Introduction: Antineutrophil cytoplasmic antibody-associated vasculitis (AAV) with renal involvement primarily affects the renal cortex and presents with key histopathologic findings of a pauci-immune necrotizing and crescentic glomerulonephritis. Infrequently reported and poorly characterized is renal medullary angiitis (RMA), a pathologic variant of AAV primarily involving the renal medulla. This study seeks to describe the presentation and treatment outcomes of RMA. Methods: In this single-center cohort, renal pathology samples classified as AAV with renal involvement underwent secondary review to determine if they met histopathologic criteria for RMA. Demographic, clinical, and laboratory data were obtained via electronic medical record review. Descriptive statistical analysis was performed on key variables. Results: Of the 136 kidney biopsy samples classified as AAV with renal involvement, histopathologic features of RMA were present in 13 cases. The mean (SD) age at the time of RMA diagnosis was 65 (19) years, and 54% were female. Most cases presented with extrarenal manifestations of disease. Initial median (IQR) estimated glomerular filtration rate and proteinuria on presentation were 16 (10–19) mL/min/1.73 m2 and 1,100 (687–2,437) mg, respectively. The primary histologic features were high degrees of interstitial inflammation comprised leukocytes, neutrophils, plasma cells, and eosinophils along with either interstitial hemorrhage or necrosis. All patients were treated with glucocorticoids in combination with either cyclophosphamide, rituximab, or mycophenolate. All patients achieved disease remission. During a median (IQR) follow-up of 42 (14–68) months, 1 patient reached ESKD and 1 patient died. Conclusions: In this single-center case series, we identified the presence of RMA in 9.5% of AAV samples that underwent secondary review. RMA presented with severe impairment in renal function and multisystem disease. Standard of care immunosuppression for AAV was effective for remission induction in RMA. It remains unclear whether standard prognostication tools are useful in this population.

Journal Section:
Research Article
Keywords:
Antineutrophil cytoplasmic antibody vasculitis, Renal medullary angiitis, Outcomes

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a rare autoimmune multisystem disease characterized by inflammation of small blood vessels, notably involving the kidneys [1]. The histologic hallmark of kidney involvement is a pauci-immune necrotizing and crescentic glomerulonephritis. Classification schemes for prognostication of ANCA-associated glomerulonephritis have been developed and primarily focus on the cortex and typify lesions as sclerotic, focal, crescentic, or mixed, dependent on percentage and features of the involved glomeruli [2]. Less commonly reported and discussed are lesions involving the vasa recta and medulla. Renal medullary angiitis (RMA) is one such presentation that is rarely reported. RMA has been previously characterized by Hendricks et al. [3] as interstitial hemorrhage and necrosis in the medulla with associated polymorphonuclear leukocyte infiltration, along with the presence of karyorrhectic debris. Case reports and series have been previously published that sought to describe the histopathologic and serologic features of medullary angiitis [3]. However, there is limited information published on the clinical presentation and treatment outcomes of RMA. In this single-center case series, we will seek to highlight the proportion of cases, the clinical and histologic presentations, and treatment outcomes in AAV patients with kidney biopsy findings of RMA.

Patients with a diagnosis of AAV who underwent a kidney biopsy between the years 2000 and 2022 were identified from the Johns Hopkins renal pathology database. Biopsies that were classified and stored as pauci-immune AAV after review by the renal pathologist of record at time of case presentation were identified. Biopsy specimens with characterization of both the cortex and medulla were included in this study. These selected cases underwent secondary review by an independent renal pathologist to determine if additional histopathologic evidence of RMA was present or could be excluded. RMA is classified as a lesion involving primarily the medulla and vasa recta. RMA was defined utilizing morphologic criterion described by Hendricks et al., with histopathologic features of interstitial hemorrhage and necrosis in the medulla with associated polymorphonuclear leukocyte infiltration and the presence of karyorrhectic debris 3. Glomerular lesions were evaluated for the presence of cellular crescents, fibrinoid necrosis, fibrous crescents, endocapillary and mesangial cell proliferation, segmental and global glomerulosclerosis. Normal glomeruli did not exhibit any active (cellular or fibrous crescents, necrosis, karyorrhexis, endocapillary proliferation, mesangial cell proliferation), or chronic lesions (global or segmental scarring). Demographic, clinical, laboratory data and treatment details were extracted by electronic medical record review. Remission was defined clinically by improvement or stabilization of serum creatinine, resolution of hematuria, and the absence of extrarenal signs of vasculitis. Estimated glomerular filtration rate (eGFR) was measured using the CKD-EPI 2021 race-free formula [4]. Proteinuria was calculated by spot urine protein to creatinine ratio, measured in units of mg/dL. Renal risk scores for each case were calculated by incorporating percentage of normal glomeruli, degree of interstitial fibrosis, and eGFR measurement at the time of diagnosis [5]. Descriptive statistical analysis was performed utilizing Microsoft Excel (Version 2308). The study was approved by the Johns Hopkins Institutional Review Board (study IRB No. 00368120).

Case Presentations and Results

We identified 136 kidney biopsies classified as pauci-immune AAV with characterization of both the cortex and medulla. Of those, 13 were found to have met additional histopathologic criteria for RMA (9.5%). Baseline clinical and serologic characteristics are noted in Table 1. The mean (SD) age at time of diagnosis was 65 (19) years, and 54% were female. One patient was ANCA negative, while 6 were positive for MPO ANCA and 6 for PR3 ANCA. Clinical manifestations of extrarenal vasculitis were present in 9 patients. The median (IQR) eGFR at time of diagnosis was 16 (10–19) mL/min/1.73 m2 with corresponding serum creatinine of 3.7 (3.2–5.7) mg/dL. The median (IQR) proteinuria at the time of diagnosis was 1,100 (687–2,437) mg. The median (IQR) duration of follow-up was 42 (14–68) months.

Table 1.

Clinical, demographic, and serologic information at time of RMA diagnosis

Case numberAge at diagnosisSexANCA serotypeExtrarenal involvementeGFR at diagnosisEntry serum creatinineProteinuria at entry
1 71 Female MPO N/A 15 3.2 0 
2 62 Female PR3 Lungs, ears, joints, systemic 13 3.7 500 
3 18 Female MPO N/A 41 1.8 171 
4 36 Male PR3 Sinus, joints 17 4.3 1,220 
5 94 Male MPO Lungs 16 3.6 1,100 
6 61 Female MPO Ears, sinus, eyes 7 6.6 5,790 
7 72 Female PR3 Lung, sinus, nerves, systemic 30 1.8 3,750 
8 75 Male PR3 Ears, heart, nerves, systemic 10 5.7 1,008 
9 77 Female MPO N/A 19 2.5 1,100 
10 65 Male MPO Lung, heart, skin, systemic 19 3.4 2,000 
11 78 Male Negative N/A 16 3.8 3,977 
12 73 Male PR3 Lung, sinus 4 9.9 750 
13 65 Female PR3 Lung, sinus 3 11 N/A 
Case numberAge at diagnosisSexANCA serotypeExtrarenal involvementeGFR at diagnosisEntry serum creatinineProteinuria at entry
1 71 Female MPO N/A 15 3.2 0 
2 62 Female PR3 Lungs, ears, joints, systemic 13 3.7 500 
3 18 Female MPO N/A 41 1.8 171 
4 36 Male PR3 Sinus, joints 17 4.3 1,220 
5 94 Male MPO Lungs 16 3.6 1,100 
6 61 Female MPO Ears, sinus, eyes 7 6.6 5,790 
7 72 Female PR3 Lung, sinus, nerves, systemic 30 1.8 3,750 
8 75 Male PR3 Ears, heart, nerves, systemic 10 5.7 1,008 
9 77 Female MPO N/A 19 2.5 1,100 
10 65 Male MPO Lung, heart, skin, systemic 19 3.4 2,000 
11 78 Male Negative N/A 16 3.8 3,977 
12 73 Male PR3 Lung, sinus 4 9.9 750 
13 65 Female PR3 Lung, sinus 3 11 N/A 

Antineutrophilic cytoplasmic antibody (ANCA) serotype is listed as either myeloperoxidase (MPO) or proteinase-3 (PR3). Extrarenal involvement lists additional organ systems involved at time of RMA diagnosis. eGFR is in units of mL/min/1.73 m2. Creatinine is measured in units of milligrams. Proteinuria was measured in units of milligrams.

View Large

Details and depiction of renal histopathology are presented in Table 2 and Figure 1, respectively. The median (IQR) number of glomeruli in the RMA cases was 11 (4–14). The mean (SD) percentage of normal glomeruli was 37.5 (23.4%). Cellular crescents were absent in all sampled glomeruli from 5 biopsies. The median (IQR) number of active crescents in the remaining 8 biopsies was 1 (0–5). Eight patients were noted to have at least mild or greater degrees of interstitial fibrosis and tubular atrophy; however, this could not be quantified in 3 of the samples due to severe inflammation. The majority of our cases had high degrees of interstitial inflammation comprised leukocytes, polymorphonuclear cells, plasma cells, and eosinophils, with 9 of the 13 cases having at least diffuse to severe interstitial involvement. All cases were noted to have the presence of either interstitial hemorrhage or necrosis, with 11 cases (85%) having both lesions. Four patients had arteritis. Mean renal risk score at time of biopsy was 3.8 (3.4).

Table 2.

Histologic findings in 13 cases of RMA

Case numberNumber of glomeruli on specimenPercent normal glomeruliFibrinoid necrosisNumber of active crescentsFibrous crescentsPresence of arteritisIFTA, %Degree of interstitial inflammationSignificant tubular injury
1 11 54 0 0 0 No 40 Severe LPNE No 
2 11 27 7 1 0 No Not significant Moderate LPNE Yes 
3 17 29 8 9 0 No Not significant Mild LPN Yes 
4 12 17 10 6 0 No 10 Diffuse NE Yes 
5 11 36 2 0 0 No 75 Diffuse LPNE Yes 
6 4 50 2 1 0 Yes N/Aa Diffuse PNE No 
7 14 43 6 1 0 Yes 5 Focal LPNE Yes 
8 3 33 2 1 0 Yes N/Aa Diffuse LN N/Aa 
9 4 0 0 0 0 No 30 Diffuse LPN Yes 
10 1 100 0 0 0 No N/Aa Diffuse N No 
11 5 40 0 0 0 No 10 Mild LPNE Yes 
12 14 29 0 5 1 Yes 30 Diffuse LPNE Yes 
13 14 29 7 6 0 No 30 Focal L Yes 
Case numberNumber of glomeruli on specimenPercent normal glomeruliFibrinoid necrosisNumber of active crescentsFibrous crescentsPresence of arteritisIFTA, %Degree of interstitial inflammationSignificant tubular injury
1 11 54 0 0 0 No 40 Severe LPNE No 
2 11 27 7 1 0 No Not significant Moderate LPNE Yes 
3 17 29 8 9 0 No Not significant Mild LPN Yes 
4 12 17 10 6 0 No 10 Diffuse NE Yes 
5 11 36 2 0 0 No 75 Diffuse LPNE Yes 
6 4 50 2 1 0 Yes N/Aa Diffuse PNE No 
7 14 43 6 1 0 Yes 5 Focal LPNE Yes 
8 3 33 2 1 0 Yes N/Aa Diffuse LN N/Aa 
9 4 0 0 0 0 No 30 Diffuse LPN Yes 
10 1 100 0 0 0 No N/Aa Diffuse N No 
11 5 40 0 0 0 No 10 Mild LPNE Yes 
12 14 29 0 5 1 Yes 30 Diffuse LPNE Yes 
13 14 29 7 6 0 No 30 Focal L Yes 

Number of glomeruli on specimen refers to the total number of glomeruli seen on a sample review. Percent normal glomeruli are those without active or chronic lesions. Fibrinoid necrosis, number of active crescents, and fibrous crescents are a count of the number of glomeruli affected. Interstitial fibrosis and tubular atrophy (IFTA) listed as a percentage of renal cortical area involvement. Degree of interstitial inflammation was qualified based on the presence of lymphocytes (L), polymorphonuclear (P), neutrophils (N), and eosinophils (E). Significant tubular injury was a qualitative assessment made by independent renal pathologist assessment.

aCould not be assessed.

View Large
Fig. 1.
Four panel image demonstrating characteristic features of RMA. Image 1 demonstrating the interstitial space with varied presence of hemosiderin-laden macrophages. Image 2 with hemosiderin-laden macrophages demarcated with a black arrow. Image 3 highlights the presence of intracapillary neutrophils (black arrow) and intracapillary neutrophils (blue arrow). Image 4 showing the presence of extravasated red blood cells (black arrow). H and E stain. ×200 magnification.
View largeDownload slide

Four panel image demonstrating characteristic features of RMA. Image 1 demonstrating the interstitial space with varied presence of hemosiderin-laden macrophages. Image 2 with hemosiderin-laden macrophages demarcated with a black arrow. Image 3 highlights the presence of intracapillary neutrophils (black arrow) and intracapillary neutrophils (blue arrow). Image 4 showing the presence of extravasated red blood cells (black arrow). H and E stain. ×200 magnification.

Fig. 1.
Four panel image demonstrating characteristic features of RMA. Image 1 demonstrating the interstitial space with varied presence of hemosiderin-laden macrophages. Image 2 with hemosiderin-laden macrophages demarcated with a black arrow. Image 3 highlights the presence of intracapillary neutrophils (black arrow) and intracapillary neutrophils (blue arrow). Image 4 showing the presence of extravasated red blood cells (black arrow). H and E stain. ×200 magnification.
View largeDownload slide

Four panel image demonstrating characteristic features of RMA. Image 1 demonstrating the interstitial space with varied presence of hemosiderin-laden macrophages. Image 2 with hemosiderin-laden macrophages demarcated with a black arrow. Image 3 highlights the presence of intracapillary neutrophils (black arrow) and intracapillary neutrophils (blue arrow). Image 4 showing the presence of extravasated red blood cells (black arrow). H and E stain. ×200 magnification.

Close modal

Induction and maintenance therapies with clinical outcomes are included in Table 3. All patients were treated with pulse methylprednisolone 500 or 1,000 mg daily for 3 days and prednisone taper in combination with either cyclophosphamide (n = 6), rituximab (n = 7), and mycophenolate (n = 1). All patients achieved disease remission. Eleven patients received maintenance immunosuppression. The median (IQR) eGFR at 6-month follow-up for all cases was 38 (34–54) mL/min/1.73 m2 and at 12 months was 46 (34–55) mL/min/1.73 m2. There were no disease relapses during the follow-up period. One individual passed away during follow-up due to a cerebrovascular accident. One patient developed ESKD within the 12-month period of follow-up.

Table 3.

Induction and maintenance treatment regimens of patients in our study with renal function at different time intervals and clinical outcomes

Case numberInduction treatmentMaintenance treatmentRenal risk score5 at diagnosiseGFR at diagnosiseGFR at 6 monthseGFR at 12 monthsRelapse at follow-upClinical/renal outcome
1 Pulse steroids + MMF None 5 15 37 34 No  
2 Pulse steroids + CYC Azathioprine, methotrexate 4 13 51 46 No  
3 Pulse steroids + CYC Azathioprine 0 41 56 95 No  
4 Pulse steroids Azathioprine 6 17 35 33 No  
5 Pulse steroids N/A 2 16 N/A N/A No Death due to CVA 
6 Pulse steroids Rituximab 9 7 73 64 No  
7 Pulse steroids + CYC Rituximab 0 30 40 48 No  
8 Pulse steroids Rituximab 3 10 16 17 No  
9 Pulse steroids Rituximab 8 19 33 N/A No  
10 Pulse steroids Rituximab 0 19 27 31 No  
11 Pulse steroids + CYC Azathioprine 0 16 34 38 No  
12 Pulse steroids + CYC Rituximab 9 4 ESKD ESKD No  
13 Pulse steroids + CYC Rituximab 5 3 55 55 No  
Case numberInduction treatmentMaintenance treatmentRenal risk score5 at diagnosiseGFR at diagnosiseGFR at 6 monthseGFR at 12 monthsRelapse at follow-upClinical/renal outcome
1 Pulse steroids + MMF None 5 15 37 34 No  
2 Pulse steroids + CYC Azathioprine, methotrexate 4 13 51 46 No  
3 Pulse steroids + CYC Azathioprine 0 41 56 95 No  
4 Pulse steroids Azathioprine 6 17 35 33 No  
5 Pulse steroids N/A 2 16 N/A N/A No Death due to CVA 
6 Pulse steroids Rituximab 9 7 73 64 No  
7 Pulse steroids + CYC Rituximab 0 30 40 48 No  
8 Pulse steroids Rituximab 3 10 16 17 No  
9 Pulse steroids Rituximab 8 19 33 N/A No  
10 Pulse steroids Rituximab 0 19 27 31 No  
11 Pulse steroids + CYC Azathioprine 0 16 34 38 No  
12 Pulse steroids + CYC Rituximab 9 4 ESKD ESKD No  
13 Pulse steroids + CYC Rituximab 5 3 55 55 No  

Pulse steroids consisted of 3 doses of either 500 mg or 1,000 mg methylprednisolone administered via infusion. Mycophenolate mofetil (MMF) and cyclophosphamide (CYC) were given via oral administration. Azathioprine was given via oral administration. Rituximab was administered via infusion. Renal risk score reported as a numeric value. eGFR reported in units of mL/min/1.73 m2.

ESKD, end-stage kidney disease; CVA, cerebrovascular accident.

View Large

In this single-center case series, we identified 13 cases of RMA out of 136 biopsies (9.5%) that were initially classified as AAV with renal involvement. Our case series demonstrates that RMA presents with severely impaired kidney function and multisystem involvement at time of diagnosis. The utilization of induction and maintenance therapies commonly prescribed in the treatment of non-RMA AAV [6] yielded positive improvements in eGFR and achieved disease remission.

Longitudinal comparisons of outcome between RMA and non-RMA were limited in this study, due to an inability to acquire complete data on the 126 non-RMA AAV cases in this cohort. For this reason, renal outcomes in this cohort were compared to the existing body of the literature. Incidence rates of ESKD following diagnosis of non-RMA AAV have been reported as 8% within the first 6 months of diagnosis [7], 20% over the first few years of diagnosis [6, 7], and up to 28% over a 5-year follow-up period [8]. This is likely similar to the rates of ESKD seen from this RMA cohort, with 1 case developing ESKD at 12 months, representing approximately 8% of our cases.

The median age at time of RMA diagnosis in this cohort was 71 (62–75) years, which overlaps with the mean age of diagnosis of non-RMA renal vasculitis [9]. This RMA cohort presented with severely depressed renal function, which is a common feature of non-RMA AAV. These cases were responsive to standard of care induction and maintenance therapies in non-RMA renal vasculitis [7], with notable improvement in GFR seen at 6 months. All patients, excluding the patient with ESKD and the patient who died, were in the same or had improvement in CKD group by eGFR using KDIGO criteria [10] at 6-month follow-up. Despite the histopathologic and clinical differences seen in the presentation of RMA, we demonstrate that RMA has a similar treatment response to standard of care immunosuppression and carries a similar risk of developing ESKD as non-RMA AAV.

There is paucity of literature on the incidence, presentation, and outcomes of RMA, which may be due to limited renal medullary sampling, misclassification of disease, or an underreporting of this distinct presentation. These barriers served as a limitation within this study, where we noted wide variability in the amount of medullary tissue present for secondary review. Samples where medullary tissue was limited may have lacked the representativeness to diagnose RMA despite its presence, resulting in an underestimation of prevalence and diagnosis. Prognostication tools have been developed for predicting renal outcomes in AAV with renal involvement. Brix et al. have developed one such renal risk score, which takes into consideration the degree and severity of glomerular involvement, interstitial fibrosis and tubular atrophy, and severity of GFR reduction at time of presentation 5. However, given the limited glomerular involvement seen in RMA, it is unclear if these prognostic tools can be validated for use in this unique variant. Further studies are needed to validate whether existing prognostication tools are accurate for use in RMA or whether novel tools will be needed.

RMA is a seemingly rare but likely an underdiagnosed and underreported histopathologic variant of ANCA-associated renal vasculitis. Increased awareness of this disease process will help emphasize the importance of evaluating histology of the medulla to improve the recognition of this disease variant and eventually grow the body of literature. This single-center case series in RMA is unique from others in not only capturing the histopathologic, clinical, and demographic features at time of diagnosis, but further reports on induction and maintenance therapies with longitudinal follow-up. This study also demonstrates that, despite being a unique variant of AAV with renal involvement with possible unique pathophysiology, RMA responds similarly to induction and maintenance therapies used in non-RMA AAV and likely carries similar rates of developing ESKD or death.

The study was approved by the Johns Hopkins Institutional Review Board (Johns Hopkins University, study IRB No. 00368120). The need for written informed consent was waived by the Johns Hopkins Institutional Review Board.

Grant Kirby, Antonio Salas, Abdulrahman Alabdulsalam, and Alana Dasgupta have no conflicts of interest to declare. Duvuru Geetha is a consultant to Amgen, ChemoCentryx, Aurinia Inc., GSK, Calliditas, and Otsuka.

Duvuru Geetha is supported by the Johns Hopkins Center for Innovative Medicine. Grant Kirby is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH) under Award No. T32DK007732.

Grant Kirby: data extraction, analysis, writing of initial draft, and editing of draft. Antonio Salas: data extraction, analysis, and writing of initial draft. Abdulrahman Alabdulsalam and Alana Dasgupta: data extraction, pathology review, analysis, writing of initial draft, and editing of draft. Duvuru Geetha: conceptualization, data curation, analysis, review, and editing of draft.

All data generated or analyzed during this study are included in this article. Further inquiries can be directed to the corresponding author.

1.
Yates
M
,
Watts
R
.
ANCA-associated vasculitis
.
Clin Med
.
2017
;
17
(
1
):
60
–
4
.
Google Scholar
Crossref
Search ADS
 
2.
Berden
AE
,
Ferrario
F
,
Hagen
EC
,
Jayne
DR
,
Jennette
JC
,
Joh
K
, et al.
Histopathologic classification of ANCA-associated glomerulonephritis
.
J Am Soc Nephrol
.
2010
;
21
(
10
):
1628
–
36
Epub 2010 Jul 8.
Google Scholar
Crossref
Search ADS
PubMed
 
3.
Hendricks
AR
,
Harris
AA
,
Walker
PD
,
Larsen
CP
.
Renal medullary angiitis: a case series from a single institution
.
Hum Pathol
.
2013
;
44
(
4
):
521
–
5
Epub 2012 Oct 15.
Google Scholar
Crossref
Search ADS
PubMed
 
4.
Inker
LA
,
Eneanya
ND
,
Coresh
J
,
Tighiouart
H
,
Wang
D
,
Sang
Y
, et al.
New creatinine-and cystatin C–based equations to estimate GFR without race
.
N Engl J Med
.
2021
;
385
(
19
):
1737
–
49
.
Google Scholar
Crossref
Search ADS
PubMed
 
5.
Brix
SR
,
Noriega
M
,
Tennstedt
P
,
Vettorazzi
E
,
Busch
M
,
Nitschke
M
, et al.
Development and validation of a renal risk score in ANCA-associated glomerulonephritis
.
Kidney Int
.
2018
;
94
(
6
):
1177
–
88
Epub 2018 Oct 29.
Google Scholar
Crossref
Search ADS
PubMed
 
6.
Walsh
M
,
Merkel
PA
,
Peh
CA
,
Szpirt
WM
,
Puéchal
X
,
Fujimoto
S
, et al,
PEXIVAS Investigators
.
Plasma exchange and glucocorticoids in severe ANCA-associated vasculitis
.
N Engl J Med
.
2020
;
382
(
7
):
622
–
31
.
Google Scholar
Crossref
Search ADS
PubMed
 
7.
Booth
AD
,
Almond
MK
,
Burns
A
,
Ellis
P
,
Gaskin
G
,
Neild
GH
, et al.
Outcome of ANCA-associated renal vasculitis: a 5-year retrospective study
.
Am J Kidney Dis
.
2003
;
41
(
4
):
776
–
84
.
Google Scholar
Crossref
Search ADS
PubMed
 
8.
Robson
J
,
Doll
H
,
Suppiah
R
,
Flossmann
O
,
Harper
L
,
Höglund
P
, et al.
Damage in the ANCA-associated vasculitides: long-term data from the European Vasculitis Study group (EUVAS) therapeutic trials
.
Ann Rheum Dis
.
2015
;
74
(
1
):
177
–
84
.
Google Scholar
Crossref
Search ADS
PubMed
 
9.
Harper
L
,
Savage
CO
.
ANCA-associated renal vasculitis at the end of the twentieth century: a disease of older patients
.
Rheumatology
.
2005
;
44
(
4
):
495
–
501
Epub 2004 Dec 21.
Google Scholar
Crossref
Search ADS
PubMed
 
10.
Kidney Disease Improving Global Outcomes KDIGO Glomerular Diseases Work Group
.
KDIGO 2021 clinical practice guideline for the management of glomerular diseases
.
Kidney Int
.
2021
;
100
(
4S
):
S1
–
276
.
PubMed
 
© 2024 The Author(s). Published by S. Karger AG, Basel
Open Access License / Drug Dosage / Disclaimer
This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
2024
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License .
Attribution-NonCommercial