Skip to main content

Main menu

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • Podcasts
    • Subject Collections
    • Archives
    • ASN Meeting Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Trainees
    • Peer Review Program
    • Prize Competition
  • About CJASN
    • About CJASN
    • Editorial Team
    • CJASN Impact
    • CJASN Recognitions
  • More
    • Alerts
    • Advertising
    • Feedback
    • Reprint Information
    • Subscriptions
  • ASN Kidney News
  • Other
    • JASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology

User menu

  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
American Society of Nephrology
  • Other
    • JASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology
  • Subscribe
  • My alerts
  • Log in
  • My Cart
Advertisement
American Society of Nephrology

Advanced Search

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • Podcasts
    • Subject Collections
    • Archives
    • ASN Meeting Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Trainees
    • Peer Review Program
    • Prize Competition
  • About CJASN
    • About CJASN
    • Editorial Team
    • CJASN Impact
    • CJASN Recognitions
  • More
    • Alerts
    • Advertising
    • Feedback
    • Reprint Information
    • Subscriptions
  • ASN Kidney News
  • Visit ASN on Facebook
  • Follow CJASN on Twitter
  • CJASN RSS
  • Community Forum
Original ArticlesAcute Kidney Injury /Acute Renal Failure
You have accessRestricted Access

Assessment of KDIGO Definitions in Patients with Histopathologic Evidence of Acute Renal Disease

Rong Chu, Cui Li, Suxia Wang, Wanzhong Zou, Gang Liu and Li Yang
CJASN July 2014, 9 (7) 1175-1182; DOI: https://doi.org/10.2215/CJN.06150613
Rong Chu
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Cui Li
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Suxia Wang
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Wanzhong Zou
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Gang Liu
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Li Yang
Renal Division, Department of Medicine, Peking University First Hospital; Peking University Institute of Nephrology; Key Laboratory of Renal Disease, Ministry of Health of China; and Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data Supps
  • Info & Metrics
  • View PDF
Loading

Abstract

Background and objectives AKI is a clinical syndrome with various causes involving glomerular, interstitial, tubular, and vascular compartments of the kidney. Acute kidney disease (AKD) is a new concept that includes both AKI and the conditions associated with subacute decreases in GFR (AKD/non-AKI). This study aimed to investigate the correlation between AKI/AKD defined by clinical presentation and diffuse histologic criteria for acute abnormalities based on renal biopsy.

Design, setting, participants, & measurements All 303 patients who were histologically diagnosed as having acute tubular necrosis (ATN), acute tubulointerstitial nephritis, cellular crescentic GN, acute thrombotic microangiopathy, or complex lesions on renal biopsy from January 2009 to December 2011 were enrolled in the study. The 2012 Kidney Disease Improving Global Outcomes AKD/AKI definitions were applied to classify patients as follows: AKI, AKD/non-AKI, non-AKD, or unclassified.

Results A total of 273 patients (90.1%) met the AKD criteria; 198 patients (65.3%) were classified as having AKI according to serum creatinine (SCr) and urine output criteria. The urine output criteria added 4.3% to the SCr criteria and reclassified 6.7% of the AKI cases into higher stages. Of patients with ATN on pathology, 79.2% met AKI criteria; this was a higher percentage than for those who had other individual pathologic lesions (50%–64%). The major cause of not being defined as having AKI was a slower SCr increase than that required by the definition of AKI (98, 93.3%). Patients with AKI had more severe clinical conditions and worse short-term renal outcome than those in the non-AKI group.

Conclusions Diffuse, acute abnormality defined by renal biopsy and AKI defined by clinical presentation are two different entities. Most patients who have diffuse acute histologic findings met the criteria for AKD, whereas only two thirds met the definition of AKI.

  • acute kidney inury
  • acute kidney disease
  • diagnosis
  • pathology

Introduction

The diagnosis of AKI and its various stages, either by the RIFLE (risk, injury, failure, loss of function, ESRD) classification (1) or the Acute Kidney Injury Network (AKIN) criteria (2), has been validated in various hospitalized populations to have strong predictive value for both short-term and long-term outcomes (3). Recently, the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guideline for AKI proposed a modified definition of AKI based on RIFLE and AKIN criteria that makes up a new conceptual definition for acute kidney disease (AKD). AKD was defined to include clinical conditions of acute (AKI) or subacute decreases in GFR (i.e., GFR<60 ml/min per 1.73 m2 for <3 months or decrease in GFR by ≥35% or increase in serum creatinine [SCr] by >50% for <3 months) (4).

The AKI and AKD definitions describe clinical states that result from various causes and are characterized by various types of histologic damage. A kidney disease can be clinically defined as “acute” on the basis of the clinical course. Pathologically, it may manifest with “acute” lesions, such as cellular crescents, tubular necrosis, and leukocyte infiltrates. Nevertheless, the relationship between clinical acute course and pathologic acute lesions is not well understood.

To date, few studies have related clinical AKI or AKD diagnoses to parenchymal pathologic changes present on renal biopsy because in many cases the clinical designation of AKI or AKD is not informed by a kidney biopsy. In a previous pilot study, we studied 740 cases for which a renal biopsy was done in 2011. Altogether, 131 cases were defined as AKD (17.7%), of which 62 cases were defined as AKI (8.4%). Among these patients with AKD/AKI, the most common pathologic changes included acute tubulointerstitial nephritis (ATIN), acute tubular necrosis (ATN), cellular crescentic GN (CCGN), and thrombotic microangiopathy (TMA), accounting for 30%, 22%, 23%, and 9% of AKD cases and 29%, 29%, 26%, and 8% of AKI cases, respectively (L. Yang et al., unpublished data). These data suggest that these four broad types of renal parenchymal acute lesions account for 84% of AKD cases and 92% of AKI cases in our renal biopsy population. To better define the relationship between clinical AKI/AKD criteria and renal parenchymal acute lesions, we conducted a retrospective study of 2119 patients and evaluated clinical-pathologic correlations in 303 patients who had presented with evidence for acute lesions of ATIN, ATN, CCGN, or TMA documented on renal biopsy. We asked the following question: Of these patients with histologic evidence for acute injury, how many fulfilled the clinical criteria for AKI or AKD?

Materials and Methods

Patients

This study adhered to the principles of the Declaration of Helsinki and was approved by the Committee on Research Ethics of Peking University First Hospital. Patients who underwent renal biopsy from January 1, 2009, to December 31, 2011, in the Renal Division of Peking University First Hospital were screened. The renal biopsy specimens were examined by light microscopy with hematoxylin-eosin, periodic acid–Schiff, Masson’s trichrome, and periodic acid-methenamine silver staining; immunofluorescence; and electron microscopy. Patients who were identified as having ATN, ATIN, CCGN, and TMA were enrolled in the study (Figure 1). Patients from other medical departments, including intensive care units (ICUs), were not included according to the study design.

Figure 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1.

Flowchart of patient enrollment. ATN, acute tubular necrosis; ATIN, acute tubulointerstitial nephritis; CCGN, cellular crescentic GN; G, glomeruli; TIN, tubulointerstitial nephritis; TMA, thrombotic microangiopathy.

Pathologic Diagnostic and Inclusion Criteria

The indication for kidney biopsy included rapidly progressive GN; acute nephritic syndrome; unexplained acute renal failure; nephrotic syndrome (especially in patients older than age 40 years); and non-nephrotic proteinuria of more than 1 g/d or with glomerular hematuria, decreased renal function, or clinical or serologic evidence of a systemic disease.

CCGN.

At least 50% of the glomeruli had cellular crescents, and ≤40% of the glomeruli were sclerotic, which included global glomerulosclerosis and fibrous crescent (5,6). A cellular crescent was defined as an extracapillary cell proliferation with cells occupying ≥10% of the lesion, including both segmental and circumferential involvement (7).

ATN.

Patients were included when any of the following was found: loss of tubular brush border, tubular necrosis, intraluminal proteinaceous cellular debris or casts, tubular dilatation with flattening of tubular epithelium, or proliferation of the tubular cells (8) involving ≥50% of the area of biopsy specimens.

ATIN.

At least 50% of the parenchymal area had interstitial inflammation, with <25% of the area having interstitial fibrosis (8).

TMA.

Thrombosis of the glomerular capillaries and arterioles and onion skin–like thickening of small arteries were detected under light microscopy with ≤40% of the glomeruli sclerotic. Widening of the subendothelial area was detected by electron microscopy (8).

Complex Lesions.

A combination of at least two types of the above-mentioned categories.

Scoring.

Scores were developed for classifying the tubular brush border loss, necrosis, and atrophy; interstitial edema; inflammation; and fibrosis according to the Banff working classification (9,10). A 0–4+ scale was applied as follows: 0=no lesion, 1+=<25%, 2+=>25%–50%, 3+=>50%–75%, and 4+=>75% of parenchyma affected by the lesion.

Clinical Data Collection and Grouping

Disease history, age, sex, weight, BP, underlying diseases, dialysis and urine volume, hemoglobin, SCr, and the length of hospital stay and costs were recorded. Patients were classified into clinical groups of AKI, AKD/non-AKI, non-AKD, or unclassified according to the 2012 KIDGO AKI SCr and urine output (UO) criteria and AKD definition (3). AKD is a broader concept that comprises both AKI and AKD/non-AKI.

AKI Group.

The diagnostic criteria for AKI were an abrupt increase in SCr by ≥0.3 mg/dl within 48 hours or to ≥1.5 times baseline that occurred within the prior 7 days and/or a decline of UO to ≤12 ml/kg per 24 hours for 24 hours. A modified 24-hour UO criterion was applied because hourly UO was not available in these non-ICU patients. Patients with UO≤12 ml/kg per 24 hours for 24 hours were allocated to AKI stage 2; those who had UO≤7.2 ml/kg per hours for 24 hours were defined as AKI stage 3. Baseline SCr was defined as the lowest value among the following: the SCr value that was measured at a time closest to admission within the prior 1 year, the minimum SCr value within 3 months before admission, or the minimum SCr value during the hospital stay.

In all, 262 patients had baseline SCr, of which 93 patients had no baseline CKD, 134 patients were at CKD stage 1, 16 patients were at stage 2, and 19 patients were at stage 3. In 34 patients who had no records of SCr tests with no suspected CKD, a back-estimation of baseline SCr was made from the Modification of Diet in Renal Disease formula, assuming an eGFR of 75 ml/min per 1.73 m2 (4).

AKD/Non-AKI Group.

Patients who had developed a GFR<60 ml/min per 1.73 m2 or had a decrease in GFR by ≥35%, or had an increase in SCr by >50% within 3 months before admission (4), but did not meet the AKI criteria were placed in the AKD/non-AKI group.

Non-AKD Group.

Patients who had GFR≥60 ml/min per 1.73 m2 or developed GFR<60 ml/min per 1.73 m2 over more than 3 months, presenting a slower SCr rise than that required by AKD definition, were classified into the non-AKD group.

Unclassified Group.

Patients who had GFR<60 ml/min per 1.73 m2, with history of proteinuria and/or hematuria of >3 months, but had no records of SCr measurements could not be identified as having acute or chronic kidney insufficiency.

Renal Outcome for Patients with AKD at Hospital Discharge

An eGFR was calculated using the CKD-Epidemiology Collaboration equation (11,12), from which CKD stage was assessed at discharge to evaluate renal outcome. CKD stages 1–2 at discharge was defined as a good outcome; CKD stages 3–5 was regarded as a poor outcome.

Statistical Analyses

SPSS software, version 16.0 (IBM, Chicago, IL), was used for statistical analyses. Quantitative data are expressed as mean±SD or median with 25th, 75th percentiles. Categorical data are expressed as frequency (percentage). For comparison of clinical and pathologic parameters among different groups, nonparametric variables were analyzed by the Mann–Whitney test or the Kruskal–Wallis test, and categorical variables were analyzed by Pearson two-tailed test or Fisher exact test, whenever appropriate. To determine the association of clinical factors, such as age, sex, comorbid conditions, oliguria, systolic BP, baseline SCr, RRT, AKI stage, hemoglobin, nephrotic syndrome, and pathologic changes, with AKI classification and renal outcome of patients with AKD at time of discharge, we used univariate logistic regression analysis followed by multivariate logistic regression with stepwise backward inclusion of variables to minimize the number of covariates in the model. P values were two sided, and P<0.05 was considered to indicate statistical significance.

Results

Patient Enrollment, Clinical Diagnosis, and Grouping

Of 2119 biopsy specimens, 303 cases (159 men and 144 women, age 45.7±17.1 years) met the pathologic enrollment criteria (Figure 2). The renal pathologic diagnoses included ATIN in 107 cases (35.3%), CCGN in 89 (29.4%), ATN in 77 (25.4%), TMA in 22 (7.3%), and complex lesions in 8 (2.6%). Altogether 273 patients (90.1%) met AKD criteria, of whom 198 patients (65.3% of total) were classified as having AKI, with 32 at stage 1 (16.2%), 14 at stage 2 (7.1%), and 152 at stage 3 (76.8%). Seven patients (2.3%) were grouped as unclassified because their disease course was difficult to determine.

Figure 2.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 2.

Clinical grouping of patients with renal parenchymal acute lesions.

Effect of UO Criteria on AKI Diagnosis and Staging

On the basis of SCr criteria, 185 patients (61.1%) were identified as having AKI. Seventy-one (23.4%) met the UO criteria for AKI, of whom 13 (4.3%) did not meet SCr criteria. These 13 patients, including 7 who had inadequate SCr records and 6 who showed relatively slow increases in SCr levels, presented with rapid decreases in UO and therefore were diagnosed and staged by UO criteria. In addition, implementing UO criteria increased AKI stage over that defined by the SCr criteria in another 13 patients (Table 1). All the 19 patients who did not meet SCr criteria because of a relatively slow increase in SCr or were graded lower by the SCr criteria presented with nephrotic syndrome. Body weight increased by 10.5±7.6 kg (median increase, 8.25 [interquartile range, 5.0–15.0 kg]) during the disease course, with significantly decreased serum albumin of 1.52±0.32 g/dl.

View this table:
  • View inline
  • View popup
Table 1.

AKI diagnosis and staging by serum creatinine/urinary output criteria

Applicability of AKD/AKI Definition in Various Pathologic Groups

AKI definition identified all patients with complex lesions and more cases from the ATN group (79.2%) than any other individual pathologic groups (50.0%–64.0%; P=0.02) (Figure 3). The AKD criteria characterized a large percentage of patients with ATN (94.8%), ATIN (93.5%), and CCGN (88.7%). AKI stage did not significantly differ among different pathologic groups, except for a higher proportion of RRT prescription in the CCGN group (P<0.001).

Figure 3.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 3.

Acute diffuse abnormality defined by renal biopsy and AKI defined by clinical presentation are two different entities. (A) No significant difference was seen in the composition of various pathological changes among different clinical groups. (B) AKI definition identified all patients with complex lesions and more cases from the ATN group than any other individual pathological groups. In addition, 2.2% of patients with cellular crescent GN (CCGN) and 22.7% of patients with thrombotic microangiopathy (TMA) were grouped as unclassified. AKD, acute kidney disease.

Reasons for Not Meeting the AKI Definition

We then investigated the reasons for not meeting the AKI definition in a sizable percentage (34.7% [105 of 303]) of patients. A slower SCr increase than that required by the AKI definition was the major cause (93.3% [98 of 105]). Another reason was unavailable disease records (7 patients [6.7%], unclassified group).

We further looked into factors that might contribute to the slower increase in SCr. Patients who had the slowest SCr increase (non-AKD group) were younger and had milder renal dysfunction than patients who were identified as having AKD/non-AKI or AKI (Table 2). Unfortunately, by multiple logistic regression analysis, we could not define any factors significantly associated with AKI classification. None of the pathologic lesion scores were related to AKI diagnosis. This is understandable because we included only patients with severe tissue damage (i.e., >50% of the parenchymal area was affected).

View this table:
  • View inline
  • View popup
Table 2.

Clinical characteristics of patients in different clinical groups

Patients Classified with AKI Had the Highest Severity of Injury

Patients in the AKI group presented the highest SCr value at biopsy and at peak, the highest hospital costs, the longest hospital stay, and the worst renal outcome at discharge compared with those in the groups of AKD/non-AKI or non-AKD (Table 2). Patients with AKI stage 1 and stage 2 had similar clinical features (Table 3). In total, 113 patients required RRT (Table 2), presenting with the highest systolic BP, the highest SCr value, the highest hospital costs, the longest hospital stay, and the worst renal outcome; 45.3% remained on dialysis at discharge (Tables 3 and 4). Two patients who required RRT in the AKI group died: 1 of pulmonary infection and 1 of cerebral hemorrhage. This relatively low mortality rate in RRT recipients (1.8% [2 of 113]) is, at least in part, due to the fact that patients in the ICU were excluded.

View this table:
  • View inline
  • View popup
Table 3.

Clinical characteristics of patients in various AKI stages

View this table:
  • View inline
  • View popup
Table 4.

Renal outcome of patients with AKI who required RRT in various pathologic groups

We then investigated the factors related to renal outcome at time of discharge. On multiple logistic regression analysis, age (odds ratio [OR], 1.69 per 10-year increment; 95% confidence interval [95% CI], 1.28 to 2.22; P<0.001), underlying cardiovascular diseases, diabetes, or hypertension (OR, 2.37; 95% CI, 1.09 to 5.18; P=0.03), baseline SCr (OR, 1.08; 95% CI, 1.04 to 1.12; P<0.001), and RRT (OR, 8.41; 95% CI, 2.78 to 25.43; P<0.01) were independent risk factors for worse renal outcome at discharge.

Discussion

The current AKI definitions and staging criteria mainly derive from patients in the ICU, in whom the predominant cause of AKI was related to ischemia, toxins, and severe sepsis (13–15). The present study aimed to assess KDIGO AKI/AKD definitions in patients with indications for kidney biopsy who had various documented diffuse acute pathologic kidney lesions.

Of the 303 patients with diffuse parenchymal acute renal pathologic injury, only 198 (65.3%) were classified as having clinical AKI. The reliability of clinical AKI recognition varied with different kinds of pathologic lesions, with a much better concordance in ATN than in ATIN, CCGN, or TMA. Further analyses revealed that the major reason for not meeting the AKI criteria was the slower decrease in GFR, reflecting underlying pathophysiologic processes in various pathologic injuries. It is not surprising that patients who most commonly met the AKI criteria most often had abrupt loss of GFR after acute tubular injury, where the definition was derived. In cases of ATIN, CCGN, and TMA, however, where maladaptive immunity plays major roles in the tissue damage, the loss of GFR was less aggressive but more progressive than in ATN cases and thus was not in accordance with AKI criteria, which focuses more on the speed than the length of the disease course. In the present study, 20.8% of the patients with ATN were not classified as having AKI because of a slower GFR loss as well. Our study did not include patients in the ICU, in whom the cause and pathogenesis of ATN are generally complex and occur in the setting of severe clinical conditions (16). ATN in the non-ICU unit, such as the cases in our study, is usually induced by causes such as drugs or milder ischemia and, thus, may be less severe and less aggressive compared with ATN cases in the ICU.

Another possible reason that some patients with diffuse acute pathology did not meet the AKI criteria may be the presence of “renal reserve” (17), the “resting” extra excretory capacity that the kidney can call upon in times of stress. When the kidney is damaged and filtration capacity is lost, this unused reserve would be depleted before the resting GFR falls (17). Vaidya et al. demonstrated that SCr value does not increase until the renal parenchyma is significantly injured (18). This can easily explain why younger patients tended not to meet AKI/AKD criteria in our study. In addition, patients who had nephrotic syndrome and significant edema were less likely to meet AKI criteria. In these patients, the increase in SCr could be slowed by dilution. These results re-emphasize the limitation of SCr in detecting AKIs.

UO criteria were important for fine-tuning the diagnosis and staging of AKI in our cohort. Recent studies have shown that UO is a sensitive and early marker for AKI in patients in the ICU and has additional roles in AKI staging (19,20). There is still controversy, however, about the application of UO criteria, especially in non-ICU patients. In the present study, a modified 24-hour UO criterion was applied; this added 4.3% to the SCr criteria and reclassified 6.7% of the patients with AKI into higher stages. It was of particular use for the patients who had insufficient SCr records and those who had nephrotic syndrome.

Because the major reason for not meeting AKI criteria was the less aggressive GFR loss, it is not surprising that a much higher proportion of patients (92.1%) were classified as having AKD, with good agreement among the groups with various pathologic lesions. Furthermore, even though the patients in the AKD/non-AKI group presented with slower GFR declines, they had similar durations of hospital stay, total costs, and renal outcome at discharge compared with those who had AKI stages 1 and 2. This study, to our knowledge, is the first application and validation of the KDIGO AKI/AKD definitions in patients with acute parenchymal kidney diseases. Our results suggest that the operational AKD definition could identify kidney injury at an earlier stage, especially in patients with pathologic lesions other than ATN.

Our study has limitations related to the retrospective observational design in a single center. The major limitation is the selection bias that stems from retrospectively evaluating clinical-pathologic correlations in patients who had presented with evidence for acute lesions of ATIN, ATN, CCGN, or TMA on renal biopsy. This design excluded information from patients who were too sick to undergo biopsy or had contraindications for renal biopsy. Moreover, these patients are more likely to have met the AKI definition. Although we did consider the limitation of using SCr to detect acute pathologic injury, it is important to also highlight the limitation of using the kidney biopsy specimens for the same (e.g., because of inadequate tissue sampling). An additional limitation of our study is that the pathologic criteria, 40% and 25% cutoffs for sclerotic and interstitial fibrosis, may not completely exclude chronic processes. The use of the Modification of Diet in Renal Disease formula to back-estimate baseline SCr may have also limited the accuracy because it has not been validated in the Chinese population. The short-term outcomes evaluated by our study is another limitation. Many of the preceding limitations may be addressed by a multicenter, prospective investigative study conducted over a longer term.

In conclusion, the KDIGO definition of AKD detects most patients with a broad range of acute renal parenchymal histologic injuries on kidney biopsy. The AKI and AKD/non-AKI clinical courses reflect different type of renal abnormality, and the AKI criteria help distinguish patients with more severe renal dysfunction and worse outcomes.

Disclosures

None.

Acknowledgments

This work was supported by National Natural Science Foundation of China grant 81070549 and Beijing Training Program for the Talents 20110009001000002 to L.Y.

Footnotes

  • Published online ahead of print. Publication date available at www.cjasn.org.

  • Received June 11, 2013.
  • Accepted March 13, 2014.
  • Copyright © 2014 by the American Society of Nephrology

References

  1. ↵
    1. Bellomo R,
    2. Ronco C,
    3. Kellum JA,
    4. Mehta RL,
    5. Palevsky P,
    6. Acute Dialysis Quality Initiative workgroup
    : Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 8: R204–R212, 2004pmid:15312219
    OpenUrlCrossRefPubMed
  2. ↵
    1. Mehta RL,
    2. Kellum JA,
    3. Shah SV,
    4. Molitoris BA,
    5. Ronco C,
    6. Warnock DG,
    7. Levin A,
    8. Acute Kidney Injury Network
    : Acute Kidney Injury Network: Report of an initiative to improve outcomes in acute kidney injury. Crit Care 11: R31, 2007pmid:17331245
    OpenUrlCrossRefPubMed
  3. ↵
    1. Ricci Z,
    2. Cruz D,
    3. Ronco C
    : The RIFLE criteria and mortality in acute kidney injury: A systematic review. Kidney Int 73: 538–546, 2008pmid:18160961
    OpenUrlCrossRefPubMed
  4. ↵
    1. National Kidney Foundation
    : Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2: 19–36, 2012
    OpenUrlCrossRefPubMed
  5. ↵
    1. Haas M
    : Histologic subclassification of IgA nephropathy: a clinicopathologic study of 244 cases. Am J Kidney Dis 29: 829–842, 1997pmid:9186068
    OpenUrlCrossRefPubMed
  6. ↵
    1. Roberts IS,
    2. Cook HT,
    3. Troyanov S,
    4. Alpers CE,
    5. Amore A,
    6. Barratt J,
    7. Berthoux F,
    8. Bonsib S,
    9. Bruijn JA,
    10. Cattran DC,
    11. Coppo R,
    12. D’Agati V,
    13. D’Amico G,
    14. Emancipator S,
    15. Emma F,
    16. Feehally J,
    17. Ferrario F,
    18. Fervenza FC,
    19. Florquin S,
    20. Fogo A,
    21. Geddes CC,
    22. Groene HJ,
    23. Haas M,
    24. Herzenberg AM,
    25. Hill PA,
    26. Hogg RJ,
    27. Hsu SI,
    28. Jennette JC,
    29. Joh K,
    30. Julian BA,
    31. Kawamura T,
    32. Lai FM,
    33. Li LS,
    34. Li PK,
    35. Liu ZH,
    36. Mackinnon B,
    37. Mezzano S,
    38. Schena FP,
    39. Tomino Y,
    40. Walker PD,
    41. Wang H,
    42. Weening JJ,
    43. Yoshikawa N,
    44. Zhang H,
    45. Working Group of the International IgA Nephropathy Network and the Renal Pathology Society
    : The Oxford classification of IgA nephropathy: Pathology definitions, correlations, and reproducibility. Kidney Int 76: 546–556, 2009pmid:19571790
    OpenUrlCrossRefPubMed
  7. ↵
    1. Berden AE,
    2. Ferrario F,
    3. Hagen EC,
    4. Jayne DR,
    5. Jennette JC,
    6. Joh K,
    7. Neumann I,
    8. Noël LH,
    9. Pusey CD,
    10. Waldherr R,
    11. Bruijn JA,
    12. Bajema IM
    : Histopathologic classification of ANCA-associated glomerulonephritis. J Am Soc Nephrol 21: 1628–1636, 2010pmid:20616173
    OpenUrlAbstract/FREE Full Text
  8. ↵
    1. Jennette JC,
    2. Olson JL,
    3. Schwartz MM,
    4. Silva FG
    : Hepinstall's Pathology of the Kidney, 6th Ed., Philadelphia, PA, Lippincott Williams & Wilkins, 2007
  9. ↵
    1. Racusen LC,
    2. Solez K,
    3. Colvin RB,
    4. Bonsib SM,
    5. Castro MC,
    6. Cavallo T,
    7. Croker BP,
    8. Demetris AJ,
    9. Drachenberg CB,
    10. Fogo AB,
    11. Furness P,
    12. Gaber LW,
    13. Gibson IW,
    14. Glotz D,
    15. Goldberg JC,
    16. Grande J,
    17. Halloran PF,
    18. Hansen HE,
    19. Hartley B,
    20. Hayry PJ,
    21. Hill CM,
    22. Hoffman EO,
    23. Hunsicker LG,
    24. Lindblad AS,
    25. Yamaguchi Y,
    26. Mihatsch MJ,
    27. Nadasdy TR,
    28. Nickerson PR,
    29. Steenolsen T,
    30. Papadimitriou JC,
    31. Randhawa PS,
    32. Rayner DC,
    33. Roberts I,
    34. Rose SN,
    35. Rush DD,
    36. Madrigal LS,
    37. Salomon DR,
    38. Sund SE,
    39. Taskinen EO,
    40. Trpkov KL,
    41. Yamaguchi Y
    : The Banff 97 working classification of renal allograft pathology. Kidney Int 55: 713–723, 1999pmid:9987096
    OpenUrlCrossRefPubMed
  10. ↵
    1. Solez K,
    2. Colvin RB,
    3. Racusen LC,
    4. Haas M,
    5. Sis B,
    6. Mengel M,
    7. Halloran PF,
    8. Baldwin W,
    9. Banfi G,
    10. Collins AB,
    11. Cosio F,
    12. David DS,
    13. Drachenberg C,
    14. Einecke G,
    15. Fogo AB,
    16. Gibson IW,
    17. Glotz D,
    18. Iskandar SS,
    19. Kraus E,
    20. Lerut E,
    21. Mannon RB,
    22. Mihatsch M,
    23. Nankivell BJ,
    24. Nickeleit V,
    25. Papadimitriou JC,
    26. Randhawa P,
    27. Regele H,
    28. Renaudin K,
    29. Roberts I,
    30. Seron D,
    31. Smith RN,
    32. Valente M
    : Banff 07 classification of renal allograft pathology: Updates and future directions. Am J Transplant 8: 753–760, 2008pmid:18294345
    OpenUrlCrossRefPubMed
  11. ↵
    1. Levey AS,
    2. Stevens LA,
    3. Schmid CH,
    4. Zhang YL,
    5. Castro AF 3rd.,
    6. Feldman HI,
    7. Kusek JW,
    8. Eggers P,
    9. Van Lente F,
    10. Greene T,
    11. Coresh J,
    12. CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration)
    : A new equation to estimate glomerular filtration rate. Ann Intern Med 150: 604–612, 2009pmid:19414839
    OpenUrlCrossRefPubMed
  12. ↵
    1. Kong X,
    2. Ma Y,
    3. Chen J,
    4. Luo Q,
    5. Yu X,
    6. Li Y,
    7. Xu J,
    8. Huang S,
    9. Wang L,
    10. Huang W,
    11. Wang M,
    12. Xu G,
    13. Zhang L,
    14. Zuo L,
    15. Wang H,
    16. Chinese eGFR Investigation Collaboration
    : Evaluation of the Chronic Kidney Disease Epidemiology Collaboration equation for estimating glomerular filtration rate in the Chinese population. Nephrol Dial Transplant 28: 641–651, 2013pmid:23197682
    OpenUrlCrossRefPubMed
  13. ↵
    1. Plataki M,
    2. Kashani K,
    3. Cabello-Garza J,
    4. Maldonado F,
    5. Kashyap R,
    6. Kor DJ,
    7. Gajic O,
    8. Cartin-Ceba R
    : Predictors of acute kidney injury in septic shock patients: An observational cohort study. Clin J Am Soc Nephrol 6: 1744–1751, 2011pmid:21734090
    OpenUrlAbstract/FREE Full Text
    1. Lopes JA,
    2. Jorge S,
    3. Resina C,
    4. Santos C,
    5. Pereira A,
    6. Neves J,
    7. Antunes F,
    8. Prata MM
    : Acute renal failure in patients with sepsis. Crit Care 11: 411, 2007pmid:17466080
    OpenUrlCrossRefPubMed
  14. ↵
    1. Bagshaw SM,
    2. Lapinsky S,
    3. Dial S,
    4. Arabi Y,
    5. Dodek P,
    6. Wood G,
    7. Ellis P,
    8. Guzman J,
    9. Marshall J,
    10. Parrillo JE,
    11. Skrobik Y,
    12. Kumar A,
    13. Cooperative Antimicrobial Therapy of Septic Shock (CATSS) Database Research Group
    : Acute kidney injury in septic shock: Clinical outcomes and impact of duration of hypotension prior to initiation of antimicrobial therapy. Intensive Care Med 35: 871–881, 2009pmid:19066848
    OpenUrlCrossRefPubMed
  15. ↵
    1. Liaño F,
    2. Junco E,
    3. Pascual J,
    4. Madero R,
    5. Verde E,
    6. The Madrid Acute Renal Failure Study Group
    : The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. Kidney Int Suppl 66: S16–S24, 1998pmid:9580541
    OpenUrlCrossRefPubMed
  16. ↵
    1. Thomas DM,
    2. Coles GA,
    3. Williams JD
    : What does the renal reserve mean? Kidney Int 45: 411–416, 1994pmid:8164427
    OpenUrlCrossRefPubMed
  17. ↵
    1. Vaidya VS,
    2. Ozer JS,
    3. Dieterle F,
    4. Collings FB,
    5. Ramirez V,
    6. Troth S,
    7. Muniappa N,
    8. Thudium D,
    9. Gerhold D,
    10. Holder DJ,
    11. Bobadilla NA,
    12. Marrer E,
    13. Perentes E,
    14. Cordier A,
    15. Vonderscher J,
    16. Maurer G,
    17. Goering PL,
    18. Sistare FD,
    19. Bonventre JV
    : Kidney injury molecule-1 outperforms traditional biomarkers of kidney injury in preclinical biomarker qualification studies. Nat Biotechnol 28: 478–485, 2010pmid:20458318
    OpenUrlCrossRefPubMed
  18. ↵
    1. Macedo E,
    2. Malhotra R,
    3. Bouchard J,
    4. Wynn SK,
    5. Mehta RL
    : Oliguria is an early predictor of higher mortality in critically ill patients. Kidney Int 80: 760–767, 2011pmid:21716258
    OpenUrlCrossRefPubMed
  19. ↵
    1. Han SS,
    2. Kang KJ,
    3. Kwon SJ,
    4. Wang SJ,
    5. Shin SH,
    6. Oh SW,
    7. Na KY,
    8. Chae DW,
    9. Kim S,
    10. Chin HJ
    : Additional role of urine output criterion in defining acute kidney injury. Nephrol Dial Transplant 27: 161–165, 2012pmid:21712492
    OpenUrlCrossRefPubMed
PreviousNext
Back to top

In this issue

Clinical Journal of the American Society of Nephrology: 9 (7)
Clinical Journal of the American Society of Nephrology
Vol. 9, Issue 7
July 07, 2014
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
View Selected Citations (0)
Print
Download PDF
Sign up for Alerts
Email Article
Thank you for your help in sharing the high-quality science in CJASN.
Enter multiple addresses on separate lines or separate them with commas.
Assessment of KDIGO Definitions in Patients with Histopathologic Evidence of Acute Renal Disease
(Your Name) has sent you a message from American Society of Nephrology
(Your Name) thought you would like to see the American Society of Nephrology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Assessment of KDIGO Definitions in Patients with Histopathologic Evidence of Acute Renal Disease
Rong Chu, Cui Li, Suxia Wang, Wanzhong Zou, Gang Liu, Li Yang
CJASN Jul 2014, 9 (7) 1175-1182; DOI: 10.2215/CJN.06150613

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Request Permissions
Share
Assessment of KDIGO Definitions in Patients with Histopathologic Evidence of Acute Renal Disease
Rong Chu, Cui Li, Suxia Wang, Wanzhong Zou, Gang Liu, Li Yang
CJASN Jul 2014, 9 (7) 1175-1182; DOI: 10.2215/CJN.06150613
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Abstract
    • Materials and Methods
    • Results
    • Discussion
    • Disclosures
    • Acknowledgments
    • Footnotes
    • References
  • Figures & Data Supps
  • Info & Metrics
  • View PDF

More in this TOC Section

Original Articles

  • Smoking Cessation and Coronary Artery Calcification in CKD
  • Estimated Loss of Lifetime Employment Duration for Patients Undergoing Maintenance Dialysis in Taiwan
  • Neural Epidermal Growth Factor–Like 1 Protein–Positive Membranous Nephropathy in Chinese Patients
Show more Original Articles

Acute Kidney Injury /Acute Renal Failure

  • Acute Respiratory Distress Syndrome and Risk of AKI among Critically Ill Patients
  • Derivation of Urine Output Thresholds That Identify a Very High Risk of AKI in Patients with Septic Shock
Show more Acute Kidney Injury /Acute Renal Failure

Cited By...

  • AKI!Now Initiative: Recommendations for Awareness, Recognition, and Management of AKI
  • Drug-Induced Acute Interstitial Nephritis
  • Inhibition of Reticulon-1A-Mediated Endoplasmic Reticulum Stress in Early AKI Attenuates Renal Fibrosis Development
  • Google Scholar

Similar Articles

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Keywords

  • acute kidney inury
  • Acute kidney disease
  • diagnosis
  • pathology

Articles

  • Current Issue
  • Early Access
  • Subject Collections
  • Article Archive
  • ASN Meeting Abstracts

Information for Authors

  • Submit a Manuscript
  • Trainee of the Year
  • Author Resources
  • ASN Journal Policies
  • Reuse/Reprint Policy

About

  • CJASN
  • ASN
  • ASN Journals
  • ASN Kidney News

Journal Information

  • About CJASN
  • CJASN Email Alerts
  • CJASN Key Impact Information
  • CJASN Podcasts
  • CJASN RSS Feeds
  • Editorial Board

More Information

  • Advertise
  • ASN Podcasts
  • ASN Publications
  • Become an ASN Member
  • Feedback
  • Follow on Twitter
  • Password/Email Address Changes
  • Subscribe to ASN Journals

© 2021 American Society of Nephrology

Print ISSN - 1555-9041 Online ISSN - 1555-905X

Powered by HighWire