LN+

 

LN-

 

χ²

 

P

LN+LN-
Acute, %3971776,20,09,881<0,005
Subacute, %39717781,731,1140,957<0,001
Chronic, %39717712,168,9191,497<0,001

Table 3: The nature of the course of SLE in the study groups.

Similarly, in the group with LN, a significantly higher degree of disease activity was naturally observed - high activity was detected in almost every third patient (30.4%), compared with patients without kidney damage (19.4%). This is also evidenced by the higher SELENA-SLEDAI disease activity index – 14.2±0.4 versus 6.9±0.3 points (p<0.001). Predictably, in patients with LN, the estimated GFR was much lower than in individuals without kidney damage (71.4 and 92.5 ml/min, respectively). In the presence of chronic kidney disease, stage 1 prevailed in persons without LN (other causes of CKD), and late stages (3-5) were observed predominantly in LN and accounted for more than a third of cases (36.4%) (Table 4).

 

CKD stage

Number of observations

 

LN+

 

LN-

 

χ²

 

P

LN+LN-
I, %38914238,469,039,158<0,001 
II, %38914225,221,80,637>0,05 
III, %38914222,47,814,725<0,001 
IV, %3891429,51,49,962<0,01 
V, %3891424,50,06,566<0,05 

Table 4: CKD stages in the study groups.

In the group of people with LN, as expected, the presence of proteinuria was more often noted (97.7% versus 8.5% in the group without LN), and its level both in a single portion and when calculating the daily amount was significantly higher.  In LN, hematuria (56.9% and 2.3%, respectively), leukocyturia (51.8% and 9.5%, respectively), and casts (31.8% and 1.1%, respectively) were significantly more common (Tables 5 and 6).In the biochemical analysis of blood in LN, there were significantly higher levels of creatinine (136.4 versus 78.3 µmol/l, respectively), total cholesterol (6.64 versus 5.24 mmol/l) and low-density lipoproteins (4.25 versus 2.89 mmol/l) with lower blood concentrations of total protein (65.5 versus 77.2 g/l) and albumin (41.7 and 48.9 g/l). In the general blood test, the average hemoglobin level was significantly lower in the group with LN (109.7 versus 117.5 g/L), as was the percentage of lymphocytes (25.7 versus 28.7%), with a higher level of leukocytes (6.7 x 109/L and 5.7 x 109/L). Immunological blood parameters showed no significant differences in the study groups, except for a higher frequency of detection of antiphospholipid antibodies in the group of patients without lupus nephritis (p <0.05).

 

Parameter

Number of observations

 

LN+

 

LN-

 

t -criteria

 

P

LN+LN-
GFR, ml/min3149671,4±2,192,5±2,7-5,199<0,001
Urine protein, g/l3791481,76±0,130,02±0,0048,692<0,001
Daily proteinuria, g209202,31±0,210,06±0,013,246<0,001
Serum creatinine, µmol/l31296136,4±7,678,3±2,84,233<0,001
Total serum protein, g|l38515665,5±0,677,2±0,8-10,379<0,001
Serum albumin, g/l3699241,7±0,748,4±0,8-5,563<0,001
Total cholesterol, mmol/l253556,64±0,135,24±0,164,695<0,001
Low-density lipoprotein cholesterol, mmol/l125224,25±0,152,89±0,203,783<0,001
Hemoglobin, g/l397179109,7±1,1117,5±1,4-4,041<0,001
Leukocytes, 109/l3931806,7±0,185,7±0,23,319<0,001
Lymphocytes, %2929025,7±0,728,7±1,1-2,282<0,05
Platelets, 109/l278101247,3±5,7251,3±9,1-0,365>0,05
ESR, mm|h39017530,2±1,027,8±1,41,38>0,05
Antibodies to C1q, U/ml4242201,3±40,0149,6±34,60,977>0,05

Table 5: Comparison of laboratory parameters in groups of patients with LN and without LN.

 

Parameter

Number of observations

 

LN+

 

LN-

 

t -criteria

 

P

LN+LN-
Hematuria, %39717756,92,314,376<0,001
Leukocyturia, %39216951,89,510,257<0,001
Casta, %39017731,81,18,645<0,001
C3, %1653568,568,60,0001>0,05
C4, %1623555,660,00,231>0,05
CH50, %866777,974,60,225>0,05
Anti-dsDNA antibodies, %34616677,572,91,367>0,05
АNА, %2489384,391,42,888>0,05
Antibodies to phospholipids, %1143847,465,83,874<0,05

Table 6: Comparison of laboratory parameters in groups of patients with LN and without LN.

Patients with LN had hypertension significantly more often (49.9% versus 21.1%), but secondary APS was detected less frequently (Table 7).

 

Parameter

Number of observations

 

LN+

 

LN-

 

χ²

 

P

LN+LN-
Patients with arterial hypertension, %39717749,921,142,446<0>
Patients with APS, %3971778,69,432,393<0>

Table 7: Comorbid conditions in patients with SLE.

LN was more often accompanied by such extrarenal manifestations of SLE as anemia (49.8% versus 28.3%), lymphopenia (18.1% versus 6.1%), and stomatitis (4.0% versus 1.1%). At the same time, the absence of LN was significantly more often accompanied by skin manifestations (51.7% versus 37.2%), photosensitivity phenomena (7.8% versus 2.0%), signs of arthritis (37.8% versus 21.9%) and arthralgia (45.6% versus 36.9%), Raynaud's syndrome (19.4% versus 11.6%) (Table 8).

 

Parameter

Number of observations

 

LN+

 

LN-

 

χ²

 

P

LN+LN-
Arthritis, %39717721,937,816,009<0,001
Arthralgia, %39717736,945,63,851<0,05
Body temperature increasement, %39717723,429,42,425>0,05
Myalgia, %3971772,01,10,589>0,05
APS, %3971778,69,432,394<0,001
Central nervous system involvement, %3971775,36,10,165>0,05
Lymphadenopathy, %39717714,318,31,517>0,05
Pneumonitis, %3971777,85,60,938>0,05
Photosensitivity, %3971772,07,811,261<0,001
Erythema, %39717737,251,710,691<0,001
Alopecia, %39717714,318,31,517>0,05
Lupus-carditis, %39717720,622,80,35>0,05
Stomatitis, %3971774,01,13,476<0,05
Weight loss, %39717714,318,31,517>0,05
Gastrointestinal tract involvement, %3971773,02,80,024>0,05
Serositis, %3971779,66,11,887>0,05
Capillaritis, %3971774,85,00,014>0,05
Raynaud's syndrome, %39717711,619,46,398<0,05
Sjögren's syndrome, %3971772,31,10,878>0,05
Anemia, %39717749,828,323,181<0,001
Leukopenia, %39717723,425,60,325>0,05
Lymphopenia, %39717718,16,114,927<0,001
Thrombocytopenia, %3971779,88,30,314>0,05
        

Table 8: Frequency of clinical manifestations of SLE in the study groups.

At the onset of SLE, the picture of extrarenal lesions that accompanied LN or preceded its development was somewhat different: signs of arthritis (45.3% versus 33.6%), lymphadenopathy (11.8% versus 4.8%), and anemia (17.8% versus 4.9%) prevailed. Differences between groups in other clinical manifestations were not statistically significant (Table 9).

 

Parameter

Number of observations

 

LN+

 

LN-

 

χ²

 

P

LN+LN-
Arthritis, %33812545,333,65,095<0,05
Arthralgia, %33812513,915,20,125>0,05
Body temperature increasement, %33812541,432,82,848>0,05
Myalgia, %3381253,93,20,107>0,05
APS, %3381253,35,61,343>0,05
Central nervous system involvement, %3381252,72,40,025>0,05
Lymphadenopathy, %33812511,84,85,046<0,05
Photosensitivity, %3381251,52,40,456>0,05
Erythema, %33812533,430,40,382>0,05
Alopecia, %33812511,88,01,393>0,05
Lupus-carditis, %3381255,42,40,0089>0,05
Weight loss, %3381258,95,61,332>0,05
Gastrointestinal tract involvement, %3381251,51,60,009>0,05
Serositis, %3381254,73,20,519>0,05
Raynaud's syndrome, %3381256,55,60,134>0,05
Anemia, %33812513,91,614,602<0,0001
Leukopenia, %33812510,74,83,787>0,05
Lymphopenia, %3381254,40,83,619>0,05
Thrombocytopenia, %3381258,64,02,813>0,05

Table 9: Frequency of clinical manifestations of SLE in the study groups at the onset of the disease.

At the time of the patient’s initial examination, the duration of LN averaged 5.9±0.6 years. At the onset of the disease, kidney damage was noted in almost every second person (47.2%). In a number of patients, the first clinical and laboratory manifestations of LN were only changes in urine tests (hematuria, leukocyturia, casts and slight proteinuria - no more than 0.5 g/day). Isolated urinary syndrome (IUS) was observed in 33.5% of cases. In another 11%, isolated proteinuria was detected, not exceeding 3.0 g/day. Thus, in 44.5% of patients (almost half!) the first manifestations of LN concerned only abnormal urine tests, i.e. latent course of nephritis without extrarenal manifestations, which indicates the need for a careful study of urinary tests (general analysis, Nechiporenko test, daily proteinuria) at the initial diagnosis of SLE. In a third of patients (32.1%), LN debuted with the classic nephritic (acute nephritic) syndrome, manifested in most cases by hematuria, casts, moderate or slight proteinuria (usually no more than 1.5 g/day), increased blood pressure and periodically decreased GFR. Almost one in ten (9.2%) had signs of nephrotic syndrome, and in 5% of cases a diagnosis of acute kidney injury (AKI, 1.3%) and rapidly progressive glomerulonephritis (RPGN, 3.7%) was established. Finally, a combination of nephrotic syndrome and RPGN (5.5%), as well as nephrotic and acute nephritic syndromes (3.7%) was found in a number of individuals (Table 10).

Clinical and laboratory syndromeNumber of patientsNumber of casesFrequency, %
UTI2187333,5
Proteinuria2182411,0
Acute nephritic syndrome2187032,1
Nephrotic syndrome218209,2
RPGN21883,7
AKI21831,3
Nephrotic syndrome + RPGN218125,5
Nephrotic syndrome + acute nephritic syndrome21883,7
Total 218100

Table 10: Variants of the onset of LN and their frequency.

Based on histomorphological data obtained after nephrobiopsies in patients with SLE, the most common types of LN are IV (50.3%) and III (25.6%). In 14.1%, “pure” class V was diagnosed. The remaining options were found much less frequently (Table 11).

LN morphological classNumber of nephrobiopsies, n (total 199)Frequency, %
II105
III5125,6
IV10050,3
V2814,1
VI31,5
III+V21,0
IV+V10,5
Not informative42

Table 11: Morphological types of kidney damage in patients with SLE according to the ISN/RPS classification (2003).

A total of 317 cases of exacerbation of LN were recorded during observation in patients with SLE. The table below shows the types of exacerbations and their frequency. (Table 12)

Type of exacerbationNumber of patientsNumber of casesFrequency, %
UTI2034319,3
Proteinuria2036618,5
Acute nephritic syndrome2039425,2
Nephrotic syndrome203257,0
RPGN203227,6
AKI20361,1
Nephrotic syndrome + RPGN203328,7
Nephrotic syndrome + acute nephritic syndrome203251,4
Nephrotic syndrome +AKI203411,2
Total203317100

Table 12: Variants of exacerbations of LN and its frequency.

Just as in the onset of LN, a significant portion of exacerbations are represented by latent changes (IUS and proteinuria), accounting for 37.8% of all exacerbations. In these cases, there were no extrarenal signs (increased blood pressure and edema), and exacerbation was established by the increase (appearance) and persistent (at least three tests) persistence of proteinuria and changes in urinary sediment. Acute nephritic syndrome was observed in a quarter of cases. However, in contrast to the debut manifestations of LN, more severe variants were much more common - RPGN (7.6%) and combinations of nephrotic syndrome with RPGN (8.7%) and AKI (11.2%), amounting to a total of 27.5% (i.e., in every fourth patient with LN). These types of exacerbations, according to the literature, are serious predictors of adverse outcomes (development of late stages of CKD, initiation of renal replacement therapy, deaths).In the treatment of patients in both groups, almost 100% used glucocorticosteroids (GCS), the average dosage of which in patients with LN was 20.3 mg/day, and in the other group - 12.9 mg/day (p <0>

 

Parameter

Number of observations

 

LN+

 

LN-

 

t -criteria

 

P

LN+LN-
GCS per os, mg/daily33212520,3±0,712,9±0,76,210<0,001

Table 13: Average dosage of prescribed corticosteroids in the study groups.

There was a more frequent use of GCS pulse therapy in the group of patients with LN (26.1% compared to 12.8%). In more than half (53.1%) of patients with LN, immunosuppressive therapy was added to the treatment –  azathioprine (27.6%) and cyclophosphamide (17.1%). In the group of patients without LN, cytostatics agents were prescribed much less frequently (azathioprine - 16.0%). Angiotensin-converting enzyme inhibitors (ACEIs) (58.1% vs. 26.0%) and angiotensin II receptor blockers (ARBs) (7.3% vs. 0.0%) were used significantly more often in LN, taking into account their antihypertensive and renoprotective effects. However, in the absence of immune complex kidney damage, hydroxychloroquine (HCQ) was more widely used (54.4% versus 44.1%), although without significant differences. Antiplatelet drugs (36.0% vs. 22.4%) were also more often prescribed to patients with LN; no significant differences could be detected with regard to anticoagulant therapy (16.2% vs. 10.4%). However, plasmapheresis sessions were more often performed in the group without lupus nephritis (in 20.3% and 4.7% of cases, respectively). In 3.7% of patients with LN, methods of renal replacement therapy were used (sessions of hemodialysis, hemodiafiltration, peritoneal dialysis and kidney transplantation) (Table 14).

ParameterNumber of observationsLN+LN-χ²P
 LN+LN-
GCS pulse therapy, %33312526,112,89,259<0,005
Hydroxychloroquine, %33312544,154,43,838>0,05
Cyclophosphamide,%33312517,10,024,438<0,001
Azathioprine, %33312527,616,06,651<0,05
Mycophenolate mofetil, %2545011,50,06,375<0,05
ACEIs, %2545058,126,017,042<0,001
BRA, %254507,30,03,864<0,05
Heparin, %33312516,210,42,462>0,05
Antiplatelet agents, %33312536,022,47,726<0,05
Plasmapheresis, %234794,720,318,124<0,001
Hemodialysis, %3331253,30,04,231<0,05
Kidney transplantation, %234500,40,00,214>0,05

Table 14: Frequency of use of various therapeutic agents in the study groups.

Among patients under dynamic observation (from 1 month to 20 years), the development of complications associated with both the underlying disease and the therapy was studied. A total of 49 such complications (19.3%) were identified, 36 in the group with LN and 13 without kidney damage. The most common changes (8 cases) were changes in the musculoskeletal system (aseptic necrosis of bone tissue), which were observed only in the group of patients with LN and were probably associated with a higher dose of corticosteroids used. Infectious complications come in second place in frequency (7 cases in the LN group and 5 cases in people without LN). This is followed by a complication in the form of osteoporosis with symptoms of vertebral compression fractures (6 cases in the LN group and 4 cases in the absence of LN). Five cases of Cushing syndrome have been described (all in individuals with LN). Complications from the cardiovascular system in the form of myocardial infarction and acute cerebrovascular accident were noted in 5 cases (3 and 2, respectively). In 4 cases, patients developed glaucoma (2 and 2, respectively), in 2 - a steroid gastric ulcer, in one - drug-induced stomatitis, etc. (all in the LN group). One patient from the group without kidney damage was diagnosed with ovarian cancer. Apparently, the vast majority of the described complications are associated with the drug therapy and, above all, with the prescription of GCS. When studying disease outcomes, the end points were patient death and “renal” death, i.e. development of end-stage chronic renal failure and/or transfer of the patient to renal replacement therapy. According to the data obtained, the presence of LN is an extremely unfavorable factor. If in the group of patients without kidney damage the rate of adverse outcomes was 1.7%, then in the presence of LN this figure reached 20.7%. Mortality in the group of people with LN was 9.9%, while the death of patients associated specifically with the presence of nephritis (end-stage CKD) occurred almost 2 times more often than deaths associated with other causes (cardiovascular and infectious complications, gastrointestinal bleeding, etc.). In addition to these cases, end-stage CKD was noted in 7.8% of cases, and taking into account deaths - in almost 15% (14.1%).  An important end point in assessing the outcome of renal pathology is a persistent (at least 3 months) doubling of blood creatinine levels compared to the initial level, indicating the steady progression of CKD. In the study group of patients, this figure was 3.3%; these individuals are potential candidates for the use of renal replacement therapy methods in the near future. 12.7% were treated with program hemodialysis, 7% of patients underwent kidney transplantation. (Table 15)

ParameterLN+LN-
Number of patients, n396172
Doubling of serum creatinine level, n (%)13 (3,3)0
End-stage CKD (including those receiving RRT), n (%)31 (7,8)0
LN-associated death, n (%)25 (6,3)0
Death from other causes, n (%)13 (3,3)3 (1,7)
Total number of adverse outcomes, n (%)82 (20,7)3 (1,7)
Duration of observation, months48,6±3,025,3±4,3

Table 15: Adverse outcomes in patients with and without LN.

Finally, the number of hospitalizations appears to be an important socioeconomic indicator. It turned out that during the observation period in the presence of LN it averaged 2.09±0.3, and in the absence of kidney damage - 1.43±0.3 (p=0.0033). (Table 16)

 

Parameter

Number of observations

 

LN+

 

LN-

 

t -criteria*

 

P

LN+LN-
Number of hospitalizations,n237392,091,432,999=0,0033

Table 16: Comparison of normalized number of hospitalizations per year between patients with and without LN.

Discussion and conclusions

Systemic lupus erythematosus is a fairly rare disease. Its highest incidence and prevalence are reported in North America, with rates of 23.2 and 241 per 100,000 population, respectively. In the United States, there are more than 250,000 patients suffering from SLE [13]. However, worldwide, the overall incidence of SLE varies widely, ranging from 4 to 250 cases per 100,000 population [14]. According to our earlier study, in Minsk the incidence of SLE was 4-5, and the prevalence was 18-20 patients per 100,000 urban adult population [15]. The clinical forms and course of SLE are diverse and often become severe, accompanied by serious complications and even deaths. In such situations, there is a need to prescribe active therapy using high doses of GCS and immunosuppressive drugs, the administration of which may be accompanied by severe side effects. LN, along with damage to the central nervous system, is the cause of complications and unfavorable outcomes of SLE, but is much more common than neurolupus. For the first time, using a large material, we tried to give a comprehensive (clinical, laboratory and morphological) assessment of patients with LN, to analyze the features of the course of nephritis and its outcomes. A retrospective and prospective analysis of 574 cases of SLE over a more than 30-year period revealed a high incidence of lupus nephritis (69.2%), probably associated with the predominance of inpatients in whom exacerbation of LN was one of the indications for hospitalization. The study showed an increase in cases of LN as the duration of the underlying disease increased. Accordingly, the observation time for patients with LN turned out to be significantly longer than for persons without kidney damage, due to the need for more careful and frequent monitoring of the course of the disease. Among patients with LN, the acute and subacute course of the disease was significantly more common, while in patients without lupus nephritis, a chronic course of SLE was mainly observed. Disease activity, including that calculated using the SELENA-SLEDAI index, was also significantly higher in the group of patients with LN. Interestingly, the immunological activity of SLE in patients with and without LN did not have significant differences, which is at odds with a number of literature data [5, 7]. In the presence of LN, hypertension was more often observed, which is partly explained by the presence of more advanced stages of CKD. At the same time, patients with LN are significantly less likely to have secondary APS. In addition, patients with SLE without LN were significantly more likely to have symptoms such as skin manifestations, photosensitivity, arthritis and arthralgia, and Raynaud's syndrome. It is noteworthy that at the onset of the disease, kidney damage was noted in almost half of the patients with SLE (48.2%), and in many cases, the first clinical and laboratory manifestations of LN were only changes in urine tests. In more than 10% of cases, lupus nephritis debuted with manifestations of RPGN or AKI, including in combination with nephrotic syndrome. Obviously, taking into account the unfavorable prognosis and more intense immunosuppression already at the time of diagnosis of SLE, to improve patient survival, a careful analysis of available clinical and laboratory data is required: general urine analysis, analysis for daily proteinuria, determination of GFR, as well as monitoring these parameters over time. Such therapeutic tactics as nephrobiopsy makes possible early identification of lupus nephritis, as well as choosing the most rational immunosuppression, which will ultimately reduce the number of exacerbations of LN, especially in combination of RPGN and AKI or acute nephritic syndrome. In this way, it is possible to achieve a reduction in the number of hospitalizations, as well as prolongation of the patient’s “renal” and general life.  The vast majority (75%) of patients with LN have proliferative forms according to histological examination. The presence of lupus nephritis in a patient with SLE is associated with a higher incidence of complications and deaths, as well as more hospitalizations.

References

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Dr Elvira Farina

Dear Jessica, and the super professional team of the ‘Clinical Cardiology and Cardiovascular Interventions’ I am sincerely grateful to the coordinated work of the journal team for the no problem with the submission of my manuscript: “Cardiometabolic Disorders in A Pregnant Woman with Severe Preeclampsia on the Background of Morbid Obesity (Case Report).” The review process by 5 experts was fast, and the comments were professional, which made it more specific and academic, and the process of publication and presentation of the article was excellent. I recommend that my colleagues publish articles in this journal, and I am interested in further scientific cooperation. Sincerely and best wishes, Dr. Oleg Golyanovskiy.

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Dr Oleg Golyanovski

Dear Ashley Rosa, Editorial Coordinator of the journal - Psychology and Mental Health Care. " The process of obtaining publication of my article in the Psychology and Mental Health Journal was positive in all areas. The peer review process resulted in a number of valuable comments, the editorial process was collaborative and timely, and the quality of this journal has been quickly noticed, resulting in alternative journals contacting me to publish with them." Warm regards, Susan Anne Smith, PhD. Australian Breastfeeding Association.

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Dr Susan Anne Smith

Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. I appreciate the journal (JCCI) editorial office support, the entire team leads were always ready to help, not only on technical front but also on thorough process. Also, I should thank dear reviewers’ attention to detail and creative approach to teach me and bring new insights by their comments. Surely, more discussions and introduction of other hemodynamic devices would provide better prevention and management of shock states. Your efforts and dedication in presenting educational materials in this journal are commendable. Best wishes from, Farahnaz Fallahian.

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Dr Farahnaz Fallahian

Dear Maria Emerson, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. I am delighted to have published our manuscript, "Acute Colonic Pseudo-Obstruction (ACPO): A rare but serious complication following caesarean section." I want to thank the editorial team, especially Maria Emerson, for their prompt review of the manuscript, quick responses to queries, and overall support. Yours sincerely Dr. Victor Olagundoye.

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Dr Victor Olagundoye

Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. Many thanks for publishing this manuscript after I lost confidence the editors were most helpful, more than other journals Best wishes from, Susan Anne Smith, PhD. Australian Breastfeeding Association.

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Dr Susan Anne Smith

Dear Agrippa Hilda, Editorial Coordinator, Journal of Neuroscience and Neurological Surgery. The entire process including article submission, review, revision, and publication was extremely easy. The journal editor was prompt and helpful, and the reviewers contributed to the quality of the paper. Thank you so much! Eric Nussbaum, MD

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Dr Eric S Nussbaum

Dr Hala Al Shaikh This is to acknowledge that the peer review process for the article ’ A Novel Gnrh1 Gene Mutation in Four Omani Male Siblings, Presentation and Management ’ sent to the International Journal of Clinical Case Reports and Reviews was quick and smooth. The editorial office was prompt with easy communication.

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Hala Al Shaikh

Dear Erin Aust, Editorial Coordinator, Journal of General Medicine and Clinical Practice. We are pleased to share our experience with the “Journal of General Medicine and Clinical Practice”, following the successful publication of our article. The peer review process was thorough and constructive, helping to improve the clarity and quality of the manuscript. We are especially thankful to Ms. Erin Aust, the Editorial Coordinator, for her prompt communication and continuous support throughout the process. Her professionalism ensured a smooth and efficient publication experience. The journal upholds high editorial standards, and we highly recommend it to fellow researchers seeking a credible platform for their work. Best wishes By, Dr. Rakhi Mishra.

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Dr Rakhi Mishra

Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. The peer review process of the journal of Clinical Cardiology and Cardiovascular Interventions was excellent and fast, as was the support of the editorial office and the quality of the journal. Kind regards Walter F. Riesen Prof. Dr. Dr. h.c. Walter F. Riesen.

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Dr Walter F Riesen

Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. Thank you for publishing our article, Exploring Clozapine's Efficacy in Managing Aggression: A Multiple Single-Case Study in Forensic Psychiatry in the international journal of clinical case reports and reviews. We found the peer review process very professional and efficient. The comments were constructive, and the whole process was efficient. On behalf of the co-authors, I would like to thank you for publishing this article. With regards, Dr. Jelle R. Lettinga.

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Dr Jelle Lettinga

Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, I would like to express my deep admiration for the exceptional professionalism demonstrated by your journal. I am thoroughly impressed by the speed of the editorial process, the substantive and insightful reviews, and the meticulous preparation of the manuscript for publication. Additionally, I greatly appreciate the courteous and immediate responses from your editorial office to all my inquiries. Best Regards, Dariusz Ziora

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Dariusz Ziora

Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation, Auctores Publishing LLC, We would like to thank the editorial team for the smooth and high-quality communication leading up to the publication of our article in the Journal of Neurodegeneration and Neurorehabilitation. The reviewers have extensive knowledge in the field, and their relevant questions helped to add value to our publication. Kind regards, Dr. Ravi Shrivastava.

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Dr Ravi Shrivastava

Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, Auctores Publishing LLC, USA Office: +1-(302)-520-2644. I would like to express my sincere appreciation for the efficient and professional handling of my case report by the ‘Journal of Clinical Case Reports and Studies’. The peer review process was not only fast but also highly constructive—the reviewers’ comments were clear, relevant, and greatly helped me improve the quality and clarity of my manuscript. I also received excellent support from the editorial office throughout the process. Communication was smooth and timely, and I felt well guided at every stage, from submission to publication. The overall quality and rigor of the journal are truly commendable. I am pleased to have published my work with Journal of Clinical Case Reports and Studies, and I look forward to future opportunities for collaboration. Sincerely, Aline Tollet, UCLouvain.

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Dr Aline Tollet

Dear Ms. Mayra Duenas, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. “The International Journal of Clinical Case Reports and Reviews represented the “ideal house” to share with the research community a first experience with the use of the Simeox device for speech rehabilitation. High scientific reputation and attractive website communication were first determinants for the selection of this Journal, and the following submission process exceeded expectations: fast but highly professional peer review, great support by the editorial office, elegant graphic layout. Exactly what a dynamic research team - also composed by allied professionals - needs!" From, Chiara Beccaluva, PT - Italy.

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Dr Chiara Giuseppina Beccaluva

Dear Maria Emerson, Editorial Coordinator, we have deeply appreciated the professionalism demonstrated by the International Journal of Clinical Case Reports and Reviews. The reviewers have extensive knowledge of our field and have been very efficient and fast in supporting the process. I am really looking forward to further collaboration. Thanks. Best regards, Dr. Claudio Ligresti

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Dr Claudio Ligresti

Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation. “The peer review process was efficient and constructive, and the editorial office provided excellent communication and support throughout. The journal ensures scientific rigor and high editorial standards, while also offering a smooth and timely publication process. We sincerely appreciate the work of the editorial team in facilitating the dissemination of innovative approaches such as the Bonori Method.” Best regards, Dr. Matteo Bonori.

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Dr Matteo Bonori

I recommend without hesitation submitting relevant papers on medical decision making to the International Journal of Clinical Case Reports and Reviews. I am very grateful to the editorial staff. Maria Emerson was a pleasure to communicate with. The time from submission to publication was an extremely short 3 weeks. The editorial staff submitted the paper to three reviewers. Two of the reviewers commented positively on the value of publishing the paper. The editorial staff quickly recognized the third reviewer’s comments as an unjust attempt to reject the paper. I revised the paper as recommended by the first two reviewers.

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Edouard Kujawski

Dear Maria Emerson, Editorial Coordinator, Journal of Clinical Research and Reports. Thank you for publishing our case report: "Clinical Case of Effective Fetal Stem Cells Treatment in a Patient with Autism Spectrum Disorder" within the "Journal of Clinical Research and Reports" being submitted by the team of EmCell doctors from Kyiv, Ukraine. We much appreciate a professional and transparent peer-review process from Auctores. All research Doctors are so grateful to your Editorial Office and Auctores Publishing support! I amiably wish our article publication maintained a top quality of your International Scientific Journal. My best wishes for a prosperity of the Journal of Clinical Research and Reports. Hope our scientific relationship and cooperation will remain long lasting. Thank you very much indeed. Kind regards, Dr. Andriy Sinelnyk Cell Therapy Center EmCell

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Dr Andriy Sinelnyk

Dear Editorial Team, Clinical Cardiology and Cardiovascular Interventions. It was truly a rewarding experience to work with the journal “Clinical Cardiology and Cardiovascular Interventions”. The peer review process was insightful and encouraging, helping us refine our work to a higher standard. The editorial office offered exceptional support with prompt and thoughtful communication. I highly value the journal’s role in promoting scientific advancement and am honored to be part of it. Best regards, Meng-Jou Lee, MD, Department of Anesthesiology, National Taiwan University Hospital.

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Dr Meng-JouLe

Dear Editorial Team, Journal-Clinical Cardiology and Cardiovascular Interventions, “Publishing my article with Clinical Cardiology and Cardiovascular Interventions has been a highly positive experience. The peer-review process was rigorous yet supportive, offering valuable feedback that strengthened my work. The editorial team demonstrated exceptional professionalism, prompt communication, and a genuine commitment to maintaining the highest scientific standards. I am very pleased with the publication quality and proud to be associated with such a reputable journal.” Warm regards, Dr. Mahmoud Kamal Moustafa Ahmed

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Mahmoud Kamal Moustafa Ahmed

Dear Maria Emerson, Editorial Coordinator of ‘International Journal of Clinical Case Reports and Reviews’, I appreciate the opportunity to publish my article with your journal. The editorial office provided clear communication during the submission and review process, and I found the overall experience professional and constructive. Best regards, Elena Salvatore.

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Dr Elena Salvatore

Dear Mayra Duenas, Editorial Coordinator of ‘International Journal of Clinical Case Reports and Reviews Herewith I confirm an optimal peer review process and a great support of the editorial office of the present journal

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Christoph Maurer

Dear Editorial Team, Clinical Cardiology and Cardiovascular Interventions. I am really grateful for the peers review; their feedback gave me the opportunity to reflect on the message and impact of my work and to ameliorate the article. The editors did a great job in addition by encouraging me to continue with the process of publishing.

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Baciulescu Laura

Dear Cecilia Lilly, Editorial Coordinator, Endocrinology and Disorders, Thank you so much for your quick response regarding reviewing and all process till publishing our manuscript entitled: Prevalence of Pre-Diabetes and its Associated Risk Factors Among Nile College Students, Sudan. Best regards, Dr Mamoun Magzoub.

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Dr Mamoun Magzoub

International Journal of Clinical Case Reports and Reviews is a high quality journal that has a clear and concise submission process. The peer review process was comprehensive and constructive. Support from the editorial office was excellent, since the administrative staff were responsive. The journal provides a fast and timely publication timeline.

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Joel Yat Seng Wong

Dear Maria Emerson, Editorial Coordinator of International Journal of Clinical Case Reports and Reviews, What distinguishes International Journal of Clinical Case Report and Review is not only the scientific rigor of its publications, but the intellectual climate in which research is evaluated. The submission process is refreshingly free of unnecessary formal barriers and bureaucratic rituals that often complicate academic publishing without adding real value. The peer-review system is demanding yet constructive, guided by genuine scientific dialogue rather than hierarchical or authoritarian attitudes. Reviewers act as collaborators in improving the manuscript, not as gatekeepers imposing arbitrary standards. This journal offers a rare balance: high methodological standards combined with a respectful, transparent, and supportive editorial approach. In an era where publishing can feel more burdensome than research itself, this platform restores the original purpose of peer review — to refine ideas, not to obstruct them Prof. Perlat Kapisyzi, FCCP PULMONOLOGIST AND THORACIC IMAGING.

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Dr Perlat Kapisyzi

Dear Mayra Duenas, Editorial Coordinator of the journal IJCCR, I write here a little on my experience as an author submitting to the International Journal of Clinical Case Reports and Reviews (IJCCR). This was my first submission to IJCCR and my manuscript was inherently an outsider’s effort. It attempted to broadly identify and then make some sense of life’s under-appreciated mysteries. I initially had responded to a request for possible submissions. I then contacted IJCCR with a tentative topic for a manuscript. They quickly got back with an approval for the submission, but with a particular requirement that it be medically relevant. I then put together a manuscript and submitted it. After the usual back-and-forth over forms and formality, the manuscript was sent off for reviews. Within 2 weeks I got back 4 reviews which were both helpful and also surprising. Surprising in that the topic was somewhat foreign to medical literature. My subsequent updates in response to the reviewer comments went smoothly and in short order I had a series of proofs to evaluate. All in all, the whole publication process seemed outstanding. It was both helpful in terms of the paper’s content and also in terms of its efficient and friendly communications. Thank you all very much. Sincerely, Ted Christopher, Rochester, NY.

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Dr Ted Christopher

Dear Grace Pierce, Editorial Coordinator of the journal IJCCR, I had a very positive experience with Auctores - Journal throughout the publication process. The Editorial Team was highly responsive, professional, and supportive at every stage. I would like to extend my sincere thanks to the Editor: Grace Pierce, for her guidance and assistance. The peer-review process was smooth and constructive, helping improve the quality of my work. I would gladly recommend Auctores Journal to fellow researchers and authors. Dr. SABITA SINHA, Medical Oncologist, MD (Electro Homeopathy).

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Dr SABITA SINHA