Review

Volume 17, Number 2, February 2025, pages 67-75

Acute Kidney Injury in Autoimmune-Mediated Rheumatic Diseases

Acute kidney injury (AKI) is a growing concern for hospitalized and non-hospitalized patients worldwide. The incidence of AKI ranges from 5% to over 30%, depending on the region, medical specialty, and the specific medical circumstances (e.g., Eastern Asia 14.7%, Western Europe 20.1%, Southern Europe 31.5%; community-acquired 8.3%, all hospital acquired 20.9%, critical care 31.7%) [1, 2]. Patients receiving intensive care are affected in 50% or more [3], depending on the underlying disease and its treatment. An almost 100% mortality rate has been observed in patients with hematologic malignancies, chemotherapy-induced sepsis, and AKI requiring kidney replacement therapy (KRT) [4]. The diagnosis of AKI is still based on the 2012 revised “Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guidelines for acute kidney injury” [5], which provide cutoff values for changes in serum creatinine levels over time. Recent advancements in AKI biomarker research are expected to lead to a revised definition of the syndrome, which will likely involve the integration of so-called damage biomarkers [6].

Individual AKI episodes increase the risk of developing chronic kidney disease (CKD) [7-11]. In 2014, Rewa et al [12] published a review of the long-term survival of patients with AKI, highlighting the strongest reduction in probability of survival for patients with CKD stage 5D (dialysis requirement). The life expectancy of individuals with pre-existing CKD who also developed AKI was almost equally reduced. The study also found that even individuals without pre-existing CKD who experienced a single episode of AKI faced a reduced life expectancy, with the greatest decline occurring for more severe episodes (RIFLE criteria [13]). Back in 2013, Lewington et al already demonstrated that annually more people worldwide die from the direct and indirect consequences of AKI than from the combined conditions of diabetes mellitus, heart failure, breast cancer, and prostate cancer [14]. Finally, it is important to note that elderly individuals with AKI have a reduced likelihood of renal recovery when compared to younger subjects [15]. This phenomenon is presumably attributable to the elevated average morbidity observed in the elderly population. Comparable observations on renal recovery were made in the gender comparison: women have a higher risk of non-recovery than men [16]. The second aspect is relevant insofar as many inflammatory rheumatic diseases manifest themselves more frequently in women than in men, namely rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

The most common cause of AKI is transient renal hypoperfusion, leading to either pre-renal or, in prolonged cases, intra-renal AKI [17]. The latter is characterized by structural abnormalities of the tubular epithelium. In a clinical setting, renal hypoperfusion often occurs due to worsening heart failure, sepsis, and fluid or blood loss. AKI can also result from specific glomerular or tubulointerstitial diseases, especially those with a sudden onset. Obstruction of the ureters or bladder is the least common cause [18]. Several risk factors can increase the susceptibility to AKI, including pre-existing conditions such as hypertension, diabetes mellitus, heart failure, and others. The highly complex pathogenesis of AKI has been addressed by excellent review articles [6].

Autoimmune inflammatory rheumatic diseases are represented by four main groups: RA, seronegative spondyloarthritides, collagenoses, and vasculitides. Medical attention, especially among rheumatology specialists, often focuses on the impact of the disease processes on the function and structure of the musculoskeletal system. However, defined collagenoses and vasculitides are disproportionately associated with severe kidney diseases. Furthermore, it is well known that chronic inflammatory autoimmune diseases significantly increase the cardiovascular disease risk [19], ultimately also increasing the risk for CKD and potentially susceptibility to AKI. Finally, a wide range of, at times very specific, medications are meanwhile used in the treatment of inflammatory rheumatic diseases. Some of these are well-known risk factors for AKI (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs) [20]), while others have been sporadically linked with the syndrome mechanistically.

The aim of the current article is to discuss the epidemiology and etiology of AKI in inflammatory rheumatic diseases. Three perspectives will be highlighted: the impact of the underlying disease itself, the potential effects of medication therapy, and the risk of AKI in the context of latent systemic inflammation.

The following databases were searched for references: PubMed, Web of Science, Cochrane Library, and Scopus. The period lasted from 1958 until 2024. The following article types were considered: prospective, randomized and controlled clinical trials, original experimental studies, retrospective observational cohort studies, case reports, systematic and non-systematic reviews, and specific guidelines.

The following terms were utilized: 1) group 1: disease-related “inflammatory rheumatic diseases” OR “autoimmune-mediated rheumatic diseases” OR “rheumatoid arthritis” OR “spondylarthritis” OR “ankylosing spondylitis” OR “arthritis psoriatica” OR “collagenoses” OR “vasculitis” OR “vasculitides” OR “SLE” OR “systemic lupus erythematosus” OR “Sjogren’s syndrome” OR “inflammatory myopathy” OR “ANCA-associated vasculitis” OR “granulomatosis with polyangiitis” OR “microscopic polyangiitis” OR “cryoglobulinemia” OR “Henoch-Schonlein purpura” OR “IgA vasculitis” OR “polyarteriitis nodosa” OR “Behcet’s disease” OR “giant cell arteriitis”; 2) group 2: therapy-related (in variable combinations with group 1 and 3 terms): “NSAID” OR “cDMARDs” OR “bDMARDs” OR “bsDMARDs” OR “tsDMARDs”; 3) group 3: AKI-related (in variable combinations with group 1 and 2 terms) “acute renal failure” OR “acute kidney injury” OR “AKI” OR “glomerulonephritis” OR “GN” OR “ATN” OR “papillary necrosis”. Additional terms were “anti-IL6” OR “anti-IL12” OR “anti-IL12/-23” OR “anti-IL17” AND “AKI” and “oral health” OR “periodontitis”; 4) group 4: cytokine and oral health-related (predominantly in variable combinations with group 1 terms).

This section will only discuss literature on AKI as a direct manifestation of an inflammatory rheumatic disease. References will be listed chronologically, from oldest to most recent dates, if not specified otherwise. The article does not refer to rare entities (polyarteritis nodosa, Behcet’s syndrome, etc.).

RA is the most common singular entity in the realm of inflammatory rheumatic diseases, affecting approximately 2% of adults in Central Europe [21]. The primary feature of the disease process is chronic inflammation of the synovial membrane in the joints. Reports of acute deteriorations in excretory kidney function were already published in the 1980s; however, these are reports or case studies. In 1986, Bar et al [22] reported on a patient with AKI complicating RA-associated amyloidosis, while Wegelius et al [23] published a report on two patients with severe interstitial kidney edema. Interestingly, the two latter individuals did not exhibit a specific glomerular or tubular damage pattern. Instead, they showed an accumulation of hyaluronic acid (HA) in the interstitial space. This accumulation could potentially have been responsible for edema formation, as HA has a significant water-binding capacity. In conclusion, the accumulation of HA was considered to directly indicate impaired connective tissue homeostasis in RA. Another case report from 2009 [24] identified focal-segmental proliferative glomerulonephritis as the leading cause of AKI. Renal biopsy investigation did not reveal any interstitial inflammation or renal amyloidosis. A somewhat similar case was published in 2010 [25], reporting on a 40-year-old woman with RA who developed acute, oliguric kidney injury. Histologically, there were no specific tubular or interstitial abnormalities, but there was an edematous thickening of the vascular intima, accompanied by signs of ischemic damage to the glomeruli. In summary, RA can sometimes lead to AKI. The patterns of kidney damage are generally nonspecific, though glomerulonephritis may occasionally occur.

SpA encompasses five distinct entities: ankylosing spondylitis (AS), psoriatic arthritis, reactive arthritis, enteropathic arthritis, and undifferentiated SpA. Collectively, the prevalence of this group is comparable to that of RA. SpA, in general, [26] and AS, in particular, have occasionally been reported to coincide with immunoglobulin (Ig)A nephritis [27]. The pattern of IgA mesangioproliferative glomerulonephritis is also typically diagnosed in Henoch-Schonlein purpura (HSP), where extracapillary inflammation may require treatment with cyclophosphamide, as seen in other vasculitides (see “Vasculitides”). However, extracapillary proliferative glomerulonephritis, whether or not associated with mesangial IgA, is likely negligible as a cause of AKI in AS. Only 1% of all AS patients with renal involvement exhibit extracapillary changes [28]. The literature provides minimal evidence for specific kidney disease patterns in other types of spondyloarthritis. However, there are numerous references regarding kidney-related side effects of drugs used for managing disease activity and progression in SpA (see “AKI Resulting From the Anti-Rheumatic Therapy”).

Collagenoses, particularly SLE, are significantly associated with AKI. The literature on potential kidney involvement in SLE is indeed so extensive that a comprehensive review here is hardly feasible. We must refer to relevant review articles, setting aside hundreds of original manuscripts [29-32]. Lupus nephritis (LN) is likely one of those complications of inflammatory rheumatic diseases that the vast majority of physicians will be familiar with. Up to 50% of all SLE patients experience kidney involvement during the course of the disease [31]. According to the revised International Society of Nephrology/Renal Pathology Society classification for LN, LN classes III and IV are characterized by endocapillary hypercellularity and crescent formation in less than 50% (focal - class III) or more than 50% (diffuse - class IV) of all glomeruli examined by a pathologist [33]. The clinical spectrum of renal involvement in LN can encompass virtually all patterns of acute or chronic glomerular damage: isolated glomerular hematuria or proteinuria, nephrotic and nephritic syndrome, the latter with a rapid course AKI, renal hypertension, and progressive CKD [34]. Nephritic manifestations, including the potential development of AKI, are predominantly observed in LN classes III and IV [31]. These two forms also require intensified immunosuppression. The most recently updated KDIGO guidelines from 2024 [35] currently offer four distinct therapeutic regimens for remission induction in this situation, with the inclusion of belimumab as a potential first-line treatment option. Primary Sjogren’s syndrome is classically associated with dryness of the eyes and mouth, caused by autoimmune inflammation of the exocrine glands in the head region [36]. In addition to articular, cutaneous, and pulmonary complications, affected individuals are potentially at risk for renal manifestations. While renal tubular dysfunctions (such as renal tubular acidosis (RTA) types 1 and 2) are predominant, proliferative glomerulonephritis including AKI have also been reported. In 2015, the EULAR-SS Task Force Group summarized potential kidney damage patterns [37]. The prevalence of RTA was estimated at 9%, while the prevalence of all glomerulonephritides was 4%. The publication also lists the findings from 149 reported cases of glomerulonephritis associated with Sjogren’s syndrome. Crescentic rapidly progressive glomerulonephritis, typically associated with AKI, was identified in only nine individuals. A 2019 case series on patients with primary Sjogren’s syndrome and kidney involvement (n = 20) did not identify any cases of AKI, although glomerulonephritis was diagnosed in six individuals [38].

In contrast to the relatively low incidence of AKI as a direct consequence of primary Sjogren’s syndrome, systemic sclerosis, particularly the diffuse variant, is associated with a significantly increased AKI risk. The term renal crisis describes the concurrence of AKI and the histopathological finding of obliterative endarteritis within the kidney itself [39]. The vascular obstructions result from intimal hyperplasia and fibrinoid media degeneration. Serologically, affected patients are characterized by the association with RNA polymerase 3 antibodies [40]. Before the availability of angiotensin-converting enzyme (ACE) inhibitors, the mortality rate of renal crisis was high. In 2019, classification criteria for this condition were published [41]. The criteria also include possible accompanying phenomena such as thrombotic microangiopathy, which can clinically aggravate the course. Several case reports have already been published on this topic [42-44]. The combined manifestation of systemic sclerosis and anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis has also been documented in the literature, although such cases are likely to be rare [45]. Other sporadic manifestations include the pattern of membranoproliferative glomerulonephritis [46] and pauci-immune glomerulonephritis in systemic sclerosis without skin involvement [47].

Inflammatory myopathies include the following entities: idiopathic dermatomyositis (DM), juvenile dermatomyositis (jDM), idiopathic amyopathic DM (often associated with anti-MDA5), idiopathic polymyositis (PM), immune-mediated necrotizing myopathy (IMNM), anti-synthetase syndrome (ASys), paraneoplastic idiopathic poly-/dermatomyositis, inclusion body myositis, and overlap myositis [48]. Other, even rarer types have also been identified. Although glomerulonephritis has been described in a few cases of inflammatory myopathies [49], these diseases primarily pose a risk of AKI due to rhabdomyolysis [50, 51]. The unusual manifestation of thrombotic microangiopathy in PM was reported in 2021 [52].

The issue of AKI is most significant in SLE and less so in other types of collagenoses. In Sjogren’s syndrome, systemic sclerosis, or inflammatory myopathies, glomerulonephritis can cause AKI. In inflammatory myopathies, rhabdomyolysis must also be considered. In all affected patients, side effects of medication or other causes must always be considered.

Similar to the group of collagenoses, vasculitides often present an interdisciplinary challenge for rheumatologists and nephrologists. This is particularly true for ANCA-associated vasculitides (AAV), namely granulomatosis with polyangiitis and microscopic polyangiitis. The 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Antineutrophil Cytoplasmic Antibody-Associated Vasculitis distinguishes between five disease stages: nonsevere, severe, active, refractory, remission, and relapse [53]. Extrapapillary proliferative glomerulonephritis, with either focal or diffuse manifestation, is a common AAV-associated complication that was nearly always fatal before the availability of cyclophosphamide [54]. Among the types of extrapapillary proliferative glomerulonephritis, the ANCA-associated variant is the most common, accounting for 70% of cases. Immunofluorescence histology does not reveal a specific finding, which explains the term pauci-immune. It is estimated that 70-100% of all AAV patients develop a prognostically significant renal involvement over the course of the disease [55]. Clinically, most affected patients suffer from AKI.

A similar pattern of glomerular injury (extrapapillary proliferative glomerulonephritis) may occur in cryoglobulinemia (CG) of either primary or secondary origin. Immunofluorescence staining reveals granular glomerular deposition of immune complexes [56]. CG is represented by three types, with type 3 being the most prevalent [57]. Type 2 immune complexes contain monoclonal antibodies that interact with pre-existing polyclonal immunoglobulins. A significant percentage of affected patients test positive for hepatitis C [58]. Approximately 20-50% of all type 2 CG patients develop extrapapillary proliferative glomerulonephritis [58], usually resulting in AKI.

Another specific type of small-vessel vasculitis, HSP, also referred to as IgA vasculitis, is typically characterized by IgA mesangioproliferative glomerulonephritis [59]. The disease can be interpreted as a systemic form of IgA nephropathy [60]. Comparable to IgA nephropathy, kidney involvement in the context of HSP can be associated with extracapillary proliferations [60]. Clinically, this may sometimes manifest as AKI, although despite the histological findings, milder consequences of glomerular damage are also possible, such as isolated proteinuria or a non-rapidly progressive course [61].

Table 1 summarizes all discussed types of rheumatic diseases and respective risk and mechanism of kidney involvement [23-25, 27, 28, 31, 33, 37, 41-45, 49, 50, 52, 55, 58-60].

Click to view

Table 1. Patterns of Kidney Damage Associated With AKI in Patients With Inflammatory Rheumatic Diseases

Several potential NSAID side effects can impact kidney function and structure. Some of these effects are dose-dependent, while others are not. Acute adverse events include reversible pre-renal failure, which may progress to acute tubular necrosis (ATN), acute interstitial nephritis (AIN), renal vasculitis (rare), and acute papillary necrosis [62-64]. In theory, papillary necrosis can potentially cause AKI by leading to bilateral ureteral obstruction. The most common type of NSAID-induced AKI results from diminished intrarenal blood flow due to inhibited prostaglandin synthesis. This particularly affects patients whose renal blood flow is stabilized by increased intrarenal prostaglandin synthesis. This occurs in situations characterized by latent reduced blood flow to the entire body, including the kidneys, such as heart failure, sepsis, and advanced atherosclerosis with manifestation in the organ itself [65]. NSAIDs exhibit varying selectivity for cyclooxygenase (COX)-1 and COX-2 enzymes. Non-selective drugs include ibuprofen and ketoprofen, while meloxicam, diclofenac, and celecoxib show intermediate COX-2 selectivity. Highly COX-2 selective substances include rofecoxib and etoricoxib. However, it would be incorrect to assume that COX-2 selective medications do not increase the risk of AKI. Huerta et al [66] reported a three-fold increase in AKI risk in patients receiving diclofenac, ibuprofen, ketoprofen, or meloxicam compared to those not on such therapies. The overall risk increased with longer duration of therapy and higher doses. This dose-dependent effect was further confirmed by Fine et al [20], who found a 2.3-fold higher AKI risk with the use of conventional NSAIDs, including a 2.42-fold risk increase with naproxen. Rofecoxib also posed a higher risk, with a 2.31-fold increase [20]. The risk of AKI increases significantly when NSAIDs are taken in combination with certain other drugs. Specifically, diuretics, ACE inhibitors, and angiotensin receptor blockers can substantially elevate the risk when used with NSAIDs [67]. Due to the almost routine use of NSAIDs in individuals with various forms of inflammatory rheumatic diseases, the issue of NSAID-induced AKI remains highly relevant both epidemiologically and prognostically. Other potential side effects are not even mentioned, such as an increase in cardiovascular risk and gastrointestinal bleeding.

Methotrexate is the drug of first choice for RA patients requiring disease-modifying therapy. It has also been proven effective in psoriatic arthritis [68, 69]. When considering the kidney-related side effects of methotrexate, the required dose for disease control must be taken into account. In patients with hematologic-oncologic disorders, the drug dosage ranges from 1 to 15 g/m², which can lead to AKI due to acute crystalline nephropathy [70]. However, for rheumatic diseases, methotrexate is used as an anti-inflammatory and anti-progressive drug, with doses typically between 10 and 20 (up to 25) mg per week [71]. Within this dosage range, the risk of adverse effects on kidney function and structure is almost negligible.

Renal adverse events associated with azathioprine (AZA) have been reported sporadically. Bir et al published a rare case of AZA-induced AIN, which was subsequently followed by rapidly progressive AKI [72].

Sulfasalazine has also been reported to occasionally induce AIN [73].

Calcineurin inhibitors (CNIs) can act as vasoconstrictors, reducing glomerular perfusion and potentially leading to AKI in severe cases [74]. These vascular effects are dose-dependent and can be mitigated by regular monitoring of CNI blood levels. In the long term, CNIs contribute to renal fibrogenesis. They have been shown to induce transforming growth factor (TGF)-beta, a well-known key mediator of fibroblast activity and epithelial-mesenchymal transition [75].

Kidney-related side effects of anti-tumor necrosis factor (TNF)-alpha are rare. Wei et al reported the uncommon occurrence of IgA nephropathy [76], while Kaneko et al [77] documented two cases of extracapillary necrotizing glomerulonephritis in patients treated with anti-TNF-alpha. Korsten et al [78] reported adalimumab-induced granulomatous interstitial nephritis in AS. Overall, the risk of renal adverse events induced by anti-TNF-alpha is considered low. The current literature search (as of May 2024) yields no official entries for the following search terms: “AKI” and “anti-IL6” or “anti-IL12” or “anti-IL12/-23” or “anti-IL17”. The same applies to the terms “AKI” and “abatacept”. Overall, the risk of AKI induced by biological DMARDs (bDMARDs) or their corresponding biosimilars (bsDMARDs) is effectively negligible.

Targeted synthetic DMARDs (tsDMARDs) are a relatively new class of drugs, currently represented by JAK kinase inhibitors such as baricitinib, filgotinib, tofacitinib, and upadacitinib. Apremilast can also be included in this group, although it inhibits the activity of phosphodiesterase 4, leading to reduced production of TNF-alpha. The literature on JAK kinase inhibitors and AKI is sparse. However, in 2021, an experimental study using a lipopolysaccharide-induced AKI model was published [79]. This study demonstrated that kidney damage could be reduced with tofacitinib. Aside from this, no additional references can currently be identified using the terms “JAK kinase inhibitors” and “AKI”.

Initially, it seems plausible to assume that inflammatory rheumatic systemic diseases are associated with an increased risk of AKI. This theoretical increase should be suspected even if the underlying disease does not primarily involve specific renal complications. Given the data on the elevated cardiovascular risk in RA and seronegative spondyloarthropathies [19, 80], affected individuals are more likely to suffer from atherosclerosis more frequently and at an earlier stage. Atherosclerosis also affects the intrarenal arteries, potentially reducing the kidney’s overall stress tolerance. However, regarding the general risk of AKI in inflammatory rheumatic diseases, there are currently few significant references available. Levy et al [81] conducted a retrospective study on AS patients between 1996 and 2006, including 4,836 males and 3,780 females, to determine the prevalences of AKI, CKD, amyloidosis, and hypertensive renal disease. All predefined types of renal disease were 72% more prevalent in individuals with AS compared to healthy controls, particularly among younger individuals. The study does verify the hypothesis of an increased AKI risk, at least in AS patients; however, the investigation does not necessarily support the presumed association with heightened AKI susceptibility due to aggravated atherosclerosis. However, inflammatory rheumatic diseases can also contribute to morbidities beyond the cardiovascular system. These can be particularly relevant to nephrology and may increase the risk of AKI. Periodontitis for instance, a multifactorial inflammatory disease of the tissues surrounding the teeth [82], could be of particular interest. Periodontitis has been reported to be related to systemic rheumatic diseases, especially due to common risk factors [83]. Recent literature indicates potential bidirectional interrelationships between rheumatic diseases (especially RA) and periodontitis, such as the affected citrullination of antibodies caused by periodontal bacteria [84]. These bacteria, primarily Porphyromonas gingivalis, can promote autoimmune inflammatory diseases by inducing the activation of the inflammasome [85]. On the other hand, periodontal diseases are reported to be related to kidney diseases. Although not fully clarified, several mechanisms appear to connect periodontitis and chronic kidney failure [86], as supported by a recent meta-analysis [87]. Furthermore, oral bacteria can potentially cause intestinal nephritis, leading to AKI [88]. Therefore, oral and particularly periodontal inflammation might represent a further link between rheumatic diseases and kidney injury. This example highlights the potential relevance of inflammatory comorbidities and offers another field for future research. However, by applying the search terms “AKI risk” and “rheumatic diseases”, a total of 18 references were found (as of May 2024). No study provides satisfactory conclusions on the subject. Undoubtedly, there is a significant data gap that needs to be addressed in the coming years.

AKI is a potentially significant issue for patients with inflammatory rheumatic diseases. The risk of AKI is elevated not only due to possible direct kidney involvement from the underlying disease but also significantly due to the uncontrolled use of NSAIDs. It is suspected that individuals with inflammatory rheumatic diseases are already at risk of developing AKI resulting from the proatherogenic/inflammatory activity of the underlying condition itself. However, data on this latter aspect are still very limited.

Acknowledgments

None to declare.

Financial Disclosure

No funding was provided for the study.

Conflict of Interest

The authors declare that they have no conflict of interest.

Author Contributions

Daniel Patschan wrote the article. Gerhard Schmalz provided substantial information on oral health in rheumatic diseases. Wajima Safi, Friedrich Stasche, and Igor Matyukhin searched for references. Oliver Ritter assisted in writing. Susann Patschan designed the article, assisted in reference collection and writing.

Data Availability

The authors declare that data supporting the findings of this study are available within the article.

Abbreviations

AAV: ANCA-associated vasculitis; AKI: acute kidney injury; ANCA: anti-neutrophil cytoplasmic antibodies; AS: ankylosing spondylitis; ATN: acute tubular necrosis; CG: cryoglobulinemia; CKD: chronic kidney disease; COX: cyclooxygenase; DMARDs: disease-modifying anti-rheumatic drugs; bDMARDs: biologic disease-modifying anti-rheumatic drugs; bsDMARDs: biosimilar disease-modifying anti-rheumatic drugs; tsDMARDs: targeted synthetic disease-modifying anti-rheumatic drugs; DM: dermatomyositis; GN: glomerulonephritis; HA: hyaluronic acid; HSP: Henoch-Schonlein purpura; IMNM: immune-mediated necrotizing myopathy; KDIGO: Kidney Disease Improving Global Outcomes; KRT: kidney replacement therapy; LN: lupus nephritis; NSAID: non-steroidal anti-inflammatory drugs; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; SpA: spondylarthritis

1. Susantitaphong P, Cruz DN, Cerda J, Abulfaraj M, Alqahtani F, Koulouridis I, Jaber BL, et al. World incidence of AKI: a meta-analysis. Clin J Am Soc Nephrol. 2013;8(9):1482-1493.
   doi pubmed
2. Hoste EAJ, Kellum JA, Selby NM, Zarbock A, Palevsky PM, Bagshaw SM, Goldstein SL, et al. Global epidemiology and outcomes of acute kidney injury. Nat Rev Nephrol. 2018;14(10):607-625.
   doi pubmed
3. Hoste EA, Bagshaw SM, Bellomo R, Cely CM, Colman R, Cruz DN, Edipidis K, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41(8):1411-1423.
   doi pubmed
4. Heeg M, Mertens A, Ellenberger D, Muller GA, Patschan D. Prognosis of AKI in malignant diseases with and without sepsis. BMC Anesthesiol. 2013;13(1):36.
   doi pubmed
5. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract. 2012;120(4):c179-184.
   doi pubmed
6. Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Anders HJ. Acute kidney injury. Nat Rev Dis Primers. 2021;7(1):52.
   doi pubmed
7. Venkatachalam MA, Weinberg JM, Kriz W, Bidani AK. Failed tubule recovery, AKI-CKD transition, and kidney disease progression. J Am Soc Nephrol. 2015;26(8):1765-1776.
   doi pubmed
8. Ferenbach DA, Bonventre JV. Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD. Nat Rev Nephrol. 2015;11(5):264-276.
   doi pubmed
9. Polichnowski AJ. Microvascular rarefaction and hypertension in the impaired recovery and progression of kidney disease following AKI in preexisting CKD states. Am J Physiol Renal Physiol. 2018;315(6):F1513-F1518.
   doi pubmed
10. Wang Z, Zhang C. From AKI to CKD: maladaptive repair and the underlying mechanisms. Int J Mol Sci. 2022;23(18):10880.
    doi pubmed
11. Forni LG, Darmon M, Ostermann M, Oudemans-van Straaten HM, Pettila V, Prowle JR, Schetz M, et al. Renal recovery after acute kidney injury. Intensive Care Med. 2017;43(6):855-866.
    doi pubmed
12. Rewa O, Bagshaw SM. Acute kidney injury-epidemiology, outcomes and economics. Nat Rev Nephrol. 2014;10(4):193-207.
    doi pubmed
13. Bagshaw SM, George C, Bellomo R, Committe ADM. A comparison of the RIFLE and AKIN criteria for acute kidney injury in critically ill patients. Nephrol Dial Transplant. 2008;23(5):1569-1574.
    doi pubmed
14. Lewington AJ, Cerda J, Mehta RL. Raising awareness of acute kidney injury: a global perspective of a silent killer. Kidney Int. 2013;84(3):457-467.
    doi pubmed
15. Abdel-Rahman EM, Turgut F, Gautam JK, Gautam SC. Determinants of outcomes of acute kidney injury: clinical predictors and beyond. J Clin Med. 2021;10(6):1175.
    doi pubmed
16. Foley RN, Sexton DJ, Reule S, Solid C, Chen SC, Collins AJ. End-stage renal disease attributed to acute tubular necrosis in the United States, 2001-2010. Am J Nephrol. 2015;41(1):1-6.
    doi pubmed
17. Devarajan P. Update on mechanisms of ischemic acute kidney injury. J Am Soc Nephrol. 2006;17(6):1503-1520.
    doi pubmed
18. Ronco C, Bellomo R, Kellum JA. Acute kidney injury. Lancet. 2019;394(10212):1949-1964.
    doi pubmed
19. Nurmohamed MT, Heslinga M, Kitas GD. Cardiovascular comorbidity in rheumatic diseases. Nat Rev Rheumatol. 2015;11(12):693-704.
    doi pubmed
20. Fine M. Quantifying the impact of NSAID-associated adverse events. Am J Manag Care. 2013;19(14 Suppl):s267-272.
    pubmed
21. Finckh A, Gilbert B, Hodkinson B, Bae SC, Thomas R, Deane KD, Alpizar-Rodriguez D, et al. Global epidemiology of rheumatoid arthritis. Nat Rev Rheumatol. 2022;18(10):591-602.
    doi pubmed
22. Bar M, Burke M, Isakov A, Almog C. Reversible, nonoliguric acute renal failure in a patient with rheumatoid arthritis and renal amyloidosis. N Y State J Med. 1986;86(10):542-543.
    pubmed
23. Wegelius O, Klockars M. Reversible acute renal failure complicating rheumatoid arthritis. Scand J Rheumatol. 1987;16(1):161-168.
    doi pubmed
24. Dutta PK, Khan IH. Proliferative glomerulonephritis with acute renal failure-a rare manifestation in seronegative rheumatoid arthritis. Mymensingh Med J. 2009;18(1):84-87.
    pubmed
25. Marszalek A, Skoczylas-Makowska N, Kardymowicz A, Manitius J. Patient with rheumatoid arthritis and acute renal failure: a case report and review of literature. Pol J Pathol. 2010;61(4):229-233.
    pubmed
26. Champtiaux N, Liote F, El Karoui K, Vigneau C, Miceli C, Cornec-Le Gall E, Remy P, et al. Spondyloarthritis-associated IgA nephropathy. Kidney Int Rep. 2020;5(6):813-820.
    doi pubmed
27. Kamath S, Ahmed T, Rana F, Upadhyay AS. Rare case of ankylosing spondylitis complicated by IgA vasculitis. BMJ Case Rep. 2022;15(11):e252182.
    doi pubmed
28. Strobel ES, Fritschka E. Renal diseases in ankylosing spondylitis: review of the literature illustrated by case reports. Clin Rheumatol. 1998;17(6):524-530.
    doi pubmed
29. Yu C, Li P, Dang X, Zhang X, Mao Y, Chen X. Lupus nephritis: new progress in diagnosis and treatment. J Autoimmun. 2022;132:102871.
    doi pubmed
30. Almaani S, Meara A, Rovin BH. Update on lupus nephritis. Clin J Am Soc Nephrol. 2017;12(5):825-835.
    doi pubmed
31. Parikh SV, Almaani S, Brodsky S, Rovin BH. Update on lupus nephritis: core curriculum 2020. Am J Kidney Dis. 2020;76(2):265-281.
    doi pubmed
32. Anders HJ, Saxena R, Zhao MH, Parodis I, Salmon JE, Mohan C. Lupus nephritis. Nat Rev Dis Primers. 2020;6(1):7.
    doi pubmed
33. Bajema IM, Wilhelmus S, Alpers CE, Bruijn JA, Colvin RB, Cook HT, D'Agati VD, et al. Revision of the International Society of Nephrology/Renal Pathology Society classification for lupus nephritis: clarification of definitions, and modified National Institutes of Health activity and chronicity indices. Kidney Int. 2018;93(4):789-796.
    doi pubmed
34. Gasparotto M, Gatto M, Binda V, Doria A, Moroni G. Lupus nephritis: clinical presentations and outcomes in the 21st century. Rheumatology (Oxford). 2020;59(Suppl5):v39-v51.
    doi pubmed
35. Kidney Disease: Improving Global Outcomes Lupus Nephritis Work Group. KDIGO 2024 Clinical Practice Guideline for the management of LUPUS NEPHRITIS. Kidney Int. 2024;105(1S):S1-S69.
    doi pubmed
36. Baer AN, Walitt B. Update on sjogren syndrome and other causes of sicca in older adults. Rheum Dis Clin North Am. 2018;44(3):419-436.
    doi pubmed
37. Ramos-Casals M, Brito-Zeron P, Seror R, Bootsma H, Bowman SJ, Dorner T, Gottenberg JE, et al. Characterization of systemic disease in primary Sjogren's syndrome: EULAR-SS Task Force recommendations for articular, cutaneous, pulmonary and renal involvements. Rheumatology (Oxford). 2015;54(12):2230-2238.
    doi pubmed
38. Goules A, Geetha D, Arend LJ, Baer AN. Renal involvement in primary Sjogren's syndrome: natural history and treatment outcome. Clin Exp Rheumatol. 2019;37 Suppl 118(3):123-132.
    pubmed
39. Bose N, Chiesa-Vottero A, Chatterjee S. Scleroderma renal crisis. Semin Arthritis Rheum. 2015;44(6):687-694.
    doi pubmed
40. Moinzadeh P, Kuhr K, Siegert E, Blank N, Sunderkoetter C, Henes J, Krusche M, et al. Scleroderma renal crisis: risk factors for an increasingly rare organ complication. J Rheumatol. 2020;47(2):241-248.
    doi pubmed
41. Butler EA, Baron M, Fogo AB, Frech T, Ghossein C, Hachulla E, Hoa S, et al. Generation of a core set of items to develop classification criteria for scleroderma renal crisis using consensus methodology. Arthritis Rheumatol. 2019;71(6):964-971.
    doi pubmed
42. Kong W, Wang Y, Wang H, Zhou Q, Chen J, Han F. Systemic sclerosis complicated with renal thrombotic microangiopathy: a case report and literature review. BMC Nephrol. 2022;23(1):22.
    doi pubmed
43. Riley M, Der Mesropian P, Maheshwari A, Arslan ME, Visrodia P, Salman L, Peredo-Wende R, et al. Scleroderma renal crisis associated with microangiopathic hemolytic anemia in a patient with seronegative scleroderma and monoclonal gammopathy. J Investig Med High Impact Case Rep. 2022;10:23247096221074591.
    doi pubmed
44. Aterini L, Gallo M, Vadala B, Aterini S. Thrombotic microangiopathy and multiple organ failure in scleroderma renal crisis: a case report. Cureus. 2023;15(8):e44322.
    doi pubmed
45. Hughes M, Kahaleh B, Denton CP, Mason JC, Matucci-Cerinic M. ANCA in systemic sclerosis, when vasculitis overlaps with vasculopathy: a devastating combination of pathologies. Rheumatology (Oxford). 2021;60(12):5509-5516.
    doi pubmed
46. Farrukh L, Beers K, Ibrahim A, Shapiro L, Mehta S. Membranoproliferative glomerulonephritis: A rare presentation in systemic sclerosis. Clin Nephrol. 2023;100(4):185-189.
    doi pubmed
47. Shabaka A, Gatius S, Vian J, Pascual A, Rodriguez-Moreno A. Pauci-immune necrotizing glomerulonephritis as a manifestation of systemic sclerosis sine scleroderma. J Clin Rheumatol. 2021;27(1):e20-e21.
    doi pubmed
48. Lundberg IE, Fujimoto M, Vencovsky J, Aggarwal R, Holmqvist M, Christopher-Stine L, Mammen AL, et al. Idiopathic inflammatory myopathies. Nat Rev Dis Primers. 2021;7(1):86.
    doi pubmed
49. Dein EJ, Crespo-Bosque M, Timlin H, Geetha D. Double-positive with positive anti-glomerular basement membrane antibody and ANCA-positive disease in a patient with dermatomyositis. BMJ Case Rep. 2018;2018:bcr2018224475.
    doi pubmed
50. Cucchiari D, Angelini C. Renal involvement in idiopathic inflammatory myopathies. Clin Rev Allergy Immunol. 2017;52(1):99-107.
    doi pubmed
51. Hamadeh M, Boustany S, Fares J. Acute Kidney Injury Following Dermatomyositis. Clin Med Res. 2019;17(3-4):102-104.
    doi pubmed
52. Fukuda M, Mizuno H, Hiramatsu R, Sekine A, Kawada M, Hasegawa E, Yamanouchi M, et al. A case of thrombotic microangiopathy associated with polymyositis. Clin Nephrol. 2021;95(6):339-344.
    doi pubmed
53. Chung SA, Langford CA, Maz M, Abril A, Gorelik M, Guyatt G, Archer AM, et al. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Rheumatol. 2021;73(8):1366-1383.
    doi pubmed
54. Walton EW. Giant-cell granuloma of the respiratory tract (Wegener's granulomatosis). Br Med J. 1958;2(5091):265-270.
    doi pubmed
55. Sinico RA, Di Toma L, Radice A. Renal involvement in anti-neutrophil cytoplasmic autoantibody associated vasculitis. Autoimmun Rev. 2013;12(4):477-482.
    doi pubmed
56. Menter T, Hopfer H. Renal disease in cryoglobulinemia. Glomerular Dis. 2021;1(2):92-104.
    doi pubmed
57. Napodano C, Gulli F, Rapaccini GL, Marino M, Basile U. Cryoglobulins: Identification, classification, and novel biomarkers of mysterious proteins. Adv Clin Chem. 2021;104:299-340.
    doi pubmed
58. Chen YP, Cheng H, Rui HL, Dong HR. Cryoglobulinemic vasculitis and glomerulonephritis: concerns in clinical practice. Chin Med J (Engl). 2019;132(14):1723-1732.
    doi pubmed
59. Pillebout E, Sunderkotter C. IgA vasculitis. Semin Immunopathol. 2021;43(5):729-738.
    doi pubmed
60. Davin JC, Ten Berge IJ, Weening JJ. What is the difference between IgA nephropathy and Henoch-Schonlein purpura nephritis? Kidney Int. 2001;59(3):823-834.
    doi pubmed
61. Schinzel V, Fernandez JD, Clemente G, Fraga MM, Andrade MC, Len CA, Terreri MT. The profile and clinical outcomes of patients with renal involvement due to IgA vasculitis: is azathioprine a good option for treatment? Adv Rheumatol. 2019;59(1):21.
    doi pubmed
62. Geller SA, de Campos FPF. Renal papillary necrosis. Autops Case Rep. 2013;3(4):69-71.
    doi pubmed
63. Klomjit N, Ungprasert P. Acute kidney injury associated with non-steroidal anti-inflammatory drugs. Eur J Intern Med. 2022;101:21-28.
    doi pubmed
64. Murray MD, Brater DC. Effects of NSAIDs on the kidney. Prog Drug Res. 1997;49:155-171.
    doi pubmed
65. Kane-Gill SL, Sileanu FE, Murugan R, Trietley GS, Handler SM, Kellum JA. Risk factors for acute kidney injury in older adults with critical illness: a retrospective cohort study. Am J Kidney Dis. 2015;65(6):860-869.
    doi pubmed
66. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3):531-539.
    doi pubmed
67. Lapi F, Azoulay L, Yin H, Nessim SJ, Suissa S. Concurrent use of diuretics, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers with non-steroidal anti-inflammatory drugs and risk of acute kidney injury: nested case-control study. BMJ. 2013;346:e8525.
    doi pubmed
68. Nash P, Lubrano E, Cauli A, Taylor WJ, Olivieri I, Gladman DD. Updated guidelines for the management of axial disease in psoriatic arthritis. J Rheumatol. 2014;41(11):2286-2289.
    doi pubmed
69. Mease P. Update on treatment of psoriatic arthritis. Bull NYU Hosp Jt Dis. 2012;70(3):167-171.
    pubmed
70. Perazella MA, Luciano RL. Review of select causes of drug-induced AKI. Expert Rev Clin Pharmacol. 2015;8(4):367-371.
    doi pubmed
71. Bianchi G, Caporali R, Todoerti M, Mattana P. Methotrexate and rheumatoid arthritis: current evidence regarding subcutaneous versus oral routes of administration. Adv Ther. 2016;33(3):369-378.
    doi pubmed
72. Bir K, Herzenberg AM, Carette S. Azathioprine induced acute interstitial nephritis as the cause of rapidly progressive renal failure in a patient with Wegener's granulomatosis. J Rheumatol. 2006;33(1):185-187.
    pubmed
73. Augusto JF, Sayegh J, Simon A, Croue A, Chennebault JM, Cousin M, Subra JF. A case of sulphasalazine-induced DRESS syndrome with delayed acute interstitial nephritis. Nephrol Dial Transplant. 2009;24(9):2940-2942.
    doi pubmed
74. Goldberg RJ, Weng FL, Kandula P. Acute and chronic allograft dysfunction in kidney transplant recipients. Med Clin North Am. 2016;100(3):487-503.
    doi pubmed
75. Olyaei AJ, de Mattos AM, Bennett WM. Nephrotoxicity of immunosuppressive drugs: new insight and preventive strategies. Curr Opin Crit Care. 2001;7(6):384-389.
    doi pubmed
76. Wei SS, Sinniah R. Adalimumab (TNF alpha Inhibitor) therapy exacerbates IgA glomerulonephritis acute renal injury and induces lupus autoantibodies in a psoriasis patient. Case Rep Nephrol. 2013;2013:812781.
    doi pubmed
77. Kaneko K, Nanki T, Hosoya T, Mizoguchi F, Miyasaka N. Etanercept-induced necrotizing crescentic glomerulonephritis in two patients with rheumatoid arthritis. Mod Rheumatol. 2010;20(6):632-636.
    doi pubmed
78. Korsten P, Sweiss NJ, Nagorsnik U, Niewold TB, Grone HJ, Gross O, Muller GA. Drug-induced granulomatous interstitial nephritis in a patient with ankylosing spondylitis during therapy with adalimumab. Am J Kidney Dis. 2010;56(6):e17-21.
    doi pubmed
79. Yun Y, Chen J, Wang X, Li Y, Hu Z, Yang P, Qin L. Tofacitinib ameliorates lipopolysaccharide-induced acute kidney injury by blocking the JAK-STAT1/STAT3 signaling pathway. Biomed Res Int. 2021;2021:8877056.
    doi pubmed
80. Papagoras C, Voulgari PV, Drosos AA. Atherosclerosis and cardiovascular disease in the spondyloarthritides, particularly ankylosing spondylitis and psoriatic arthritis. Clin Exp Rheumatol. 2013;31(4):612-620.
    pubmed
81. Levy AR, Szabo SM, Rao SR, Cifaldi M, Maksymowych WP. Estimating the occurrence of renal complications among persons with ankylosing spondylitis. Arthritis Care Res (Hoboken). 2014;66(3):440-445.
    doi pubmed
82. Kinane DF, Stathopoulou PG, Papapanou PN. Periodontal diseases. Nat Rev Dis Primers. 2017;3:17038.
    doi pubmed
83. de Pablo P, Chapple IL, Buckley CD, Dietrich T. Periodontitis in systemic rheumatic diseases. Nat Rev Rheumatol. 2009;5(4):218-224.
    doi pubmed
84. Gonzalez-Febles J, Sanz M. Periodontitis and rheumatoid arthritis: What have we learned about their connection and their treatment? Periodontol 2000. 2021;87(1):181-203.
    doi pubmed
85. Lin J, Huang D, Xu H, Zhan F, Tan X. Macrophages: A communication network linking Porphyromonas gingivalis infection and associated systemic diseases. Front Immunol. 2022;13:952040.
    doi pubmed
86. Parsegian K, Randall D, Curtis M, Ioannidou E. Association between periodontitis and chronic kidney disease. Periodontol 2000. 2022;89(1):114-124.
    doi pubmed
87. Serni L, Caroti L, Barbato L, Nieri M, Serni S, Cirami CL, Cairo F. Association between chronic kidney disease and periodontitis. A systematic review and metanalysis. Oral Dis. 2023;29(1):40-50.
    doi pubmed
88. Raina R, Ale S, Chaturvedi T, Fraley L, Novak R, Tanphaichitr N. Infection associated acute interstitial nephritis; a case report. J Nephropathol. 2017;6(2):53-57.
    doi pubmed

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