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Medscape
07-07-2025
- Health
- Medscape
Fast Five Quiz: Management of MPA
Microscopic polyangiitis (MPA) represents one category within the antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV), alongside granulomatosis with polyangiitis (GPA) and eosinophilic GPA (EGPA). MPA is associated with distinct presentations, organ involvement, and worse prognosis than EGPA and GPA; treatment strategies must be customized according to disease severity, affected organs, and individual patient characteristics. What do you know about the management of MPA? Check your knowledge with this quick quiz. Although renal involvement is common in ANCA vasculitis owing to a high concentration of blood vessels, subtypes of ANCA vasculitis have distinct patterns of extrarenal involvement. These varying clinical presentations correlate with different antibody profiles: MPA commonly associates with myeloperoxidase (MPO) serology while GPA generally presents with proteinase 3 (PR3) serology. Following renal involvement, the pulmonary system is a commonly involved organ system in MPA; cutaneous involvement and neurologic manifestations are also common. MPA typically shows fewer manifestations in the ear, nose, and throat region and eyes than other subtypes. Cardiovascular system and gastrointestinal system involvement are more often seen in EGPA, though patients with MPA can experience cardiovascular and gastrointestinal symptoms. Learn more about renal involvement in MPA. The latest Kidney Disease Improving Global Outcomes (KDIGO) and European Alliance of Associations for Rheumatology (EULAR) guidelines recommend beginning plasma exchange in patients with MPA when serum creatinine rises above > 300 µmol/L (equivalent to 3.4 mg/dL, as stated by KDIGO). This is supported by a recent meta-analysis that reported plasma exchange reduces the risk for end-stage kidney disease at 12 months; the same serum creatinine level for initiation was recommended by the researchers. However, they noted that plasma exchange was not found to improve the combined endpoint of "death and/or end-stage kidney disease." Additionally, KDIGO also recommends plasma exchange for patients requiring dialysis or those with diffuse alveolar hemorrhage and hypoxemia, but EULAR specifically recommends against routine use of plasma exchange for diffuse alveolar hemorrhage in patients with MPA and GPA. Learn more about creatinine monitoring in MPA. The latest KDIGO guidelines recommend considering discontinuation of immunosuppressive therapy in patients with MPA who have remained on dialysis for 3 months without extrarenal disease manifestations. This approach acknowledges that patients with MPO-ANCA-associated vasculitis (which is most strongly associated with MPA) who have kidney failure without involvement of other organs face minimal relapse risk. Supporting this, the EULAR cites research demonstrating that patients who are dependent on dialysis and in remission without immunosuppression are significantly more likely to experience serious infectious or cardiovascular complications from continued treatment than suffer disease recurrence; they specifically recommend weighing benefits and harms in continuing immunosuppressive therapy in the MPA subtype of ANCA. Learn more about immunosuppressive therapy in MPA. According to a recent review citing data from KDIGO, patients with MPA typically have the worst kidney prognosis due to the chronic damage associated with this subtype. Further, patients with EGPA less often have kidney involvement than GPA or MPA and usually have better kidney prognosis. Kidney prognosis is generally worse in patients with MPA than those with GPA as well. KDIGO also cites previously developed prognostic scoring systems (which include sclerotic, focal, crescentic, and mixed class), depending on most of the glomeruli histology. For example, focal class (> 50% normal glomeruli) is associated with a favorable outcome, while sclerotic class (≥ 50% sclerotic glomeruli) is associated with poorer outcomes. Learn more about prognosis in MPA. Both KDIGO and EULAR guidelines recommend a tapering schedule of 4-5 months after initiating glucocorticoids in patients with MPA, reaching a reduced dose (listed as " 5 mg prednisolone equivalent" per day) by that point. Tapering schedule is generally based on weight and disease severity. For example, for patients weighing > 75 kg (165 lb), EULAR suggests starting at 75 mg, then tapering to 40 mg by week 2, then lowering the dose by approximately 25% every 2 weeks until reaching 5 mg by week 19. This is the same tapering schedule recommended by KDIGO; the full tapering schedule for this weight and others can be found here. Clinical evidence supporting this strategy comes from the PEXIVAS trial, which demonstrated that lowering steroid exposure by 40% during the initial 6 months maintained therapeutic effectiveness while significantly decreasing serious infection rates compared to conventional dosing. This accelerated reduction strategy effectively balances inflammatory control with minimizing steroid-related complications. Learn more about glucocorticoids in MPA.
Medscape
03-07-2025
- Health
- Medscape
Fast Five Quiz: Management of GPA
Granulomatosis with polyangiitis (GPA) is a variant of anti-neutrophil cytoplasmic antibody ( ANCA)-associated vasculitis that most commonly presents with proteinase 3 (PR3) serology and distinct clinical features that necessitates swift identification and therapeutic intervention. Prompt treatment plays a crucial role in minimizing permanent organ damage, particularly in the renal and pulmonary systems. What do you know about the management of GPA? Check your knowledge with this quick quiz. The latest guidelines from the Kidney Disease Improving Global Outcomes (KDIGO) and European Alliance of Associations for Rheumatology (EULAR) both recommend initiating immunosuppressive therapy in patients with suspected PR3 positive ANCA vasculitis, which is indicative of GPA, even if clinicians are still awaiting biopsy results. Further, EULAR specifically acknowledges that collecting biopsies might not be feasible for each patient with ANCA vasculitis and treatment should 'not be delayed while awaiting histological information.' Learn more about biopsy for GPA. KDIGO recommends maintaining therapeutic intervention for 18 months to 4 years following successful remission, which is similar to the EULAR guidelines recommending maintenance therapy for 24-48 months in patients with GPA. They also state, 'longer duration of therapy should be considered in relapsing patients or those with an increased risk of relapse, but should be balanced against patient preferences and risks of continuing immunosuppression.' Learn more about remission maintenance in GPA. Infection is a significant concern in ANCA vasculitis, especially regarding immunosuppressive therapies including glucocorticoids that are used to manage the clinical manifestations of the disease. Recent research has shown that chronic nasal carriage of S aureus is significantly higher in patients with the GPA subtype; it has also been shown to be associated with increased endonasal activity and risk for relapse. Although M catarrhalis, H influenzae, and S pneumoniae do not appear to have a specific association with GPA, data have shown that infection is among the most common causes of death in GPA. Learn more about infection in GPA. Data indicate that the GPA subtype is an independent risk factor for disease recurrence. Additionally, KDIGO also considers lower serum creatinine, more extensive disease, PR3 histology (which is associated with higher relapse rates than MPO-positive disease commonly seen in MPA) and ear, nose, and throat involvement as 'baseline factors' for disease recurrence. Factors after diagnosis include history of relapse, ANCA positivity at the end of induction, and rise in ANCA. Treatment-related relapse factors include lower cyclophosphamide exposure, immunosuppressive withdrawal, and glucocorticoid withdrawal. Learn more about prognosis in GPA. To ensure disease does not recur into the transplanted tissue, KDIGO specifically recommends delaying kidney transplantation until patients have achieved complete clinical remission for at least 6 months. Further, ANCA positivity or negativity should not factor into this decision, with KDIGO stating, 'the persistence of ANCA should not delay transplantation.' Although a serum creatinine of > 4 mg/dL is a significant predictor of relapse, guidelines recommend considering combination of a monoclonal antibody and an alkylating agent for this indication. Similarly, induction and maintenance of dialysis should also be done under various separate conditions. Learn more about kidney transplantation for GPA. Editor's Note: This article was created using several editorial tools, including generative AI models, as part of the process. Human review and editing of this content were performed prior to publication.
Los Angeles Times
04-06-2025
- General
- Los Angeles Times
Acute Kidney Injury: From Early Signs to Chronic Risk
Acute kidney injury (AKI) isn't just a short-term problem—it's the start of a longer kidney health journey. AKI was previously called 'acute renal failure' or 'renal failure' but the terminology has evolved to reflect the spectrum of kidney injury. AKI occurs when the kidneys suddenly stop filtering waste products from the blood and the kidney function changes rapidly. This complication is very different from diseases such as Polycystic Kidney Disease, which is a genetic disease and genetic disorder caused by gene mutations passed from biological parents to their children. Whether it happens in the ICU or outpatient clinic AKI carries a big burden: increased risk of hospitalization, long term dialysis and even premature death. AKI is common in hospitalized patients and patients admitted to hospital and impacts outcomes and length of stay. Recognizing it early, treating it promptly and understanding the link to chronic kidney disease (CKD) is key to preserving kidney function and better patient outcomes. AKI and CKD are both forms of renal disease and show the continuum between acute and chronic conditions. Let's look at how AKI is classified, how to detect it early and what modern tools and strategies are helping clinicians change the trajectory from injury to recovery. AKI is classified by where the problem starts: The KDIGO clinical practice guideline (Kidney Disease: Improving Global Outcomes) defines AKI using changes in serum creatinine levels and urine output. The urine output criteria are also used in AKI staging, such as less than 0.5 mL/kg/h for specified durations. The Acute Kidney Injury Network (AKIN) is another classification system that incorporates both serum creatinine and urine output criteria. Early detection and classification are key, with identification of renal dysfunction and monitoring of glomerular filtration rate (GFR) as key measures of kidney health. But while these have been the clinical mainstays, they aren't always fast or specific enough to catch injury early. Serum creatinine level and blood urea nitrogen are traditional markers for assessing renal function but both have limitations in sensitivity and specificity. That's where newer biomarkers like neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and cystatin C come in. These tools are changing early detection, helping clinicians distinguish between mild, reversible cases and more severe or ongoing damage [2] [3]. A 2021 article highlights the importance of fluid balance, electrolyte monitoring and timely renal replacement therapy (RRT) when AKI is confirmed [3]. In the outpatient space, some reviews suggest early medication adjustment and specialist referrals can reduce complications in patients managed outside the hospital [4]. In the context of pathophysiology blood clots can cause vascular obstruction leading to AKI and red blood cells may be seen in kidney biopsies in certain conditions such as anticoagulant-related nephropathy. [5] Prevention starts by identifying who's most at risk. People with diabetes, hypertension, chronic heart failure, or advanced age are more likely to develop AKI—especially during acute illnesses or when exposed to nephrotoxic medications like NSAIDs or contrast agents. Both patient-related and treatment-related risk factors such as underlying chronic diseases, recent infections, trauma or major surgeries play a key role in increasing the likelihood of AKI. According to a 2020 Journal of Clinical Medicine review, risk mitigation means taking a proactive, team-based approach: monitor hydration, avoid nephrotoxins and assess kidney function during high-risk scenarios like surgery or infection [7]. It's especially important to identify high risk patients, such as those undergoing major procedures like cardiac surgery and tailor perioperative management strategies to prevent renal complications. Hospital-based strategies such as standardized monitoring protocols and early nephrology involvement can also reduce AKI rates as emphasized by the American Journal of Kidney Diseases Core Curriculum [11]. In a more recent 2025 article in Lakartidningen Swedish clinicians advocate for a streamlined system to identify and intervene early in AKI cases, especially in older adults or those with fluctuating blood pressure [10]. Relying solely on serum creatinine to assess kidney health is a bit like using a smoke detector after the fire's already burning. Biomarkers offer a more sensitive way to detect kidney injury before significant function is lost. Blood tests are essential for detecting changes in kidney function and guiding the management of AKI patients. A 2022 review in Medicina presents compelling evidence that biomarkers can guide both diagnosis and risk stratification, helping clinicians decide when to intensify care or when to hold off on aggressive treatments [6]. These biomarkers also help distinguish between transient AKI (due to things like dehydration) and persistent AKI, which is more likely to result in long-term damage. This distinction is critical when managing critically ill patients or adjusting medications like ACE inhibitors and diuretics. One of the biggest changes in kidney medicine over the past decade is that AKI doesn't always resolve cleanly. Many patients recover creatinine levels but their kidneys never return to full health. This transitional phase, called acute kidney disease (AKD), spans from 7 to 90 days after AKI onset. Renal recovery after AKI depends on factors such as the severity of injury, underlying comorbidities and the presence of biomarkers indicating renal repair mechanisms. A 2022 Nephron review calls AKD the 'missing link' between AKI and CKD, emphasizing the need for follow-up labs and patient education [8]. If kidney function hasn't bounced back within that 90-day window CKD is usually diagnosed. New research in the Yonsei Medical Journal shows how early post-discharge care—such as nephrology visits, medication reviews and blood pressure control—can slow progression to irreversible kidney damage [9]. Kidney disease progression after AKI increases the risk of developing chronic renal failure, chronic kidney failure, end stage kidney disease and end stage renal disease. Meanwhile a 2024 American Journal of Physiology review looks into the biological mechanisms behind this progression. It points to inflammation, fibrosis (scarring) and microvascular injury as key drivers—and possible therapeutic targets—of the AKI-to-CKD transition [12]. Cardiovascular disease is also a major cause of morbidity and mortality in patients with a history of AKI. When it comes to managing AKI a few core principles apply across both hospital and outpatient settings: The Acute Dialysis Quality Initiative (ADQI) has developed consensus guidelines and classification systems for AKI management. The sooner these are implemented the better the chances of preventing permanent kidney damage and the slide to CKD. Acute kidney injury is more than a short term health crisis—it's a long term disease. As we learn more about AKI we have more opportunity to intervene early, personalize care and protect long term kidney health. By using advanced biomarkers, prevention focused strategies and recognizing AKD as a key phase clinicians can change the story for thousands of patients with kidney injury every year. [1] Rahman, M., Shad, F., & Smith, M. C. (2012). Acute kidney injury: a guide to diagnosis and management. American family physician, 86(7), 631–639. [2] Mercado, M. G., Smith, D. K., & Guard, E. L. (2019). Acute Kidney Injury: Diagnosis and Management. American family physician, 100(11), 687–694. [3] Kellum, J. A., Romagnani, P., Ashuntantang, G., Ronco, C., Zarbock, A., & Anders, H. J. (2021). Acute kidney injury. Nature reviews. Disease primers, 7(1), 52. [4] Jacob, J., Dannenhoffer, J., & Rutter, A. (2020). Acute Kidney Injury. Primary care, 47(4), 571–584. [5] Neyra, J. A., & Chawla, L. S. (2021). Acute Kidney Disease to Chronic Kidney Disease. Critical care clinics, 37(2), 453–474. [6] Yoon, S. Y., Kim, J. S., Jeong, K. H., & Kim, S. K. (2022). Acute Kidney Injury: Biomarker-Guided Diagnosis and Management. Medicina (Kaunas, Lithuania), 58(3), 340. [7] Gameiro, J., Fonseca, J. A., Outerelo, C., & Lopes, J. A. (2020). Acute Kidney Injury: From Diagnosis to Prevention and Treatment Strategies. Journal of clinical medicine, 9(6), 1704. [8] Levey A. S. (2022). Defining AKD: The Spectrum of AKI, AKD, and CKD. Nephron, 146(3), 302–305. [9] Koh, E. S., & Chung, S. (2024). Recent Update on Acute Kidney Injury-to-Chronic Kidney Disease Transition. Yonsei medical journal, 65(5), 247–256. [10] Bell, M., M Öberg, C., & Ewert Broman, M. (2025). Akut njurskada – prevention och behandling [Acute kidney injury - prevention and treatment]. Lakartidningen, 122, 23182. [11] Moore, P. K., Hsu, R. K., & Liu, K. D. (2018). Management of Acute Kidney Injury: Core Curriculum 2018. American journal of kidney diseases : the official journal of the National Kidney Foundation, 72(1), 136–148. [12] Zhang, T., Widdop, R. E., & Ricardo, S. D. (2024). Transition from acute kidney injury to chronic kidney disease: mechanisms, models, and biomarkers. American journal of physiology. Renal physiology, 327(5), F788–F805.
