Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury

doi:10.21203/rs.3.rs-4878222/v1

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Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury

https://doi.org/10.21203/rs.3.rs-4878222/v1

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Introduction: Acute kidney injury (AKI) is no longer considered a single hit disease but part of a spectrum that culminates in adverse renal and cardiovascular outcomes. What are the renal biopsy findings of patient with persistent AKI/AKD (acute kidney disease)? Are there renal biopsy characteristics which predict renal recovery. These are the questions that this study addresses.

Methodology: A retrospective study was conducted analyzing all patients who underwent a renal biopsy with a diagnosis of acute kidney injury from January 2021 to January 2023 from the online hospital database. Patients with other glomerular disease and transplant patients were excluded from this cohort. The clinical and renal biopsy characteristics were analyzed for their correlation with renal recovery.

Results: Of 420 patients screened, 54 were included in the study. Most patients had stage 3 AKI. The median follow up in this study was 80.50 days. Among those on dialysis, 55.6% of patients became free of KRT (kidney replacement therapy). 92.6% of the study population had diffuse tubular involvement on the renal biopsy. Clinical recovery correlated with the degree of vasculature involvement on the renal biopsy. Interstitial fibrosis and tubular atrophy corelated with progression to CKD. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score correlated with independence from KRT.

Conclusion: Specific findings on the renal biopsy such as atherosclerotic changes correlate negatively with long-term recovery in AKI and renal biopsy findings of interstitial fibrosis and tubular atrophy may help to prognosticate progression to CKD.. Among clinical characteristics, the presence of co-morbidities and pre-existing CKD correlates negatively with renal recovery.

AKI (acute kidney injury) the term provides a convenient label to categorize a heterogenous cluster of illness all of which have differing courses and outcomes. Of the total number of renal biopsies, acute kidney injury occupies 31.7% among hospitalised patients(1). There is an increased risk, about 2–7 fold times, of bleed associated with biopsies in an acute hospitalised setting as opposed to patients undergoing routine out-patient non emergent biopsies(2). The lack of a proper etiological diagnosis for AKI particularly when underlying causes of injury are occult, along with ambiguity on the use of drugs or toxins often forces the clinician to take on the risk of the kidney biopsy. The histopathological findings on a biopsy for acute kidney injury that actually correlate with renal recovery are unknown. This study aims to evaluate the value of the renal biopsy done for AKI in terms of its use in prognostication and renal recovery.

Acute kidney injury has evolved from being considered a single hit disease to being a part of a continuum that ultimately results in CKD(3). The etiologies of AKI in the west are very different from those seen in third world countries where snake bite and diarrhoea are still of major concern. Is all AKI similar in its outcome leading to a steady progression to CKD? Is the prognosis same in a younger population with a single event of AKI and no other co-morbidities? Does a renal biopsy done in this setting really prognosticate recovery equally for all etiologies? These are some of the questions this study aims to answer.

A retrospective cohort study was conducted in a tertiary level hospital in South India including all patients between the time period of 2021–2023 January with a diagnosis of acute kidney injury who underwent a renal biopsy.

Inclusion criteria:

Adult patients with a biopsy proven diagnosis of AKI on the kidney biopsy

Exclusion criteria

Concomitant glomerular disease

Transplant patients

Children

These specific exclusion criteria of transplant and glomerular disease were chosen since in these subsets, the renal recovery may correlate with the specific glomerular pathology such as rejection or treatment of the glomerular disease rather than the AKI alone. In children outcome variables may need to be modified and the etiology of AKI is different than that seen in adults

Data was collected from the hospital database. Certain key words were used to identify AKI on the renal biopsy reports: “acute tubular injury, acute tubular necrosis, cortical necrosis, severe tubular injury, diffuse tubular injury”. Patients who had these key words in their biopsy reports, were then screened for their eligibility into the study. Data was analysed for demography, presence and etiology of AKI as per KDIGO criteria, co-morbidities, use of dialysis and recovery parameters, death and recurrence of AKI. Specific outcome parameters were defined. The renal biopsy findings were available on the online database and these were used to correlate with specific parameters of clinical recovery. The renal biopsy data were reviewed by both a nephrologist and trained renal pathologist.

Outcome parameters

The primary outcome of the study was to evaluate the correlation between the renal biopsy report and recovery from AKI at maximum follow up.

Secondary outcomes

To identify the recovery rate and follow up rate of patients with acute kidney injury

To identify clincial risk factors associated with poor renal recovery and progression to CKD such as age, BMI, presence of co-morbidities, requirement and duration of KRT.

Definitions used in this study

AKI: As defined by the KDIGO 2012 criteria(4). Refer to supplementary table 4 for criteria for baseline creatinine.

Co-morbidities were evaluated using the Charlston co-morbidity(6) and the AKI risk prediction score(7) was also checked for these patients.

Renal recovery was defined as follows

Complete recovery: Return to baseline creatinine or normal creatinine value

Partial recovery: Fall in the stage of AKI

Non-resolving AKI: AKI that does not resolve within 72 hours(8)

Resolving AKI: resolved within 72 hours

MAKE (Major adverse kidney events) events(9) are defined as: either death, new requirement for dialysis or worsening of kidney function denoted by > 25% decline in eGFR from baseline. MAKE events were considered at 30 days, 60 days and 90 days

Kellum classification(10) was also used for assessing different types of renal recovery

This study was reviewed by the institutional review board of this hospital and approved. The IRB number is IRB Min no15967.

Statistical analysis

Mean and standard deviation was reported for all the continuous variables following normality and Median and IQR (Inter Quartile Range) was reported for all the continuous variables not following normality. Frequency and percentage were reported for all the categorical variables. The parametric t-test was performed to compare the continuous variables following normality for two groups and Mann-Whitney test was performed to compare the continuous variables not following normality for two groups. Normality of the variable was assessed using rule of thumb. The Pearson Chi-square test was performed to find the association between the categorical variables. The Pie chart was plotted to show that etiology of acute kidney injury and indication for renal biopsy. The bar charts was plotted to show that frequency of outcome measures in AKI, various Kellum classes of AKI and frequency of various biopsy findings in AKI. The p-value less than 0.05 shows the statistical significance. Statistical analysis was performed using Statistical Package for Social Science (SPSS) version 21. 25.0 (IBM statistic, New York, USA).

The consort diagram of the study (Fig. 1) shows that out of 420 patients identified on screening, only 54 were finally included. The majority of patients excluded were patients with concomitant glomerular disease. The patient population consisted of patients with drug or toxin induced AKI (the majority) followed by septic patients and those with snake bite AKI (Table 1). The mean age of patients was 44.9 years. Most were of normal BMI and only 61.1% of them had no known co-morbidities. About 70% of this population required dialysis and 96.3% of them had stage 3 AKI. Patient were followed by for a median of 80.50 days. Time to achieve nadir creatinine was 57 days. The mean duration of hospitalisation was 17.87 days. Among those who were on dialysis, the average time spent on dialysis was 21 days and 55.6%% became free of KRT eventually. The most commonly used modality in this study was IHD (intermittent hemodialysis) in 89.47% of patients (Table 2). Of the total number of patients, 72.2% of patients had microhematuria and proteinuria was present in 39% of patients. Most of the renal biopsies (76%), were done for an etiological evaluation of renal dysfunction when a clear diagnosis as to the cause of AKI was not present or an alternate etiology like Acute tubule-interstitial diagnosis or rapidly progressive glomerulonephritis was entertained, while 24% were done for prognostication.

Table 1

Baseline characteristics on the study population
Characteristic	Frequency N = 54
Age Mean (Standard Deviation)	44.91 (SD14.04)
Gender: Male : female n (%)	34(63%):20(37%)
Average BMI Mean (SD) Median (IQR) BMI: underweight : <18.5kg/m2 BMI normal weight: 18.5-24.9kg/m2 BMI Overweight: 25-29.9kg/m2 BMI obese > 30kg/m2	22.47 (SD45.83) 21.8 (19.52–23.55) 7 (16.7) 26 (61.9%) 6 (14.3%) 3 (7.1%)
Co-morbidities Diabetes Hypertension Pre-existing CKD Chronic liver disease Cardiovascular disease Burns or trauma Major surgery Others	14 (25.9%) 18 (33.3%) 6 (11.1%) (5 stage 3 and 1 stage 4) 3 (5.6%) 0 1 (1.9%) 0 13 (24.07%)
Charlston co-morbidity score 0 score – no co-morbids Mild (score 1,2) Moderate (score 3,4) Severe (5 and above)	33 (61.1) 13 (24.1) 4 (7.4) 4 (7.4)
Cause of AKI Urinary tract infection Pigment related AKI Poisoning Drug or toxin induced Snake bite AKI Pancreatitis Sepsis Hypovolemia Hypercalcemia Hepato-renal syndrome	1 1 2 19 6 1 13 8 2 1
Stage of AKI Stage 1: Stage 2: Stage 3:	0 2 (3.7%) 52 (96.3%)
Requirement of dialysis Yes No	38 (70.4%) 16 (29.6%)
Number of patients on mechanical ventilation	8 (14.8%)
Number of patients on inotropes	5 (9.3%)
AKI risk prediction score Low (0-2.9) Moderate (3-8.9) High (9-11.5) Very high (more than 11.5)	22 (40.7) 30 (55.6) 2 (3.7)
Site of admission Outpatient Ward ICU	0 37 (68.5%) 17 (31.5%)
Duration of hospitalization Mean (SD) Median (IQR)	17.87 (SD45.22) 10 (5.75–17.25)
Mean Admission creatinine	6.65 (5.13)
Days to reach maximum creatinine value Mean (SD) Median (IQR)	134.72 (SD188.57) 4 (1–14)
Nadir creatinine Mean (SD) Median (IQR)	2.61 (SD2.52) 1.51 (0.93–3.86)
Days to reach nadir value of creatinine Mean (SD) Median (IQR)	134.72 (SD188.57) 57 (15.75–177.50)
Duration of follow up Mean (SD) Median (IQR)	186.68 (SD249.19) 80.50 (24.50-229.25)
Creatinine at maximum follow up Mean (SD) Median (IQR)	3.67 (SD4.49) 1.69 (0.94–5.24)

Table 2

Details of the use of dialysis for AKI
Characteristic	Frequency (percentage)
Number of patients on KRT	38 (70.4%)
Type of KRT used (n = 38) IHD SLED CRRT	(Some patients used multiple modalities) 34 (89.47%) 5 (13.16%) 1 (2.63%)
Number of sessions	5.45
Number of days on KRT Mean (SD) Median	22.48 (SD4.83) 21.8 (0–18.00)
Number of patients who became free of KRT	30 (55.6%)

When looking at various outcome measures of AKI, the incidence of MAKE events at 30 days was found to be 7.4% which decreased to 3.7% at 60 and 90 days (Fig. 2). All patients in this cohort had persistent AKI (i.e., persisting beyond 48 hours). Partial recovery was seen in 33.3% and complete recovery in 38.9%. Overall, 72.2% of patients showed some form of renal recovery. Only 1 patient died in this cohort. Most patients (98.1%) had AKD (acute kidney disease) and 44.4% of them were labelled as CKD (chronic kidney disease) subsequently. Most patients were classified as Kellum class 4 i.e., without complete recovery at hospital discharge but showing some form of renal recovery. Among the clinical features, the cause of AKI, presence of pre-existing CKD and Charleston co-morbidity score seemed to correlate negatively with independence from KRT (Table 3). Among the laboratory parameters the admission creatinine and maximum creatinine and days taken to reach the nadir correlated negatively with independence from KRT and complete recovery of the renal injury. Presence or absence of AKD did not seem to have any bearing on long term renal recovery of independence from KRT.

Table 3

Table representing correlation of various clinical characteristics with outcome measures of AKI
Variable	P value for partial recovery	Complete recovery P value	Independence from KRT P Value	Transitioned to CKD P value	Composite of renal recovery and independence from KRT P value
Age	0.201	0.637	0.829	0.715	0.874
Gender	0.84	0.480	0.950	0.553	0.328
BMI	0.432	0.524	0.373	0.324	0.769
Stage of AKI	0.54	0.147	0.193	1	1
Cause of AKI	0.39	0.12	0.38	0.006	0.86
Requirement of KRT	0.14	0.089	< 0.001	0.235	0.734
Co-morbidities Diabetes Hypertension Pre-existing CKD Stage of CKD CLD Burns or trauma Major surgery	0.18 0.54 0.65 0.767 0.25 1 0.418	0.77 0.55 0.386 0.778 1 0.389 0.017	0.890 0.245 0.005 0.005 0.575 1 0.720	0.115 0.051 0.027 0.056 1 0.42 0.012	0.407 0.487 0.018 0.018 1 1 0.356
Charlston co-morbidity score	0.08	0.507	0.005	0.038	0.537
Mechanical ventilation	0.70	1	0.277	1	1
Inotropes requirement	1	0.144	1	0.442	0.306
AKI risk prediction score	1	0.628	0.238	0.273	0.341
Admission creatinine	0.811	0.579	0.009	0.826	0.441
Maximum creatinine	0.970	0.785	0.001	0.411	0.983
Days to reach maximum creatinine value	0.800	0.175	0.841	0.180	0.820
nadir value of creatinine	0.130	< 0.001	0.251	< 0.001	0.002
Days to reach nadir value of creatinine	0.419	0.028	0.009	0.653	< 0.001
Type of KRT used	0.44	0.078	< 0.001	0.126	0.227
Number of sessions	0.428	0.046	< 0.001	0.067	0.880
Number of days on KRT	0.483	0.039	< 0.001	0.062	0.970
Free of KRT	0.004	0.851	----	0.609	-----
Kellum class	0.102	< 0.001	< 0.001	0.002	< 0.001
AKD	1	0.389	0.444	0.442	1

The frequency of various biopsy findings in acute kidney injury is presented in Fig. 3. 92.6% of patients had diffuse involvement of tubules on renal biopsy. Cortical involvement in the form of cortical necrosis was seen in 5.6% of patients. The most frequent finding on the renal biopsy was dilatation of tubules followed by flattening of the tubular lining epithelium. 77.8% of cases the brush border was damaged. Chronic vascular sclerotic changes were present in 61.1% of patients. Interstitial fibrosis and tubular atrophy (IFTA) was present in 50% of patients. The association of diabetes with glomerulosclerosis on the kidney biopsy in this setting was not significant (p value 0.568) however, hypertension was significantly associated with glomerulosclerosis (p value of 0.203). The presence of IFTA was significantly correlated with diabetes (p value 0.295) but not associated with presence of hypertension (p value of 0.614). Vascular changes were not significantly associated with diabetes or hypertension in this setting (p value 0.758 and 0.713 respectively). Pre-exiting CKD was significantly correlated with both presence of glomerulosclerosis, IFTA and atherosclerosis. Severe degrees of glomerular injury are generally absent in cases of acute kidney injury. The only biopsy finding which correlated with independence from KRT was presence of sloughing (Table 4). Recovery both complete and partial, had a correlation with presence of chronic vascular sclerotic changes. IFTA correlated with progression to chronic kidney disease. Presence of vacuolization on the renal biopsy correlated with complete recovery.

Table 4

Correlation of biopsy findings with various outcome measures in AKI
Variable	P value for partial recovery	Complete recovery P value	Independence from KRT p value	Transitioned to CKD p value	Composite of renal recovery and independence from KRT P value
Site of involvement Cortex or Medulla	0.543	0.274	0.579	0.243	0.121
Tubular changes due to AKI
Degree of involvement Focal or Diffuse-	1	0.638	1	1	1
Presence of sloughing	1	0.97	0.016	0.728	0.708
Presence of flattening	1.00	1	1	0.618	1
Presence of dilation of tubules	1	0.287	1	1	0.564
Presence of necrosis of tubules	0.30	0.117	0.359	0.152	0.485
Regenerative changes noted on biopsy	1	0.253	0.415	0.373	0.071
Presence of Vacuolization of tubules	0.512	0.028	0.890	0.708	0.261
Loss of brush border	1	0.747	0.272	0.470	0.714
Denudation of the tubular basement membrane	1	0.389	1	0.442	1
Tubular cell calcification	1	0.723	0.165	0.680	1
Interstitial changes due to AKI
Interstitial edema	0.846	0.272	0.667	0.388	0.556
IFTA more than 25%	0.634	0.066	0.565	0.008	1
Glomerular changes due to AKI
Glomerulosclerosis more than 25%	0.549	0.518	0.677	0.320	0.179
Vascular changes identified
Arteriosclerosis	0.016	0.003	0.534	0.027	0.495

The exact prognostic value of a kidney biopsy in the setting of AKI has not been studied previously. This study looks at both clinical and renal biopsy prognostic variables in renal recovery from AKI in the setting of a developing country where the etiology and setting of AKI is often different from that seen in the developed world.

The patient population

The transplant and glomerulonephritis cohorts have been included in other research on AKI(10). However, when looking at the pathology of AKI it was essential to exclude these patients since glomerulonephritis cause specific pathological changes in the kidney which might confound the interpretation of the extent of involvement of the acute kidney injury on the renal biopsy. The most common cause of AKI in this cohort was drug or toxin induced acute kidney injury and septic AKI (Table 1). In data from the Indian society of nephrology AKI registry, sepsis (34.7%) and tropical fevers (9.8%) were considered to be the most common etiology of community acquired AKI followed by AKI associated with liver disease (9.1%) (12). Snake bite AKI is also fairly common in these regions. The difference is the etiological diagnosis in this study when compared to others on AKI is likely because only patients who underwent a kidney biopsy were included. The co-morbidity profile (Table 1) is similar to that observed in the ISN registry with hypertension being the most common co-morbidity and diabetes following closely. When compared to data from developed nations, it is noted that AKI in the developing world occurs more frequently in younger patients with fewer co-morbidities as opposed to the developed world where older populations with more number of comorbidities develop AKI(13). The cohort in this research study were individuals who had severe AKI, that is most of them required dialysis and more than 95% of them had stage 3 AKI. This data is in keeping with prospective studies done in India where more than 50% of patients have AKI stage 3(12, 14).

Follow up and outcome measures

Patients were followed up for a median of 80.50 days (Table 1). Data from other studies showed that only about 13-37.3%(14) of patients with AKI remain on follow up with a nephrologist among Medicare patients(15). Follow up needs to be streamlined for better patient outcomes especially in high-risk patients.

Traditionally it is considered that recovery from AKI follows 4 steps, initiation, maintenance, polyuria and restitution. Renal recovery is expected to occur within 3 month, if it doesn’t if is labelled CKD(16). In this study however, although most patients who stop dialysis do so over a mean of 22.48 days, recovery takes much longer with nadir creatinine generally being achieved over a period of 57 days or more. This is in keeping with data from the mayo clinic services, most patients were able to discontinue dialysis before 6 months while the remaining recovered over a period of 12 months. This may be an important take home message from this data, that recovery occurs slowly and can be anticipated even after 3 months.

A majority (55.6%) of patients on dialysis became free of dialysis during the course of their treatment (Table 2). When compared to western data, this number is low in that among 50% of AKD patients who have survived their initial hospitalisation, only 30% generally required continuation of KRT(17). The higher number in this cohort maybe due to the selection bias of patients. Patients who are likely to not recover AKI, were more likely to require kidney biopsies for prognostication or to provide an alternate diagnosis for the kidney injury.

The clinical characteristic that correlated with renal recovery and outcome measures such as independence from KRT (Table 3) is similar to those documented in another study where underlying CKD and presence of co-morbidities corelate poorly for these measures(18). It is interesting to note that labelling the disease as AKD does not portend a poor prognosis for renal recovery. Another interesting finding is that not just the nadir creatinine that correlates with composite measures of renal recovery but also the time to achieve the nadir. This may give us an early clue likelihood of renal recovery even before nadir creatinine is achieved.

The urine sediment

Pre-renal AKI is known to have a bland sediment, while in ATN urine may show hematuria and muddy brown casts. Automated analysers are less sensitive and specific to detect these casts when compared with a nephrologist interpretation of the urine sediment(19). In this cohort, automated analysers were used to assess urine and the difficulty is often differentiating a severe AKI which has caused ATN from a glomerular disease. This may be a contributing factor to the number of biopsies that were done in the acute phase of the illness to rule out a glomerular disorder.

Outcome measures of AKI

When it comes to measuring renal recovery, there is no dearth of outcome measures(20). The myriad different interpretations of renal recovery and measures make comparing data between studies difficult. Some examples of renal recovery measures that are used in various studies are MAKE DC, 30, 60,90 and 1 year events, while others look at partial recovery (defined variably in different studies) vs. complete recovery. Still other studies look at AKI as transient or persistent based on a 48-hour window. To make the results comparable, we looked at all these outcome variables in AKI, MAKE 30 events were very low, as were MAKE 60, and 90 events (Fig. 2). In data from another trial the incidence of MAKE is approximately 30%(21). These may represent a selection bias in that only patients who survived this initial episode of AKI and were fit for biopsy were included in this study. However, it should be remembered that, most of this cohort were dialysis requiring AKI and the number of MAKE events is much lower than expected. One possible reason is the etiology of AKI which is different than the west and the lower co-morbidity burden of this population. Kellum et al suggested a novel method of quantifying recovery based on timing and degree of recovery. This classification showed the pattern of renal recovery and in other data proved to predict long term outcomes(22). In this cohort the Kellum classes had good correlation with other measures of renal recovery such as complete recovery and independence from KRT (Table 3).

Biopsy findings in AKI

The relative frequency of biopsy findings is shown in Fig. 3. In a systematic review of biopsy findings in AKI, A similar pattern to this one was noted by Wen et al(23). As in this study, tubular sloughing was a common finding followed by epithelial cell flattening and simplification. Very little data is available worldwide correlating biopsy findings with clinically significant outcomes for AKI. One such study was a post-mortem analysis of patients who underwent kidney biopsy for acute kidney injury in COVID-19 patients(24). The only histopathological finding that correlated with severity of AKI and recovery was presence of pigmented casts.

This study provides new insight and findings into correlation of biopsy findings with renal recovery and independence from KRT. As can be expected, chronic vascular sclerotic changes on the renal biopsy have significant correlation with renal recovery (Table 4). This is possibly because the pathophysiology of acute kidney injury is closely linked to renal vasoconstriction, endothelial injury and activation of inflammatory pathways(25). It makes sense that poor blood supply with arteriosclerotic vessels would play an important role in renal recovery. Vacuolisation is commonly seen in drug and toxin induced AKI due to ART (anti-retroviral therapy), CNI (calcineurin inhibitors) and contrast media and hence probably has a specific correlation with etiology and renal recovery(26). Interstitial fibrosis and tubular atrophy in several glomerular diseases has been liked to disease progression(27).

This study is a first-of-its-kind cohort study looking at renal biopsy findings and correlating them with renal recovery however, the selection bias of the study, to include only biopsy proven AKI, will limit the generalisability of the data to all AKI.

Renal recovery occurs slowly with nadir creatinine being achieved over a mean of 57 days. Clinical characteristics associated negatively with independence from KRT include presence of pre-existing CKD and the Charleston comorbidity index. Renal biopsy findings that corelate positively with progression to CKD include presence of interstitial fibrosis and tubular atrophy. Chronic vascular sclerotic changes on a renal biopsy have significant negative correlation with renal recovery. The degree of glomerular damage does not correlate with recovery from AKI.

Disclosure:

Dr Jose et al have no conflicts of interest to disclose

Funding:

No external funding was used for this study

Author Contribution

NJ, SR, RK, JJ and SSR wrote the main manuscript and prepared figuresATJ, JJE, SV, SA, VGD reviewed and edited the manuscript

Acknowledgement

I acknowledge Mr Srinivasan statistician working in christian medical college for his help with the statisitics

Data sharing:

all the data that support the findings is included in the manuscript.

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No competing interests reported.

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Looking backward at the future of AKI: A retrospective cohort study on the clinic-pathological variables affecting renal recovery after acute kidney injury

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