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Home > Books > Lupus - Diagnostics and Developments
Open access peer-reviewed chapter
Written By
Abire Allaoui, Rita Aniq Filali, Amine Khalfaoui and Abdelhamid Naitlho
Submitted: 17 July 2024 Reviewed: 19 September 2024 Published: 21 November 2024
DOI: 10.5772/intechopen.1007408
From the Edited Volume
Lupus - Diagnostics and Developments
Rizwan Ahmad
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Abstract
Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) have revolutionized the treatment of diabetic nephropathy. Their application was expanded to include other disorders, such as cardiovascular disease. Lupus nephritis is a significant complication of systemic lupus. Within the first 3years of the disease, one-third of patients develop lupus nephritis. It is recognized as a leading cause of morbidity and mortality. Lupus nephritis therapy has improved with the use of corticosteroids, immunosuppressants such cyclophosphamide, mycophenolate mofetil, calcineurin inhibitors, and rituximab over the years. However, existing medications do not address all needs in the management of Lupus nephritis (LN) and are not always effective. According to new research, SGLT-2i may have potential for treating lupus nephritis due to their pleiotropic effects (anti-inflammatory, immunological, and hemodynamic implications). Recent trials using SGLT-2i in animals and humans have yielded encouraging outcomes in lupus nephritis. This review will explore the role of SGLT-2i in the management of lupus nephritis in addition to immunosuppressive medication.
Keywords
- SGTL2 inhibitors
- lupus
- lupus nephritis
- treatment
- proteinuria
Author Information
Abire Allaoui*
- Internal Medicine Department, Mohammed VI University of Health and Sciences, Casablanca, Morocco
- Clinical Immunology, Autoimmunity and Inflammation Laboratory (LICIA), Faculty of Medicine and Pharmacy, Hassan II University, Casablanca, Morocco
- Mohammed VI Center of Research and Innovation, Rabat, Morocco
Rita Aniq Filali
- Internal Medicine Department, Mohammed VI University of Health and Sciences, Casablanca, Morocco
Amine Khalfaoui
- Nephrology Department, Mohammed VI University of Health and Sciences, Casablanca, Morocco
Abdelhamid Naitlho
- Internal Medicine Department, Mohammed VI University of Health and Sciences, Casablanca, Morocco
*Address all correspondence to: abire.allaoui@gmail.com
1. Introduction
Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease with alternating periods of remission and flares [1]. Approximately 33–50% of SLE patients develop organ involvement within 5years of diagnosis [2]. The incidence and prevalence of SLE and LN differ based on the specific population under investigation and the diagnostic criteria employed to identify SLE and LN [2, 3]. Lupus nephritis (LN) is one of SLE’s most common and severe complications [3]. Glomerulonephritis is the most prevalent type of LN. LN can progress to end-stage renal disease [3]. LN was linked to higher rates of illness and death, while SLE patients who did not develop LN had favorable overall outcomes in terms of survival [3]. Our understanding of the genetic and pathogenetic bases for LN has significantly advanced in recent decades [3, 4]. It is crucial to consider key risk factors to effectively assess and address progressive kidney disease. These include clinical parameters (proteinuria, glomerular filtration rate, complement levels, anti-dsDNA titer, and presence of antiphospholipid antibodies), kidney biopsy classification, and adherence to therapy [4].
Current treatments do not meet all needs in the management of LN and are not uniformly effective; they also carry significant risks and side effects, underscoring the need for novel therapeutic approaches [4]. While glucocorticoids and immunosuppressive agents such cyclophosphamide, mycophenolate mofetil, calcineurin inhibitors, and B-cell depletion therapy, remain the standard of care for LN, non-immunosuppressive therapies, such as renin-angiotensin-aldosterone system inhibitors, have always been part of the therapeutic arsenal of LN.
The concept of clinical response lacks unanimity, and there is an urgent need for uniform protocols to establish therapy response. A comprehensive response is typically achieved when the spot urinary protein-to-creatinine ratio is below 500mg/g, the serum creatinine level reverts to the previous baseline or becomes normal, and there are less than five red blood cells per high-power field and no red blood cell casts in the urinary sediment. A partial response is achieved when the amount of protein in the urine decreases by more than 50% to a level that is below the threshold for kidney damage. This is indicated by a spot urinary protein-to-creatinine ratio of less than 3g/g. Additionally, the serum creatinine level should be 15–25% higher or lower than the initial level. The number of red blood cells per high-power field should be less than 50% of the initial count, and there should be no red blood cell casts in the urine sediment [3]. Despite, all the advancements in the LN treatment, LN remains a substantial cause of morbidity and death among patients with SLE, and achieving clinical remission is not always possible.
Cardiovascular complications are also common and a leading cause of death in patients with SLE and LN. Patients with LN have multiple risk factors for cardiovascular complications, such as diabetes, dyslipidemia, and vascular inflammation [5].
Emerging evidence suggests that sodium-glucose cotransporter 2 inhibitors (SGLT-2i), a class of drugs primarily used to manage type 2 diabetes (T2D) and heart failure, may hold promise for treating lupus nephritis. These agents block reabsorption of glucose in the kidneys, leading to increased urinary glucose excretion and improved glycemic control [6]. Beyond their effects on blood sugar, SGLT2 inhibitors have demonstrated anti-inflammatory, antioxidant, and renoprotective properties that may be beneficial in autoimmune kidney diseases such as LN [7]. The unique renal and cardiac protective effects of SGLT2is in patients with chronic kidney disease (CKD) offer an attractive opportunity for SLE/LN management.
2. Sodium-glucose cotransporter 2
Sodium-glucose cotransporter 2 (SGTL2) belongs to a large family of membrane proteins located in the intestinal tract and proximal tubule, and is responsible for the transport of glucose, amino acids, vitamins, and some ions across the membrane of the epithelial intestine and proximal tubule in the kidneys. SGLT1 is predominantly found in the gastrointestinal tract, while SGLT2 is a renal protein, primarily expressed in the proximal tubule and accounts for 80–90% of glucose reabsorption, with the remaining 10–20% reabsorbed by SGLT1 [8]. SGLT-2 proteins have the physiological function of reabsorbing filtered glucose from the tubular lumen. Upon the discovery of the SGLT proteins, scientists found that phlorizin, an SGLT inhibitor, had been extensively researched for more than 150years. However, it was only in recent decades that scientists uncovered its precise mechanism of action [7]. Phlorizin is derived from the root bark of the apple tree. In 1933, a limited number of individuals had a brief trial of the substance, during which scientists observed its ability to raise glucose levels in urine, decrease blood glucose levels, and inhibit the reabsorption of glucose. Its effect extended beyond the kidney. Due to its ability to impede glucose absorption in the intestine, limited oral absorption, and interference with glucose transport zones, it was considered inappropriate for human usage [7]. However, research on phlorizin played a crucial role in comprehending the functioning of sodium-glucose transporters, and scientists hypothesized that it might interfere with the activity of SGLTs. In 1995, researchers discovered that phlorizin effectively blocked the activity of both SGLT1 and SGLT2 [7]. Phlorizin’s negative effects can be attributed to the presence of SGLT1 in several tissues and its crucial function in glucose absorption in the intestine. As scientists gained additional knowledge about phlorizin and SGLTs, they became intrigued by the potential of employing phlorizin as a basis for developing a diabetes treatment. Subsequent research efforts in the following decades were dedicated to enhancing the efficacy, selectivity, and duration of action of phlorizin derivatives targeted at SGLT2. This study led to the identification and evaluation of enhanced SGLT2 inhibitors [7].
Currently, four classes of SGLT-2i exist (canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin), which reduce the reabsorption of filtered glucose, decrease the renal threshold for glucose, and promote urinary glucose excretion [9].
3. The revolution of SGLT-2i
Canagliflozin was the first SGLT-2 inhibitor approved on March 29, 2013, to be used in adult patients with type 2 diabetes to enhance blood glucose control in addition to diet and exercise [7]. These insulin-independent antihyperglycemic medications are now known to be pleiotropic agents with significant metabolic, cardiovascular, and renal benefits [9].
In addition to lowering glycated hemoglobin (HbA1c), fasting and postprandial plasma glucose levels, body weight, and blood pressure, SGLT2 inhibitors reduce the risk of a range of cardiovascular and renal outcomes, without increasing the risk of hypoglycemia [7].
Large clinical trials in patients with T2D with established cardiovascular disease or cardiovascular risk factors, heart failure, and CKD have shown that SGLT2 inhibitors confer cardiovascular and kidney protection [8]. In May of 2023, the FDA expanded the indication of dapagliflozin to include heart failure across the entire spectrum of left ventricular ejection fraction. This includes heart failure with mildly reduced ejection fraction (HFmrEF) and preserved ejection fraction (HFpEF) [8].
Four cardiovascular outcome trials showed that SGLT-2is has important effects on slowing the decline rate of the estimated glomerular filtration rate and decreasing albuminuria, in addition to a significant reduction in cardiovascular events. The nephroprotective efficacy of SGLT2is was extended to non-diabetic chronic kidney diseases such as IgA nephropathy [10]. Nephropathy reduces renal workload, thereby reducing intraglomerular pressure and regulating blood pressure [9, 10]. This has solved the management difficulties in patients with CKD and congestive heart failure [10].
SGLT2is are also used in Off-label indications such as the management of obesity in combination with glucagon-like peptide-1 receptor agonists and nonalcoholic fatty liver disease (NAFLD), as adjunctive therapy in patients with type 2 diabetes and NAFLD [7, 8].
In addition to its pleiotropic effects, SGLT-2is has been reported to be able to block lipopolysaccharide-induced and NOD-like receptor family pyrin domain containing 3 (NLRP3)-mediated inflammatory responses and regulate macrophage polarization via interplay with mammalian target of rapamycin (mTOR) and AMP-activated protein kinase pathways [10, 11]; hence, the promising effect of SGLT-2is to reducing inflammation, modulate endothelial dysfunction, and decelerate atherosclerosis, which are all impaired in the pathophysiology of SLE. Some recent studies with a small effective have found an antiproteinuric effect of empagliflozin in patients with LN [11].
4. Mechanistic effects of SGTL-2i
4.1 Renal effects
The effects of SGTL-2i on glomerular hemodynamic pathways have been analyzed in numerous studies, either in experimental models or in patients. SGLT2 inhibitors have demonstrated a reduction in hyperfiltration by inhibiting sodium reabsorption in the proximal tubule and have also shown an afferent renal arterial vasoconstriction and vasodilation of the renal efferent arteriole, similar to how angiotensin-converting enzyme inhibitors and angiotensin receptor blockers work [8], in addition to a decrease in intraglomerular pressure by restoring distal sodium delivery and therefore normalizing tubuloglomerular feedback [8, 12, 13].
Under hyperglycemic conditions, increased SGLT2 expression increases sodium and glucose reabsorption, which increases ATP-dependent tubular workload and oxygen consumption, both of which can result in hypoxia. As SGLT-2i reduces tubular workload, oxygen consumption, and hypoxia by reducing glucose and sodium reabsorption, they may also reduce the risk of acute kidney injury events and proximal biomarkers of acute kidney injury, such as kidney injury molecule-1 [8]. Interestingly, clinical studies have confirmed that EPO expression increases following SGLT2 inhibition [14, 15]. Therefore, it was not surprising to see that the risk of anemia, which was an independent predictor of renal and cardiovascular outcomes, and the start of anemia treatment were significantly reduced with canagliflozin in a sizable multi-national kidney outcome trial [16].
4.2 Effects on blood pressure
The systolic and diastolic blood pressures were reduced by approximately 4 and 2mmHg, respectively, by SGLT-2i. It is likely that SGLT-2i lowers blood pressure through different contributing variables [8]. Increased natriuresis and osmotic diuresis in conjunction with decreases in extracellular volume and plasma volume are believed to be responsible for SGLT-2i’s ability to control blood pressure, and according to human clinical trials, SGLT-2i has a positive impact on blood pressure variability, endothelial function, and arterial stiffness [8, 13, 17]. These results suggest that sympathoinhibition may be a modulator of the beneficial effects of SGLT-2i on the kidneys and perhaps the cardiovascular system [8].
4.3 Effects in non-diabetic patients
In patients with CKD, the DAPA-CKD trial demonstrated a decreased risk of kidney failure, hospitalization for heart failure or death from cardiovascular causes, and all-cause mortality, with statistically significant effects in reducing the risk of kidney failure both in the subgroup of patients with and without type 2 diabetes [17]. Furthermore, the EMPEROR-Reduced and DAPA-HF trials showed that SGLT-2i lowered the risk of heart failure hospitalizations or cardiovascular death and slowed the progression of kidney function decline in patients with heart failure. They reduced the ejection fraction, both with and without type 2 diabetes [18, 19]. These three clinical trials showed that SGLT-2i has positive effects in patients with type 2 diabetes. If used in clinical practice, it can revolutionize the management of a wide spectrum of high-risk CKD patients [8].
4.4 Immunological effects
Unexpectedly, SGLT2i therapy also has immunological effects that go beyond metabolic effects. Through the induction of regulatory T-cell production, they have a significant effect on the development of germinal centers and creation of autoreactive plasma cells in the spleen [17].
It appears that SGLT-2i inhibits both podocyte and macrophage mTOR activation [18, 19]. The significance of mTOR blocking in patients with SLE is highlighted by the well-established roles that mTOR plays in proinflammatory lineage formation [20], podocyte and endothelial cell dysfunction [21], and adaptive immune system activation [22]. In addition to their protective effects on the kidneys and heart, SGLT-2i may function as an adjuvant immunomodulatory therapy for SLE, partly through mTOR inhibition [10].
Higher ketone body concentrations decrease monocyte production of interleukin-1b and inhibit the Nod-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome [23, 24]. These inflammatory mediators are significant inflammatory pathways that may have a major impact on the onset and course of renal disease [25]. Some clinical trials with SGLT-2i in patients with type 2 diabetes have revealed important effects on inflammatory mediators, including decreases in urine IL-6 and MCP-1, as well as serum tumor necrosis factor receptor 1 and IL-6 [8, 17].
Finally, SGLT2is can inhibit apoptosis and the production of reactive oxygen species and attenuates glomerular atrophy, kidney fibrosis, and kidney dysfunction [18, 19].
5. Proof of concept
A study conducted in 2023 confirmed the renoprotective effect of SGLT2 inhibitors in lupus mice, underscoring the role of non-immunosuppressive treatment in improving renal function in classic autoimmune kidney diseases, such as LN [20]. The levels of mouse anti-dsDNA IgG-specific antibodies, serum creatinine, and proteinuria markedly decreased. From a histological perspective, glomerular and tubulointerstitial damage was reduced by empagliflozin administration [20].
An observational international cohort study found that the use of SGLT2i in the management of glomerular/systemic autoimmune diseases with proteinuria was associated with a significant reduction in proteinuria, irrespective of the underlying disease [21]. An SGLT2i (empagliflozin) add-on to sustained immunosuppressive treatment showed a promising reduction in proteinuria (~50% reduction within 8weeks) in a small case series of five active individuals with LN [10].
Another small study (n=9) showed significantly reduced proteinuria in patients with lupus nephritis [20].
In a recent cohort study of a total of 31,790 patients, the propensity matched 1775 matched pairs of SGLT2i users and nonusers (N=3550), the patients had a mean age of 57years, with 85% of them being women. This study showed that SGLT2i use was associated with a significantly lower risk of incident lupus nephritis (AHR, 0.55; 95% CI, 0.40–0.77), dialysis (AHR, 0.55; 95% CI, 0.40–0.77), kidney transplant (AHR, 0.14; 95% CI, 0.03–0.62), heart failure (AHR, 0.65; 95% CI, 0.53–0.78), and all-cause mortality (AHR, 0.35; 95% CI, 0.26–0.47) than SGLT2i non-use in patients with SLE and type 2 diabetes [22]. Since individuals with systemic lupus face a greater risk of developing cardiovascular illness as a result of systemic inflammation, it seems that SGLT2i could potentially provide the additional advantage of decreasing the risk of heart failure in this particular group of patients [22]. The use of SGLT2 inhibitors in systemic lupus erythematosus provides both kidney-protective and heart-protective advantages.
Considering this evidence, SGLT2i have been recommended as a treatment adjuvant for LN in the recent KDIGO recommendations for LN management published in 2024 [23].
6. Overrated expectations?
In a trial, 38 patients with LN were treated with dapagliflozin add-on therapy, and the safety profile as a primary endpoint was acceptable; however, the secondary endpoints revealed no improvement in SLE Disease Activity Index scores or proteinuria (among 17 patients with LN) [10]. The authors proposed two major explanations. First, <50% of the patients with LN were on renin-angiotensin-aldosterone system inhibitors, which has been postulated to be required for SGLT2is to enhance their action. Another possible reason might be attributed to the fact that the participants had a relatively long LN duration and were resistant to several immunosuppressants in the past [10].
7. Concerns of using SGTL2i in LN
7.1 Increased risk for infections in lupus
Urinary tract infections are a typical side effect of SGLT2is because they increase glucose availability in the urinary tract [22]. Urinary tract infections are a concern for SLE patients because they are prone to various infections. Nonetheless, only one patient (2.63%) experienced urinary tract infections in a trial, which was not higher than that in non-SLE large-scale clinical trials [10].
As SGLT-2 inhibitors also increase the risk of genital mycotic infections, both male and female patients with a history of these illnesses should be closely monitored [23].
Therefore, patients undergoing SGLT-2i therapy should be closely monitored for clinical features of urinary tract infections, such as dysuria, urinary frequency, urgency, and suprapubic discomfort. If present, urinalysis should be performed to rule out infections [24].
7.2 Vascular problems
Before initiating canagliflozin and ertugliflozin, patients should be screened for risk factors for lower limb amputations, such as peripheral vascular disease, history of amputations, and neuropathy, especially in patients with SLE, and should be routinely monitored for infections or ulcer formations of the lower extremities, as non-traumatic lower limb amputations have been reported [25].
7.3 Osteoporosis
SGLT2 inhibitors are associated with increased incidence of bone fractures. Increased fracture risk has been observed with canagliflozin, occurring 12weeks after treatment initiation [26]. Potential mechanisms for fracture include volume contraction leading to dizziness and falls, and possible effects on calcium, phosphate, and vitamin D homeostasis, leading to a reduction in bone mineral density [27]. This risk can increase in patients with SLE treated with corticosteroids.
8. Conclusion
Currently, there is little data supporting the use of iSGLT-2 in lupus nephritis; the studies were small observational series and case studies with positive effects on renal and cardiovascular protection. Further randomized experiments are required to confirm these encouraging results. On SGTL-2i, this specific patient group should be regularly monitored for osteoporosis and the risk of genital and urinary infections.
Acknowledgments
All authors acknowledge Dr. Amine Azzaz for his assistance in providing us with articles published about sodium-glucose cotransporter 2 inhibitors (SGLT-2i) in Lupus nephritis.
Notes/thanks/other declarations
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Written By
Abire Allaoui, Rita Aniq Filali, Amine Khalfaoui and Abdelhamid Naitlho
Submitted: 17 July 2024 Reviewed: 19 September 2024 Published: 21 November 2024
© The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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